sync

008252c8-5656-408f-9f9f-d1664f73a7e1.json

@@ -0,0 +1,50 @@
+{
+ "id": "008252c8-5656-408f-9f9f-d1664f73a7e1",
+ "disease": {
+  "id": "H00409",
+  "names": [
+   "Type 2 diabetes mellitus"
+  ],
+  "dbLinks": {
+   "icd10": [
+    "E11"
+   ],
+   "mesh": [
+    "D003924"
+   ]
+  },
+  "category": "Metabolic disease; Endocrine disease"
+ },
+ "article": {
+  "id": "12351479",
+  "text": "OBJECTIVE:\nTo determine whether components of the metabolic syndrome precede the 5-year incidence of cardiovascular disease and diabetes.\n\nRESEARCH DESIGN AND METHODS:\nA population of individuals aged 43-84 years was evaluated from 1988 to 1990 and again 5 years later. Medical history, blood pressure, and laboratory measures were obtained at both examinations following the same protocols. Subjects without diabetes were classified according to level of glycemia, high blood pressure, high-risk lipid levels, high uric acid levels, and proteinuria at baseline. History of incident myocardial infarction, angina, stroke, and diabetes was obtained at follow-up.\n\nRESULTS:\nOf the 4,423 subjects without diabetes, 6.9% had elevated levels of glycemia, 18.4% had high blood pressure, 82.7% had high-risk lipid levels (either high serum total cholesterol or low HDL cholesterol or high ratio of these two levels), 27% had elevated uric acid levels, 33.2% had high BMI, and 3.3% had proteinuria (\u003e or =30 mg/dl). The risk of incident cardiovascular disease 5 years later increased with the number of the components present; 2.5% of those with one component developed cardiovascular disease, whereas 14.9% of those with four or more components developed cardiovascular disease. Of those with one component, diabetes developed in 1.1% 5 years later, whereas diabetes developed in 17.9% of those with four or more components.\n\nCONCLUSIONS:\nComponents of the metabolic syndrome are common and are associated with incident cardiovascular disease and diabetes after 5 years. Interventions to alter BMI, lipid levels, and blood pressure may decrease incident diabetes and cardiovascular disease."
+ },
+ "questions": [
+  {
+   "id": "ad9f6434-15af-436c-8e80-5d31b010ac51",
+   "text": "what are the risk factors of Type 2 diabetes mellitus?",
+   "answers": [
+    {
+     "answer_start": 1432,
+     "text": "Components of the metabolic syndrome"
+    },
+    {
+     "answer_start": 721,
+     "text": "elevated levels of glycemia"
+    },
+    {
+     "answer_start": 760,
+     "text": "high blood pressure"
+    },
+    {
+     "answer_start": 791,
+     "text": "high-risk lipid levels (either high serum total cholesterol or low HDL cholesterol or high ratio of these two levels)"
+    },
+    {
+     "answer_start": 955,
+     "text": "high BMI"
+    }
+   ]
+  }
+ ]
+}

02551e49-54f9-4d1a-a797-476104decd03.json

@@ -0,0 +1,43 @@
+{
+ "id": "02551e49-54f9-4d1a-a797-476104decd03",
+ "disease": {
+  "id": "H00079",
+  "names": [
+   "Asthma"
+  ],
+  "dbLinks": {
+   "icd10": [
+    "J45"
+   ],
+   "mesh": [
+    "D001249"
+   ]
+  },
+  "category": "Immune system disease",
+  "description": "Asthma is a complex syndrome with many clinical phenotypes in both adults and children. Its major characteristics include a variable degree of airflow obstruction, bronchial hyperresponsiveness, and airway inflammation. Inhaled allergens encounter antigen presenting cells (APC) that line the airway. Upon recognition of the antigen and activation by APC, naive T cells differentiate into TH2 cells. Activated TH2 stimulate the formation of IgE by B cells. IgE molecules bind to IgE receptors located on mast cells. The crosslinking of mast-cell-bound IgE by allergens leads to the release of biologically active mediators (histamine, leukotrienes) by means of degranulation and, so, to the immediate symptoms of allergy. Mast cells also release chemotactic factors that contribute to the recruitment of inflammatory cells, particularly eosinophils, whose proliferation and differentiation from bone marrow progenitors is promoted by IL-5. The activation of eosinophils leads to release of toxic granules and oxygen free radicals that lead to tissue damage and promote the development of chronic inflammation."
+ },
+ "article": {
+  "id": "17050892",
+  "text": "BACKGROUND:\nReduced lung function in early infancy has been associated with later obstructive airway diseases. We assessed whether reduced lung function shortly after birth predicts asthma 10 years later.\n\nMETHODS:\nWe conducted a prospective birth cohort study of healthy infants in which we measured lung function shortly after birth with the use of tidal breathing flow-volume loops (the fraction of expiratory time to peak tidal expiratory flow to total expiratory time [t(PTEF)/t(E)]) in 802 infants and passive respiratory mechanics, including respiratory-system compliance, in 664 infants. At 10 years of age, 616 children (77%) were reassessed by measuring lung function, exercise-induced bronchoconstriction, and bronchial hyperresponsiveness (by means of a methacholine challenge) and by conducting a structured interview to determine whether there was a history of asthma or current asthma.\n\nRESULTS:\nAs compared with children whose t(PTEF)/t(E) shortly after birth was above the median, children whose t(PTEF)/t(E) was at or below the median were more likely at 10 years of age to have a history of asthma (24.3% vs. 16.2%, P=0.01), to have current asthma (14.6% vs. 7.5%, P=0.005), and to have severe bronchial hyperresponsiveness, defined as a methacholine dose of less than 1.0 micromol causing a 20% fall in the forced expiratory volume in 1 second (FEV1) (9.1% vs. 4.9%, P=0.05). As compared with children whose respiratory-system compliance was above the median, children with respiratory compliance at or below the median more often had a history of asthma (27.4% vs. 14.8%; P=0.001) and current asthma (15.0% vs. 7.7%, P=0.009), although this measure was not associated with later measurements of lung function. At 10 years of age, t(PTEF)/t(E) at birth correlated weakly with the maximal midexpiratory flow rate (r=0.10, P=0.01) but not with FEV1 or forced vital capacity.\n\nCONCLUSIONS:\nReduced lung function at birth is associated with an increased risk of asthma by 10 years of age."
+ },
+ "questions": [
+  {
+   "id": "a8b372a0-70f9-446c-b705-b229e08cb70e",
+   "text": "What are the risk factors of Asthma?",
+   "answers": [
+    {
+     "answer_start": 1907,
+     "text": "Reduced lung function at birth"
+    },
+    {
+     "answer_start": 998,
+     "text": "children whose t(PTEF)/t(E) was at or below the median"
+    },
+    {
+     "answer_start": 1480,
+     "text": "children with respiratory compliance at or below the median"
+    }
+   ]
+  }
+ ]
+}

03063f69-25c7-4f99-af64-34e0c16638db.json

@@ -0,0 +1,38 @@
+{
+ "id": "03063f69-25c7-4f99-af64-34e0c16638db",
+ "disease": {
+  "id": "H00409",
+  "names": [
+   "Type 2 diabetes mellitus"
+  ],
+  "dbLinks": {
+   "icd10": [
+    "E11"
+   ],
+   "mesh": [
+    "D003924"
+   ]
+  },
+  "category": "Metabolic disease; Endocrine disease"
+ },
+ "article": {
+  "id": "7888928",
+  "text": "OBJECTIVE:\nTo examine the association between smoking, alcohol consumption, and the incidence of non-insulin dependent diabetes mellitus in men of middle years and older.\n\nDESIGN:\nCohort questionnaire study of men followed up for six years from 1986.\n\nSETTING:\nThe health professionals' follow up study being conducted across the United States.\n\nSUBJECTS:\n41,810 male health professionals aged 40-75 years and free of diabetes, cardiovascular disease, and cancer in 1986 and followed up for six years.\n\nMAIN OUTCOME MEASURE:\nIncidence of non-insulin dependent diabetes mellitus diagnosed in the six years.\n\nRESULTS:\nDuring 230,769 person years of follow up 509 men were newly diagnosed with diabetes. After controlling for known risk factors men who smoked 25 or more cigarettes daily had a relative risk of diabetes of 1.94 (95% confidence interval 1.25 to 3.03) compared with non-smokers. Men who consumed higher amounts of alcohol had a reduced risk of diabetes (P for trend \u003c 0.001). Compared with abstainers men who drank 30.0-49.9 g of alcohol daily had a relative risk of diabetes of 0.61 (95% confidence interval 0.44 to 0.91).\n\nCONCLUSIONS:\nCigarette smoking may be an independent, modifiable risk factor for non-insulin dependent diabetes mellitus. Moderate alcohol consumption among healthy people may be associated with increased insulin sensitivity and a reduced risk of diabetes."
+ },
+ "questions": [
+  {
+   "id": "2c3fd709-0411-444f-8d0e-293a10e37339",
+   "text": "what are the risk factors of type 2 diabetes mellitus?",
+   "answers": [
+    {
+     "answer_start": 742,
+     "text": "men who smoked 25 or more cigarettes daily"
+    },
+    {
+     "answer_start": 1150,
+     "text": "Cigarette smoking"
+    }
+   ]
+  }
+ ]
+}

030e07f4-3960-4b5d-b42b-1baa0c4cb5bd.json

@@ -0,0 +1,38 @@
+{
+ "id": "030e07f4-3960-4b5d-b42b-1baa0c4cb5bd",
+ "disease": {
+  "id": "H00409",
+  "names": [
+   "Type 2 diabetes mellitus"
+  ],
+  "dbLinks": {
+   "icd10": [
+    "E11"
+   ],
+   "mesh": [
+    "D003924"
+   ]
+  },
+  "category": "Metabolic disease; Endocrine disease"
+ },
+ "article": {
+  "id": "11889155",
+  "text": "Insulin resistance is common in adults with polycystic ovary syndrome (PCOS). Although recent data demonstrate that insulin resistance is present in the early stages of PCOS, the prevalence of insulin resistance in adolescents with PCOS has not been determined. Likewise, the prevalence of impaired glucose tolerance (IGT) or type 2 diabetes mellitus (DM) in adolescent cohorts has not been established. In this study we sought to obtain preliminary data regarding the prevalence of IGT and DM in adolescents with PCOS and to assess the ability of screening tests to predict these abnormalities within this population. Twenty-seven adolescents with PCOS underwent oral glucose tolerance tests. Plasma glucose and insulin levels were obtained at baseline, and glucose was measured 2 h after a 75-g glucose challenge. The 2-h plasma glucose level was used to categorize subjects as having IGT or the provisional diagnosis of DM. Eight of our 27 subjects had IGT, and 1 had previously undiagnosed DM. These abnormalities were seen among lean and obese subjects. Fasting plasma glucose levels and simple measures of insulin resistance were suboptimal predictors of IGT and DM within our cohort. As in adults, our results indicate that adolescents with PCOS are at increased risk for IGT and DM and that the 2-h plasma glucose level after an oral glucose challenge appears to be the most reliable screening test for these abnormalities. Our results need to be corroborated by future studies that determine the prevalence of abnormalities in glucose tolerance among large populations of adolescents, both with and without PCOS. However, as DM may be preventable by lifestyle modifications, we would recommend that adolescents with PCOS undergo periodic screening for abnormal glucose tolerance using 2-h postchallenge plasma glucose levels."
+ },
+ "questions": [
+  {
+   "id": "265016af-0f85-4011-9891-5c1f9a6dc332",
+   "text": "what are the risk factors of Type 2 diabetes mellitus?",
+   "answers": [
+    {
+     "answer_start": 1231,
+     "text": "adolescents with PCOS"
+    },
+    {
+     "answer_start": 44,
+     "text": "polycystic ovary syndrome (PCOS)"
+    }
+   ]
+  }
+ ]
+}

039ecaa9-9b14-4d71-8373-19bc54f60418.json

@@ -0,0 +1,38 @@
+{
+ "id": "039ecaa9-9b14-4d71-8373-19bc54f60418",
+ "disease": {
+  "id": "H00409",
+  "names": [
+   "Type 2 diabetes mellitus"
+  ],
+  "dbLinks": {
+   "icd10": [
+    "E11"
+   ],
+   "mesh": [
+    "D003924"
+   ]
+  },
+  "category": "Metabolic disease; Endocrine disease"
+ },
+ "article": {
+  "id": "12610050",
+  "text": "OBJECTIVE:\nInsulin resistance (IR) and the metabolic syndrome (MS) are associated with type 2 diabetes and adverse cardiovascular disease (CVD) risk factor profiles. Whether IR and MS predict CVD independently of diabetes and other CVD risk factors is not known. This study examines whether IR and/or presence of MS are independently associated with CVD in nondiabetic American Indians (AI).\n\nRESEARCH DESIGN AND METHODS:\nWe examined 2283 nondiabetic AI who were free of CVD at the baseline examination of the Strong Heart Study (SHS). CVD risk factors were measured, IR was quantified using the homeostasis model assessment (HOMA), and MS as defined by the National Cholesterol Education Program Adult Treatment Panel (ATP III) was assessed for each participant. Incident CVD and diabetes were ascertained during follow-up.\n\nRESULTS:\nMS was present in 798 individuals (35%), and 181 participants (7.9%) developed CVD over 7.6 +/- 1.8 years of follow-up. Age, BMI, waist circumference, and triglyceride levels increased and HDL cholesterol decreased across tertiles of HOMA-IR. Risk of diabetes increased as a function of baseline HOMA-IR (6.3, 14.6, and 30.1%; P \u003c 0.001) and MS (12.8 vs. 24.5%). In Cox models adjusted for CVD risk factors, risk of CVD did not increase either as a function of baseline HOMA-IR or MS, but individual CVD risk factors predicted subsequent CVD.\n\nCONCLUSIONS:\nAmong nondiabetic AI in the SHS, HOMA-IR and MS both predict diabetes, but neither predicts CVD independently of other established CVD risk factors."
+ },
+ "questions": [
+  {
+   "id": "b78ca6d5-3d16-4b44-be9d-e0d2bd8fb1bd",
+   "text": "what are the risk factors of Type 2 diabetes mellitus?",
+   "answers": [
+    {
+     "answer_start": 11,
+     "text": "Insulin resistance (IR)"
+    },
+    {
+     "answer_start": 43,
+     "text": "metabolic syndrome (MS) "
+    }
+   ]
+  }
+ ]
+}

03b94b86-3d51-4507-8fa2-fe337d186e02.json

@@ -0,0 +1,43 @@
+{
+ "id": "03b94b86-3d51-4507-8fa2-fe337d186e02",
+ "disease": {
+  "id": "H00038",
+  "names": [
+   "Melanoma"
+  ],
+  "dbLinks": {
+   "icd10": [
+    "C43"
+   ],
+   "mesh": [
+    "D008545"
+   ]
+  },
+  "category": "Cancer",
+  "description": "Melanoma is a form of skin cancer that has a poor prognosis and which is on the rise in Western populations. Melanoma arises from the malignant transformation of pigment-producing cells, melanocytes. The only known environmental risk factor is exposure to ultraviolet (UV) light and in people with fair skin the risk is greatly increased. Melanoma pathogenesis is also driven by genetic factors. Oncogenic NRAS mutations activate both effector pathways Raf-MEK-ERK and PI3K-Akt. The Raf-MEK-ERK pathway may also be activated via mutations in the BRAF gene. The PI3K-Akt pathway may be activated through loss or mutation of the inhibitory tumor suppressor gene PTEN. These mutations arise early during melanoma pathogenesis and are preserved throughout tumor progression. Melanoma development has been shown to be strongly associated with inactivation of the p16INK4a/cyclin dependent kinases 4 and 6/retinoblastoma protein (p16INK4a/CDK4,6/pRb) and p14ARF/human double minute 2/p53 (p14ARF/HMD2/p53) tumor suppressor pathways. MITF and TP53 are implicated in further melanoma progression."
+ },
+ "article": {
+  "id": "24876226",
+  "text": "BACKGROUND:\nFew prospective studies have examined the relationship between sun exposure, other potential risk factors, and risk of different skin cancers [including basal cell carcinoma (BCC), squamous cell carcinoma (SCC), and melanoma] simultaneously.\n\nMETHODS:\nWe evaluated the association between a number of potential risk factors and skin cancer risk in a cohort of 108,916 US women, the Nurses' Health Study II (1989-2009).\n\nRESULTS:\nDuring 2.05 million years of follow-up, we identified 6,955, 880, and 779 diagnoses of BCC, SCC, and melanoma, respectively. Compared with participants in the lowest quintile of cumulative ultraviolet flux in adulthood, participants in the highest quintile had multivariable-adjusted relative risks (RR) of 2.35 (Ptrend \u003c 0.0001) for BCC, 2.53 (Ptrend = 0.009) for SCC, and 0.68 (Ptrend = 0.38) for melanoma. In contrast, the RRs were 1.68 (95% CI, 1.55-1.82) for BCC, 1.68 (95% CI, 1.34-2.11) for SCC, and 1.80 (95% CI, 1.42-2.28) for melanoma for participants with ≥5 blistering sunburns when compared with participants without sunburn between ages 15 and 20 years. We found significant interactions between family history of melanoma, number of blistering sunburns between ages 15 and 20 years and BCC risk, and between sunburn reaction as a child/adolescent and SCC risk (all Pinteraction \u003c 0.05).\n\nCONCLUSION:\nIn a cohort of U.S. women, we found that sun exposures in both early life and adulthood were predictive of BCC and SCC risks, whereas melanoma risk was predominantly associated with sun exposure in early life.\n\nIMPACT:\nOur results may have potential implications for the prevention of skin cancers. Cancer Epidemiol Biomarkers Prev; 23(6); 1080-9. ©2014 AACR."
+ },
+ "questions": [
+  {
+   "id": "f66e889f-0816-4ea9-a296-fef0b984d9d2",
+   "text": "What are the risk factors of Melanoma?",
+   "answers": [
+    {
+     "answer_start": 1008,
+     "text": "≥5 blistering sunburns"
+    },
+    {
+     "answer_start": 1151,
+     "text": "family history of melanoma"
+    },
+    {
+     "answer_start": 1179,
+     "text": "number of blistering sunburns between ages 15 and 20 years"
+    }
+   ]
+  }
+ ]
+}

