new cls

10709885.json

@@ -0,0 +1,8 @@
+{
+ "id": "10709885",
+ "label": 1,
+ "article": {
+  "id": "10709885",
+  "text": "Coeliac disease has emerged as a public health problem. The aim of the present study was to analyse trends in the occurrence of symptomatic coeliac disease in Swedish children from 1973 to 1997, and to explore any temporal relationship to changes in infant dietary patterns. We established a population-based prospective incidence register of coeliac disease in 1991, and, in addition, retrospective data from 1973 were collected. A total of 2151 cases fulfilled the diagnostic criteria. Furthermore. We collected national data on a yearly basis on duration of breastfeeding, intake of gluten-containing cereals and recommendations on when and how to introduce gluten into the diet of infants. From 1985 to 1987 the annual incidence rate in children below 2 y of age increased fourfold to 200-240 cases per 100000 person years, followed from 1995 by a sharp decline to the previous level of 50-60 cases per 100000 person years. This epidemic pattern is quite unique for a chronic disease of immunological pathogenesis, suggesting that prevention could be possible. The ecological observations made in this study are compatible with the epidemic being the result, at least in part, of a change in and an interplay among three factors within the area of infant feeding, i.e. amount of gluten given, age at introduction of gluten, and whether breastfeeding was ongoing or not when gluten was introduced. Other factor(s) may also have contributed, and the search for these should be intensified."
+ }
+}

11080708.json

@@ -0,0 +1,8 @@
+{
+ "id": "11080708",
+ "label": 1,
+ "article": {
+  "id": "11080708",
+  "text": "BACKGROUND:\nEvents occurring during fetal life may affect the development of the immune and respiratory systems and increase the risk of asthma and allergic diseases.\n\nOBJECTIVES:\nWe sought to elaborate the relations between the occurrence of pregnancy complications and other pregnancy-related conditions and the risk of bronchial obstruction during the first 2 years of life and the occurrence of asthma and allergic rhinitis by the age of 4 years. Pregnancy complications were considered both as predictors of the health outcomes and as possible effects caused by other prenatal factors.\n\nMETHODS:\nA population-based, 4-year, cohort study was carried out involving 2531 children born in Oslo, Norway. We collected information on maternally related (hyperemesis, hypertension, and preeclampsia) and uterus-related complications in pregnancy (antepartum hemorrhage, preterm contractions, insufficient placenta, and restricted growth of the uterus) and the child's health and environmental exposures at birth and at 6, 12, 18, and 24 months and 4 years of age. The outcomes of interest were bronchial obstruction during the first 2 years and asthma and allergic rhinitis at the age of 4 years.\n\nRESULTS:\nIn a logistic regression analysis adjusting for potential confounders, uterus-related, but not other pregnancy-related, complications increased the risk of bronchial obstruction (odds ratio [OR], 2.1; 95% confidence interval [CI], 1.3-3.4), asthma (OR, 3.0; 95% CI, 1.8-5.4), and allergic rhinitis (OR, 2.9; 95% CI, 1.6-5.2). These relations were similar in children of atopic and nonatopic parents.\n\nCONCLUSIONS:\nUterus-related complications in pregnancy increase the risk of having asthma and allergic rhinitis in childhood."
+ }
+}

11312420.json

@@ -0,0 +1,8 @@
+{
+ "id": "11312420",
+ "label": 1,
+ "article": {
+  "id": "11312420",
+  "text": "BACKGROUND:\nOral methoxsalen (psoralen) and ultraviolet A radiation (PUVA) is a highly effective therapy for psoriasis and many other skin conditions. It is carcinogenic. Previously we reported an increased risk of melanoma that first emerged 15 years after first treatment.\n\nOBJECTIVE:\nOur purpose is to present additional data concerning the associations of previous exposure to PUVA, the passage of time, and the risk of malignant melanoma.\n\nMETHODS:\nWe have prospectively studied a cohort of 1380 patients first treated with PUVA in 1975 and 1976. We have documented the occurrence of melanoma and in this report compare the observed and expected incidence of melanoma in this cohort, particularly melanomas developing since our earlier report (ie, after March 1996).\n\nRESULTS:\nSince 1975, 23 patients have developed 26 invasive or in situ cutaneous melanomas. In an average of 2.25 years since our last report, we detected 7 additional invasive melanomas (incidence rate ratio, 8.4; 95% confidence interval, 3.4-17.3).\n\nCONCLUSION:\nBeginning 15 years after first exposure to PUVA, an increased risk of melanoma is observed in our cohort of PUVA-treated patients. This risk is greater in patients exposed to high doses of PUVA, appears to be increasing with the passage of time, and should be considered in determining the risks and benefits of this therapy."
+ }
+}

11522737.json

@@ -0,0 +1,8 @@
+{
+ "id": "11522737",
+ "label": 1,
+ "article": {
+  "id": "11522737",
+  "text": "BACKGROUND \u0026 AIMS:\nResults concerning an association between cholecystectomy and right-sided colon cancer are inconsistent. Little is known about the relation between cholecystectomy and small bowel cancer. Therefore, we evaluated cholecystectomy and risk of bowel cancer.\n\nMETHODS:\nCholecystectomized patients, identified through the Swedish Inpatient Register, from 1965 through 1997, were followed up for subsequent cancer. The standardized incidence ratio (SIR) estimated relative risk.\n\nRESULTS:\nIn total, 278,460 cholecystectomized patients, contributing 3,519,682 person-years, were followed up for a maximum of 33 years after surgery. Cholecystectomized patients had an increased risk of proximal intestinal adenocarcinoma, which gradually declined with increasing distance from the common bile duct. The risk was significantly increased for adenocarcinoma (SIR, 1.77; 95% confidence interval [CI], 1.37-2.24) and carcinoids of the small bowel (SIR, 1.71; 95% CI, 1.39-2.08), and right-sided colon cancer (SIR, 1.16; 95% CI, 1.08-1.24). No association was found with more distal bowel cancer. The gradient was further pronounced when surgery of the common bile duct was included. The associations remained increased up to 33 years after cholecystectomy. No differences between sexes were found.\n\nCONCLUSIONS:\nCholecystectomy increases the risk of intestinal cancer, a risk that declines with increasing distance from the common bile duct. Changes in the intestinal exposure to bile might be the underlying biological mechanism."
+ }
+}

11976167.json

@@ -0,0 +1,8 @@
+{
+ "id": "11976167",
+ "label": 1,
+ "article": {
+  "id": "11976167",
+  "text": "BACKGROUND:\nCeliac disease, or permanent gluten-sensitive enteropathy, is an immunologic disease strictly dependent on exposure to wheat gluten or related proteins in rye and barley.\n\nOBJECTIVE:\nThe aim of this study was to explore whether breast-feeding and the mode of introducing dietary gluten influence the risk of celiac disease in childhood.\n\nDESIGN:\nA population-based incident case-referent study of Swedish children, 627 cases with celiac disease and 1254 referents, was conducted; 78% of the matched sets were included in the final analyses. A questionnaire was used to assess patterns of food introduction to infants. Models were built, based on current epidemiologic and immunologic knowledge of celiac disease, to study the potential influence of dietary patterns on disease risk and were evaluated by conditional logistic regression in multivariate analyses.\n\nRESULTS:\nThe risk of celiac disease was reduced in children aged \u003c2 y if they were still being breast-fed when dietary gluten was introduced [adjusted odds ratio (OR): 0.59; 95% CI: 0.42, 0.83]. This effect was even more pronounced in infants who continued to be breast-fed after dietary gluten was introduced (OR: 0.36; 95% CI: 0.26, 0.51). The risk was greater when gluten was introduced in the diet in large amounts (OR: 1.5; 95% CI: 1.1, 2.1) than when introduced in small or medium amounts. In older children, these risk factors were of no or only minor importance.\n\nCONCLUSIONS:\nThe gradual introduction of gluten-containing foods into the diet of infants while they are still being breast-fed reduces the risk of celiac disease in early childhood and probably also during the subsequent childhood period."
+ }
+}

12093765.json

@@ -0,0 +1,8 @@
+{
+ "id": "12093765",
+ "label": 1,
+ "article": {
+  "id": "12093765",
+  "text": "BACKGROUND:\nInterleukin (IL)-18 plays a central role in orchestrating the cytokine cascade and accelerates atherosclerosis and plaque vulnerability in animal models. However, epidemiological data evaluating the role of IL-18 levels in atherosclerosis are lacking.\n\nMETHODS AND RESULTS:\nIn a prospective study of 1229 patients with documented coronary artery disease, we measured baseline serum concentrations of IL-18 and other markers of inflammation. During the follow-up period (median, 3.9 years), 95 patients died of cardiovascular causes. Median serum concentrations of IL-18 were significantly higher among patients who had a fatal cardiovascular event than among those who did not (68.4 versus 58.7 pg/mL; P\u003c0.0001). The hazard risk ratio of future cardiovascular death increased with increasing quartiles of IL-18 (hazard risk ratio, 1.46; 95% CI 1.21 to 1.76; P for trend \u003c0.0001). After adjustment for most potential confounders, including the strong predictor ejection fraction as well as the inflammatory variables IL-6, high-sensitive C-reactive protein, and fibrinogen, this relation remained almost unchanged, such that patients within the highest quartile of IL-18 had a 3.3-fold increase in hazard risk compared with those in the first quartile (95% CI, 1.3 to 8.4, P=0.01). This relation was observed in patients with stable angina and patients with unstable angina at baseline.\n\nCONCLUSIONS:\nSerum IL-18 level was identified as a strong independent predictor of death from cardiovascular causes in patients with coronary artery disease regardless of the clinical status at admission. This result strongly supports recent experimental evidence of IL-18-mediated inflammation leading to acceleration and vulnerability of atherosclerotic plaques."
+ }
+}