03c10014-aab4-422f-9401-5df2267318ec.json

@@ -0,0 +1,39 @@
+{
+ "id": "03c10014-aab4-422f-9401-5df2267318ec",
+ "disease": {
+  "id": "H00038",
+  "names": [
+   "Melanoma"
+  ],
+  "dbLinks": {
+   "icd10": [
+    "C43"
+   ],
+   "mesh": [
+    "D008545"
+   ]
+  },
+  "category": "Cancer",
+  "description": "Melanoma is a form of skin cancer that has a poor prognosis and which is on the rise in Western populations. Melanoma arises from the malignant transformation of pigment-producing cells, melanocytes. The only known environmental risk factor is exposure to ultraviolet (UV) light and in people with fair skin the risk is greatly increased. Melanoma pathogenesis is also driven by genetic factors. Oncogenic NRAS mutations activate both effector pathways Raf-MEK-ERK and PI3K-Akt. The Raf-MEK-ERK pathway may also be activated via mutations in the BRAF gene. The PI3K-Akt pathway may be activated through loss or mutation of the inhibitory tumor suppressor gene PTEN. These mutations arise early during melanoma pathogenesis and are preserved throughout tumor progression. Melanoma development has been shown to be strongly associated with inactivation of the p16INK4a/cyclin dependent kinases 4 and 6/retinoblastoma protein (p16INK4a/CDK4,6/pRb) and p14ARF/human double minute 2/p53 (p14ARF/HMD2/p53) tumor suppressor pathways. MITF and TP53 are implicated in further melanoma progression."
+ },
+ "article": {
+  "id": "26103029",
+  "text": "IMPORTANCE:\nThe target for the oral erectile dysfunction drugs, phosphodiesterase type 5 (PDE5) inhibitors, is part of a pathway implicated in the development of malignant melanoma. An increased risk of melanoma in sildenafil users was recently reported.\n\nOBJECTIVE:\nTo examine the association between use of PDE5 inhibitors and melanoma risk, including data on specific PDE5 inhibitors, number of prescriptions, and melanoma stage.\n\nDESIGN, SETTING, AND PARTICIPANTS:\nNationwide, population-based, nested case-control study in the Swedish Prescribed Drug Register, the Swedish Melanoma Register, and other health care registers and demographic databases in Sweden, including 4065 melanoma cases diagnosed from 2006 through 2012 and 5 randomly selected controls per case with matching year of birth.\n\nEXPOSURES:\nNumber of filled prescriptions for the PDE5 inhibitors sildenafil and vardenafil or tadalafil.\n\nMAIN OUTCOMES AND MEASURES:\nRisk of melanoma; overall and by stage and risk of basal cell carcinoma in multivariable logistic regression analyses.\n\nRESULTS:\nOf 4065 melanoma cases, 435 men (11%) had filled prescriptions for PDE5 inhibitors, as did 1713 men of 20,325 controls (8%). In multivariable analysis, there was an increased risk of melanoma in men taking PDE5 inhibitors (OR, 1.21 [95% CI, 1.08-1.36]). The most pronounced increase in risk was observed in men who had filled a single prescription (OR, 1.32 [95% CI, 1.10-1.59]; exposure rate, 4% for cases vs 3% for controls), but was not significant among men with multiple filled prescriptions (for 2-5 prescriptions: OR, 1.14 [95% CI, 0.95-1.37], 4% for cases and 3% for controls; for ≥6 prescriptions: OR, 1.17 [95% CI, 0.95-1.44], 3% for cases vs 2% for controls). PDE5 inhibitors were significantly associated with melanoma stage 0 (OR, 1.49 [95% CI, 1.22-1.83], 13% for cases vs 8% for controls) and stage I (OR, 1.21 [95% CI, 1.02-1.43], 12% for cases vs 10% for controls), but not stage II through IV (OR, 0.83 [95% CI, 0.63-1.09], 6% for cases vs 7% for controls). The risk estimates were similar for sildenafil and vardenafil or tadalafil. PDE5 inhibitor use was also associated with an increased risk of basal cell carcinoma (OR, 1.19 [95% CI, 1.14-1.25], 9% for cases vs 8% for controls). Men taking PDE5 inhibitors had a higher educational level and annual income, factors that were also significantly associated with melanoma risk.\n\nCONCLUSIONS AND RELEVANCE:\nIn a Swedish cohort of men, the use of PDE5 inhibitors was associated with a modest but statistically significant increased risk of malignant melanoma. However, the pattern of association (eg, the lack of association with multiple filled prescriptions) raises questions about whether this association is causal."
+ },
+ "questions": [
+  {
+   "id": "fb0f9948-9bca-457c-b987-fcc734259374",
+   "text": "What are the risk factors of Melanoma?",
+   "answers": [
+    {
+     "answer_start": 2473,
+     "text": "use of PDE5 inhibitors"
+    },
+    {
+     "answer_start": 1260,
+     "text": "men taking PDE5 inhibitors"
+    }
+   ]
+  }
+ ]
+}

03e788ac-cd54-4c16-98a9-fbcd7b0ac5d3.json

@@ -0,0 +1,46 @@
+{
+ "id": "03e788ac-cd54-4c16-98a9-fbcd7b0ac5d3",
+ "disease": {
+  "id": "H00408",
+  "names": [
+   "Type 1 diabetes mellitus"
+  ],
+  "dbLinks": {
+   "icd10": [
+    "E10"
+   ],
+   "mesh": [
+    "D003922"
+   ]
+  },
+  "category": "Metabolic disease; Immune system disease; Endocrine disease"
+ },
+ "article": {
+  "id": "9165223",
+  "text": "The relationship between the incidence of childhood-onset insulin-dependent diabetes mellitus and levels of nitrate in drinking water in the former Yorkshire Regional Health Authority was investigated by means of an ecological analysis. A population-based register contributed 1797 0-16-year-olds diagnosed with diabetes between 1978 and 1994. Nitrate data were based on 9330 samples of drinking water tested between 1990 and 1995 in 148 water supply zones, for which 1991 census small area statistics were taken on population density, ethnicity and socio-economic status. Diabetes incidence was positively associated with raised mean nitrate levels with a standardised incidence ratio of 115 in zones with greater than 14.85 mg.1-1 (chi2 = 26.81, 1 df, p \u003c 0.001). Significant negative trends were found between standardised incidence ratios and proportion of non-whites in the population (chi2 = 33.57, 1 df, p \u003c 0.001), childhood population density (chi2 = 30.81, 1 df, p \u003c 0.001) and the Townsend deprivation score (chi2 = 33.89, 1 df, p \u003c 0.001). Poisson regression modelling, adjusting for the other factors, showed a significant increase in relative incidence rate ratio from a baseline of 1 at nitrate levels below 3.22 mg.1-1 to 1.27 (95% confidence interval 1.09, 1.48) for mean nitrate levels above 14.85 mg.1-1. An association between higher nitrate levels in domestic drinking water and incidence of childhood diabetes has been demonstrated. This was not explained by the ethnic composition of the population, population density or socioeconomic status. Nitrate in drinking water may be a precursor of chemicals which are toxic to the pancreas."
+ },
+ "questions": [
+  {
+   "id": "7027e957-4d75-47cb-926d-e84f8dbebe31",
+   "text": "What are the risk factors of Type 1 diabetes mellitus?",
+   "answers": [
+    {
+     "answer_start": 847,
+     "text": "proportion of non-whites in the population"
+    },
+    {
+     "answer_start": 992,
+     "text": "Townsend deprivation score"
+    },
+    {
+     "answer_start": 1347,
+     "text": "higher nitrate levels in domestic drinking water"
+    },
+    {
+     "answer_start": 1567,
+     "text": "Nitrate in drinking water"
+    }
+   ]
+  }
+ ]
+}

041e9e0a-7de7-4121-a69d-17677c5fb5e1.json

@@ -0,0 +1,46 @@
+{
+ "id": "041e9e0a-7de7-4121-a69d-17677c5fb5e1",
+ "disease": {
+  "id": "H00031",
+  "names": [
+   "Breast cancer"
+  ],
+  "dbLinks": {
+   "icd10": [
+    "C50"
+   ],
+   "mesh": [
+    "D001943"
+   ]
+  },
+  "category": "Cancer"
+ },
+ "article": {
+  "id": "18666209",
+  "text": "BACKGROUND:\nThe Gail model has been commonly used to estimate a woman's risk of breast cancer within a certain time period. High bone mineral density (BMD) is also a significant risk factor for breast cancer, but it appears to play no role in the Gail model. The objective of the current study was to investigate whether hip BMD predicts postmenopausal breast cancer risk independently of the Gail score.\n\nMETHODS:\nIn this prospective study, 9941 postmenopausal women who had a baseline hip BMD and Gail score from the Women's Health Initiative were included in the analysis. Their average age was 63.0 +/- 7.4 years at baseline.\n\nRESULTS:\nAfter an average of 8.43 years of follow-up, 327 incident breast cancer cases were reported and adjudicated. In a multivariate Cox proportional hazards model, the hazards ratios (95% confidence interval [95% CI]) for incident breast cancer were 1.35 (95% CI, 1.05-1.73) for high Gail score (\u003eor=1.67%) and 1.25 (95% CI, 1.11-1.40) for each unit of increase in the total hip BMD T-score. Restricting the analysis to women with both BMD and a Gail score above the median, a sharp increase in incident breast cancer for women with the highest BMD and Gail scores was found (P \u003c .05).\n\nCONCLUSIONS:\nThe contribution of BMD to the prediction of incident postmenopausal breast cancer across the entire population was found to be independent of the Gail score. However, among women with both high BMD and a high Gail score, there appears to be an interaction between these 2 factors. These findings suggest that BMD and Gail score may be used together to better quantify the risk of breast cancer."
+ },
+ "questions": [
+  {
+   "id": "48e36c34-b11a-41f1-849f-63789c476ac5",
+   "text": "What are the risk factors of Breast Cancer?",
+   "answers": [
+    {
+     "answer_start": 914,
+     "text": "high Gail score (\u003eor=1.67%)"
+    },
+    {
+     "answer_start": 975,
+     "text": "each unit of increase in the total hip BMD T-score"
+    },
+    {
+     "answer_start": 1172,
+     "text": "highest BMD and Gail scores"
+    },
+    {
+     "answer_start": 124,
+     "text": "High bone mineral density (BMD)"
+    }
+   ]
+  }
+ ]
+}

04a49704-1bf6-45ce-b36d-87003e0402fb.json

@@ -0,0 +1,34 @@
+{
+ "id": "04a49704-1bf6-45ce-b36d-87003e0402fb",
+ "disease": {
+  "id": "H01730",
+  "names": [
+   "Myocardial infarction"
+  ],
+  "dbLinks": {
+   "icd10": [
+    "I21"
+   ],
+   "mesh": [
+    "D009203"
+   ]
+  },
+  "category": "Cardiovascular disease"
+ },
+ "article": {
+  "id": "33626252",
+  "text": "BACKGROUND:\nMost data regarding the association between the glycemic index and cardiovascular disease come from high-income Western populations, with little information from non-Western countries with low or middle incomes. To fill this gap, data are needed from a large, geographically diverse population.\n\nMETHODS:\nThis analysis includes 137,851 participants between the ages of 35 and 70 years living on five continents, with a median follow-up of 9.5 years. We used country-specific food-frequency questionnaires to determine dietary intake and estimated the glycemic index and glycemic load on the basis of the consumption of seven categories of carbohydrate foods. We calculated hazard ratios using multivariable Cox frailty models. The primary outcome was a composite of a major cardiovascular event (cardiovascular death, nonfatal myocardial infarction, stroke, and heart failure) or death from any cause.\n\nRESULTS:\nIn the study population, 8780 deaths and 8252 major cardiovascular events occurred during the follow-up period. After performing extensive adjustments comparing the lowest and highest glycemic-index quintiles, we found that a diet with a high glycemic index was associated with an increased risk of a major cardiovascular event or death, both among participants with preexisting cardiovascular disease (hazard ratio, 1.51; 95% confidence interval [CI], 1.25 to 1.82) and among those without such disease (hazard ratio, 1.21; 95% CI, 1.11 to 1.34). Among the components of the primary outcome, a high glycemic index was also associated with an increased risk of death from cardiovascular causes. The results with respect to glycemic load were similar to the findings regarding the glycemic index among the participants with cardiovascular disease at baseline, but the association was not significant among those without preexisting cardiovascular disease.\n\nCONCLUSIONS:\nIn this study, a diet with a high glycemic index was associated with an increased risk of cardiovascular disease and death. (Funded by the Population Health Research Institute and others.)."
+ },
+ "questions": [
+  {
+   "id": "c6c65161-d4d8-4390-982f-1e1ad65f2aa7",
+   "text": "What are the risk factors of Myocardial infarction?",
+   "answers": [
+    {
+     "answer_start": 1910,
+     "text": "diet with a high glycemic index"
+    }
+   ]
+  }
+ ]
+}

04b50bc5-9c21-4313-9f41-e6f9e7ddd036.json

@@ -0,0 +1,43 @@
+{
+ "id": "04b50bc5-9c21-4313-9f41-e6f9e7ddd036",
+ "disease": {
+  "id": "H00079",
+  "names": [
+   "Asthma"
+  ],
+  "dbLinks": {
+   "icd10": [
+    "J45"
+   ],
+   "mesh": [
+    "D001249"
+   ]
+  },
+  "category": "Immune system disease",
+  "description": "Asthma is a complex syndrome with many clinical phenotypes in both adults and children. Its major characteristics include a variable degree of airflow obstruction, bronchial hyperresponsiveness, and airway inflammation. Inhaled allergens encounter antigen presenting cells (APC) that line the airway. Upon recognition of the antigen and activation by APC, naive T cells differentiate into TH2 cells. Activated TH2 stimulate the formation of IgE by B cells. IgE molecules bind to IgE receptors located on mast cells. The crosslinking of mast-cell-bound IgE by allergens leads to the release of biologically active mediators (histamine, leukotrienes) by means of degranulation and, so, to the immediate symptoms of allergy. Mast cells also release chemotactic factors that contribute to the recruitment of inflammatory cells, particularly eosinophils, whose proliferation and differentiation from bone marrow progenitors is promoted by IL-5. The activation of eosinophils leads to release of toxic granules and oxygen free radicals that lead to tissue damage and promote the development of chronic inflammation."
+ },
+ "article": {
+  "id": "22952297",
+  "text": "RATIONALE:\nAlthough epidemiological studies suggest that exposure to maternal smoking during fetal and early life increases the risk of childhood wheezing and asthma, previous studies were not able to differentiate the effects of prenatal from postnatal exposure.\n\nOBJECTIVES:\nTo assess the effect of exposure to maternal smoking only during pregnancy on wheeze and asthma among preschool-age children.\n\nMETHODS:\nA pooled analysis was performed based on individual participant data from eight European birth cohorts. Cohort-specific effects of maternal smoking during pregnancy, but not during the first year, on wheeze and asthma at 4 to 6 years of age were estimated using logistic regression and then combined using a random effects model. Adjustments were made for sex, parental education, parental asthma, birth weight, and siblings.\n\nMEASUREMENTS AND MAIN RESULTS:\nAmong the 21,600 children included in the analysis, 735 children (3.4%) were exposed to maternal smoking exclusively during pregnancy but not in the first year after birth. In the pooled analysis, maternal smoking only during pregnancy was associated with wheeze and asthma at 4 to 6 years of age, with adjusted odds ratios of 1.39 (95% confidence interval, 1.08-1.77) and 1.65 (95% confidence interval, 1.18-2.31), respectively. The likelihood to develop wheeze and asthma increased statistically significantly in a linear dose-dependent manner in relation to maternal daily cigarette consumption during the first trimester of pregnancy.\n\nCONCLUSIONS:\nMaternal smoking during pregnancy appears to increase the risk of wheeze and asthma among children who are not exposed to maternal smoking after birth."
+ },
+ "questions": [
+  {
+   "id": "3f68731e-9e28-4e20-9f7c-784fbb742b2e",
+   "text": "What are the risk factors of Asthma?",
+   "answers": [
+    {
+     "answer_start": 1068,
+     "text": "maternal smoking only during pregnancy"
+    },
+    {
+     "answer_start": 1432,
+     "text": "maternal daily cigarette consumption during the first trimester of pregnancy"
+    },
+    {
+     "answer_start": 1524,
+     "text": "Maternal smoking during pregnancy"
+    }
+   ]
+  }
+ ]
+}

0532f382-af42-4e7d-b059-cc5831307410.json

@@ -0,0 +1,41 @@
+{
+ "id": "0532f382-af42-4e7d-b059-cc5831307410",
+ "disease": {
+  "id": "M2023_04_26_16_38_52",
+  "names": [
+   "Migraine"
+  ],
+  "dbLinks": {
+   "icd10": [
+    "G43"
+   ],
+   "icd11": [
+    "8A80"
+   ],
+   "mesh": [
+    "C10.228.140.546.399.750"
+   ]
+  },
+  "description": "Migraine is a chronic neurological disorder characterized by recurrent episodes of unilateral, pulsatile headaches associated with autonomic symptoms such as nausea, vomiting, photophobia, and phonophobia. The pathophysiology of migraine is multifactorial and involves complex interactions between genetic, environmental, and neurochemical factors that modulate cerebral vascular tone and nociception. Migraine attacks can be triggered by a variety of factors, including stress, hormonal changes, sleep disturbances, and certain foods or medications. Treatment options for migraine include pharmacotherapy for acute attacks, preventive medications for frequent or severe headaches, and lifestyle modifications to avoid triggers. In refractory cases, interventional therapies such as nerve blocks or neuromodulation techniques may be considered."
+ },
+ "article": {
+  "id": "23636092",
+  "text": "Migraine is a common disabling disorder with a significant genetic component, characterized by severe headache and often accompanied by nausea, vomiting, and light sensitivity. We identified two families, each with a distinct missense mutation in the gene encoding casein kinase Iδ (CKIδ), in which the mutation cosegregated with both the presence of migraine and advanced sleep phase. The resulting alterations (T44A and H46R) occurred in the conserved catalytic domain of CKIδ, where they caused reduced enzyme activity. Mice engineered to carry the CKIδ-T44A allele were more sensitive to pain after treatment with the migraine trigger nitroglycerin. CKIδ-T44A mice also exhibited a reduced threshold for cortical spreading depression (believed to be the physiological analog of migraine aura) and greater arterial dilation during cortical spreading depression. Astrocytes from CKIδ-T44A mice showed increased spontaneous and evoked calcium signaling. These genetic, cellular, physiological, and behavioral analyses suggest that decreases in CKIδ activity can contribute to the pathogenesis of migraine."
+ },
+ "questions": [
+  {
+   "id": "ae99a30d-5e0f-4158-8efe-2d523a3f4f02",
+   "text": "what are the risk factors of Migraine?",
+   "answers": [
+    {
+     "answer_start": 1032,
+     "text": "decreases in CKIδ activity"
+    },
+    {
+     "answer_start": 265,
+     "text": "casein kinase Iδ (CKIδ)"
+    }
+   ]
+  }
+ ]
+}