14519706.json

@@ -0,0 +1,8 @@
+{
+ "id": "14519706",
+ "label": 1,
+ "article": {
+  "id": "14519706",
+  "text": "CONTEXT:\nDietary factors modifying type 1 diabetes mellitus (DM) risk have been proposed, but little is known if they trigger the islet autoimmunity that precedes clinical disease.\n\nOBJECTIVE:\nTo determine whether breastfeeding duration, food supplementation, or age at introduction of gluten-containing foods influences the risk of developing islet autoantibodies.\n\nDESIGN AND SETTING:\nProspective natural history cohort study conducted from 1989 to 2003 in inpatient/outpatient clinics in Germany.\n\nPARTICIPANTS:\nThe BABYDIAB study follows newborn children of parents with type 1 DM. Eligibility requirements were met in 1610 children. Blood samples were obtained at birth, age 9 months, 2, 5, and 8 years. Dropout rate was 14.4% by age 5 years. Breastfeeding data were obtained by prospective questionnaires (91% complete), and food supplementation data were obtained by family interview (72% for food supplementation and 80% for age of gluten introduction).\n\nMAIN OUTCOME MEASURE:\nDevelopment of islet autoantibodies (insulin, glutamic acid decarboxylase, or IA-2 antibodies) in 2 consecutive blood samples.\n\nRESULTS:\nLife-table islet autoantibody frequency was 5.8% (SE, 0.6%) by age 5 years. Reduced total or exclusive breastfeeding duration did not significantly increase the risk of developing islet autoantibodies. Food supplementation with gluten-containing foods before age 3 months, however, was associated with significantly increased islet autoantibody risk (adjusted hazard ratio, 4.0; 95% confidence interval, 1.4-11.5; P =.01 vs children who received only breast milk until age 3 months). Four of 17 children who received gluten foods before age 3 months developed islet autoantibodies (life-table 5-year risk, 24%; SE, 10%). All 4 children had the high-risk DRB1*03/04,DQB1*0302 genotype. Early exposure to gluten did not significantly increase the risk of developing celiac disease-associated autoantibodies. Children who first received gluten foods after age 6 months did not have increased risks for islet or celiac disease autoantibodies.\n\nCONCLUSION:\nEnsuring compliance to infant feeding guidelines is a possible way to reduce the risk of development of type 1 DM autoantibodies."
+ }
+}

15898094.json

@@ -0,0 +1,8 @@
+{
+ "id": "15898094",
+ "label": 1,
+ "article": {
+  "id": "15898094",
+  "text": "BACKGROUND:\nExposure to occupational hazards among firefighters may lead to increased mortality from cancer, lung, or heart disease.\n\nMETHODS:\nAge- and gender-adjusted mortality rates of 34,796 male and 2,017 female Florida professional firefighters between 1972 and 1999 were compared with the Florida general population.\n\nRESULTS:\nOne thousand four hundred eleven male and 38 female firefighter deaths with known causes were identified. In male firefighters, mortality due to all causes and most non-malignant diseases was significantly less than expected. There was no excess overall mortality from cancer, but excesses existed for male breast cancer [standardized mortality ratio (SMR = 7.41; 95% confidence interval (CI): 1.99-18.96) and thyroid cancer (SMR = 4.82; 95% CI: 1.30-12.34)]. Mortality from bladder cancer was increased and approached statistical significance (SMR = 1.79; 95% CI: 0.98-3.00). Firefighters certified between 1972 and 1976 had excess mortality from bladder cancer (SMR = 1.95; 95% CI: 1.04-3.33). Female firefighters had similar morality patterns to Florida women except for atherosclerotic heart disease (SMR = 3.85; 95% CI: 1.66-7.58).\n\nCONCLUSIONS:\nExcess mortality risk from bladder cancer may be related to occupational exposure during firefighting. The thyroid cancer and breast cancer risk in males, as well as the excess risk of cardiovascular disease mortality noted in females warrant further investigation."
+ }
+}

16364180.json

@@ -0,0 +1,8 @@
+{
+ "id": "16364180",
+ "label": 0,
+ "article": {
+  "id": "16364180",
+  "text": "Recent consensus statements demonstrate the breadth of the chronic rhinosinusitis (CRS) differential diagnosis. However, the classification and mechanisms of different CRS phenotypes remains problematic."
+ }
+}

16434451.json

@@ -0,0 +1,8 @@
+{
+ "id": "16434451",
+ "label": 1,
+ "article": {
+  "id": "16434451",
+  "text": "CONTEXT:\nPolycystic ovary syndrome (PCOS) is associated with menstrual and reproductive abnormalities, insulin resistance, and obesity.\n\nOBJECTIVE:\nThe objective of this study was to determine the prevalence of diagnosed PCOS and its association with cardiovascular risk factors.\n\nSETTING:\nThe study is set in an integrated health care delivery system in northern California.\n\nPATIENTS:\nA total of 11,035 women with PCOS were identified by one or more outpatient diagnoses of PCOS using health plan databases. An age-matched sample of women without PCOS was also selected.\n\nOUTCOME MEASURES:\nPrevalence of PCOS and targeted cardiovascular risk factors [hypertension, dyslipidemia, diabetes mellitus, and body mass index (BMI)] were measured.\n\nRESULTS:\nDuring 2002-2004, the prevalence of diagnosed PCOS among female members aged 25-34 yr was 2.6% (95% confidence interval 1.6-1.7%). Women with diagnosed PCOS were more likely than those without PCOS to be obese [BMI \u003e or = 30 mg/m(2); odds ratio (OR) 4.21, 3.96-4.47]. Furthermore, PCOS was associated with diabetes (OR 2.45, confidence interval 2.16-2.79), hypertension (OR 1.41, 1.31-1.51) and known dyslipidemia (OR 1.53, 1.39-1.68), even after adjusting for BMI and known confounders. Among women with PCOS, compared with whites, Blacks and Hispanics were more likely and Asians less likely to be obese; Asians and Hispanics were more likely to have diabetes; and Blacks were more likely and Hispanics less likely to have hypertension.\n\nCONCLUSIONS:\nWithin a large, community-based population receiving health care, diagnosed PCOS was highly prevalent and associated with a much higher frequency of cardiovascular risk factors that varied by race/ethnicity. Our prevalence estimates likely underestimate the true prevalence of PCOS. Further studies are needed to explore racial/ethnic differences and the extent to which PCOS contributes to future cardiovascular risk."
+ }
+}

16495934.json

@@ -0,0 +1,8 @@
+{
+ "id": "16495934",
+ "label": 1,
+ "article": {
+  "id": "16495934",
+  "text": "We directly compared risk factors between 214 histologically confirmed melanomas (CMM), 215 basal-cell carcinomas (BCC) and 139 squamous-cell carcinomas (SCC) in a multiple case-case-control study with 349 controls from patients without dermatological disease admitted to the same hospitals. Subjects with fair hair had a significant risk increase for all types of tumours at a comparable level (OR(adj) for blonde hair: CMM 2.3; SCC 2.4; BCC 2.3). The effect of pale eyes was significant and similar for CMM and BCC (OR(adj) 2.6). Intermittent sun exposure measured in hours spent at beach during holidays was significant for both CMM (OR(adj) 2.6 for more than 7000 lifelong hours) and BCC (OR(adj) 2.1 for more than 7000 lifelong hours), while SCC exhibited a significant risk increase for chronic exposure to sunlight measured in hours of outdoor work (OR(adj) 2.2 for more than 6000 lifelong hours). In the case-case comparison using a multinomial logistic regression model, we found a statistically significant risk difference for pale eyes, and number of naevi in the CMM group, compared to other skin cancers. For intermittent sun exposure, there was a significant risk difference of BCC when compared to the risk of SCC. Factors influencing risk of SCC are different, with chronic exposure to sun playing a major role in causing this type of carcinoma."
+ }
+}

16845665.json

@@ -0,0 +1,8 @@
+{
+ "id": "16845665",
+ "label": 1,
+ "article": {
+  "id": "16845665",
+  "text": "BACKGROUND:\nThe familial risk of bladder cancer (BC) is not well understood and, to date, little attention has been paid to the joint effect of smoking and family history in modifying the risk of BC. The authors investigated the role of family history in association with the risk of BC.\n\nMETHODS:\nCase and control probands were identified as part of an on-going BC case-control study. The relative risk associated with a family history of BC was estimated.\n\nRESULTS:\nIn total, 713 cases and 658 controls were included. In a case-control analysis, compared with individuals who never smoked and who had no family history of BC, probands who had smoked and who also had a positive family history were at 5.31-fold increased risk of BC (P for interaction = .04). The 713 case probands and the 658 controls reported 5160 and 4816 first-degree relatives, respectively. Compared with never-smoking relatives who had probands diagnosed with BC at an older age (age \u003e65 years), ever-smoking relatives who had probands diagnosed at a younger age (ages 40-65 years) showed a 6.89-fold (95% confidence interval, from 2.25-fold to 21.12-fold) increased risk. Similar results were obtained for the joint effects of family history of BC and smoking. CONCLUSIONS. The current results indicated that a positive family history of BC may have interacted with smoking habits to increase the risk of BC in the study population."
+ }
+}