05d967dc-437a-463c-9d91-34696585b7a9.json

@@ -0,0 +1,39 @@
+{
+ "id": "05d967dc-437a-463c-9d91-34696585b7a9",
+ "disease": {
+  "id": "H00079",
+  "names": [
+   "Asthma"
+  ],
+  "dbLinks": {
+   "icd10": [
+    "J45"
+   ],
+   "mesh": [
+    "D001249"
+   ]
+  },
+  "category": "Immune system disease",
+  "description": "Asthma is a complex syndrome with many clinical phenotypes in both adults and children. Its major characteristics include a variable degree of airflow obstruction, bronchial hyperresponsiveness, and airway inflammation. Inhaled allergens encounter antigen presenting cells (APC) that line the airway. Upon recognition of the antigen and activation by APC, naive T cells differentiate into TH2 cells. Activated TH2 stimulate the formation of IgE by B cells. IgE molecules bind to IgE receptors located on mast cells. The crosslinking of mast-cell-bound IgE by allergens leads to the release of biologically active mediators (histamine, leukotrienes) by means of degranulation and, so, to the immediate symptoms of allergy. Mast cells also release chemotactic factors that contribute to the recruitment of inflammatory cells, particularly eosinophils, whose proliferation and differentiation from bone marrow progenitors is promoted by IL-5. The activation of eosinophils leads to release of toxic granules and oxygen free radicals that lead to tissue damage and promote the development of chronic inflammation."
+ },
+ "article": {
+  "id": "16141442",
+  "text": "BACKGROUND:\nAlthough research has shown that early life exposure to household endotoxin protects against development of allergies, studies are less clear on the relationship between household endotoxin exposure and prevalence of wheezing and asthma. We assayed 2,552 house dust samples in a representative nationwide sam- ple to explore relationships between endotoxin exposures and risk factors for asthma, asthma symptoms, and medication use.\n\nMETHODS:\nHouse dust was vacuum-sampled from five locations within homes and assayed for endotoxin. Health, demographic, and housing information was assessed through questionnaire and on-site evaluation of 2,456 residents of 831 homes selected to represent the demographics of the United States.\n\nRESULTS:\nEndotoxin concentration (EU/mg) and load (EU/m(2)) were highly correlated (r = 0.73-0.79). Geometric mean endotoxin concentrations were as follows (in EU/mg): bedroom floors, 35.3 (5th-95th percentile, 5.0-260); bedding, 18.7 (2.0-142); family room floors, 63.9 (11.5-331); sofas, 44.8 (6.4-240); and kitchen floors, 80.5 (9.8-512). Multivariate analysis demonstrated significant relationships between increasing endotoxin levels and diagnosed asthma, asthma symptoms in the past year, current use of asthma medications, and wheezing among residents of the homes. These relationships were strongest for bedroom floor and bedding dust and were observed in adults only. Modeling the joint effect of bedding and bedroom floor endotoxin on recent asthma symptoms yielded an adjusted odds ratio of 2.83 (95% confidence interval, 1.01-7.87). When stratified by allergy status, allergic subjects with higher endotoxin exposure were no more likely to have diagnosed asthma or asthma symptoms than nonallergic subjects.\n\nCONCLUSION:\nThis study demonstrates that household endotoxin exposure is a significant risk factor for increased asthma prevalence."
+ },
+ "questions": [
+  {
+   "id": "c80ed6a6-6cc7-4559-96f5-4df4be5eb15d",
+   "text": "What are the risk factors of Asthma?",
+   "answers": [
+    {
+     "answer_start": 1804,
+     "text": "household endotoxin exposure"
+    },
+    {
+     "answer_start": 1153,
+     "text": "increasing endotoxin levels"
+    }
+   ]
+  }
+ ]
+}

05db10b1-2fd8-435a-a5be-1363f8684bd1.json

@@ -0,0 +1,42 @@
+{
+ "id": "05db10b1-2fd8-435a-a5be-1363f8684bd1",
+ "disease": {
+  "id": "H00022",
+  "names": [
+   "Bladder cancer"
+  ],
+  "dbLinks": {
+   "icd10": [
+    "C67"
+   ],
+   "mesh": [
+    "D001749"
+   ]
+  },
+  "category": "Cancer"
+ },
+ "article": {
+  "id": "11545456",
+  "text": "BACKGROUND:\nUsing a combined analysis of 11 case-control studies from Europe, we have investigated the relationship between cigarette smoking and bladder cancer in women.\n\nMETHODS:\nAvailable smoking information on 685 female bladder cancer cases and 2416 female controls included duration of smoking habit, number of cigarettes smoked per day, and time since cessation of smoking habit for ex-smokers.\n\nRESULTS:\nThere was an increasing risk of bladder cancer with increasing duration of smoking, ranging from approximately a two-fold increased risk for a duration of less than 10 years (odds ratio (OR) = 1.9, 95% confidence interval (CI) 1.1-3.1) to over a four-fold increased risk for a duration of greater than 40 years (OR = 4.1, 95% CI 3.0-5.5). A dose-response relationship was observed between number of cigarettes smoked per day and bladder cancer up to a threshold limit of 15-20 cigarettes per day, OR = 3.8 (95% CI 2.7-5.4), after which no increased risk was observed. An immediate decrease in risk of bladder cancer was observed for those who gave up smoking. This decrease was over 30% in the immediate 1-4 years after cessation, OR = 0.68 (95% CI 0.38-1.2). However, even after 25 years the decrease in risk did not reach the level of the never-smokers, OR = 0.27 (95% CI 0.21-0.35).\n\nCONCLUSION:\nThe proportion of bladder cancer cases among women attributable to ever smoking was 0.30, (0.25-0.35) and to current smoking was 0.18 (0.14-0.22). These attributable proportions are less than those observed among men, although they are likely to increase in the future as the smoking-related disease epidemic among women matures."
+ },
+ "questions": [
+  {
+   "id": "3135a5e9-427a-4716-947d-430f9066c6af",
+   "text": "What are the risk factors of Bladder Cancer?",
+   "answers": [
+    {
+     "answer_start": 464,
+     "text": "increasing duration of smoking"
+    },
+    {
+     "answer_start": 1378,
+     "text": "ever smoking"
+    },
+    {
+     "answer_start": 1420,
+     "text": "current smoking"
+    }
+   ]
+  }
+ ]
+}

061d870f-1d33-45e1-9a4c-f7f888e336b0.json

@@ -0,0 +1,46 @@
+{
+ "id": "061d870f-1d33-45e1-9a4c-f7f888e336b0",
+ "disease": {
+  "id": "H00408",
+  "names": [
+   "Type 1 diabetes mellitus"
+  ],
+  "dbLinks": {
+   "icd10": [
+    "E10"
+   ],
+   "mesh": [
+    "D003922"
+   ]
+  },
+  "category": "Metabolic disease; Immune system disease; Endocrine disease"
+ },
+ "article": {
+  "id": "14519705",
+  "text": "CONTEXT:\nDietary exposures in infancy have been implicated, albeit inconsistently, in the etiology of type 1 diabetes mellitus (DM).\n\nOBJECTIVE:\nTo examine the association between cereal exposures in the infant diet and appearance of islet autoimmunity (IA).\n\nDESIGN:\nBirth cohort study conducted from 1994 to 2002 with a mean follow-up of 4 years.\n\nSETTING:\nNewborn screening for HLA was done at St Joseph's Hospital in Denver, Colo. First-degree relatives of type 1 DM individuals were recruited from the Denver metropolitan area.\n\nPARTICIPANTS:\nWe enrolled 1183 children at increased type 1 DM risk, defined as either HLA genotype or having a first-degree relative with type 1 DM, at birth and followed them prospectively. We obtained exposure and outcome measures for 76% of enrolled children. Participants had variable lengths of follow-up (9 months to 9 years).\n\nMAIN OUTCOME MEASURES:\nBlood draws for the detection of insulin autoantibody, glutamic acid decarboxylase autoantibody, or IA-2 autoantibody were performed at 9, 15, and 24 months and annually thereafter. Children with IA (n = 34) were defined as those testing positive for at least 1 of the autoantibodies on 2 or more consecutive visits and who tested positive or had diabetes on their most recent visit.\n\nRESULTS:\nChildren initially exposed to cereals between ages 0 and 3 months (hazard ratio [HR], 4.32; 95% confidence interval [CI], 2.0-9.35) and those who were exposed at 7 months or older (HR, 5.36; 95% CI, 2.08-13.8) had increased hazard of IA compared with those who were exposed during the fourth through sixth month, after adjustment for HLA genotype, family history of type 1 DM, ethnicity, and maternal age. In children who were positive for the HLA-DRB1*03/04,DQB8 genotype, adjusted HRs were 5.55 (95% CI, 1.92-16.03) and 12.53 (95% CI, 3.19-49.23) for initial cereal exposure between ages 0 to 3 months and at 7 months or older, respectively.\n\nCONCLUSION:\nThere may be a window of exposure to cereals in infancy outside which initial exposure increases IA risk in susceptible children."
+ },
+ "questions": [
+  {
+   "id": "c54996c9-73e7-4025-b6b1-dde8c060d4d1",
+   "text": "What are the risk factors of Type 1 diabetes mellitus?",
+   "answers": [
+    {
+     "answer_start": 1286,
+     "text": "Children initially exposed to cereals between ages 0 and 3 months"
+    },
+    {
+     "answer_start": 1422,
+     "text": "those who were exposed at 7 months or older"
+    },
+    {
+     "answer_start": 1695,
+     "text": "children who were positive for the HLA-DRB1*03/04,DQB8 genotype"
+    },
+    {
+     "answer_start": 1968,
+     "text": "exposure to cereals in infancy"
+    }
+   ]
+  }
+ ]
+}

074019cb-a9f4-47ef-80c0-80367a653174.json

@@ -0,0 +1,49 @@
+{
+ "id": "074019cb-a9f4-47ef-80c0-80367a653174",
+ "disease": {
+  "id": "H00020",
+  "names": [
+   "Colorectal cancer"
+  ],
+  "dbLinks": {
+   "icd10": [
+    "C18",
+    "C19",
+    "C20"
+   ],
+   "mesh": [
+    "D015179"
+   ]
+  },
+  "category": "Cancer",
+  "description": "Colorectal cancer (CRC) is the second largest cause of cancer-related deaths in Western countries. CRC arises from the colorectal epithelium as a result of the accumulation of genetic alterations in defined oncogenes and tumour suppressor genes (TSG). Two major mechanisms of genomic instability have been identified in sporadic CRC progression. The first, known as chromosomal instability (CIN), results from a series of genetic changes that involve the activation of oncogenes such as K-ras and inactivation of TSG such as p53, DCC/Smad4, and APC. The second, known as microsatellite instability (MSI), results from inactivation of the DNA mismatch repair genes MLH1 and/or MSH2 by hypermethylation of their promoter, and secondary mutation of genes with coding microsatellites, such as transforming growth factor receptor II (TGF-RII) and BAX. Hereditary syndromes have germline mutations in specific genes (mutation in the tumour suppressor gene APC on chromosome 5q in FAP, mutated DNA mismatch repair genes in HNPCC)."
+ },
+ "article": {
+  "id": "24037561",
+  "text": "BACKGROUND:\nIncreasing evidence suggests that diabetes mellitus (DM) is associated with increased cancer incidence and mortality. Several mechanisms involved in diabetes, such as promotion of cell proliferation and decreased apoptosis, may foster carcinogenesis. This study investigated the association between DM and cancer incidence and cancer-specific mortality in patients with breast and colorectal carcinoma.\n\nMETHODS:\nA meta-analysis of controlled trials, prospective cohort studies and pooled cohort studies published after 2007 was conducted. Embase, PubMed and the Cochrane Library were searched. Summary hazard ratios (HRs) were calculated using a random-effects model. Sensitivity and subgroup analyses were performed to adjust for confounders, mode of DM assessment and follow-up time.\n\nRESULTS:\nTwenty studies were included to investigate the association between DM and breast and colorectal cancer incidence and cancer-specific mortality. The studies predominantly comprised patients with type II DM. The overall HR for breast cancer incidence was 1·23 (95 per cent confidence interval 1·12 to 1·34) and that for colorectal cancer was 1·26 (1·14 to 1·40) in patients with DM compared with those without diabetes. The overall HR was 1·38 (1·20 to 1·58) for breast cancer- and 1·30 (1·15 to 1·47) for colorectal cancer-specific mortality in patients with DM compared with those without diabetes.\n\nCONCLUSION:\nThis meta-analysis indicated that DM is a risk factor for breast and colorectal cancer, and for cancer-specific mortality."
+ },
+ "questions": [
+  {
+   "id": "821c8fe4-809d-4e4a-9a81-0533ec758d0f",
+   "text": "What are the risk factors of Colorectal Cancer?",
+   "answers": [
+    {
+     "answer_start": 990,
+     "text": "patients with type II DM"
+    },
+    {
+     "answer_start": 1173,
+     "text": "patients with DM"
+    },
+    {
+     "answer_start": 1456,
+     "text": "DM"
+    },
+    {
+     "answer_start": 46,
+     "text": "diabetes mellitus (DM)"
+    }
+   ]
+  }
+ ]
+}

07d8bf30-1ff4-463c-b4e7-09241fdfe69e.json

@@ -0,0 +1,35 @@
+{
+ "id": "07d8bf30-1ff4-463c-b4e7-09241fdfe69e",
+ "disease": {
+  "id": "H00056",
+  "names": [
+   "Alzheimer disease",
+   "Dementia due to Alzheimer disease"
+  ],
+  "dbLinks": {
+   "icd10": [
+    "G30"
+   ],
+   "mesh": [
+    "D000544"
+   ]
+  },
+  "category": "Neurodegenerative disease"
+ },
+ "article": {
+  "id": "8113792",
+  "text": "Almost all patients \u003e 40 years of age with Down's syndrome (DS) develop the pathology characteristic of Alzheimer's disease: abundant beta-amyloid plaques and neurofibrillary tangles. We have investigated the gene expression of beta-amyloid protein precursor (APP) and tau in DS and age-matched control brains and found that levels of both mRNAs were significantly elevated in DS. Such up-regulation was not observed in two other neuronal proteins. A correlation between total APP and tau mRNA levels was also found in DS brain but distinct from the pattern observed in normal brain. Although a proportionality existed between APP-695 mRNA and three-repeat tau mRNA in DS, the proportionality between APP-751 mRNA and four-repeat tau mRNA, which is normally present, was not observed. Thus, DS brains are primarily characterized by the up-regulation of tau mRNA as well as APP mRNA and disruption of the coordinate expression between APP-751 and four-repeat tau."
+ },
+ "questions": [
+  {
+   "id": "5e05a017-96ba-4e63-8c92-85faa233dc56",
+   "text": "What are the risk factors of Alzheimer disease?",
+   "answers": [
+    {
+     "answer_start": 11,
+     "text": "patients \u003e 40 years of age with Down's syndrome (DS)"
+    }
+   ]
+  }
+ ]
+}

07f11fd4-babc-46d7-bf8d-4394fa354e74.json

@@ -0,0 +1,34 @@
+{
+ "id": "07f11fd4-babc-46d7-bf8d-4394fa354e74",
+ "disease": {
+  "id": "H01730",
+  "names": [
+   "Myocardial infarction"
+  ],
+  "dbLinks": {
+   "icd10": [
+    "I21"
+   ],
+   "mesh": [
+    "D009203"
+   ]
+  },
+  "category": "Cardiovascular disease"
+ },
+ "article": {
+  "id": "11416288",
+  "text": "In a follow up of elderly Framingham men and women, and after multivariate adjustment, the total/high-density lipoprotein-cholesterol ratio remained highly associated with the incidence of coronary heart disease in both sexes, whereas total cholesterol level was associated with coronary heart disease only in women. Whereas total cholesterol values decline in the very elderly, and the association of coronary heart disease with total cholesterol level alone is weaker in the elderly than among those of middle age, the total/high-density lipoprotein-cholesterol ratio remains a strong predictor of coronary heart disease. In assessing the elderly for coronary risk, lipid measurements should include high-density lipoprotein-cholesterol and cholesterol determinations."
+ },
+ "questions": [
+  {
+   "id": "d4d51f7a-2b33-4a5a-bb6e-6fb8650ef4d4",
+   "text": "What are the risk factors of Myocardial infarction?",
+   "answers": [
+    {
+     "answer_start": 521,
+     "text": "total/high-density lipoprotein-cholesterol ratio "
+    }
+   ]
+  }
+ ]
+}

085f5b41-4786-4417-8b47-73bb742cf2f1.json

@@ -0,0 +1,34 @@
+{
+ "id": "085f5b41-4786-4417-8b47-73bb742cf2f1",
+ "disease": {
+  "id": "H00409",
+  "names": [
+   "Type 2 diabetes mellitus"
+  ],
+  "dbLinks": {
+   "icd10": [
+    "E11"
+   ],
+   "mesh": [
+    "D003924"
+   ]
+  },
+  "category": "Metabolic disease; Endocrine disease"
+ },
+ "article": {
+  "id": "17679132",
+  "text": "BACKGROUND:\nHemoglobin A1c (HbA1c) is a marker of cumulative glycemic exposure over the preceding 2- to 3-month period. Whether mild elevations of this biomarker provide prognostic information for development of clinically evident type 2 diabetes and cardiovascular disease among individuals at usual risk for these disorders is uncertain.\n\nMETHODS:\nWe examined baseline HbA1c levels as a predictor of incident clinical diabetes and cardiovascular disease (nonfatal myocardial infarction, coronary revascularization procedure, ischemic stroke, or death from cardiovascular causes) in a prospective cohort study beginning in 1992 of 26,563 US female health professionals aged 45 years or more without diagnosed diabetes or vascular disease (median follow-up 10.1 years).\n\nRESULTS:\nDuring follow-up, 1238 cases of diabetes and 684 cardiovascular events occurred. In age-adjusted analyses using quintiles of HbA1c, a risk gradient was observed for both incident diabetes and cardiovascular disease. After multivariable adjustment, HbA1c remained a strong predictor of diabetes but was no longer significantly associated with incident cardiovascular disease. In analyses of threshold effects, adjusted relative risks for incident diabetes in HbA1c categories of less than 5.0%, 5.0% to 5.4%, 5.5% to 5.9%, 6.0% to 6.4%, 6.5% to 6.9%, and 7.0% or more were 1.0, 2.9, 12.1, 29.3, 28.2, and 81.2, respectively. Risk associations persisted after additional adjustment for C-reactive protein and after excluding individuals developing diabetes within 2 and 5 years of follow-up.\n\nCONCLUSIONS:\nThese prospective findings suggest that HbA1c levels are elevated well in advance of the clinical development of type 2 diabetes, supporting recent recommendations for lowering of diagnostic thresholds for glucose metabolic disorders. In contrast, the association of HbA1c with incident cardiovascular events is modest and largely attributable to coexistent traditional risk factors."
+ },
+ "questions": [
+  {
+   "id": "6f0c3d34-9e6b-41a7-a9cd-c983e4fe6af7",
+   "text": "what are the risk factors of type 2 diabetes mellitus?",
+   "answers": [
+    {
+     "answer_start": 1028,
+     "text": "HbA1c"
+    }
+   ]
+  }
+ ]
+}