16864817.json

@@ -0,0 +1,8 @@
+{
+ "id": "16864817",
+ "label": 1,
+ "article": {
+  "id": "16864817",
+  "text": "OBJECTIVE:\nTo assess the influence of the body mass index (BMI) on the prevalence and severity of chronic daily headache (CDH) and its most frequent subtypes, transformed migraine (TM) and chronic tension-type headache (CTTH).\n\nMETHODS:\nThe authors gathered information on headache, medical features, height, and weight using a computer-assisted telephone interview. Participants were divided into five categories, based on BMI: underweight (\u003c18.5), normal weight (18.5 to 24.9), overweight (25 to 29.9), obese (30 to 34.9), and morbidly obese (\u003e35). The prevalence and severity of CDH, TM, and CTTH were assessed. Multivariate analyses modeling these diagnoses as a function of BMI were conducted.\n\nRESULTS:\nAmong 30,215 participants, the prevalence of CDH was 4.1%; 1.3% had TM and 2.8% CTTH. In contrast with the normal weight group (3.9%), the prevalence of CDH was higher in obese (5.0% [odds ratio (OR) = 1.3, 95% CI = 1.1-1.6]) and morbidly obese (6.8% [OR = 1.8, 95% CI = 1.4 to 2.2]). BMI had a strong influence on the prevalence of TM, which ranged from 0.9% of the normal weighted to 1.2% of the overweight (OR = 1.4 [1.1 to 1.8]), 1.6% of the obese (OR = 1.7 [1.2 to 2.43]), and 2.5% of the morbidly obese (OR = 2.2 [1.5 to 3.2]). The effects of the BMI on the prevalence of CTTH were just significant in the morbidly obese group. Adjusted analyses showed that obesity was associated with CDH and TM but not CTTH.\n\nCONCLUSIONS:\nChronic daily headache and obesity are associated. Obesity is a stronger risk factor for transformed migraine than for chronic tension-type headache."
+ }
+}

17040332.json

@@ -0,0 +1,8 @@
+{
+ "id": "17040332",
+ "label": 1,
+ "article": {
+  "id": "17040332",
+  "text": "Review of epidemiological and clinical studies suggests that sleep disorders are disproportionately observed in specific headache diagnoses (eg, migraine, tension-type, cluster) and other nonspecific headache patterns (ie, chronic daily headache, \"awakening\" or morning headache). Interestingly, the sleep disorders associated with headache are of varied types, including obstructive sleep apnea (OSA), periodic limb movement disorder, circadian rhythm disorder, insomnia, and hypersomnia. Headache, particularly morning headache and chronic headache, may be consequent to, or aggravated by, a sleep disorder, and management of the sleep disorder may improve or resolve the headache. Sleep-disordered breathing is the best example of this relationship. Insomnia is the sleep disorder most often cited by clinical headache populations. Depression and anxiety are comorbid with both headache and sleep disorders (especially insomnia) and consideration of the full headache-sleep-affective symptom constellation may yield opportunities to maximize treatment. This paper reviews the comorbidity of headache and sleep disorders (including coexisting psychiatric symptoms where available). Clinical implications for headache evaluation are presented. Sleep screening strategies conducive to headache practice are described. Consideration of the spectrum of sleep-disordered breathing is encouraged in the headache population, including awareness of potential upper airway resistance syndrome in headache patients lacking traditional risk factors for OSA. Pharmacologic and behavioral sleep regulation strategies are offered that are also compatible with treatment of primary headache."
+ }
+}

17164760.json

@@ -0,0 +1,8 @@
+{
+ "id": "17164760",
+ "label": 1,
+ "article": {
+  "id": "17164760",
+  "text": "In a prospective cohort study, a close to two-fold elevated risk of bladder cancer was found among men reporting a history of gonorrhoea (relative risk=1.92, 95% CI=1.10-3.33). Our finding warrants further examination of the role of gonorrhoea in bladder carcinogenesis."
+ }
+}

17311987.json

@@ -0,0 +1,8 @@
+{
+ "id": "17311987",
+ "label": 0,
+ "article": {
+  "id": "17311987",
+  "text": "Perforin is a cytolytic protein expressed mainly in activated cytotoxic lymphocytes and natural killer cells. Inherited perforin mutations account for 20% to 40% of familial hemophagocytic lymphohistiocytosis, a fatal disease of early childhood characterized by the absence of functional perforin. Aplastic anemia, the paradigm of immune-mediated bone marrow failure syndromes, is characterized by hematopoietic stem cell destruction by activated T cells and Th1 cytokines. We examined whether mutations in the perforin gene occurred in acquired aplastic anemia. Three nonsynonymous PRF1 mutations among 5 unrelated patients were observed. Four of 5 patients with the mutations showed some hemophagocytosis in the bone marrow at diagnosis. Perforin protein levels in these patients were very low or absent, and perforin granules were completely absent. Natural killer (NK) cell cytotoxicity from these patients was significantly decreased. Our data suggest that PRF1 genetic alterations help explain the aberrant proliferation and activation of cytotoxic T cells and may represent genetic risk factors for bone marrow failure."
+ }
+}

17427485.json

@@ -0,0 +1,8 @@
+{
+ "id": "17427485",
+ "label": 0,
+ "article": {
+  "id": "17427485",
+  "text": "Clinically silent adrenal masses (incidentaloma) are incidentally discovered lesions when noninvasive imaging methods (ultrasonography--USG, computer tomography--CT, magnetic resonance imaging--MRI) are performed for the reason other than known or suspected adrenal disease. Most of studies report the prevalence of adrenal incidentaloma range between 1 and 10% in radiological series."
+ }
+}

17634245.json

@@ -0,0 +1,8 @@
+{
+ "id": "17634245",
+ "label": 1,
+ "article": {
+  "id": "17634245",
+  "text": "OBJECTIVES:\nAir pollution has been associated with an increased risk for lung cancer. We examined whether long-term air pollution is associated with bladder cancer risk.\n\nMETHODS:\nInformation from a case-control study in Spain that included 1219 incident cases and 1271 hospital controls was used. Information on residential history including several indicators of exposure to air pollution and other potential risk factors was collected in a face-to-face computerised personal interview. Odds ratios (OR) and 95% confidence intervals (95% CI) were adjusted for age, gender, region, smoking, occupation, water contaminants and diet.\n\nRESULTS:\nLiving more than 40 years in a city with a population of more than 100 000 was associated with an increased risk for bladder cancer overall (OR 1.30, 95% CI 1.04 to 1.63). Emissions of polycyclic aromatic hydrocarbons and diesel from industries near the residence, as evaluated by experts, were associated with an increased risk (OR 1.29, 95% CI 0.85 to 1.98), while lower or no excess risks were observed for other pollution-related variables. Odds ratios among never smokers tended to be higher than among smokers.\n\nCONCLUSIONS:\nThe small to moderate positive associations found for several indices of air pollution and bladder cancer, while suggestive of excess risk, require further evaluation in other settings."
+ }
+}

17646581.json

@@ -0,0 +1,8 @@
+{
+ "id": "17646581",
+ "label": 1,
+ "article": {
+  "id": "17646581",
+  "text": "BACKGROUND:\nConsumption of soft drinks has been linked to obesity in children and adolescents, but it is unclear whether it increases metabolic risk in middle-aged individuals.\n\nMETHODS AND RESULTS:\nWe related the incidence of metabolic syndrome and its components to soft drink consumption in participants in the Framingham Heart Study (6039 person-observations, 3470 in women; mean age 52.9 years) who were free of baseline metabolic syndrome. Metabolic syndrome was defined as the presence of \u003e or = 3 of the following: waist circumference \u003e or = 35 inches (women) or \u003e or = 40 inches (men); fasting blood glucose \u003e or = 100 mg/dL; serum triglycerides \u003e or = 150 mg/dL; blood pressure \u003e or = 135/85 mm Hg; and high-density lipoprotein cholesterol \u003c 40 mg/dL (men) or \u003c 50 mg/dL (women). Multivariable models included adjustments for age, sex, physical activity, smoking, dietary intake of saturated fat, trans fat, fiber, magnesium, total calories, and glycemic index. Cross-sectionally, individuals consuming \u003e or = 1 soft drink per day had a higher prevalence of metabolic syndrome (odds ratio [OR], 1.48; 95% CI, 1.30 to 1.69) than those consuming \u003c 1 drink per day. On follow-up (mean of 4 years), new-onset metabolic syndrome developed in 717 of 4033 participants (17.8%) consuming \u003c 1 drink/day and in 433 of 2006 persons (21.6%) [corrected] consuming \u003e or = 1 soft drink/day [corrected] Consumption of \u003e or = 1 soft drink per day was associated with increased odds of developing metabolic syndrome (OR, 1.44; 95% CI, 1.20 to 1.74), obesity (OR, 1.31; 95% CI, 1.02 to 1.68), increased waist circumference (OR, 1.30; 95% CI, 1.09 to 1.56), impaired fasting glucose (OR, 1.25; 95% CI, 1.05 to 1.48), higher blood pressure (OR, 1.18; 95% CI, 0.96 to 1.44), hypertriglyceridemia (OR, 1.25; 95% CI, 1.04 to 1.51), and low high-density lipoprotein cholesterol (OR, 1.32; 95% CI 1.06 to 1.64).\n\nCONCLUSIONS:\nIn middle-aged adults, soft drink consumption is associated with a higher prevalence and incidence of multiple metabolic risk factors."
+ }
+}