097cbfac-e787-4450-a4f7-f169b5350ee3.json

@@ -0,0 +1,38 @@
+{
+ "id": "097cbfac-e787-4450-a4f7-f169b5350ee3",
+ "disease": {
+  "id": "H00408",
+  "names": [
+   "Type 1 diabetes mellitus"
+  ],
+  "dbLinks": {
+   "icd10": [
+    "E10"
+   ],
+   "mesh": [
+    "D003922"
+   ]
+  },
+  "category": "Metabolic disease; Immune system disease; Endocrine disease"
+ },
+ "article": {
+  "id": "7589885",
+  "text": "The risk of developing diabetes is higher in offspring of fathers than of mothers with insulin-dependent diabetes mellitus (IDDM). The reasons for this sex differential are unclear, as early studies were often selected and relatively small. We conducted a prospective study on the risk of IDDM in a cohort of 9,453 offspring from 5,255 Finnish parents with diabetes diagnosed before age 30 years. Age of first admission to the hospital was considered to be the age of diagnosis of IDDM in the offspring; IDDM occurred in 248 offspring. The risk of IDDM tended to be lower in the offspring of the same gender as the diabetic parent (adjusted risk ratio (RR) 0.78; p = 0.50). When offspring were of same gender as the diabetic parent, male offspring had a higher risk of IDDM than female offspring (RR 2.28; 95% confidence interval 1.53-3.38), whereas if the gender of the diabetic parent and the offspring were different, the risk in male offspring was lower (RR 0.43; 95% confidence interval 0.31-0.62). For the offspring of diabetic fathers, the cumulative risk by the age of 20 was higher (7.6%) than for those with diabetic mothers (3.5%) (p \u003c 0.0001). In a multivariate analysis statistically significant predictors of IDDM in the offspring were the sex of the parent, the year of birth and the birth order of the offspring. The risk of IDDM in the offspring increased by 9% per year of birth cohort. By age 20, the cumulative risk of developing IDDM in the offspring of diabetic parents was 5.3%, 10 times higher than in the background population. It is likely that genetic factors seem to have played a major role in the continuous increase of IDDM incidence in Finnish children."
+ },
+ "questions": [
+  {
+   "id": "901f48c7-6a7a-4abc-a811-2ed7a654299a",
+   "text": "What are the risk factors of Type 1 diabetes mellitus?",
+   "answers": [
+    {
+     "answer_start": 1353,
+     "text": "offspring"
+    },
+    {
+     "answer_start": 1462,
+     "text": "offspring of diabetic parents"
+    }
+   ]
+  }
+ ]
+}

0a4d6add-0662-43be-b84a-5cd360f338af.json

@@ -0,0 +1,36 @@
+{
+ "id": "0a4d6add-0662-43be-b84a-5cd360f338af",
+ "disease": {
+  "id": "H01714",
+  "names": [
+   "Chronic obstructive pulmonary disease (COPD)",
+   "Emphysema"
+  ],
+  "dbLinks": {
+   "icd10": [
+    "J43",
+    "J44"
+   ],
+   "mesh": [
+    "D029424"
+   ]
+  },
+  "category": "Lung disease"
+ },
+ "article": {
+  "id": "26541532",
+  "text": "Recent studies suggest that males with chronic obstructive pulmonary disease (COPD) have more emphysema than females. It is not known if these differences persist across degrees of COPD severity. Our aim was to identify sex-specific differences in quantitative emphysema within COPD subgroups based on COPD severity.We included non-Hispanic white and African-American subjects from the COPDGene study with at least 10 pack-years of smoking and COPD Global Initiative for Chronic Obstructive Lung Disease (GOLD) spirometry grade II or greater. We examined sex-specific differences in log-transformed emphysema (log per cent low-attenuation area (%LAA)) by GOLD spirometry grade among subjects with early-onset COPD (\u003c55 years old) and advanced emphysema (\u003e25% emphysema).Compared with females, males had higher log %LAA: overall (1.97±1.4 versus 1.69±1.6, β=0.32 (0.04), p=1.34×10(-14)), and among non-Hispanic white (p=8.37×10(-14)) and African-American subjects (p=0.002). Females with early-onset COPD, severe emphysema and GOLD grade IV COPD had similar emphysema as males, but markedly fewer pack-years smoking (early-onset, p=0.01; severe emphysema and GOLD grade IV, p\u003c0.001).This study identifies subsets of female smokers with COPD who are particularly susceptible to parenchymal destruction."
+ },
+ "questions": [
+  {
+   "id": "53dcb947-f557-44e7-aa13-95a647b58d50",
+   "text": "What are the risk factors for Chronic obstructive pulmonary disease (COPD)?",
+   "answers": [
+    {
+     "answer_start": 1215,
+     "text": "female smokers"
+    }
+   ]
+  }
+ ]
+}

0ae2dfe1-b4f1-4098-8f4a-3b23038c29f9.json

@@ -0,0 +1,50 @@
+{
+ "id": "0ae2dfe1-b4f1-4098-8f4a-3b23038c29f9",
+ "disease": {
+  "id": "H01730",
+  "names": [
+   "Myocardial infarction"
+  ],
+  "dbLinks": {
+   "icd10": [
+    "I21"
+   ],
+   "mesh": [
+    "D009203"
+   ]
+  },
+  "category": "Cardiovascular disease"
+ },
+ "article": {
+  "id": "10080459",
+  "text": "OBJECTIVE:\nTo assess the relationship between dysglycemia and myocardial infarction in nondiabetic individuals.\n\nBACKGROUND:\nNondiabetic hyperglycemia may be an important cardiac risk factor. The relationship between myocardial infarction and glucose, insulin, abdominal obesity, lipids and hypertension was therefore studied in South Asians-a group at high risk for coronary heart disease and diabetes.\n\nMETHODS:\nDemographics, waist/hip ratio, fasting blood glucose (FBG), insulin, lipids and glucose tolerance were measured in 300 consecutive patients with a first myocardial infarction and 300 matched controls.\n\nRESULTS:\nCases were more likely to have diabetes (OR 5.49; 95% CI 3.34, 9.01), impaired glucose tolerance (OR 4.08; 95% CI 2.31, 7.20) or impaired fasting glucose (OR 3.22; 95% CI 1.51, 6.85) than controls. Cases were 3.4 (95% CI 1.9, 5.8) and 6.0 (95% CI 3.3, 10.9) times more likely to have an FBG in the third and fourth quartile (5.2-6.3 and \u003e6.3 mmol/1); after removing subjects with diabetes, impaired glucose tolerance and impaired fasting glucose, cases were 2.7 times (95% CI 1.5-4.8) more likely to have an FBG \u003e5.2 mmol/l. A fasting glucose of 4.9 mmol/l best distinguished cases from controls (OR 3.42; 95% CI 2.42, 4.83). Glucose, abdominal obesity, lipids, hypertension and smoking were independent multivariate risk factors for myocardial infarction. In subjects without glucose intolerance, a 1.2 mmol/l (21 mg/dl) increase in postprandial glucose was independently associated with an increase in the odds of a myocardial infarction of 1.58 (95% CI 1.18, 2.12).\n\nCONCLUSIONS:\nA moderately elevated glucose level is a continuous risk factor for MI in nondiabetic South Asians with either normal or impaired glucose tolerance."
+ },
+ "questions": [
+  {
+   "id": "7a353a7a-9da9-43b1-93e4-e4852d0fb260",
+   "text": "What are the risk factors of Myocardial infarction?",
+   "answers": [
+    {
+     "answer_start": 1610,
+     "text": "moderately elevated glucose level"
+    },
+    {
+     "answer_start": 1260,
+     "text": "abdominal obesity"
+    },
+    {
+     "answer_start": 1279,
+     "text": "lipids"
+    },
+    {
+     "answer_start": 1287,
+     "text": "hypertension"
+    },
+    {
+     "answer_start": 1304,
+     "text": "smoking"
+    }
+   ]
+  }
+ ]
+}

0b840514-c1a2-4e20-bc5b-8162fca8321e.json

@@ -0,0 +1,42 @@
+{
+ "id": "0b840514-c1a2-4e20-bc5b-8162fca8321e",
+ "disease": {
+  "id": "H02123",
+  "names": [
+   "Celiac disease"
+  ],
+  "dbLinks": {
+   "icd10": [
+    "K90.0"
+   ],
+   "mesh": [
+    "D002446"
+   ]
+  },
+  "category": "Digestive system disease"
+ },
+ "article": {
+  "id": "26453955",
+  "text": "BACKGROUND \u0026 AIMS:\nEarly nutrition may affect the risk of celiac disease. We investigated whether amount of gluten in diet until 2 years of age increases risk for celiac disease.\n\nMETHODS:\nWe performed a 1-to-3 nested case-control study of 146 cases, resulting in 436 case-control pairs matched for sex, birth year, and HLA genotype generated from Swedish children at genetic risk for celiac disease. Newborns were annually screened for tissue transglutaminase autoantibodies (tTGA). If tested tTGA positive, time point of seroconversion was determined from frozen serum samples taken every 3 months. Celiac disease was confirmed by intestinal biopsies. Gluten intake was calculated from 3-day food records collected at ages 9, 12, 18 and 24 months. Odds ratios (OR) were calculated through conditional logistic regression.\n\nRESULTS:\nBreastfeeding duration (median, 32 wk) and age at first introduction to gluten (median, 22 wk) did not differ between cases and tTGA-negative controls. At the visit before tTGA seroconversion, cases reported a larger intake of gluten than controls (OR, 1.28; 95% confidence interval [CI], 1.13-1.46; P = .0002). More cases than controls were found in the upper third tertile (ie, \u003e5.0 g/d) before they tested positive for tTGA seroconversion than controls (OR, 2.65; 95% CI, 1.70-4.13; P \u003c .0001). This finding was similar in children homozygous for DR3-DQ2 (OR, 3.19; 95% CI, 1.61-6.30; P = .001), heterozygous for DR3-DQ2 (OR, 2.24; 95% CI, 1.08-4.62; P = .030), and for children not carrying DR3-DQ2 (OR, 2.43; 95% CI, 0.90-6.54; P = .079).\n\nCONCLUSIONS:\nThe amount of gluten consumed until 2 years of age increases the risk of celiac disease at least 2-fold in genetically susceptible children. These findings may be taken into account for future infant feeding recommendations."
+ },
+ "questions": [
+  {
+   "id": "7c4d8c08-fc66-42eb-a53f-3a8cbade06c2",
+   "text": "What are the risk factors of Celiac disease?",
+   "answers": [
+    {
+     "answer_start": 1592,
+     "text": "The amount of gluten consumed until 2 years of age"
+    },
+    {
+     "answer_start": 1044,
+     "text": "larger intake of gluten"
+    },
+    {
+     "answer_start": 1189,
+     "text": "upper third tertile (ie, \u003e5.0 g/d)"
+    }
+   ]
+  }
+ ]
+}

0c99389b-42d3-4255-976b-03bcbf58ea87.json

@@ -0,0 +1,45 @@
+{
+ "id": "0c99389b-42d3-4255-976b-03bcbf58ea87",
+ "disease": {
+  "id": "H00020",
+  "names": [
+   "Colorectal cancer"
+  ],
+  "dbLinks": {
+   "icd10": [
+    "C18",
+    "C19",
+    "C20"
+   ],
+   "mesh": [
+    "D015179"
+   ]
+  },
+  "category": "Cancer",
+  "description": "Colorectal cancer (CRC) is the second largest cause of cancer-related deaths in Western countries. CRC arises from the colorectal epithelium as a result of the accumulation of genetic alterations in defined oncogenes and tumour suppressor genes (TSG). Two major mechanisms of genomic instability have been identified in sporadic CRC progression. The first, known as chromosomal instability (CIN), results from a series of genetic changes that involve the activation of oncogenes such as K-ras and inactivation of TSG such as p53, DCC/Smad4, and APC. The second, known as microsatellite instability (MSI), results from inactivation of the DNA mismatch repair genes MLH1 and/or MSH2 by hypermethylation of their promoter, and secondary mutation of genes with coding microsatellites, such as transforming growth factor receptor II (TGF-RII) and BAX. Hereditary syndromes have germline mutations in specific genes (mutation in the tumour suppressor gene APC on chromosome 5q in FAP, mutated DNA mismatch repair genes in HNPCC)."
+ },
+ "article": {
+  "id": "15956652",
+  "text": "BACKGROUND:\nCurrent evidence suggests that high red meat intake is associated with increased colorectal cancer risk. High fish intake may be associated with a decreased risk, but the existing evidence is less convincing.\n\nMETHODS:\nWe prospectively followed 478 040 men and women from 10 European countries who were free of cancer at enrollment between 1992 and 1998. Information on diet and lifestyle was collected at baseline. After a mean follow-up of 4.8 years, 1329 incident colorectal cancers were documented. We examined the relationship between intakes of red and processed meat, poultry, and fish and colorectal cancer risk using a proportional hazards model adjusted for age, sex, energy (nonfat and fat sources), height, weight, work-related physical activity, smoking status, dietary fiber and folate, and alcohol consumption, stratified by center. A calibration substudy based on 36 994 subjects was used to correct hazard ratios (HRs) and 95% confidence intervals (CIs) for diet measurement errors. All statistical tests were two-sided.\n\nRESULTS:\nColorectal cancer risk was positively associated with intake of red and processed meat (highest [\u003e160 g/day] versus lowest [\u003c20 g/day] intake, HR = 1.35, 95% CI = 0.96 to 1.88; Ptrend = .03) and inversely associated with intake of fish (\u003e80 g/day versus \u003c10 g/day, HR = 0.69, 95 % CI = 0.54 to 0.88; Ptrend\u003c.001), but was not related to poultry intake. Correcting for measurement error strengthened the associations between colorectal cancer and red and processed meat intake (per 100-g increase HR = 1.25, 95% CI =1.09 to 1.41, Ptrend = .001 and HR = 1.55, 95% CI = 1.19 to 2.02, Ptrend = .001 before and after calibration, respectively) and for fish (per 100 g increase HR = 0.70, 95% CI = 0.57 to 0.87, Ptrend\u003c.001 and HR = 0.46, 95% CI = 0.27 to 0.77, Ptrend = .003; before and after correction, respectively). In this study population, the absolute risk of development of colorectal cancer within 10 years for a study subject aged 50 years was 1.71% for the highest category of red and processed meat intake and 1.28% for the lowest category of intake and was 1.86% for subjects in the lowest category of fish intake and 1.28% for subjects in the highest category of fish intake.\n\nCONCLUSIONS:\nOur data confirm that colorectal cancer risk is positively associated with high consumption of red and processed meat and support an inverse association with fish intake."
+ },
+ "questions": [
+  {
+   "id": "0c197850-f433-48ce-97d6-32fad36b4bfb",
+   "text": "What are the risk factors of Colorectal Cancer?",
+   "answers": [
+    {
+     "answer_start": 2334,
+     "text": "high consumption of red and processed meat"
+    },
+    {
+     "answer_start": 1114,
+     "text": "intake of red and processed meat (highest [\u003e160 g/day]"
+    },
+    {
+     "answer_start": 1506,
+     "text": "red and processed meat intake (per 100-g"
+    }
+   ]
+  }
+ ]
+}

0d195070-7f03-447f-9a14-ba2273db9665.json

@@ -0,0 +1,35 @@
+{
+ "id": "0d195070-7f03-447f-9a14-ba2273db9665",
+ "disease": {
+  "id": "H00079",
+  "names": [
+   "Asthma"
+  ],
+  "dbLinks": {
+   "icd10": [
+    "J45"
+   ],
+   "mesh": [
+    "D001249"
+   ]
+  },
+  "category": "Immune system disease",
+  "description": "Asthma is a complex syndrome with many clinical phenotypes in both adults and children. Its major characteristics include a variable degree of airflow obstruction, bronchial hyperresponsiveness, and airway inflammation. Inhaled allergens encounter antigen presenting cells (APC) that line the airway. Upon recognition of the antigen and activation by APC, naive T cells differentiate into TH2 cells. Activated TH2 stimulate the formation of IgE by B cells. IgE molecules bind to IgE receptors located on mast cells. The crosslinking of mast-cell-bound IgE by allergens leads to the release of biologically active mediators (histamine, leukotrienes) by means of degranulation and, so, to the immediate symptoms of allergy. Mast cells also release chemotactic factors that contribute to the recruitment of inflammatory cells, particularly eosinophils, whose proliferation and differentiation from bone marrow progenitors is promoted by IL-5. The activation of eosinophils leads to release of toxic granules and oxygen free radicals that lead to tissue damage and promote the development of chronic inflammation."
+ },
+ "article": {
+  "id": "1728015",
+  "text": "The relationship between parental smoking and both subsequent development of asthma and subsequent lung function (before age 12) was studied in more than 700 children enrolled before age 5. Children of mothers with 12 or fewer years of education and who smoked 10 or more cigarettes per day were 2.5 times more likely (95% confidence interval 1.42 to 4.59; P = .0018) to develop asthma and had 15.7% lower maximal midexpiratory flow (P less than .001) than children of mothers with the same education level who did not smoke or smoked fewer than 10 cigarettes per day. These relationships were independent of self-reported respiratory symptoms in parents. There was no association between maternal smoking and subsequent incidence of asthma or maximal midexpiratory flow among children of mothers with more than 12 years of education. It is concluded that children of lower socioeconomic status may be at considerable risk of developing asthma if their mothers smoke 10 or more cigarettes per day. It is speculated that recently reported increases in prevalence of childhood asthma may be in part related to the increased prevalence of smoking among less educated women."
+ },
+ "questions": [
+  {
+   "id": "ca7c2279-304b-428f-83df-565adc95c86b",
+   "text": "What are the risk factors of Asthma?",
+   "answers": [
+    {
+     "answer_start": 190,
+     "text": "Children of mothers with 12 or fewer years of education and who smoked 10 or more cigarettes per day"
+    }
+   ]
+  }
+ ]
+}