17671226.json

@@ -0,0 +1,8 @@
+{
+ "id": "17671226",
+ "label": 1,
+ "article": {
+  "id": "17671226",
+  "text": "Cigarette smoking is a major risk factor for bladder cancer and a prominent point source of 4-aminobiphenyl (4-ABP), a recognized human bladder carcinogen. 4-ABP-hemoglobin (Hb) adducts are established biomarkers of 4-ABP exposure in humans. The role of environmental tobacco smoke (ETS) in the etiology of bladder cancer is largely unknown. As part of a large population-based bladder cancer study in Los Angeles County, California, lifetime exposure to ETS was ascertained for 148 cases and 292 control subjects who had never used any tobacco products over their lifetime. 4-ABP-Hb adducts were quantitatively measured on 230 control subjects. Female lifelong nonsmokers living with two or more smokers during childhood were significantly related to risk of bladder cancer [odds ratio (OR), 3.08; 95% confidence interval (95% CI), 1.16-8.22]. During adulthood, approximately 2-fold risks were seen among women living with a spouse/domestic partner who smoked for \u003e or =10 years or having a coworker who smoked in an indoor environment for \u003e or =10 years. When all sources of ETS exposure were combined, a statistically significant, dose-dependent association (P for trend = 0.03) was noted in women, with the OR for the highest category of ETS exposure being 5.48 (95% CI, 1.06-28.36). Levels of 4-ABP-Hb adducts varied by ETS exposure status among female control subjects. Mean level was lowest in women never exposed to ETS (16.4 pg/g Hb) and highest in those with current ETS exposure (23.6 pg/g Hb). ETS exposure was associated with neither bladder cancer risk nor 4-ABP-Hb adduct levels in male lifelong nonsmokers. In conclusion, ETS is a risk factor for bladder cancer in women who were lifelong nonusers of any tobacco products."
+ }
+}

17684133.json

@@ -0,0 +1,8 @@
+{
+ "id": "17684133",
+ "label": 1,
+ "article": {
+  "id": "17684133",
+  "text": "The relationship between family history of cancer in first-degree relatives and risk of bladder cancer was examined in the Spanish Bladder Cancer Study. Information on family history of cancer was obtained for 1,158 newly diagnosed bladder cancer cases and 1,244 controls included in 18 hospitals between 1998 and 2001. A total of 464 (40.1%) cases and 436 (35.1%) controls reported a family history of cancer in \u003e/=1 relative [odds ratio (OR), 1.32; 95% confidence interval (95% CI), 1.11-1.59]; the OR was 1.23 (95% CI, 1.01-1.50) among those with only one relative affected and 1.67 (95% CI, 1.23-2.29) among those with \u003e/=2 affected relatives (P(trend) = 0.0004). A greater risk of bladder cancer was observed among those diagnosed at age \u003c/=45 years (OR, 2.67; 95% CI, 1.10-6.50) compared with those diagnosed over age 45 years (OR, 1.27; 95% CI, 1.06-1.52). The OR of bladder cancer among subjects reporting a family history of cancer of the bladder was 2.34 (95% CI, 0.95-5.77). Statistically significant associations emerged between bladder cancer risk and family history of cancer of the esophagus, lung, prostate, and brain. The OR of bladder cancer for those reporting family history of bladder cancer was 4.76 (95% CI, 1.25-18.09) among NAT2-slow acetylators and 1.17 (95% CI, 0.17-7.86) among NAT2-rapid/intermediate acetylators (P(interaction) = 0.609). Among individuals with GSTM1 null and present genotypes, the corresponding ORs were 2.91 (95% CI, 0.44-19.09) and 4.21 (95% CI, 1.26-14.14), respectively (P(interaction) = 0.712). Limitations of our study are small sample size in subgroup analyses, reliability of family history data, and possible residual confounding by shared environmental exposures. Overall, our findings support the hypothesis that genetic factors play a role in bladder cancer etiology. Whether these correspond to low-penetrance cancer-predisposing polymorphisms acting together and/or interacting with environmental factors warrants further research."
+ }
+}

17891891.json

@@ -0,0 +1,8 @@
+{
+ "id": "17891891",
+ "label": 1,
+ "article": {
+  "id": "17891891",
+  "text": "Using the fixed-effect model, the author quantitatively estimated the risks of cancers of the colon, bladder, kidneys, and brain as well as non-Hodgkin's lymphoma and leukemia among firefighters. The risk of these six cancers was not markedly elevated when cohort mortality studies were considered. When all mortality studies were considered, however, there was a mild increase in risk for kidney cancer and non-Hodgkin's lymphoma, with a summary relative risk (sumRR) of 1.22 (95% confidence interval [CI] = 1.02-1.43) and 1.40 (95% CI = 1.20-1.60), respectively. A subcohort analysis based on duration of employment revealed that firefighters with 30 or more years of employment had a significantly increased mortality risk for colon cancer, sumRR of 1.51 (95% CI = 1.05-2.11); kidney cancer, sumRR of 6.25 (95% CI = 1.70-16.00); brain cancer, sumRR of 2.53 (95% CI = 1.27 7.07); and leukemia, sumRR of 2.87 (95% CI = 1.43-5.14). After firefighters had 40 or more years of employment, their risk of mortality was significantly increased for colon cancer, sumRR of 4.71 (95% CI = 2.03-9.27); kidney cancer, sumRR of 36.12 (95% CI = 4.03-120.42); and bladder cancer, sumRR of 5.7 (95% CI = 1.56-14.63). The risk for non-Hodgkin's lymphoma was elevated but not significantly so among firefighters with 20 or more years of employment, with sumRR of 1.72 (95% CI = 0.90-3.31). Kidney cancer risk was significantly elevated as early as the second decade of employment."
+ }
+}

17932376.json

@@ -0,0 +1,8 @@
+{
+ "id": "17932376",
+ "label": 1,
+ "article": {
+  "id": "17932376",
+  "text": "RATIONALE:\nRisk factors for asthma among farm women are understudied.\n\nOBJECTIVES:\nWe evaluated pesticide and other occupational exposures as risk factors for adult-onset asthma.\n\nMETHODS:\nStudying 25,814 farm women in the Agricultural Health Study, we used self-reported history of doctor-diagnosed asthma with or without eczema and/or hay fever to create two case groups: patients with atopic asthma and those with nonatopic asthma. We assessed disease-exposure associations with polytomous logistic regression.\n\nMEASUREMENTS AND MAIN RESULTS:\nAt enrollment (1993-1997), 702 women (2.7%) reported a doctor's diagnosis of asthma after age 19 years (282 atopic, 420 nonatopic). Growing up on a farm (61% of all farm women) was protective for atopic asthma (odds ratio [OR], 0.55; 95% confidence interval [CI], 0.43-0.70) and, to a lesser extent, for nonatopic asthma (OR, 0.83; 95%CI, 0.68-1.02; P value for difference = 0.008). Pesticide use was almost exclusively associated with atopic asthma. Any use of pesticides on the farm was associated only with atopic asthma (OR, 1.46; 95% CI, 1.14-1.87). This association with pesticides was strongest among women who had grown up on a farm. Women who grew up on farms and did not apply pesticides had the lowest overall risk of atopic asthma (OR, 0.41; 95% CI, 0.27-0.62) compared with women who neither grew up on farms nor applied pesticides. A total of 7 of 16 insecticides, 2 of 11 herbicides, and 1 of 4 fungicides were significantly associated with atopic asthma; only permethrin use on crops was associated with nonatopic asthma.\n\nCONCLUSIONS:\nThese findings suggest that pesticides may contribute to atopic asthma, but not nonatopic asthma, among farm women."
+ }
+}

18311140.json

@@ -0,0 +1,8 @@
+{
+ "id": "18311140",
+ "label": 1,
+ "article": {
+  "id": "18311140",
+  "text": "Our genome-wide association study of celiac disease previously identified risk variants in the IL2-IL21 region. To identify additional risk variants, we genotyped 1,020 of the most strongly associated non-HLA markers in an additional 1,643 cases and 3,406 controls. Through joint analysis including the genome-wide association study data (767 cases, 1,422 controls), we identified seven previously unknown risk regions (P \u003c 5 x 10(-7)). Six regions harbor genes controlling immune responses, including CCR3, IL12A, IL18RAP, RGS1, SH2B3 (nsSNP rs3184504) and TAGAP. Whole-blood IL18RAP mRNA expression correlated with IL18RAP genotype. Type 1 diabetes and celiac disease share HLA-DQ, IL2-IL21, CCR3 and SH2B3 risk regions. Thus, this extensive genome-wide association follow-up study has identified additional celiac disease risk variants in relevant biological pathways."
+ }
+}

1833349.json

@@ -0,0 +1,8 @@
+{
+ "id": "1833349",
+ "label": 1,
+ "article": {
+  "id": "1833349",
+  "text": "Case-control studies of Alzheimer's disease were re-analysed to examine the association of Alzheimer's disease with family history in first degree relatives of dementia, Down's syndrome and Parkinson's disease. Overall, the relative risk of Alzheimer's disease for those with at least one first degree relative with dementia was 3.5 (95% confidence interval 2.6-4.6). Stratification according to age of onset of Alzheimer's disease showed that the relative risk decreased with increasing onset age. However, among patients with an onset of disease after 80 years, there were still significantly more subjects with one or more first degree relatives with dementia as compared to controls (relative risk 2.6; 95% confidence interval 1.3-5.2). The relative risk of Alzheimer's disease was significantly lower in patients who had one first degree relative with dementia (relative risk 2.6; 95% confidence interval 2.0-3.5) as compared to those who had two or more affected relatives (relative risk 7.5; 95% confidence interval 3.3-16.7). Furthermore, the re-analysis showed a significant association between Alzheimer's disease and family history of Down's syndrome (relative risk 2.7; 95% confidence interval 1.2-5.7), which was strongest in those patients who had a positive family history of dementia. The relative risk of Alzheimer's disease for those with a positive family history of Parkinson's disease was 2.4 (95% confidence interval 1.0-5.8)."
+ }
+}