0dce1a7d-02ab-45fd-9dd0-742ec2fb9a5a.json

@@ -0,0 +1,39 @@
+{
+ "id": "0dce1a7d-02ab-45fd-9dd0-742ec2fb9a5a",
+ "disease": {
+  "id": "H00630",
+  "names": [
+   "Rheumatoid arthritis"
+  ],
+  "dbLinks": {
+   "icd10": [
+    "M05"
+   ],
+   "mesh": [
+    "D001172"
+   ]
+  },
+  "category": "Immune system disease",
+  "description": "Rheumatoid arthritis (RA) is a common autoimmune disease that primarily manifests as chronic inflammatory arthropathy. Persistent synovitis leads to cartilage destruction, bone erosions and periarticular decalcification, subsequently resulting in impaired joint function. It is more common between the ages of 35 and 50 years, affecting three times more women than men. Susceptibility to RA is genetically determined with multiple genes contributing. Inheritance of HLA DRB1 alleles encoding a distinctive five-amino-acid sequence known as the \"shared epitope\" (SE) is the best characterized genetic risk factor. The mechanism by which the SE alleles contribute to the development of RA is not very clear. It has been postulated that the presence of these conserved sequences in the antigen-binding groove alters the way antigenic peptides are bound to and presented to T-cell lymphocytes. This, in turn, may trigger abnormal immune responses and lead to RA."
+ },
+ "article": {
+  "id": "19151010",
+  "text": "BACKGROUND:\nPrevious studies have reported an interaction between ever cigarette smoking and the presence of the human leukocyte antigen (HLA)-DRB1 shared epitope (SE) genotype and rheumatoid arthritis (RA) risk. To address the effect of dosage, a case-control study nested within two prospective cohorts to determine the interaction between heavy smoking and the HLA-SE was conducted.\n\nMETHODS:\nBlood was obtained from 32 826 women in the Nurses' Health Study and 29 611 women in the Nurses' Health Study II. Incident RA diagnoses were validated by chart review. Controls were matched for age, menopausal status and postmenopausal hormone use. High-resolution HLA-DRB1 genotyping was performed for SE alleles. HLA-SE, smoking, HLA-SE* smoking interactions and RA risk, were assessed using conditional logistic regression models, adjusted for age and reproductive factors. Additive and multiplicative interactions were tested.\n\nRESULTS:\nIn all, 439 Caucasian matched pairs were included. Mean age at RA diagnosis was 55.2 years; 62% of cases were seropositive. A modest additive interaction was observed between ever smoking and HLA-SE in seropositive RA risk. A strong additive interaction (attributable proportion due to interaction (AP) = 0.50; p\u003c0.001) and significant multiplicative interaction (p = 0.05) were found between heavy smoking (\u003e10 pack-years) and any HLA-SE in seropositive RA risk. The highest risk was in heavy smokers with double copy HLA-SE (odds ratio (OR) 7.47, 95% CI 2.77 to 20.11).\n\nCONCLUSIONS:\nA strong gene-environment interaction was observed between HLA-SE and smoking when stratifying by pack-years of smoking rather than by ever smoking. Future studies should assess cumulative exposure to cigarette smoke when testing for gene-smoking interactions."
+ },
+ "questions": [
+  {
+   "id": "05bfd05d-f100-431b-aba0-bca6a5fef11b",
+   "text": "What are the risk factors of Rheumatoid arthritis?",
+   "answers": [
+    {
+     "answer_start": 1425,
+     "text": "heavy smokers with double copy HLA-SE"
+    },
+    {
+     "answer_start": 1330,
+     "text": "heavy smoking (\u003e10 pack-years) and any HLA-SE"
+    }
+   ]
+  }
+ ]
+}

0dfcd9e7-b11c-44f0-a175-ac24a015ad1d.json

@@ -0,0 +1,41 @@
+{
+ "id": "0dfcd9e7-b11c-44f0-a175-ac24a015ad1d",
+ "disease": {
+  "id": "H00020",
+  "names": [
+   "Colorectal cancer"
+  ],
+  "dbLinks": {
+   "icd10": [
+    "C18",
+    "C19",
+    "C20"
+   ],
+   "mesh": [
+    "D015179"
+   ]
+  },
+  "category": "Cancer",
+  "description": "Colorectal cancer (CRC) is the second largest cause of cancer-related deaths in Western countries. CRC arises from the colorectal epithelium as a result of the accumulation of genetic alterations in defined oncogenes and tumour suppressor genes (TSG). Two major mechanisms of genomic instability have been identified in sporadic CRC progression. The first, known as chromosomal instability (CIN), results from a series of genetic changes that involve the activation of oncogenes such as K-ras and inactivation of TSG such as p53, DCC/Smad4, and APC. The second, known as microsatellite instability (MSI), results from inactivation of the DNA mismatch repair genes MLH1 and/or MSH2 by hypermethylation of their promoter, and secondary mutation of genes with coding microsatellites, such as transforming growth factor receptor II (TGF-RII) and BAX. Hereditary syndromes have germline mutations in specific genes (mutation in the tumour suppressor gene APC on chromosome 5q in FAP, mutated DNA mismatch repair genes in HNPCC)."
+ },
+ "article": {
+  "id": "15644546",
+  "text": "CONTEXT:\nDiabetes is a serious and costly disease that is becoming increasingly common in many countries. The role of diabetes as a cancer risk factor remains unclear.\n\nOBJECTIVE:\nTo examine the relationship between fasting serum glucose and diabetes and risk of all cancers and specific cancers in men and women in Korea.\n\nDESIGN, SETTING, AND PARTICIPANTS:\nTen-year prospective cohort study of 1,298,385 Koreans (829,770 men and 468,615 women) aged 30 to 95 years who received health insurance from the National Health Insurance Corp and had a biennial medical evaluation in 1992-1995 (with follow-up for up to 10 years).\n\nMAIN OUTCOME MEASURES:\nDeath from cancer and registry-documented incident cancer or hospital admission for cancer.\n\nRESULTS:\nDuring the 10 years of follow-up, there were 20,566 cancer deaths in men and 5907 cancer deaths in women. Using Cox proportional hazards models and controlling for smoking and alcohol use, the stratum with the highest fasting serum glucose (\u003e or =140 mg/dL [\u003e or =7.8 mmol/L]) had higher death rates from all cancers combined (hazard ratio [HR], 1.29; 95% confidence interval [CI], 1.22-1.37 in men and HR, 1.23; 95% CI, 1.09-1.39 in women) compared with the stratum with the lowest level (\u003c90 mg/dL [\u003c5.0 mmol/L]). By cancer site, the association was strongest for pancreatic cancer, comparing the highest and lowest strata in men (HR, 1.91; 95% CI, 1.52-2.41) and in women (HR, 2.05; 95% CI, 1.43-2.93). Significant associations were also found for cancers of the esophagus, liver, and colon/rectum in men and of the liver and cervix in women, and there were significant trends with glucose level for cancers of the esophagus, colon/rectum, liver, pancreas, and bile duct in men and of the liver and pancreas in women. Of the 26,473 total cancer deaths in men and women, 848 were estimated as attributable to having a fasting serum glucose level of less than 90 mg/dL. For cancer incidence, the general patterns reflected those found for mortality. For persons with a diagnosis of diabetes or a fasting serum glucose level greater than 125 mg/dL (6.9 mmol/L), risks for cancer incidence and mortality were generally elevated compared with those without diabetes.\n\nCONCLUSION:\nIn Korea, elevated fasting serum glucose levels and a diagnosis of diabetes are independent risk factors for several major cancers, and the risk tends to increase with an increased level of fasting serum glucose."
+ },
+ "questions": [
+  {
+   "id": "900c0189-83b0-4f6c-8355-474572099505",
+   "text": "What are the risk factors of Colorectal Cancer?",
+   "answers": [
+    {
+     "answer_start": 2238,
+     "text": "elevated fasting serum glucose levels"
+    },
+    {
+     "answer_start": 2282,
+     "text": "diagnosis of diabetes"
+    }
+   ]
+  }
+ ]
+}

0ecb1c40-6106-4355-b746-5ad68883f618.json

@@ -0,0 +1,38 @@
+{
+ "id": "0ecb1c40-6106-4355-b746-5ad68883f618",
+ "disease": {
+  "id": "H00022",
+  "names": [
+   "Bladder cancer"
+  ],
+  "dbLinks": {
+   "icd10": [
+    "C67"
+   ],
+   "mesh": [
+    "D001749"
+   ]
+  },
+  "category": "Cancer"
+ },
+ "article": {
+  "id": "21673031",
+  "text": "BACKGROUND:\nDespite an increase in the number of molecular epidemiological studies conducted in recent years to evaluate the association between human papillomavirus (HPV) infection and risk of bladder cancer, the studies remain inconclusive.\n\nMETHODS:\nThe prevalence of HPV in bladder cancer was estimated by pooling data from 52 studies, taking into consideration the heterogeneity from major related parameters including study region, histological type, HPV DNA specimen, publication calendar period, and detection method. Moreover, the association of HPV infection with bladder cancer was tested by a meta-analysis with 19 case-control studies.\n\nRESULTS:\nAn HPV prevalence of 16.88% (95% confidence interval [CI], 15.53%-18.31%) among the bladder cancer cases was revealed, most of whom were high-risk HPV types (15.82% [95% CI, 14.37%-17.36%]). The prevalence varied by region, types of HPV DNA specimen, and polymerase chain reaction primers used. A significantly increased risk of bladder cancer was shown for the positivity of overall HPV (odds ratio, 2.84 [95% CI, 1.39-5.80]), which was also infuenced by HPV type, study region, HPV DNA specimen, and detection method.\n\nCONCLUSIONS:\nInfection of high-risk HPV types, especially HPV16, may play a role in bladder carcinogenesis."
+ },
+ "questions": [
+  {
+   "id": "7abdf9e5-9724-4df5-b751-a002ca4f5e3b",
+   "text": "What are the risk factors of Bladder Cancer?",
+   "answers": [
+    {
+     "answer_start": 662,
+     "text": "HPV"
+    },
+    {
+     "answer_start": 1193,
+     "text": "Infection of high-risk HPV types, especially HPV16"
+    }
+   ]
+  }
+ ]
+}

0f2d9b8c-69e1-4d80-949a-73b137424464.json

@@ -0,0 +1,41 @@
+{
+ "id": "0f2d9b8c-69e1-4d80-949a-73b137424464",
+ "disease": {
+  "id": "H00020",
+  "names": [
+   "Colorectal cancer"
+  ],
+  "dbLinks": {
+   "icd10": [
+    "C18",
+    "C19",
+    "C20"
+   ],
+   "mesh": [
+    "D015179"
+   ]
+  },
+  "category": "Cancer",
+  "description": "Colorectal cancer (CRC) is the second largest cause of cancer-related deaths in Western countries. CRC arises from the colorectal epithelium as a result of the accumulation of genetic alterations in defined oncogenes and tumour suppressor genes (TSG). Two major mechanisms of genomic instability have been identified in sporadic CRC progression. The first, known as chromosomal instability (CIN), results from a series of genetic changes that involve the activation of oncogenes such as K-ras and inactivation of TSG such as p53, DCC/Smad4, and APC. The second, known as microsatellite instability (MSI), results from inactivation of the DNA mismatch repair genes MLH1 and/or MSH2 by hypermethylation of their promoter, and secondary mutation of genes with coding microsatellites, such as transforming growth factor receptor II (TGF-RII) and BAX. Hereditary syndromes have germline mutations in specific genes (mutation in the tumour suppressor gene APC on chromosome 5q in FAP, mutated DNA mismatch repair genes in HNPCC)."
+ },
+ "article": {
+  "id": "23896379",
+  "text": "BACKGROUND:\nThe p.I1307K adenomatous polyposis coli (APC) gene variant, prevalent among Ashkenazi Jews, may increase the risk for colorectal neoplasia. We studied the clinical importance of screening for this polymorphism in 3305 Israelis undergoing colonoscopy.\n\nPATIENTS AND METHODS:\nClinical data regarding potential risk factors for colorectal cancer (CRC) were collected from individuals undergoing colonoscopic examination at the Tel-Aviv medical center. The APC p.I1307K was detected using real-time PCR (polymerase chain reaction) from DNA extracted from peripheral mononuclear cells.\n\nRESULTS:\nThe overall prevalence of the p.I1307K polymorphism was 8.0% (10.1% among Ashkenazi and 2.7% among Sephardic Jews, p\u003c0.001). The overall adjusted odds ratio (OR) for colorectal neoplasia among carriers was 1.51 (95% confidence intervals (CI), 1.16-1.98). Among average risk Ashkenazi Jews, the adjusted OR was 1.75 (95% CI 1.26-2.45). A multiplicative interaction was identified between Ashkenazi ethnicity and APC p.I1307K carrier status (P(INTERACTION) = 0.055). The histopathological features of adenomas and carcinomas did not differ between carriers and non-carriers.\n\nCONCLUSIONS:\nThe APC p.I1307K gene variant is an important risk factor for colorectal neoplasia in average risk Ashkenazi Jews. Carriers in this group should be considered for screening colonoscopy at the age of 40, to be repeated every 5 years, similar to recommendations in individuals with family history of colorectal cancer."
+ },
+ "questions": [
+  {
+   "id": "37fdb837-2683-431f-a3b1-6a37323088f8",
+   "text": "What are the risk factors of Colorectal Cancer?",
+   "answers": [
+    {
+     "answer_start": 1194,
+     "text": "APC p.I1307K gene variant"
+    },
+    {
+     "answer_start": 633,
+     "text": "p.I1307K polymorphism"
+    }
+   ]
+  }
+ ]
+}

0f315ae2-b4c2-41d2-bcad-9af73252d1f3.json

@@ -0,0 +1,39 @@
+{
+ "id": "0f315ae2-b4c2-41d2-bcad-9af73252d1f3",
+ "disease": {
+  "id": "H00630",
+  "names": [
+   "Rheumatoid arthritis"
+  ],
+  "dbLinks": {
+   "icd10": [
+    "M05"
+   ],
+   "mesh": [
+    "D001172"
+   ]
+  },
+  "category": "Immune system disease",
+  "description": "Rheumatoid arthritis (RA) is a common autoimmune disease that primarily manifests as chronic inflammatory arthropathy. Persistent synovitis leads to cartilage destruction, bone erosions and periarticular decalcification, subsequently resulting in impaired joint function. It is more common between the ages of 35 and 50 years, affecting three times more women than men. Susceptibility to RA is genetically determined with multiple genes contributing. Inheritance of HLA DRB1 alleles encoding a distinctive five-amino-acid sequence known as the \"shared epitope\" (SE) is the best characterized genetic risk factor. The mechanism by which the SE alleles contribute to the development of RA is not very clear. It has been postulated that the presence of these conserved sequences in the antigen-binding groove alters the way antigenic peptides are bound to and presented to T-cell lymphocytes. This, in turn, may trigger abnormal immune responses and lead to RA."
+ },
+ "article": {
+  "id": "22736291",
+  "text": "OBJECTIVE:\nTo examine the relationship of Porphyromonas gingivalis to the presence of autoantibodies in individuals at risk of rheumatoid arthritis (RA).\n\nMETHODS:\nStudy participants included the following: 1) a cohort enriched in subjects with HLA-DR4 and 2) subjects at risk of RA by virtue of having a first-degree relative with RA. None of the study subjects satisfied the American College of Rheumatology 1987 classification criteria for RA. Autoantibodies measured included anti-citrullinated protein antibody (ACPA; by second-generation anti-cyclic citrullinated peptide antibody enzyme-linked immunosorbent assay [ELISA]) and rheumatoid factor (RF; by nephelometry or ELISA for IgA, IgM, or IgG isotype). Individuals were considered autoantibody positive (n = 113) if they had ≥1 RA-related autoantibody; individuals were further categorized as high risk (n = 38) if they had ACPA or positive findings ≥2 assays for RF. Autoantibody-negative individuals (n = 171) served as a comparator group. Antibody to P gingivalis, P intermedia, and F nucleatum were measured. Associations of bacterial antibodies with group status were examined using logistic regression.\n\nRESULTS:\nAnti-P gingivalis concentrations were higher in high-risk (P = 0.011) and autoantibody positive group (P = 0.010) than in the autoantibody negative group. There were no group differences in anti-P intermedia or anti-F nucleatum concentrations. After multivariable adjustment, anti-P gingivalis concentrations (but not anti-P intermedia or anti-F nucleatum) were significantly associated with autoantibody-positive and high-risk status (P \u003c 0.05).\n\nCONCLUSION:\nImmunity to P gingivalis, but not P intermedia or F nucleatum, is significantly associated with the presence of RA-related autoantibodies in individuals at risk of RA. These results support the hypothesis that infection with P gingivalis may play a central role in the early loss of tolerance to self antigens that occurs in the pathogenesis of RA."
+ },
+ "questions": [
+  {
+   "id": "20386f3f-0817-445b-b7a7-6ad83e072bce",
+   "text": "What are the risk factors of Rheumatoid arthritis?",
+   "answers": [
+    {
+     "answer_start": 1179,
+     "text": "Anti-P gingivalis concentrations"
+    },
+    {
+     "answer_start": 1849,
+     "text": "infection with P gingivalis"
+    }
+   ]
+  }
+ ]
+}

0f6c198f-8a63-476f-9377-1660e6735e58.json

@@ -0,0 +1,43 @@
+{
+ "id": "0f6c198f-8a63-476f-9377-1660e6735e58",
+ "disease": {
+  "id": "H00630",
+  "names": [
+   "Rheumatoid arthritis"
+  ],
+  "dbLinks": {
+   "icd10": [
+    "M05"
+   ],
+   "mesh": [
+    "D001172"
+   ]
+  },
+  "category": "Immune system disease",
+  "description": "Rheumatoid arthritis (RA) is a common autoimmune disease that primarily manifests as chronic inflammatory arthropathy. Persistent synovitis leads to cartilage destruction, bone erosions and periarticular decalcification, subsequently resulting in impaired joint function. It is more common between the ages of 35 and 50 years, affecting three times more women than men. Susceptibility to RA is genetically determined with multiple genes contributing. Inheritance of HLA DRB1 alleles encoding a distinctive five-amino-acid sequence known as the \"shared epitope\" (SE) is the best characterized genetic risk factor. The mechanism by which the SE alleles contribute to the development of RA is not very clear. It has been postulated that the presence of these conserved sequences in the antigen-binding groove alters the way antigenic peptides are bound to and presented to T-cell lymphocytes. This, in turn, may trigger abnormal immune responses and lead to RA."
+ },
+ "article": {
+  "id": "25926142",
+  "text": "OBJECTIVES:\nTo assess whether HOUSES (HOUsing-based index of socioeconomic status (SES)) is associated with risk of and mortality after rheumatoid arthritis (RA).\n\nDESIGN:\nWe conducted a population-based case-control study which enrolled population-based RA cases and their controls without RA.\n\nSETTING:\nThe study was performed in Olmsted County, Minnesota.\n\nPARTICIPANTS:\nStudy participants were all residents of Olmsted County, Minnesota, with RA identified using the 1987 American College of Rheumatology criteria for RA from 1 January 1988, to 31 December 2007, using the auspices of the Rochester Epidemiology Project. For each patient with RA, one control was randomly selected from Olmsted County residents of similar age and gender without RA.\n\nPRIMARY AND SECONDARY OUTCOME MEASURE:\nThe disease status was RA cases and their matched controls in relation to HOUSES as an exposure. As a secondary aim, post-RA mortality among only RA cases was an outcome event. The associations of SES measured by HOUSES with the study outcomes were assessed using logistic regression and Cox models. HOUSES, as a composite index, was formulated based on a summed z-score for housing value, square footage and number of bedrooms and bathrooms.\n\nRESULTS:\nOf the eligible 604 participants, 418 (69%) were female; the mean age was 56±15.6 years. Lower SES, as measured by HOUSES, was associated with the risk of developing RA (0.5±3.8 for controls vs -0.2±3.1 for RA cases, p=0.003), adjusting for age, gender, calendar year of RA index date, smoking status and BMI. The lowest quartile of HOUSES was significantly associated with increased post-RA mortality compared to higher quartiles of HOUSES (HR 1.74; 95% CI 1.10 to 2.74; p=0.017) in multivariate analysis.\n\nCONCLUSIONS:\nLower SES, as measured by HOUSES, is associated with increased risk of RA and mortality after RA. HOUSES may be a useful tool for health disparities research concerning rheumatological outcomes when conventional SES measures are unavailable."
+ },
+ "questions": [
+  {
+   "id": "33148eba-29a3-402d-807a-674e0c3f01d7",
+   "text": "What are the risk factors of Rheumatoid arthritis?",
+   "answers": [
+    {
+     "answer_start": 1335,
+     "text": "Lower SES, as measured by HOUSES"
+    },
+    {
+     "answer_start": 61,
+     "text": "socioeconomic status (SES))"
+    },
+    {
+     "answer_start": 1767,
+     "text": "Lower SES, as measured by HOUSES"
+    }
+   ]
+  }
+ ]
+}