18591432.json

@@ -0,0 +1,8 @@
+{
+ "id": "18591432",
+ "label": 1,
+ "article": {
+  "id": "18591432",
+  "text": "BACKGROUND:\nPrediction of coronary heart disease (CHD) and cerebrovascular disease (CeVD) can aid healthcare providers and prevention programs. Previous reports have focused on traditional cardiovascular risk factors; less information has been available on the role of overweight and obesity.\n\nMETHODS AND RESULTS:\nBaseline data from 4780 Framingham Offspring Study adults with up to 24 years of follow-up were used to assess risk for a first CHD event (angina pectoris, myocardial infarction, or cardiac death) alone, first CeVD event (acute brain infarction, transient ischemic attack, and stroke-related death) alone, and CHD and CeVD events combined. Accelerated failure time models were developed for the time of first event to age, sex, cholesterol, high-density lipoprotein cholesterol, diabetes mellitus (DM), systolic blood pressure, smoking status, and body mass index (BMI). Likelihood-ratio tests of statistical significance were used to identify the best-fitting predictive functions. Age, sex, smoking status, systolic blood pressure, ratio of cholesterol to high-density lipoprotein cholesterol, and presence of DM were highly related (P\u003c0.01 for all) to the development of first CHD events, and all of the above except sex and DM were highly related to the first CeVD event. BMI also significantly predicted the occurrence of CHD (P=0.05) and CeVD (P=0.03) in multivariable models adjusting for traditional risk factors. The magnitude of the BMI effect was reduced but remained statistically significant when traditional variables were included in the prediction models.\n\nCONCLUSIONS:\nGreater BMI, higher systolic blood pressure, higher ratio of cholesterol to high-density lipoprotein cholesterol, and presence of DM were all predictive of first CHD events, and all but the presence of DM were predictive of first CeVD events. These results suggest that common pathophysiological mechanisms underlie the roles of BMI, DM, and systolic blood pressure as predictors for first CHD and CeVD events."
+ }
+}

19240061.json

@@ -0,0 +1,8 @@
+{
+ "id": "19240061",
+ "label": 1,
+ "article": {
+  "id": "19240061",
+  "text": "OBJECTIVE:\nOur previous coeliac disease genome-wide association study (GWAS) implicated risk variants in the human leucocyte antigen (HLA) region and eight novel risk regions. To identify more coeliac disease loci, we selected 458 single nucleotide polymorphisms (SNPs) that showed more modest association in the GWAS for genotyping and analysis in four independent cohorts.\n\nDESIGN:\n458 SNPs were assayed in 1682 cases and 3258 controls from three populations (UK, Irish and Dutch). We combined the results with the original GWAS cohort (767 UK cases and 1422 controls); six SNPs showed association with p\u003c1 x 10(-04) and were then genotyped in an independent Italian coeliac cohort (538 cases and 593 controls).\n\nRESULTS:\nWe identified two novel coeliac disease risk regions: 6q23.3 (OLIG3-TNFAIP3) and 2p16.1 (REL), both of which reached genome-wide significance in the combined analysis of all 2987 cases and 5273 controls (rs2327832 p = 1.3 x 10(-08), and rs842647 p = 5.2 x 10(-07)). We investigated the expression of these genes in the RNA isolated from biopsies and from whole blood RNA. We did not observe any changes in gene expression, nor in the correlation of genotype with gene expression.\n\nCONCLUSIONS:\nBoth TNFAIP3 (A20, at the protein level) and REL are key mediators in the nuclear factor kappa B (NF-kappaB) inflammatory signalling pathway. For the first time, a role for primary heritable variation in this important biological pathway predisposing to coeliac disease has been identified. Currently, the HLA risk factors and the 10 established non-HLA risk factors explain approximately 40% of the heritability of coeliac disease."
+ }
+}

19244173.json

@@ -0,0 +1,8 @@
+{
+ "id": "19244173",
+ "label": 1,
+ "article": {
+  "id": "19244173",
+  "text": "BACKGROUND:\nWith the exception of breast cancer, little is known about the effect of moderate intakes of alcohol, or of particular types of alcohol, on cancer risk in women.\n\nMETHODS:\nA total of 1,280,296 middle-aged women in the United Kingdom enrolled in the Million Women Study were routinely followed for incident cancer. Cox regression models were used to calculate adjusted relative risks and 95% confidence intervals (CIs) for 21 site-specific cancers according to amount and type of alcoholic beverage consumed. All statistical tests were two-sided.\n\nRESULTS:\nA quarter of the cohort reported drinking no alcohol; 98% of drinkers consumed fewer than 21 drinks per week, with drinkers consuming an average of 10 g alcohol (1 drink) per day. During an average 7.2 years of follow-up per woman 68,775 invasive cancers occurred. Increasing alcohol consumption was associated with increased risks of cancers of the oral cavity and pharynx (increase per 10 g/d = 29%, 95% CI = 14% to 45%, Ptrend \u003c .001), esophagus (22%, 95% CI = 8% to 38%, Ptrend = .002), larynx (44%, 95% CI = 10% to 88%, Ptrend = .008), rectum (10%, 95% CI = 2% to 18%, Ptrend = .02), liver (24%, 95% CI = 2% to 51%, Ptrend = .03), breast (12%, 95% CI = 9% to 14%, Ptrend \u003c .001), and total cancer (6%, 95% CI = 4% to 7%, Ptrend \u003c .001). The trends were similar in women who drank wine exclusively and other consumers of alcohol. For cancers of the upper aerodigestive tract, the alcohol-associated risk was confined to current smokers, with little or no effect of alcohol among never and past smokers (P(heterogeneity) \u003c .001). Increasing levels of alcohol consumption were associated with a decreased risk of thyroid cancer (Ptrend = .005), non-Hodgkin lymphoma (Ptrend = .001), and renal cell carcinoma (Ptrend = .03).\n\nCONCLUSIONS:\nLow to moderate alcohol consumption in women increases the risk of certain cancers. For every additional drink regularly consumed per day, the increase in incidence up to age 75 years per 1000 for women in developed countries is estimated to be about 11 for breast cancer, 1 for cancers of the oral cavity and pharynx, 1 for cancer of the rectum, and 0.7 each for cancers of the esophagus, larynx and liver, giving a total excess of about 15 cancers per 1000 women up to age 75."
+ }
+}

19454285.json

@@ -0,0 +1,8 @@
+{
+ "id": "19454285",
+ "label": 1,
+ "article": {
+  "id": "19454285",
+  "text": "BACKGROUND \u0026 AIMS:\nCeliac disease (CD) is a common chronic disorder of the small intestine, resulting from aberrant cellular responses to gluten peptides, and often remains undiagnosed. It is a complex genetic disorder, although 95% of the patients carry the risk heterodimer human leukocyte antigen (HLA)-DQ2. Genome-wide association studies on CD have identified 9 non-HLA loci that also contribute to CD risk, most of which are shared with other immune-related diseases. Our aim is to predict the genetic risk for CD using HLA and non-HLA risk alleles.\n\nMETHODS:\nWe selected 10 independent polymorphisms in 2,308 cases and 4,585 controls from Dutch, UK, and Irish populations and categorized the individuals into 3 risk groups, based on their HLA-DQ2 genotype. We used the summed number of non-HLA risk alleles per individual to analyze their cumulative effect on CD risk, adjusting for gender and population group in logistic regression analysis. We validated our findings in 436 Italian cases and 532 controls.\n\nRESULTS:\nCD cases carried more non-HLA risk alleles than controls: individuals carrying \u003e or = 13 risk alleles had a higher CD risk (odds ratio, 6.2; 95% confidence interval, 4.1-9.3) compared with those carrying 0-5 risk alleles. Combining HLA and non-HLA risk genotypes in one model increases sensitivity by 6.2% compared with using only HLA for identification of high-risk individuals with slight decrease in specificity.\n\nCONCLUSIONS:\nWe can use non-HLA risk factors for CD to improve identification of high-risk individuals. Our risk model is a first step toward better diagnosis and prognosis in high-risk families and population-based screening."
+ }
+}

19500688.json

@@ -0,0 +1,8 @@
+{
+ "id": "19500688",
+ "label": 1,
+ "article": {
+  "id": "19500688",
+  "text": "BACKGROUND \u0026 AIMS:\nSusceptibility to celiac disease (CD) is related to HLA-DQ2 and DQ8 alleles and the heterodimers they encode. The objective of this study was to stratify risk for CD on the basis of HLA-DQ genotype.\n\nMETHODS:\nDNA from 10,191 subjects who are at risk for CD was analyzed for HLA-DQ haplotypes. Individuals with CD were identified as those who tested positive for anti-endomysial immunoglobulin A (EMA+) in an immunofluorescence assay.\n\nRESULTS:\nSamples homozygous for DQ2.5 (HLA-DQA1 05-DQB1 02) or DQ2.2/DQ2.5 (HLA-DQA1 05-DQB1 02 and HLA-DQA1 0201-DQB1 02) comprised 5.38% of the total; 28.28% of these were EMA+ (95% confidence interval [CI], 24.55-32.26). Of the samples that were DQ2.5 heterozygous (HLA-DQA1 05-DQB1 02); 9.09% were EMA+ (95% CI, 7.82-10.51). Among samples in which HLA-DQ8 (HLA-DQA1 03-DQB1 0302) was detected, 8.42% of homozygotes (95% CI, 3.71-15.92) and 2.11% of heterozygotes (95% CI, 1.43-3.00) were EMA+. Samples with DQ2.2/DQ8 or DQ2.5/DQ8 comprised 5.08% of the total, and 11.78% of these were EMA+ (95% CI, 9.13-14.87). HLA-DQ2 and HLA-DQ8 were absent in 4283 samples (42.03% of the total); 0.16% of these samples were EMA+ (95% CI, 0.07-0.34).\n\nCONCLUSIONS:\nHigh-resolution, sequence-specific oligonucleotide probe typing with 35 DQA1-specific and 37 DQB1-specific probes of DNA from more than 10,000 subjects was used to stratify risk of CD in an at-risk U.S. population. DQ2 homozygosity (DQ2.5/DQ2.2+2.5) increased risk for CD, estimated by the rate of EMA positivity, compared with the entire sample population and other DQ genotypes. These data suggest a quantitative relationship between the type/proportion of DQ heterodimers and the risk of CD and identify potential immunotherapeutic targets."
+ }
+}

19515369.json

@@ -0,0 +1,8 @@
+{
+ "id": "19515369",
+ "label": 0,
+ "article": {
+  "id": "19515369",
+  "text": "Familial LCAT deficiency (FLD) is a disease characterized by a defect in the enzyme lecithin:cholesterol acyltransferase (LCAT) resulting in low HDL-C, premature corneal opacities, anemia as well as proteinuria and renal failure. We have identified the first French Canadian kindred with familial LCAT deficiency. Two brothers, presenting classical signs of FLD, were shown to be homozygous for a novel LCAT mutation. This c.102delG mutation occurs at the codon for His35 and causes a frameshift that stops transcription at codon 61 abolishing LCAT enzymatic activity both in vivo and in vitro. It has a dramatic effect on the lipoprotein profile, with an important reduction of HDL-C in both heterozygotes (22%) and homozygotes (88%) and a significant decrease in LDL-C in heterozygotes (35%) as well as homozygotes (58%). Furthermore, the lipoprotein profile differs markedly between the two affected brothers who had different APOE genotypes. We propose that APOE could be an important modifier gene explaining heterogeneity in lipoprotein profiles observed among FLD patients. Our results suggest that a LCAT-/- genotype associated with an APOE epsilon2 allele could be a novel mechanism leading to dysbetalipoproteinemia."
+ }
+}

19789839.json

@@ -0,0 +1,8 @@
+{
+ "id": "19789839",
+ "label": 1,
+ "article": {
+  "id": "19789839",
+  "text": "Although the risk for most cancers appears to be relatively low in patients with Parkinson's disease (PD), skin cancers and melanomas occur more frequently in the PD population as compared to controls. This article summarizes the findings of cohort studies on skin cancer in Parkinson's disease. Given that melanoma may precede use of L-dopa, the increased risk of melanoma for PD patients cannot be attributed to L-dopa. On the basis of these observations it may be reasonable to recommend that all patients with PD, whether treated with L-dopa or not, should undergo regular dermatological screening for neoplastic or pre-neoplastic skin lesions, especially melanoma."
+ }
+}

20212233.json

@@ -0,0 +1,8 @@
+{
+ "id": "20212233",
+ "label": 1,
+ "article": {
+  "id": "20212233",
+  "text": "OBJECTIVE:\nTo evaluate the possible association of Parkinson disease (PD) and melanoma in North America.\n\nDESIGN, SETTING, AND PATIENTS:\nThirty-one centers enrolled patients with idiopathic PD. At visit 1, a neurologist obtained a medical history. At visit 2, a dermatologist recorded melanoma risk factors, performed a whole-body examination, and performed a biopsy of lesions suggestive of melanoma for evaluation by a central dermatopathology laboratory. We compared overall prevalence of melanoma with prevalence calculated from the US Surveillance Epidemiology and End Results (SEER) cancer database and the American Academy of Dermatology skin cancer screening programs.\n\nRESULTS:\nA total of 2106 patients (mean [SD] age, 68.6 [10.6] years; duration of PD, 7.1 [5.7] years) completed the study. Most (84.8%) had received levodopa. Dermatology examinations revealed 346 pigmented lesions; dermatopathological findings confirmed 20 in situ melanomas (0.9%) and 4 invasive melanomas (0.2%). In addition, histories revealed 68 prior melanomas (3.2%). Prevalence (5-year limited duration) of invasive malignant melanoma in the US cohort of patients with PD (n = 1692) was 2.24-fold higher (95% confidence interval, 1.21-4.17) than expected in age- and sex-matched populations in the US SEER database. Age- or sex-adjusted relative risk of any melanoma for US patients was more than 7 times that expected from confirmed cases in American Academy of Dermatology skin cancer screening programs.\n\nCONCLUSIONS:\nMelanoma prevalence appears to be higher in patients with PD than in the general population. Despite difficulties in comparing other databases with this study population, the study supports increased melanoma screening in patients with PD."
+ }
+}

20231496.json

@@ -0,0 +1,8 @@
+{
+ "id": "20231496",
+ "label": 1,
+ "article": {
+  "id": "20231496",
+  "text": "OBJECTIVE:\nTo quantify the risk of subsequent primary cancers among patients with primary cutaneous malignant melanoma.\n\nDESIGN:\nPopulation-based registry study.\n\nSETTING:\nWe evaluated data from 9 cancer registries of the Surveillance, Epidemiology, and End Results program from 1973-2006.\n\nPARTICIPANTS:\nWe included 89 515 patients who survived at least 2 months after their initial melanoma diagnosis.\n\nRESULTS:\nOf the patients with melanoma, 10 857 (12.1%) developed 1 or more subsequent primary cancers. The overall risk of a subsequent primary cancer increased by 28% (observed to expected [O:E] ratio = 1.28). One quarter of the cancers were subsequent primary melanomas (O:E = 8.61). Women with head and neck melanoma and patients younger than 30 had markedly increased risks (O:E = 13.22 and 13.40, respectively) of developing a subsequent melanoma. Second melanomas were more likely to be thin than were the first of multiple primary melanomas (thickness at diagnosis \u003c1.00 mm, 77.9% vs 70.3%, respectively; P \u003c .001). Melanoma survivors had increased risk of developing several cancers; the most common cancers with elevated risks were breast, prostate, and non-Hodgkin lymphoma (O:E = 1.10, 1.15, and 1.25, respectively).\n\nCONCLUSIONS:\nMelanoma survivors have an approximately 9-fold increased risk of developing subsequent melanoma compared with the general population. The risk remains elevated more than 20 years after the initial melanoma diagnosis. This increased risk may be owing to behavioral factors, genetic susceptibility, or medical surveillance. Although the percentage of subsequent primary melanomas thicker than 1 mm is lower than for the first of multiple primary melanomas, it is still substantial. Melanoma survivors should remain under surveillance not only for recurrence but also for future primary melanomas and other cancers."
+ }
+}

20548022.json

@@ -0,0 +1,8 @@
+{
+ "id": "20548022",
+ "label": 1,
+ "article": {
+  "id": "20548022",
+  "text": "We previously investigated bladder cancer risk in a cohort of dyestuff workers who were heavily exposed to aromatic amines from 1922 through 1972. We updated the follow-up by 14 years (through 2003) for 590 exposed workers to include more than 30 years of follow-up since last exposure to aromatic amines. Expected numbers of deaths from bladder cancer and other causes were computed by use of national mortality rates from 1951 to 1980 and regional mortality rates subsequently. There were 394 deaths, compared with 262.7 expected (standardized mortality ratio = 1.50, 95% confidence interval = 1.36 to 1.66). Overall, 56 deaths from bladder cancer were observed, compared with 3.4 expected (standardized mortality ratio = 16.5, 95% confidence interval = 12.4 to 21.4). The standardized mortality ratio for bladder cancer increased with younger age at first exposure and increasing duration of exposure. Although the standardized mortality ratio for bladder cancer steadily decreased with time since exposure stopped, the absolute risk remained approximately constant at 3.5 deaths per 1000 man-years up to 29 years after exposure stopped. Excess risk was apparent 30 years or more after last exposure."
+ }
+}

20798970.json

@@ -0,0 +1,8 @@
+{
+ "id": "20798970",
+ "label": 1,
+ "article": {
+  "id": "20798970",
+  "text": "Patients with longstanding extensive colitis, both ulcerative colitis and Crohn's colitis, have an increased risk of developing colorectal cancer. Because of this risk, colonoscopic surveillance for neoplasia is recommended by most authorities. Although there has been no randomised controlled trial to demonstrate surveillance effectiveness, there are several retrospective comparative studies, which suggest that surveillance reduces colorectal cancer mortality. Over the past decade there have been a number of developments in our understanding of colitis cancer. We have discovered that the severity of colorectal inflammation is an important risk factor, in addition to other known risk factors such as the extent and duration of colitis, primary sclerosing cholangitis and a family history of colorectal cancer. Endoscopic techniques have also improved and evidence now demonstrates that pancolonic chromoendoscopy yields significantly more intraepithelial neoplasia than random biopsies. Endoscopic resection of well-circumscribed lesions is now also recognised as being an appropriate strategy, potentially reducing the number of patients requiring colectomy. It is hoped that such developments will further improve the effectiveness of colitis surveillance."
+ }
+}