0ff7571a-b33e-40b6-8dfa-28fb8d5f8183.json

@@ -0,0 +1,34 @@
+{
+ "id": "0ff7571a-b33e-40b6-8dfa-28fb8d5f8183",
+ "disease": {
+  "id": "H00031",
+  "names": [
+   "Breast cancer"
+  ],
+  "dbLinks": {
+   "icd10": [
+    "C50"
+   ],
+   "mesh": [
+    "D001943"
+   ]
+  },
+  "category": "Cancer"
+ },
+ "article": {
+  "id": "25692500",
+  "text": "BACKGROUND:\nThe influence of dietary fat upon breast cancer mortality remains largely understudied despite extensive investigation into its influence upon breast cancer risk.\n\nOBJECTIVE:\nTo conduct meta-analyses of studies to clarify the association between dietary fat and breast cancer mortality.\n\nDESIGN:\nMEDLINE and EMBASE were searched for relevant articles published up to March 2012. Risk of all-cause or breast-cancer-specific death was evaluated by combining multivariable adjusted estimates comparing highest versus lowest categories of intake; and per 20 g increase in intake of total and/or saturated fat (g/day) using random-effects meta-analyses.\n\nRESULTS:\nFifteen prospective cohort studies investigating total fat and/or saturated fat intake (g/day) and breast cancer mortality were included. There was no difference in risk of breast-cancer-specific death (n = 6; HR = 1.14; 95% CI: 0.86, 1.52; p = 0.34) or all-cause death (n = 4; HR = 1.73; 95% CI: 0.82, 3.66; p = 0.15) for women in the highest versus lowest category of total fat intake. Breast-cancer-specific death (n = 4; HR = 1.51; 95% CI: 1.09, 2.09; p \u003c 0.01) was higher for women in the highest versus lowest category of saturated fat intake.\n\nCONCLUSIONS:\nThese meta-analyses have shown that saturated fat intake negatively impacts upon breast cancer survival."
+ },
+ "questions": [
+  {
+   "id": "14baabaa-5099-456b-89cd-0fa69564a906",
+   "text": "What are the risk factors of Breast Cancer?",
+   "answers": [
+    {
+     "answer_start": 1271,
+     "text": "saturated fat intake"
+    }
+   ]
+  }
+ ]
+}

1045d2b8-9fed-4874-9117-1e569f05d480.json

@@ -0,0 +1,47 @@
+{
+ "id": "1045d2b8-9fed-4874-9117-1e569f05d480",
+ "disease": {
+  "id": "H00079",
+  "names": [
+   "Asthma"
+  ],
+  "dbLinks": {
+   "icd10": [
+    "J45"
+   ],
+   "mesh": [
+    "D001249"
+   ]
+  },
+  "category": "Immune system disease",
+  "description": "Asthma is a complex syndrome with many clinical phenotypes in both adults and children. Its major characteristics include a variable degree of airflow obstruction, bronchial hyperresponsiveness, and airway inflammation. Inhaled allergens encounter antigen presenting cells (APC) that line the airway. Upon recognition of the antigen and activation by APC, naive T cells differentiate into TH2 cells. Activated TH2 stimulate the formation of IgE by B cells. IgE molecules bind to IgE receptors located on mast cells. The crosslinking of mast-cell-bound IgE by allergens leads to the release of biologically active mediators (histamine, leukotrienes) by means of degranulation and, so, to the immediate symptoms of allergy. Mast cells also release chemotactic factors that contribute to the recruitment of inflammatory cells, particularly eosinophils, whose proliferation and differentiation from bone marrow progenitors is promoted by IL-5. The activation of eosinophils leads to release of toxic granules and oxygen free radicals that lead to tissue damage and promote the development of chronic inflammation."
+ },
+ "article": {
+  "id": "28926373",
+  "text": "BACKGROUND:\nEarly-life exposure to traffic-related air pollution exacerbates childhood asthma, but it is unclear what role it plays in asthma development.\n\nMETHODS:\nThe association between exposure to primary mobile source pollutants during pregnancy and during infancy and asthma incidence by ages 2 through 6 was examined in the Kaiser Air Pollution and Pediatric Asthma Study, a racially diverse birth cohort of 24,608 children born between 2000 and 2010 and insured by Kaiser Permanente Georgia. We estimated concentrations of mobile source fine particulate matter (PM2.5, µg/m), nitrogen oxides (NOX, ppb), and carbon monoxide (CO, ppm) at the maternal and child residence using a Research LINE source dispersion model for near-surface releases. Asthma was defined using diagnoses and medication dispensings from medical records. We used binomial generalized linear regression to model the impact of exposure continuously and by quintiles on asthma risk.\n\nRESULTS:\nControlling for covariates and modeling log-transformed exposure, a 2.7-fold increase in first year of life PM2.5 was associated with an absolute 4.1% (95% confidence interval, 1.6%, 6.6%) increase in risk of asthma by age 5. Quintile analysis showed an increase in risk from the first to second quintile, but similar risk across quintiles 2-5. Risk differences increased with follow-up age. Results were similar for NOX and CO and for exposure during pregnancy and the first year of life owing to high correlation.\n\nCONCLUSIONS:\nResults provide limited evidence for an association of early-life mobile source air pollution with childhood asthma incidence with a steeper concentration-response relationship observed at lower levels of exposure."
+ },
+ "questions": [
+  {
+   "id": "2054be89-feb5-4631-96dd-c5d471b29889",
+   "text": "What are the risk factors of Asthma?",
+   "answers": [
+    {
+     "answer_start": 1036,
+     "text": "a 2.7-fold increase in first year of life PM2.5"
+    },
+    {
+     "answer_start": 1387,
+     "text": "NOX"
+    },
+    {
+     "answer_start": 1395,
+     "text": "CO"
+    },
+    {
+     "answer_start": 1555,
+     "text": "early-life mobile source air pollution"
+    }
+   ]
+  }
+ ]
+}

1092af1a-3d9b-4ff1-b304-229710e9bf24.json

@@ -0,0 +1,44 @@
+{
+ "id": "1092af1a-3d9b-4ff1-b304-229710e9bf24",
+ "disease": {
+  "id": "H01714",
+  "names": [
+   "Chronic obstructive pulmonary disease (COPD)",
+   "Emphysema"
+  ],
+  "dbLinks": {
+   "icd10": [
+    "J43",
+    "J44"
+   ],
+   "mesh": [
+    "D029424"
+   ]
+  },
+  "category": "Lung disease"
+ },
+ "article": {
+  "id": "20335290",
+  "text": "BACKGROUND:\nOver half the world is exposed daily to the smoke from combustion of solid fuels. Chronic obstructive pulmonary disease (COPD) is one of the main contributors to the global burden of disease and can be caused by biomass smoke exposure. However, studies of biomass exposure and COPD show a wide range of effect sizes. The aim of this systematic review was to quantify the impact of biomass smoke on the development of COPD and define reasons for differences in the reported effect sizes.\n\nMETHODS:\nA systematic review was conducted of studies with sufficient statistical power to calculate the health risk of COPD from the use of solid fuel, which followed standardised criteria for the diagnosis of COPD and which dealt with confounding factors. The results were pooled by fuel type and country to produce summary estimates using a random effects model. Publication bias was also estimated.\n\nRESULTS:\nThere were positive associations between the use of solid fuels and COPD (OR=2.80, 95% CI 1.85 to 4.0) and chronic bronchitis (OR=2.32, 95% CI 1.92 to 2.80). Pooled estimates for different types of fuel show that exposure to wood smoke while performing domestic work presents a greater risk of development of COPD and chronic bronchitis than other fuels.\n\nCONCLUSION:\nDespite heterogeneity across the selected studies, exposure to solid fuel smoke is consistently associated with COPD and chronic bronchitis. Efforts should be made to reduce exposure to solid fuel by using either cleaner fuel or relatively cleaner technology while performing domestic work."
+ },
+ "questions": [
+  {
+   "id": "c0e4c431-0ec0-46c9-a0e7-628f01f37277",
+   "text": "What are the risk factors for Chronic obstructive pulmonary disease (COPD)?",
+   "answers": [
+    {
+     "answer_start": 965,
+     "text": "solid fuels"
+    },
+    {
+     "answer_start": 1126,
+     "text": "exposure to wood smoke while performing domestic work"
+    },
+    {
+     "answer_start": 1332,
+     "text": "exposure to solid fuel smoke"
+    }
+   ]
+  }
+ ]
+}

109adb5e-240a-4a5a-9059-021828d9dd30.json

@@ -0,0 +1,43 @@
+{
+ "id": "109adb5e-240a-4a5a-9059-021828d9dd30",
+ "disease": {
+  "id": "H00038",
+  "names": [
+   "Melanoma"
+  ],
+  "dbLinks": {
+   "icd10": [
+    "C43"
+   ],
+   "mesh": [
+    "D008545"
+   ]
+  },
+  "category": "Cancer",
+  "description": "Melanoma is a form of skin cancer that has a poor prognosis and which is on the rise in Western populations. Melanoma arises from the malignant transformation of pigment-producing cells, melanocytes. The only known environmental risk factor is exposure to ultraviolet (UV) light and in people with fair skin the risk is greatly increased. Melanoma pathogenesis is also driven by genetic factors. Oncogenic NRAS mutations activate both effector pathways Raf-MEK-ERK and PI3K-Akt. The Raf-MEK-ERK pathway may also be activated via mutations in the BRAF gene. The PI3K-Akt pathway may be activated through loss or mutation of the inhibitory tumor suppressor gene PTEN. These mutations arise early during melanoma pathogenesis and are preserved throughout tumor progression. Melanoma development has been shown to be strongly associated with inactivation of the p16INK4a/cyclin dependent kinases 4 and 6/retinoblastoma protein (p16INK4a/CDK4,6/pRb) and p14ARF/human double minute 2/p53 (p14ARF/HMD2/p53) tumor suppressor pathways. MITF and TP53 are implicated in further melanoma progression."
+ },
+ "article": {
+  "id": "22833605",
+  "text": "OBJECTIVE:\nTo estimate the burden of melanoma resulting from sunbed use in western Europe.\n\nDESIGN:\nSystematic review and meta-analysis.\n\nDATA SOURCES:\nPubMed, ISI Web of Science (Science Citation Index Expanded), Embase, Pascal, Cochrane Library, LILACS, and MedCarib, along with published surveys reporting prevalence of sunbed use at national level in Europe.\n\nSTUDY SELECTION:\nObservational studies reporting a measure of risk for skin cancer (cutaneous melanoma, squamous cell carcinoma, basal cell carcinoma) associated with ever use of sunbeds.\n\nRESULTS:\nBased on 27 studies ever use of sunbeds was associated with a summary relative risk of 1.20 (95% confidence interval 1.08 to 1.34). Publication bias was not evident. Restricting the analysis to cohorts and population based studies, the summary relative risk was 1.25 (1.09 to 1.43). Calculations for dose-response showed a 1.8% (95% confidence interval 0% to 3.8%) increase in risk of melanoma for each additional session of sunbed use per year. Based on 13 informative studies, first use of sunbeds before age 35 years was associated with a summary relative risk of 1.87 (1.41 to 2.48), with no indication of heterogeneity between studies. By using prevalence data from surveys and data from GLOBOCAN 2008, in 2008 in the 15 original member countries of the European Community plus three countries that were members of the European Free Trade Association, an estimated 3438 cases of melanoma could be attributable to sunbed use, most (n=2341) occurring among women.\n\nCONCLUSIONS:\nSunbed use is associated with a significant increase in risk of melanoma. This risk increases with number of sunbed sessions and with initial usage at a young age (\u003c35 years). The cancerous damage associated with sunbed use is substantial and could be avoided by strict regulations."
+ },
+ "questions": [
+  {
+   "id": "e2770142-ced4-48a0-911e-21322fd56261",
+   "text": "What are the risk factors of Melanoma?",
+   "answers": [
+    {
+     "answer_start": 1041,
+     "text": "first use of sunbeds before age 35 years"
+    },
+    {
+     "answer_start": 1543,
+     "text": "Sunbed use"
+    },
+    {
+     "answer_start": 1642,
+     "text": "number of sunbed sessions and with initial usage at a young age (\u003c35 years)"
+    }
+   ]
+  }
+ ]
+}

10cf864e-4503-405d-b363-a14c2f11fcc9.json

@@ -0,0 +1,37 @@
+{
+ "id": "10cf864e-4503-405d-b363-a14c2f11fcc9",
+ "disease": {
+  "id": "H00020",
+  "names": [
+   "Colorectal cancer"
+  ],
+  "dbLinks": {
+   "icd10": [
+    "C18",
+    "C19",
+    "C20"
+   ],
+   "mesh": [
+    "D015179"
+   ]
+  },
+  "category": "Cancer",
+  "description": "Colorectal cancer (CRC) is the second largest cause of cancer-related deaths in Western countries. CRC arises from the colorectal epithelium as a result of the accumulation of genetic alterations in defined oncogenes and tumour suppressor genes (TSG). Two major mechanisms of genomic instability have been identified in sporadic CRC progression. The first, known as chromosomal instability (CIN), results from a series of genetic changes that involve the activation of oncogenes such as K-ras and inactivation of TSG such as p53, DCC/Smad4, and APC. The second, known as microsatellite instability (MSI), results from inactivation of the DNA mismatch repair genes MLH1 and/or MSH2 by hypermethylation of their promoter, and secondary mutation of genes with coding microsatellites, such as transforming growth factor receptor II (TGF-RII) and BAX. Hereditary syndromes have germline mutations in specific genes (mutation in the tumour suppressor gene APC on chromosome 5q in FAP, mutated DNA mismatch repair genes in HNPCC)."
+ },
+ "article": {
+  "id": "15644544",
+  "text": "CONTEXT:\nConsumption of red and processed meat has been associated with colorectal cancer in many but not all epidemiological studies; few studies have examined risk in relation to long-term meat intake or the association of meat with rectal cancer.\n\nOBJECTIVE:\nTo examine the relationship between recent and long-term meat consumption and the risk of incident colon and rectal cancer.\n\nDESIGN, SETTING, AND PARTICIPANTS:\nA cohort of 148 610 adults aged 50 to 74 years (median, 63 years), residing in 21 states with population-based cancer registries, who provided information on meat consumption in 1982 and again in 1992/1993 when enrolled in the Cancer Prevention Study II (CPS II) Nutrition Cohort. Follow-up from time of enrollment in 1992/1993 through August 31, 2001, identified 1667 incident colorectal cancers. Participants contributed person-years at risk until death or a diagnosis of colon or rectal cancer.\n\nMAIN OUTCOME MEASURE:\nIncidence rate ratio (RR) of colon and rectal cancer.\n\nRESULTS:\nHigh intake of red and processed meat reported in 1992/1993 was associated with higher risk of colon cancer after adjusting for age and energy intake but not after further adjustment for body mass index, cigarette smoking, and other covariates. When long-term consumption was considered, persons in the highest tertile of consumption in both 1982 and 1992/1993 had higher risk of distal colon cancer associated with processed meat (RR, 1.50; 95% confidence interval [CI], 1.04-2.17), and ratio of red meat to poultry and fish (RR, 1.53; 95% CI, 1.08-2.18) relative to those persons in the lowest tertile at both time points. Long-term consumption of poultry and fish was inversely associated with risk of both proximal and distal colon cancer. High consumption of red meat reported in 1992/1993 was associated with higher risk of rectal cancer (RR, 1.71; 95% CI, 1.15-2.52; P = .007 for trend), as was high consumption reported in both 1982 and 1992/1993 (RR, 1.43; 95% CI, 1.00-2.05).\n\nCONCLUSIONS:\nOur results demonstrate the potential value of examining long-term meat consumption in assessing cancer risk and strengthen the evidence that prolonged high consumption of red and processed meat may increase the risk of cancer in the distal portion of the large intestine."
+ },
+ "questions": [
+  {
+   "id": "45083494-68db-4520-9939-4ff62dc01286",
+   "text": "What are the risk factors of Colorectal Cancer?",
+   "answers": [
+    {
+     "answer_start": 1007,
+     "text": "High intake of red and processed meat"
+    }
+   ]
+  }
+ ]
+}