21447005.json

@@ -0,0 +1,8 @@
+{
+ "id": "21447005",
+ "label": 0,
+ "article": {
+  "id": "21447005",
+  "text": "Autoimmune lymphoproliferative syndrome (ALPS) is a disorder of lymphocyte homeostasis. It is characterized by non-malignant lymphoproliferation autoimmunity mostly directed toward blood cells and increased risk of lymphoma. Majority of patients with ALPS harbor heterozygous germline mutations in the gene for the TNF receptor-family member Fas (CD 95, Apo-1) which are inherited in an autosomal dominant fashion. Somatic Fas mutations are the second most common genetic etiology of ALPS. Additionally mutations in the genes encoding Fas-ligand (FASLG), caspase 10 (CASP10) and caspase 8 (CASP8), NRAS and KRAS have been identified in a small number of patients with ALPS and related disorders. Approximately one-third of patients with ALPS have yet unidentified defect. ALPS was initially thought to be a very rare disease, but recent studies have shown that it may be more common than previously thought. Testing for ALPS should therefore be considered in patients with unexplained lymphadenopathy, cytopenias, and hepatosplenomegaly. There have been significant advances in the understanding of the pathophysiology of ALPS in last few years which has resulted in the development of new diagnostic criteria and a number of targeted therapies. This review describes the clinical and laboratory manifestations found in patients with ALPS, as well as the molecular basis for the disease and new advances in treatment."
+ }
+}

22294430.json

@@ -0,0 +1,8 @@
+{
+ "id": "22294430",
+ "label": 1,
+ "article": {
+  "id": "22294430",
+  "text": "Evidence concerning the role of Helicobacter pylori infection in the development of colorectal cancer remains controversial. The authors assessed the association of H. pylori seroprevalence with risk of colorectal cancer in a large population-based case-control study from Germany in 2003-2007. Serum antibodies to H. pylori in general and the cytotoxin-associated gene A protein (CagA) were measured in 1,712 incident colorectal cancer cases and 1,669 controls. The association between H. pylori seroprevalence and colorectal cancer risk was estimated by logistic regression, with adjustment for potential confounders and stratification by age group, sex, anatomic subsites, and cancer stage. Overall, H. pylori seroprevalence was higher in cases (46.1%) than in controls (40.1%), resulting in an age- and sex-adjusted odds ratio of 1.30 (95% confidence interval (CI): 1.14, 1.50). Adjustment for established colorectal cancer risk factors decreased the odds ratio to 1.26 (95% CI: 1.09, 1.47), with a further reduction to 1.18 (95% CI: 1.01, 1.38) after additional adjustment for previous colorectal endoscopy. Stratified analyses showed risk elevation to be essentially confined to left-sided colorectal cancer, with an odds ratio of 1.22 (95% CI: 1.02, 1.45), suggesting that H. pylori infection may be associated with a small yet relevant risk increase in the left colorectum."
+ }
+}

22833605.json

@@ -0,0 +1,8 @@
+{
+ "id": "22833605",
+ "label": 1,
+ "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."
+ }
+}

22905651.json

@@ -0,0 +1,8 @@
+{
+ "id": "22905651",
+ "label": 1,
+ "article": {
+  "id": "22905651",
+  "text": "BACKGROUND:\nPREVENTCD, Prevent Coeliac Disease, is an international project investigating the hypothesis of possible induction of tolerance to gluten in genetically predisposed children through introducing small quantities of gluten during the period of breastfeeding.\n\nAIM:\nTo summarise current knowledge on the possible relationship between early feeding practices and the risk of coeliac disease (CD).\n\nMETHODS:\nThe Cochrane Library, MEDLINE, and EMBASE databases were searched in May 2011, and the search was updated in January 2012, and again in July 2012.\n\nRESULTS:\nBreastfeeding (BF) and CD: some studies show a protective effect of BF, while others show no effect. No studies have shown a long-term preventive effect. BF at the time of gluten introduction and CD: Results from a meta-analysis of five observational case-control studies suggest that BF at gluten introduction is associated with a lower risk of CD compared with formula feeding. It is unclear whether BF provides a permanent protection or only delays the onset of CD. Timing of gluten introduction: The data suggest that both early (≤4 months) and late (≥7 months) introduction of gluten may increase the risk of CD. Amount of gluten at weaning (and later) and CD: One incident case-referent study documented that the introduction of gluten in large amounts compared with small or medium amounts increased the risk of CD.\n\nCONCLUSIONS:\nIn the absence of clear evidence, in order to decrease the risk of later coeliac disease, it is reasonable to avoid both early (\u003c4 months) and late (≥7 months) introduction of gluten, and to introduce gluten while the infant is still being breastfed. Future studies may clarify the remaining uncertainties."
+ }
+}

23155333.json

@@ -0,0 +1,8 @@
+{
+ "id": "23155333",
+ "label": 1,
+ "article": {
+  "id": "23155333",
+  "text": "Celiac disease (CD) is one of the most common diseases, resulting from both environmental (gluten) and genetic factors [human leukocyte antigen (HLA) and non-HLA genes]. The prevalence of CD has been estimated to approximate 0.5%-1% in different parts of the world. However, the population with diabetes, autoimmune disorder or relatives of CD individuals have even higher risk for the development of CD, at least in part, because of shared HLA typing. Gliadin gains access to the basal surface of the epithelium, and interact directly with the immune system, via both trans- and para-cellular routes. From a diagnostic perspective, symptoms may be viewed as either \"typical\" or \"atypical\". In both positive serological screening results suggestive of CD, should lead to small bowel biopsy followed by a favourable clinical and serological response to the gluten-free diet (GFD) to confirm the diagnosis. Positive anti-tissue transglutaminase antibody or anti-endomysial antibody during the clinical course helps to confirm the diagnosis of CD because of their over 99% specificities when small bowel villous atrophy is present on biopsy. Currently, the only treatment available for CD individuals is a strict life-long GFD. A greater understanding of the pathogenesis of CD allows alternative future CD treatments to hydrolyse toxic gliadin peptide, prevent toxic gliadin peptide absorption, blockage of selective deamidation of specific glutamine residues by tissue, restore immune tolerance towards gluten, modulation of immune response to dietary gliadin, and restoration of intestinal architecture."
+ }
+}

23204143.json

@@ -0,0 +1,8 @@
+{
+ "id": "23204143",
+ "label": 1,
+ "article": {
+  "id": "23204143",
+  "text": "A growing body of evidence demonstrates an association between vascular risk factors and Alzheimer's disease. This study investigated the frequency and severity of atherosclerotic plaques in the circle of Willis in Alzheimer's disease and multiple other neurodegenerative diseases. Semi-quantitative data from gross and microscopic neuropathological examinations in 1000 cases were analysed, including 410 with a primary diagnosis of Alzheimer's disease, 230 with synucleinopathies, 157 with TDP-43 proteinopathies, 144 with tauopathies and 59 with normal ageing. More than 77% of subjects with Alzheimer's disease had grossly apparent circle of Willis atherosclerosis, a percentage that was significantly higher than normal (47%), or other neurodegenerative diseases (43-67%). Age- and sex-adjusted atherosclerosis ratings were highly correlated with neuritic plaque, paired helical filaments tau neurofibrillary tangle and cerebral amyloid angiopathy ratings in the whole sample and within individual groups. We found no associations between atherosclerosis ratings and α-synuclein or TDP-43 lesion ratings. The association between age-adjusted circle of Willis atherosclerosis and Alzheimer's disease-type pathology was more robust for female subjects than male subjects. These results provide further confirmation and specificity that vascular disease and Alzheimer's disease are interrelated and suggest that common aetiologic or reciprocally synergistic pathophysiological mechanisms promote both vascular pathology and plaque and tangle pathology."
+ }
+}

23531950.json

@@ -0,0 +1,8 @@
+{
+ "id": "23531950",
+ "label": 0,
+ "article": {
+  "id": "23531950",
+  "text": "Alveolar soft-part sarcoma (ASPS) is a translocation-associated sarcoma that occurs most commonly in the lower extremities and rarely in orbit. Only 34 orbital cases have been reported in the literature, and it is often misdiagnosed due to its rare occurrence and nonspecific clinical findings."
+ }
+}

23569324.json

@@ -0,0 +1,8 @@
+{
+ "id": "23569324",
+ "label": 1,
+ "article": {
+  "id": "23569324",
+  "text": "PURPOSE:\nSite-specific risk of colorectal cancer (CRC) among survivors of endometrial cancer (EC) is not known. The objective of the present study was to assess the risk of CRC (overall and subsite specific) among EC survivors.\n\nMETHODS:\nA historical cohort study was performed by linking the Manitoba Cancer Registry and the Manitoba Health administrative databases. Each subject diagnosed with EC as her first cancer between 1987 and 2008 was age matched with up to five women with no history of invasive cancer on the index date (date of EC diagnosis). All subjects were followed up to the date of diagnosis of CRC or another cancer, death, migration, or study end point (December 31, 2009). Competing-risk proportional hazards models were used to compare the CRC incidence rates with adjustment for age, history of lower gastrointestinal endoscopy, and socioeconomic status. There were three mutually exclusive (and competing) outcomes: CRC, another primary cancer, and death.\n\nRESULTS:\nA total of 3,115 women with EC and 15,084 without EC were followed up for a total of 145,502 person-years. Women diagnosed with EC at age ≤ 50 years had an increased risk of being diagnosed with CRC (all CRC: hazard ratio [HR] = 4.41; 95% CI, 1.47 to 13.26; right-sided CRC: HR = 7.48; 95% CI, 1.29 to 43.28). There was no increased risk of all CRC among women 51 to 65 years of age or those older than 65 years at the time of EC diagnosis. However, women 51 to 65 years of age at EC diagnosis had an increased risk of right-sided CRC (HR = 2.30; 95% CI, 1.05 to 5.01).\n\nCONCLUSION:\nThis study suggests young women (age ≤ 50 years) with EC are at increased risk of CRC; risk of right-sided CRC is also increased in women 51 to 65 years old at EC diagnosis."
+ }
+}