1104a25e-028a-4579-ba25-cd5430faaa75.json

@@ -0,0 +1,35 @@
+{
+ "id": "1104a25e-028a-4579-ba25-cd5430faaa75",
+ "disease": {
+  "id": "H00079",
+  "names": [
+   "Asthma"
+  ],
+  "dbLinks": {
+   "icd10": [
+    "J45"
+   ],
+   "mesh": [
+    "D001249"
+   ]
+  },
+  "category": "Immune system disease",
+  "description": "Asthma is a complex syndrome with many clinical phenotypes in both adults and children. Its major characteristics include a variable degree of airflow obstruction, bronchial hyperresponsiveness, and airway inflammation. Inhaled allergens encounter antigen presenting cells (APC) that line the airway. Upon recognition of the antigen and activation by APC, naive T cells differentiate into TH2 cells. Activated TH2 stimulate the formation of IgE by B cells. IgE molecules bind to IgE receptors located on mast cells. The crosslinking of mast-cell-bound IgE by allergens leads to the release of biologically active mediators (histamine, leukotrienes) by means of degranulation and, so, to the immediate symptoms of allergy. Mast cells also release chemotactic factors that contribute to the recruitment of inflammatory cells, particularly eosinophils, whose proliferation and differentiation from bone marrow progenitors is promoted by IL-5. The activation of eosinophils leads to release of toxic granules and oxygen free radicals that lead to tissue damage and promote the development of chronic inflammation."
+ },
+ "article": {
+  "id": "24299467",
+  "text": "BACKGROUND:\nAntibiotic use in infancy disrupts gut microflora during a critical period for immune system development. It is hypothesized that this could predispose to the development of allergic diseases. We investigated the associations of antibiotic use in the first 2 yr of life with the development of asthma, eczema or hay fever by age 7.5 yr in a longitudinal birth cohort.\n\nMETHODS:\nSubjects were 4952 children from the Avon Longitudinal Study of Parents and Children (ALSPAC). Child antibiotic use and asthma, eczema and hay fever symptoms were maternally reported. Atopy was assessed by skin prick tests at age 7.5 yr. The total number of antibiotic courses was considered as the main exposure. Data were analysed using multivariate logistic regression.\n\nRESULTS:\nChildren reported to have taken antibiotics during infancy (0-2 yr) were more likely to have asthma at 7.5 yr (OR 1.75, 95% CI 1.40-2.17), and the odds (OR, [95% CI]) increased with greater numbers of courses: once 1.11 [0.84-1.48]; twice 1.50 [1.14-1.98]; three times 1.79 [1.34-2.40]; four times or more 2.82 [2.19-3.63]. Increased antibiotic use was also associated with higher odds of eczema and hay fever but not atopy. The effect appeared to be associated with cumulative rather than a critical period of exposure during the first 2 yr.\n\nCONCLUSIONS:\nA robust and dose-dependent association was found between antibiotic use in the first 2 yr of life and asthma at age 7.5 yr but did not appear to be mediated through an association with atopy."
+ },
+ "questions": [
+  {
+   "id": "a1d94c6a-3e85-4316-8da3-d661bfcccc1d",
+   "text": "What are the risk factors of Asthma?",
+   "answers": [
+    {
+     "answer_start": 1388,
+     "text": "antibiotic use in the first 2 yr of life"
+    }
+   ]
+  }
+ ]
+}

112ce6bc-992a-4795-8ca5-775bfbf4712a.json

@@ -0,0 +1,43 @@
+{
+ "id": "112ce6bc-992a-4795-8ca5-775bfbf4712a",
+ "disease": {
+  "id": "H00630",
+  "names": [
+   "Rheumatoid arthritis"
+  ],
+  "dbLinks": {
+   "icd10": [
+    "M05"
+   ],
+   "mesh": [
+    "D001172"
+   ]
+  },
+  "category": "Immune system disease",
+  "description": "Rheumatoid arthritis (RA) is a common autoimmune disease that primarily manifests as chronic inflammatory arthropathy. Persistent synovitis leads to cartilage destruction, bone erosions and periarticular decalcification, subsequently resulting in impaired joint function. It is more common between the ages of 35 and 50 years, affecting three times more women than men. Susceptibility to RA is genetically determined with multiple genes contributing. Inheritance of HLA DRB1 alleles encoding a distinctive five-amino-acid sequence known as the \"shared epitope\" (SE) is the best characterized genetic risk factor. The mechanism by which the SE alleles contribute to the development of RA is not very clear. It has been postulated that the presence of these conserved sequences in the antigen-binding groove alters the way antigenic peptides are bound to and presented to T-cell lymphocytes. This, in turn, may trigger abnormal immune responses and lead to RA."
+ },
+ "article": {
+  "id": "23897126",
+  "text": "OBJECTIVE:\nTo estimate familial aggregation of rheumatoid arthritis (RA) in 3 large population-representative samples and to test if familial aggregation is affected by rheumatoid factor (RF)/anti-citrullinated protein antibody (ACPA) status, type of relative, sex, and age at onset of RA.\n\nMETHODS:\nA register-based nested case-control study was performed in the Swedish total population. Data on patients with RA were ascertained through the nationwide Swedish Patient Register (n = 88,639), the clinical Swedish Rheumatology Quality Register (n = 11,519), and the Epidemiological Investigation of Rheumatoid Arthritis case-control study (n = 2,871). Data on first- and second-degree relatives were obtained through the Swedish Multigeneration Register. Familial risks were calculated using conditional logistic regression.\n\nRESULTS:\nConsistent across data sources, the familial odds ratio for RA was ∼3 in first-degree relatives of RA patients and 2 in second-degree relatives. Familial risks were similar among siblings, parents, and offspring. Familial aggregation was not modified by sex, but was higher in RA patients with early-onset disease and in RF/ACPA-positive RA patients. The observed familial risks were consistent with a heritability of ∼50% for ACPA-positive RA and ∼20% for ACPA-negative RA.\n\nCONCLUSION:\nThe pattern of risks suggests that familial factors influence RA in men and women equally and that these factors are of less importance for late-onset RA. Familial factors are more important for seropositive RA, but there is significant familial overlap between seropositive RA and seronegative RA. Even if the familial risk is assumed to be completely due to genetics, the observed risks suggest that heritability of RA is lower than previously reported, in particular for ACPA-negative RA."
+ },
+ "questions": [
+  {
+   "id": "493c4671-e046-4f87-b7c0-cb9cd58b98c9",
+   "text": "What are the risk factors of Rheumatoid arthritis?",
+   "answers": [
+    {
+     "answer_start": 23,
+     "text": "familial aggregation"
+    },
+    {
+     "answer_start": 1200,
+     "text": "familial risks"
+    },
+    {
+     "answer_start": 981,
+     "text": "Familial risks were similar among siblings, parents, and offspring"
+    }
+   ]
+  }
+ ]
+}

115b1453-6b15-4f89-88ed-4e74759220b2.json

@@ -0,0 +1,42 @@
+{
+ "id": "115b1453-6b15-4f89-88ed-4e74759220b2",
+ "disease": {
+  "id": "H00409",
+  "names": [
+   "Type 2 diabetes mellitus"
+  ],
+  "dbLinks": {
+   "icd10": [
+    "E11"
+   ],
+   "mesh": [
+    "D003924"
+   ]
+  },
+  "category": "Metabolic disease; Endocrine disease"
+ },
+ "article": {
+  "id": "18501234",
+  "text": "PURPOSE:\nThe study compares the risk of incident diabetes associated with fasting plasma glucose levels in the normal range, controlling for other risk factors.\n\nMETHODS:\nWe identified 46,578 members of Kaiser Permanente Northwest who had fasting plasma glucose levels less than 100 mg/dL between January 1, 1997, and December 31, 2000, and who did not previously have diabetes or impaired fasting glucose. After assigning subjects to 1 of 4 categories (\u003c85, 85-89, 90-94, or 95-99 mg/dL), we followed them until they developed diabetes, died, or left the health plan, or until April 30, 2007. We used Cox regression analysis to estimate the risk of incident diabetes, adjusted for age, sex, body mass index, blood pressure, lipids, smoking, cardiovascular disease, and hypertension.\n\nRESULTS:\nSubjects developed diabetes at a rate of less than 1% per year during a mean follow-up of 81.0 months. Each milligram per deciliter of fasting plasma glucose increased diabetes risk by 6% (hazard ratio [HR] 1.06, 95% confidence interval [CI], 1.05-1.07, P \u003c .0001) after controlling for other risk factors. Compared with those with fasting plasma glucose levels less than 85 mg/dL, subjects with glucose levels of 95 to 99 mg/dL were 2.33 times more likely to develop diabetes (HR 2.33; 95% CI, 1.95-2.79; P \u003c .0001). Subjects in the 90 to 94 mg/dL group were 49% more likely to progress to diabetes (HR 1.49; 95% CI, 1.23-1.79; P \u003c.0001). All other risk factors except sex were significantly associated with a diabetes diagnosis.\n\nCONCLUSIONS:\nThe strong independent association between the level of normal fasting plasma glucose and the incidence of diabetes after controlling for other risk factors suggests that diabetes risk increases as fasting plasma glucose levels increase, even within the currently accepted normal range."
+ },
+ "questions": [
+  {
+   "id": "f19c26a2-4af7-4fdd-b15d-396e1b8b5fc0",
+   "text": "what are the risk factors of Type 2 diabetes mellitus?",
+   "answers": [
+    {
+     "answer_start": 897,
+     "text": "Each milligram per deciliter of fasting plasma glucose"
+    },
+    {
+     "answer_start": 1176,
+     "text": "subjects with glucose levels of 95 to 99 mg/dL"
+    },
+    {
+     "answer_start": 1312,
+     "text": "Subjects in the 90 to 94 mg/dL group"
+    }
+   ]
+  }
+ ]
+}

116922a9-f469-4251-b6a5-a36e0b08801b.json

@@ -0,0 +1,40 @@
+{
+ "id": "116922a9-f469-4251-b6a5-a36e0b08801b",
+ "disease": {
+  "id": "H01714",
+  "names": [
+   "Chronic obstructive pulmonary disease (COPD)",
+   "Emphysema"
+  ],
+  "dbLinks": {
+   "icd10": [
+    "J43",
+    "J44"
+   ],
+   "mesh": [
+    "D029424"
+   ]
+  },
+  "category": "Lung disease"
+ },
+ "article": {
+  "id": "19800047",
+  "text": "Chronic obstructive pulmonary disease (COPD) is the fourth leading cause of death worldwide and is influenced by both genetic determinants and smoking. We identified genomic regions from 56 lung-tissue gene-expression microarrays and used them to select 889 SNPs to be tested for association with COPD. We genotyped SNPs in 389 severe COPD cases from the National Emphysema Treatment Trial and 424 cigarette-smoking controls from the Normative Aging Study. A total of 71 autosomal SNPs demonstrated at least nominal significance with COPD susceptibility (p = 3.4 x 10(-6) to 0.05). These 71 SNPs were evaluated in a family-based study of 127 probands with severe, early-onset COPD and 822 of their family members in the Boston Early-Onset COPD Study. We combined p values from the case-control and family-based analyses, setting p = 5.60 x 10(-5) as a conservative threshold for significance. Three SNPs in the iron regulatory protein 2 (IREB2) gene met this stringent threshold for significance, and four other IREB2 SNPs demonstrated combined p \u003c 0.02. We demonstrated replication of association for these seven IREB2 SNPs (all p values \u003c or = 0.02) in a family-based study of 3117 subjects from the International COPD Genetics Network; combined p values across all cohorts for the main phenotype of interest ranged from 1.6 x 10(-7) to 6.4 x 10(-4). IREB2 protein and mRNA were increased in lung-tissue samples from COPD subjects in comparison to controls. In summary, gene-expression and genetic-association results have implicated IREB2 as a COPD susceptibility gene."
+ },
+ "questions": [
+  {
+   "id": "08dcc626-6a58-4451-91c4-191bed3551db",
+   "text": "What are the risk factors for Chronic obstructive pulmonary disease (COPD)?",
+   "answers": [
+    {
+     "answer_start": 1353,
+     "text": "IREB2 protein"
+    },
+    {
+     "answer_start": 1536,
+     "text": "IREB2"
+    }
+   ]
+  }
+ ]
+}

125ce4cc-ee01-457a-9f57-41046f5b092d.json

@@ -0,0 +1,37 @@
+{
+ "id": "125ce4cc-ee01-457a-9f57-41046f5b092d",
+ "disease": {
+  "id": "M2023_04_26_16_38_52",
+  "names": [
+   "Migraine"
+  ],
+  "dbLinks": {
+   "icd10": [
+    "G43"
+   ],
+   "icd11": [
+    "8A80"
+   ],
+   "mesh": [
+    "C10.228.140.546.399.750"
+   ]
+  },
+  "description": "Migraine is a chronic neurological disorder characterized by recurrent episodes of unilateral, pulsatile headaches associated with autonomic symptoms such as nausea, vomiting, photophobia, and phonophobia. The pathophysiology of migraine is multifactorial and involves complex interactions between genetic, environmental, and neurochemical factors that modulate cerebral vascular tone and nociception. Migraine attacks can be triggered by a variety of factors, including stress, hormonal changes, sleep disturbances, and certain foods or medications. Treatment options for migraine include pharmacotherapy for acute attacks, preventive medications for frequent or severe headaches, and lifestyle modifications to avoid triggers. In refractory cases, interventional therapies such as nerve blocks or neuromodulation techniques may be considered."
+ },
+ "article": {
+  "id": "3404480",
+  "text": "We have studied the association between migraine and major depression in a group of 133 probands with major depression, a group of 82 normal community controls and 400 interviewed first-degree relatives of the probands and controls. There was a significant association between depression and migraine among both the probands and the relatives. We also found that concomitant symptoms of anxiety were prominent among the depressed persons with migraine. Both depression and migraine were strongly familial but their association did not appear to be highly transmissible. Rather, our data suggested that depression may either be a sequela of migraine or the diathesis which results in both migraine and depression."
+ },
+ "questions": [
+  {
+   "id": "7b735d6f-646f-4fc8-9831-c696e272cd95",
+   "text": "what are the risk factors of Migraine?",
+   "answers": [
+    {
+     "answer_start": 277,
+     "text": "depression"
+    }
+   ]
+  }
+ ]
+}

126f2585-0b2b-44f8-9676-81ce41451731.json

@@ -0,0 +1,42 @@
+{
+ "id": "126f2585-0b2b-44f8-9676-81ce41451731",
+ "disease": {
+  "id": "H00022",
+  "names": [
+   "Bladder cancer"
+  ],
+  "dbLinks": {
+   "icd10": [
+    "C67"
+   ],
+   "mesh": [
+    "D001749"
+   ]
+  },
+  "category": "Cancer"
+ },
+ "article": {
+  "id": "12441324",
+  "text": "BACKGROUND:\nPrevious studies have demonstrated that ingestion of arsenic in drinking water is a strong risk factor for several forms of cancer, including bladder cancer. It is not known whether arsenic-related cancers are genetically similar to cancers in unexposed individuals or what mechanisms of carcinogenesis may underlie their formation. This study was designed to compare chromosomal alterations in bladder cancers of arsenic-exposed individuals to provide insight into the mechanism of how arsenic may induce or promote cancer.\n\nMETHODS:\nA case-case study was conducted in Argentina and Chile examining chromosomal alterations in bladder tumor DNA in 123 patients who had been exposed to arsenic in their drinking water. Patients were placed into one of four arsenic exposure categories according to their average 5-year peak arsenic exposure. Patients were also classified as ever smokers or never smokers. Comparative genomic hybridization was used to identify chromosomal alterations throughout the genome. All statistical tests were two-sided.\n\nRESULTS:\nThe total number of chromosomal alterations was higher in individuals exposed to higher arsenic levels (5.7 +/- 5.1, 5.6 +/- 5.1, 7.3 +/- 7.4, and 9.1 +/- 6.5 [mean +/- standard deviation] chromosomal alterations per tumor with increasing arsenic exposure; P(trend) =.02, adjusted for stage and grade). The trend was stronger in high-grade (G2-G3) tumors (6.3 +/- 5.5, 8.3 +/- 4.7, 10.3 +/- 7.8, and 10.5 +/- 6.4 alterations per tumor; P(trend) =.01) than it was in low-grade (G1) tumors (3.5 +/- 3.1, 1.1 +/- 1.1, 2.5 +/- 2.5, and 3.6 +/- 3.2 alterations per tumor; P(trend) =.79). The mean number of chromosomal alterations also increased with tumor stage and grade (P(trend)\u003c.001) independently of arsenic exposure but was not associated with smoking history. Deletion of part or all of chromosome 17p (P(trend)\u003c.001) showed the strongest association with arsenic exposure.\n\nCONCLUSIONS:\nBladder tumors in patients with higher levels of arsenic exposure showed higher levels of chromosomal instability. Most of the chromosomal alterations associated with arsenic exposure were also associated with tumor stage and grade, raising the possibility that bladder tumors from arsenic-exposed patients may behave more aggressively than tumors from unexposed patients."
+ },
+ "questions": [
+  {
+   "id": "dae01f3c-0fcd-45e6-bcfb-fdf56e194cc9",
+   "text": "What are the risk factors of Bladder cancer?",
+   "answers": [
+    {
+     "answer_start": 1976,
+     "text": "patients with higher levels of arsenic exposure"
+    },
+    {
+     "answer_start": 2124,
+     "text": " arsenic exposure"
+    },
+    {
+     "answer_start": 1295,
+     "text": "increasing arsenic exposure"
+    }
+   ]
+  }
+ ]
+}

1274df29-3d1a-41e4-935f-639f4f8729e4.json

@@ -0,0 +1,58 @@
+{
+ "id": "1274df29-3d1a-41e4-935f-639f4f8729e4",
+ "disease": {
+  "id": "H00031",
+  "names": [
+   "Breast cancer"
+  ],
+  "dbLinks": {
+   "icd10": [
+    "C50"
+   ],
+   "mesh": [
+    "D001943"
+   ]
+  },
+  "category": "Cancer"
+ },
+ "article": {
+  "id": "23890780",
+  "text": "BACKGROUND:\nAssociations between circulating concentrations of oestrogens, progesterone, and androgens with breast cancer and related risk factors in premenopausal women are not well understood. We aimed to characterise these associations with a pooled analysis of data from seven studies.\n\nMETHODS:\nIndividual participant data for prediagnostic sex hormone and sex hormone-binding globulin (SHBG) concentrations were contributed from seven prospective studies. We restricted analyses to women who were premenopausal and younger than 50 years at blood collection, and to women with breast cancer diagnosed before age 50 years. We estimated odds ratios (ORs) with 95% CIs for breast cancer associated with hormone concentrations by conditional logistic regression in cases and controls matched for age, date of blood collection, and day of cycle, with stratification by study and further adjustment for cycle phase. We examined associations of hormones with risk factors for breast cancer in control women by comparing geometric mean hormone concentrations in categories of these risk factors, adjusted for study, age, phase of menstrual cycle, and body-mass index (BMI). All statistical tests were two-sided.\n\nFINDINGS:\nWe included data for up to 767 women with breast cancer and 1699 controls in the risk analyses. Breast cancer risk was associated with a doubling in concentrations of oestradiol (OR 1·19, 95% CI 1·06-1·35), calculated free oestradiol (1·17, 1·03-1·33), oestrone (1·27, 1·05-1·54), androstenedione (1·30, 1·10-1·55), dehydroepiandrosterone sulphate (1·17, 1·04-1·32), testosterone (1·18, 1·03-1·35), and calculated free testosterone (1·08, 0·97-1·21). Breast cancer risk was not associated with luteal phase progesterone (doubling in concentration OR 1·00, 95% CI 0·92-1·09), and adjustment for other factors had little effect on any of these ORs. Cross-sectional analyses in control women showed several associations of sex hormones with breast cancer risk factors.\n\nINTERPRETATION:\nCirculating oestrogens and androgens are positively associated with the risk for breast cancer in premenopausal women."
+ },
+ "questions": [
+  {
+   "id": "fe91b342-6c3b-4d09-8aa0-988495fa9c62",
+   "text": "What are the risk factors of Breast Cancer?",
+   "answers": [
+    {
+     "answer_start": 1357,
+     "text": "doubling in concentrations of oestradiol"
+    },
+    {
+     "answer_start": 1427,
+     "text": "calculated free oestradiol"
+    },
+    {
+     "answer_start": 1473,
+     "text": "oestrone"
+    },
+    {
+     "answer_start": 1500,
+     "text": " androstenedione"
+    },
+    {
+     "answer_start": 1536,
+     "text": "dehydroepiandrosterone sulphate"
+    },
+    {
+     "answer_start": 1587,
+     "text": "testosterone"
+    },
+    {
+     "answer_start": 2003,
+     "text": "Circulating oestrogens and androgens"
+    }
+   ]
+  }
+ ]
+}

129ebf8c-6e7f-4221-9fda-f63d23907055.json

@@ -0,0 +1,39 @@
+{
+ "id": "129ebf8c-6e7f-4221-9fda-f63d23907055",
+ "disease": {
+  "id": "H00079",
+  "names": [
+   "Asthma"
+  ],
+  "dbLinks": {
+   "icd10": [
+    "J45"
+   ],
+   "mesh": [
+    "D001249"
+   ]
+  },
+  "category": "Immune system disease",
+  "description": "Asthma is a complex syndrome with many clinical phenotypes in both adults and children. Its major characteristics include a variable degree of airflow obstruction, bronchial hyperresponsiveness, and airway inflammation. Inhaled allergens encounter antigen presenting cells (APC) that line the airway. Upon recognition of the antigen and activation by APC, naive T cells differentiate into TH2 cells. Activated TH2 stimulate the formation of IgE by B cells. IgE molecules bind to IgE receptors located on mast cells. The crosslinking of mast-cell-bound IgE by allergens leads to the release of biologically active mediators (histamine, leukotrienes) by means of degranulation and, so, to the immediate symptoms of allergy. Mast cells also release chemotactic factors that contribute to the recruitment of inflammatory cells, particularly eosinophils, whose proliferation and differentiation from bone marrow progenitors is promoted by IL-5. The activation of eosinophils leads to release of toxic granules and oxygen free radicals that lead to tissue damage and promote the development of chronic inflammation."
+ },
+ "article": {
+  "id": "1395752",
+  "text": "To determine the possibility that asymptomatic bronchial hyperresponsiveness (BHR) develops into symptomatic asthma, a two-year follow-up study was conducted in 81 students (48 male, 33 female; 11 to 17 years) who were found to have BHR in a 3,067 population survey (BHR group). Eighty-eight age-matched students (48 male, 40 female) with normal bronchial responsiveness served as control subjects. Daily symptom cards were recorded. Peak expiratory flow rate was measured for 24 h when symptoms occurred. Histamine inhalation tests were performed at the beginning of the study and at the end of the first and the second year. In the BHR group, 58 students remained bronchial hyperresponsive at the end of follow-up. Nine of 31 students with initially diagnosed bronchial asthma had their symptoms relieved entirely, but ten asymptomatic students developed asthma. The incidence of newly diagnosed asthma (12.5 percent in the BHR group or 20 percent in the asymptomatic BHR group) and the total percentage of diagnosed asthma (39.5 percent) in the BHR group were significantly higher than those (2.27 percent, 2.27 percent) in the control group. FVC and FEV1 showed no significant difference between two groups. PD20 FEV1 values in newly diagnosed asthmatics were significantly lower than those in asymptomatic students both at the beginning (3.05 +/- 1.56 mumol vs 6.14 +/- 1.60 mumol, p \u003c 0.05) or the end (3.47 +/- 1.73 mumol vs 6.55 +/- 1.51 mumol, p \u003c 0.05). The percentage of early respiratory illness was significantly higher in those with newly diagnosed asthma (80 percent) than in asymptomatic students (22.3 percent), but atopic index and the percentage of parental asthma showed no difference between two groups. In nine asthmatics whose symptoms were relieved entirely in the two-year follow-up, PD20 FEV1 was undetectable within the cumulative dose of 7.8 mumol of histamine in three students and rose from 4.58 +/- 1.85 mumol to 7.62 +/- 1.02 mumol in the remaining six. The higher the BHR, the more likely the students developed asthma. About 45 percent of asymptomatic students with PD20 \u003c or = 3.2 mumol developed asthma in the following two years and 80 percent of them had a history of early respiratory illness, suggesting that they may have subclinical or potential asthma."
+ },
+ "questions": [
+  {
+   "id": "52873524-3416-4030-a8eb-d5c1f15295b2",
+   "text": "What are the risk factors of Asthma?",
+   "answers": [
+    {
+     "answer_start": 1048,
+     "text": "BHR"
+    },
+    {
+     "answer_start": 2001,
+     "text": "BHR"
+    }
+   ]
+  }
+ ]
+}

12c9a0bd-1547-4262-b430-d5e302bf107b.json

@@ -0,0 +1,40 @@
+{
+ "id": "12c9a0bd-1547-4262-b430-d5e302bf107b",
+ "disease": {
+  "id": "H01714",
+  "names": [
+   "Chronic obstructive pulmonary disease (COPD)",
+   "Emphysema"
+  ],
+  "dbLinks": {
+   "icd10": [
+    "J43",
+    "J44"
+   ],
+   "mesh": [
+    "D029424"
+   ]
+  },
+  "category": "Lung disease"
+ },
+ "article": {
+  "id": "15249443",
+  "text": "BACKGROUND:\nFor several years, asthma and COPD have been regarded as distinct entities, with distinct clinical courses. However, despite distinctive physiologic features at the time of diagnosis, and different risk factors, the two diseases over time may develop features that are quite similar.\n\nSTUDY OBJECTIVE:\nTo evaluate the association between physician-diagnosed asthma and the subsequent development of COPD in a cohort of 3,099 adult subjects from Tucson, AZ.\n\nDESIGN AND METHODS:\nA prospective observational study. Participants completed up to 12 standard respiratory questionnaires and 11 spirometry lung function measurements over a period of 20 years. Survival curves (with time to development of COPD as the dependent variable) were compared between subjects with asthma and subjects without asthma at the initial survey.\n\nRESULTS:\nSubjects with active asthma (n = 192) had significantly higher hazard ratios than inactive (n = 156) or nonasthmatic subjects (n = 2751) for acquiring COPD. As compared with nonasthmatics, active asthmatics had a 10-times-higher risk for acquiring symptoms of chronic bronchitis (95% confidence interval [CI], 4.94 to 20.25), 17-times-higher risk of receiving a diagnosis of emphysema (95% CI, 8.31 to 34.83), and 12.5-times-higher risk of fulfilling COPD criteria (95% CI, 6.84 to 22.84), even after adjusting for smoking history and other potential confounders.\n\nCONCLUSIONS:\nPhysician-diagnosed asthma is significantly associated with an increased risk for CB, emphysema, and COPD."
+ },
+ "questions": [
+  {
+   "id": "469ac7de-a52e-499a-aada-cfd077000d62",
+   "text": "What are the risk factors for Chronic obstructive pulmonary disease (COPD)?",
+   "answers": [
+    {
+     "answer_start": 1424,
+     "text": "Physician-diagnosed asthma"
+    },
+    {
+     "answer_start": 1035,
+     "text": "active asthmatics"
+    }
+   ]
+  }
+ ]
+}

13765be1-2ba0-40a7-8584-1aedde831e27.json

@@ -0,0 +1,45 @@
+{
+ "id": "13765be1-2ba0-40a7-8584-1aedde831e27",
+ "disease": {
+  "id": "M2023_04_26_16_38_52",
+  "names": [
+   "Migraine"
+  ],
+  "dbLinks": {
+   "icd10": [
+    "G43"
+   ],
+   "icd11": [
+    "8A80"
+   ],
+   "mesh": [
+    "C10.228.140.546.399.750"
+   ]
+  },
+  "description": "Migraine is a chronic neurological disorder characterized by recurrent episodes of unilateral, pulsatile headaches associated with autonomic symptoms such as nausea, vomiting, photophobia, and phonophobia. The pathophysiology of migraine is multifactorial and involves complex interactions between genetic, environmental, and neurochemical factors that modulate cerebral vascular tone and nociception. Migraine attacks can be triggered by a variety of factors, including stress, hormonal changes, sleep disturbances, and certain foods or medications. Treatment options for migraine include pharmacotherapy for acute attacks, preventive medications for frequent or severe headaches, and lifestyle modifications to avoid triggers. In refractory cases, interventional therapies such as nerve blocks or neuromodulation techniques may be considered."
+ },
+ "article": {
+  "id": "23808359",
+  "text": "BACKGROUND:\nDisturbances in sleep are common among migraineurs, particularly those with frequent (ie, chronic) migraine. Examination of specific types of sleep disturbance and behaviors among episodic migraineurs, however, has not been sufficiently explored. Further, few studies have investigated whether sleep disturbance is attributable to comorbid affective symptomatology.\n\nOBJECTIVES:\nThe present case-control study sought to (1) assess sleep quality, daytime sleepiness, and sleep hygiene among a large sample of episodic migraineurs; (2) quantify relations between sleep disturbance and headache-related variables; and (3) determine if these relations remain after accounting for comorbid depression and anxiety.\n\nMETHODS:\nTwo hundred ninety-two undergraduate students (69.9% female, mean age = 19.19, standard deviation [SD] = 3.21 years) completed measures of sleep quality, daytime sleepiness, and sleep hygiene along with well-validated measures of depression and anxiety symptomatology. Those screening positive for migraine were subsequently administered a structured diagnostic interview to verify diagnosis of migraine consistent with the International Classification of Headache Disorders, 2nd edition. Episodic migraineurs and non-migraine controls were compared on the sleep disturbance variables, and among those with migraine, relations with headache frequency, severity, and disability were quantified with linear regression analyses.\n\nRESULTS:\nSeventy-eight (26.7%) participants met International Classification of Headache Disorders, 2nd edition criteria for episodic migraine. Compared with participants without migraine, episodic migraineurs reported poorer sleep quality (mean = 8.90 [SD = 3.39] vs 6.63 [SD = 3.02], P \u003c .0001), with 85.9% reporting clinically significant poor sleep quality (vs 62.0% of controls). Poor sleep quality was significantly associated with headache frequency and headache-related disability, accounting for proportions of variance (14.8% in frequency and 18.2% in disability, both P ≤ .001) similar to those attributable to depression and anxiety. These relationships remained significant after controlling for these affective symptoms, in which sleep quality accounted for 5.3% and 5.8% of unique variance in frequency and disability, respectively (P \u003c .05). By comparison, daytime sleepiness and poor sleep hygiene were not consistently associated with migraine or migraine-related variables.\n\nCONCLUSIONS:\nConsistent with prior studies on chronic migraine, poor sleep quality is uniquely associated with episodic migraine, and this relationship is not solely attributable to comorbid psychiatric symptomatology. Sleep quality should be preferentially assessed (vs sleepiness and sleep hygiene) when subjective self-report measures of insomnia are used in clinical headache settings. Future studies should supplement these findings by evaluating the efficacy of interventions that specifically target sleep quality and insomnia (eg, stimulus control, sleep restriction) among episodic migraineurs."
+ },
+ "questions": [
+  {
+   "id": "b52c9f8a-975f-40b8-aebf-c62ec7dd31dc",
+   "text": "what are the risk factors of Migraine?",
+   "answers": [
+    {
+     "answer_start": 2516,
+     "text": "poor sleep quality"
+    },
+    {
+     "answer_start": 1677,
+     "text": "poorer sleep quality"
+    },
+    {
+     "answer_start": 1843,
+     "text": "Poor sleep quality"
+    }
+   ]
+  }
+ ]
+}

13e5edba-789c-42bf-8102-814d2f6939fb.json

@@ -0,0 +1,35 @@
+{
+ "id": "13e5edba-789c-42bf-8102-814d2f6939fb",
+ "disease": {
+  "id": "H00056",
+  "names": [
+   "Alzheimer disease",
+   "Dementia due to Alzheimer disease"
+  ],
+  "dbLinks": {
+   "icd10": [
+    "G30"
+   ],
+   "mesh": [
+    "D000544"
+   ]
+  },
+  "category": "Neurodegenerative disease"
+ },
+ "article": {
+  "id": "18349428",
+  "text": "Air pollution is a serious environmental problem. We investigated whether residency in cities with high air pollution is associated with neuroinflammation/neurodegeneration in healthy children and young adults who died suddenly. We measured mRNA cyclooxygenase-2, interleukin-1beta, and CD14 in target brain regions from low (n = 12) or highly exposed residents (n = 35) aged 25.1 +/- 1.5 years. Upregulation of cyclooxygenase-2, interleukin-1beta, and CD14 in olfactory bulb, frontal cortex, substantia nigrae and vagus nerves; disruption of the blood-brain barrier; endothelial activation, oxidative stress, and inflammatory cell trafficking were seen in highly exposed subjects. Amyloid beta42 (Abeta42) immunoreactivity was observed in 58.8% of apolipoprotein E (APOE) 3/3 \u003c 25 y, and 100% of the APOE 4 subjects, whereas alpha-synuclein was seen in 23.5% of \u003c 25 y subjects. Particulate material (PM) was seen in olfactory bulb neurons, and PM \u003c 100 nm were observed in intraluminal erythrocytes from lung, frontal, and trigeminal ganglia capillaries. Exposure to air pollution causes neuroinflammation, an altered brain innate immune response, and accumulation of Abeta42 and alpha-synuclein starting in childhood. Exposure to air pollution should be considered a risk factor for Alzheimer's and Parkinson's diseases, and carriers of the APOE 4 allele could have a higher risk of developing Alzheimer's disease if they reside in a polluted environment."
+ },
+ "questions": [
+  {
+   "id": "bf624ae5-cb88-4e19-81eb-a4b8bb52b7ba",
+   "text": "What are the risk factors of Alzheimer disease?",
+   "answers": [
+    {
+     "answer_start": 1221,
+     "text": "Exposure to air pollution"
+    }
+   ]
+  }
+ ]
+}

141a7b68-ec2a-467f-96c8-202d39e4f148.json

@@ -0,0 +1,35 @@
+{
+ "id": "141a7b68-ec2a-467f-96c8-202d39e4f148",
+ "disease": {
+  "id": "H00056",
+  "names": [
+   "Alzheimer disease",
+   "Dementia due to Alzheimer disease"
+  ],
+  "dbLinks": {
+   "icd10": [
+    "G30"
+   ],
+   "mesh": [
+    "D000544"
+   ]
+  },
+  "category": "Neurodegenerative disease"
+ },
+ "article": {
+  "id": "28017827",
+  "text": "INTRODUCTION:\nThe presence of cerebrovascular pathology may increase the risk of clinical diagnosis of Alzheimer's disease (AD).\n\nMETHODS:\nWe examined excess risk of incident clinical diagnosis of AD (probable and possible AD) posed by the presence of lacunes and large infarcts beyond AD pathology using data from the Statistical Modeling of Aging and Risk of Transition study, a consortium of longitudinal cohort studies with more than 2000 autopsies. We created six mutually exclusive pathology patterns combining three levels of AD pathology (low, moderate, or high AD pathology) and two levels of vascular pathology (without lacunes and large infarcts or with lacunes and/or large infarcts).\n\nRESULTS:\nThe coexistence of lacunes and large infarcts results in higher likelihood of clinical diagnosis of AD only when AD pathology burden is low.\n\nDISCUSSION:\nOur results reinforce the diagnostic importance of AD pathology in clinical AD. Further harmonization of assessment approaches for vascular pathologies is required."
+ },
+ "questions": [
+  {
+   "id": "5e03abd2-096d-4a24-a4ff-008962a4357e",
+   "text": "What are the risk factors of Alzheimer disease?",
+   "answers": [
+    {
+     "answer_start": 711,
+     "text": "coexistence of lacunes and large infarcts"
+    }
+   ]
+  }
+ ]
+}

143e2668-926b-4793-9957-8bd6a408ecdc.json

@@ -0,0 +1,34 @@
+{
+ "id": "143e2668-926b-4793-9957-8bd6a408ecdc",
+ "disease": {
+  "id": "H00022",
+  "names": [
+   "Bladder cancer"
+  ],
+  "dbLinks": {
+   "icd10": [
+    "C67"
+   ],
+   "mesh": [
+    "D001749"
+   ]
+  },
+  "category": "Cancer"
+ },
+ "article": {
+  "id": "9833970",
+  "text": "Blackfoot disease is an endemic peripheral vascular disease found among people in a limited area on the southwest coast of Taiwan, where artesian well water has a high concentration of arsenic and was used since the turn of this century. This is an important public health problem and was noted by the authorities, who began improving the water supply in such communities in 1956. This enabled us to test the relationship between arsenic and malignant tumors using a specific exposed community. Study subjects were divided into four groups according to age (under or over 40 yr) and gender. Two methods were used for the estimation of the age-adjusted mortality rate ratios. First using the first time interval (1971-1973) as the standard, the mortality rate ratio for all malignant tumors was estimated from this interval through to the last interval (1992-1994) using Poisson regression. Cancers that were found to be related to arsenic in previous reports, such as liver, lung, bladder, kidney, and skin cancers, were examined and other malignant tumors except these cancers were also assessed. The same calculations were performed for all of Chiayi and Tainan counties, excluding the study areas, which were used as the local reference, and for the general population of Taiwan, which was used as a national reference group. Second, mortality rate ratios for the study area were compared to the local and national reference for the same time intervals for each disease category. From our results, significantly declining trends for mortality rate ratios of all malignant tumors with 1971-1973 as the standard were found for the study areas, especially in females. A decrease of mortality rate ratios from malignant cancers, compared to the local or national references, was found in those aged over 40 yr for both sexes. The decreases are mainly due to a fall in internal and skin cancer mortality rates. In conclusion, our results suggest that the improvement of drinking water supply to eliminate arsenic exposure from artesian well water decreased the mortality incidence of arsenic-related cancers in blackfoot disease endemic communities."
+ },
+ "questions": [
+  {
+   "id": "60886618-d012-4ab7-81f9-d37aa4605648",
+   "text": "What are the risk factors of Bladder cancer?",
+   "answers": [
+    {
+     "answer_start": 163,
+     "text": "high concentration of arsenic"
+    }
+   ]
+  }
+ ]
+}