23620537.json

@@ -0,0 +1,8 @@
+{
+ "id": "23620537",
+ "label": 1,
+ "article": {
+  "id": "23620537",
+  "text": "BACKGROUND:\nHyperuricemia is known to be a risk factor for incident type 2 diabetes mellitus, but the absolute magnitude of the association is not known. We aimed to evaluate the strength of association between hyperuricemia and the risk of developing diabetes among the US veterans with gout.\n\nMETHODS:\nPatients (age ≥ 18 years) with ≥2 clinical encounters with gout diagnoses, no history of inflammatory diseases or diabetes and two serum urate (sUA) measurements between 1 January 2002 and 1 January 2011 were selected. Diabetes was identified using International Classification of Disease-9-Clinical Modification codes, use of anti-diabetic medications or HbA1c ≥6.5%. sUA levels were assessed at 6-month cycles (hyperuricemia: sUA \u003e7 mg/dl). Accumulated hazard curves for time to first diabetes diagnosis were derived from Kaplan-Meier (KM) analysis. Risk of diabetes associated with hyperuricemia was estimated using a Cox proportional hazards model. Population attributable fraction (AF) of new-onset diabetes within 1 year was estimated using logistic regression.\n\nRESULTS:\nAmong 1923 patients, average age was 62.9 years, body mass index was 30.6 kg/m(2), and follow-up time was 80 months. Diabetes rates from KM were 19% for sUA ≤ 7 mg/dl, 23% for 7 mg/dl \u003c sUA ≤ 9 mg/dl and 27% for sUA \u003e 9 mg/dl at the end of follow-up period (P \u003c 0.001). Hyperuricemia was associated with a significantly higher risk of developing diabetes, after adjusting for confounding factors (hazard ratio: 1.19, 95% confidence interval: [1.01-1.41]). Approximately, 8.7% of all new cases of diabetes were statistically attributed to hyperuricemia.\n\nCONCLUSIONS:\nAmong veterans, hyperuricemia was associated with excess risk for developing diabetes. Approximately, 1 in 11 new cases of diabetes were statistically attributed to hyperuricemia."
+ }
+}

24101761.json

@@ -0,0 +1,8 @@
+{
+ "id": "24101761",
+ "label": 1,
+ "article": {
+  "id": "24101761",
+  "text": "OBJECTIVES:\nTiming of gluten introduction has been associated with the risk of celiac disease (CD) in children, but the optimal time window is unknown. We aimed to study the effect of age of gluten introduction on the risk of CD, adjusting for continued breastfeeding.\n\nMETHODS:\nIn The Norwegian Mother and Child Cohort Study, a prospective birth cohort including 107,000 children, CD was identified by questionnaires and by linkage to the Norwegian Patient Register. Gluten introduction was reported monthly from 0 to 6 months of age, and breastfeeding from 0 to 18 months.\n\nRESULTS:\nAfter exclusion of cases with insufficient information, 324 children with CD in a cohort of 82,167 were used in the analyses. Gluten was introduced before or at 4 months in 8.0%, 5 to 6 months in 45.3%, and after 6 months in 46.6%, whereas continued breastfeeding was stable at ≈ 78% at 6 months age. CD was diagnosed in 3.68/1000 of the infants with gluten introduction at 5 to 6 months compared with 4.15/1000 with late and 4.24/1000 with early gluten introduction. After adjustment for the child's age and gender, breastfeeding, and maternal CD, delayed gluten introduction was associated with an increased risk of CD (adjusted odds ratio, 1.27 [95% confidence interval, 1.01-1.65], P = .045). Breastfeeding \u003e12 months was also associated with increased risk (adjusted odds ratio, 1.49 [95% confidence interval, 1.01-2.21], P = .046).\n\nCONCLUSIONS:\nWe found an increased risk of CD in children introduced to gluten after 6 months and a higher risk in children breastfed after 12 months age."
+ }
+}

24164287.json

@@ -0,0 +1,8 @@
+{
+ "id": "24164287",
+ "label": 1,
+ "article": {
+  "id": "24164287",
+  "text": "BACKGROUND:\nRecent studies reported increased risks for the development of asthma in children after prenatal exposure to acid-suppressive drugs. As a result of common pathogenesis, associations could also be present for other allergic diseases.\n\nMETHODS:\nUsing the prescription database IADB.nl, we conducted a cohort study amongst 33 536 children in the Netherlands, with a maximum follow-up of 8 years. Maternal exposure was defined as ≥1 dispensed prescription for proton pump inhibitors (PPIs) and/or Histamine 2-antagonists (H2As) during pregnancy. Children were considered to have a drug-treated allergic disease if they received either ≥2 prescriptions for dermal (atopic dermatitis), inhaled (asthma) or nasal (allergic rhinitis) steroids within a 12-month period. Clustered Cox proportional hazard regression was used to estimate crude and adjusted hazard ratios (aHR) with 95% confidence intervals (95% CI).\n\nRESULTS:\nThe aHR for the development of any allergic disease was 1.37 (95% CI: 1.14-1.66) for children exposed to PPIs or H2As. Prenatal exposure to PPIs and/or H2As was associated with atopic dermatitis, asthma and allergic rhinitis with aHRs of 1.32 (95% CI 1.06-1.64), 1.57 (95% CI 1.20-2.05) and 2.40 (95% CI 1.42-4.04), respectively. The aHR for the development of two or more (aHR 2.13 95% CI: 1.43-3.19) and three allergic diseases (aHR 5.18 95% CI: 2.16-12.42) were even more elevated after prenatal exposure to PPIs or H2As.\n\nCONCLUSION:\nPrenatal exposure to PPIs and H2As appeared associated with an increased risk for the development of atopic dermatitis, asthma and allergic rhinitis in the offspring, especially with the development of multiple allergic diseases. Because our study has limitations inherent to observational studies, prospective studies are now warranted to confirm our findings."
+ }
+}

24190118.json

@@ -0,0 +1,8 @@
+{
+ "id": "24190118",
+ "label": 1,
+ "article": {
+  "id": "24190118",
+  "text": "PURPOSE:\nSteroid hormones, particularly androgens, play a major role in prostatic carcinogenesis. Personal history of severe acne, a surrogate for higher androgen activity, has been associated with an increased risk of prostate cancer (PCa), and one recent study indicated that severe teenage acne was a novel risk factor for melanoma. These findings suggest a possible relationship between PCa and risk of melanoma. We prospectively evaluated this association among US men.\n\nMETHODS:\nA total of 42,372 participants in the Health Professionals' Follow-Up Study (HPFS; 1986 to 2010) were included. Biennially self-reported PCa diagnosis was confirmed using pathology reports. Diagnosis of melanoma and nonmelanoma skin cancer (NMSC) was self-reported biennially, and diagnosis of melanoma was pathologically confirmed. We sought to confirm the association in 18,603 participants from the Physicians' Health Study (PHS; 1982 to 1998).\n\nRESULTS:\nWe identified 539 melanomas in the HPFS. Personal history of PCa was associated with an increased risk of melanoma (multivariate-adjusted hazard ratio [HR], 1.83; 95% CI, 1.32 to 2.54). Although we also detected a marginally increased risk of NMSC associated with PCa (HR, 1.08; 95% CI, 0.995 to 1.16), the difference in the magnitude of the association between melanoma and NMSC was significant (P for heterogeneity = .002). We did not find an altered risk of melanoma associated with personal history of other cancers. The association between PCa and risk of incident melanoma was confirmed in the PHS (HR, 2.17; 95% CI, 1.12 to 4.21).\n\nCONCLUSION:\nPersonal history of PCa is associated with an increased risk of melanoma, which may not be entirely a result of greater medical scrutiny."
+ }
+}

24444654.json

@@ -0,0 +1,8 @@
+{
+ "id": "24444654",
+ "label": 1,
+ "article": {
+  "id": "24444654",
+  "text": "We studied 2332 individuals with monoallelic mutations in MUTYH among 9504 relatives of 264 colorectal cancer (CRC) cases with a MUTYH mutation. We estimated CRC risks through 70 years of age of 7.2% for male carriers of monoallelic mutations (95% confidence interval [CI], 4.6%-11.3%) and 5.6% for female carriers of monoallelic mutations (95% CI, 3.6%-8.8%), irrespective of family history. For monoallelic MUTYH mutation carriers with a first-degree relative with CRC diagnosed by 50 years of age who does not have the MUTYH mutation, risks of CRC were 12.5% for men (95% CI, 8.6%-17.7%) and 10% for women (95% CI, 6.7%-14.4%). Risks of CRC for carriers of monoallelic mutations in MUTYH with a first-degree relative with CRC are sufficiently high to warrant more intensive screening than for the general population."
+ }
+}

24876226.json

@@ -0,0 +1,8 @@
+{
+ "id": "24876226",
+ "label": 1,
+ "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."
+ }
+}