Hospira, Inc. presented two studies supporting biosimilar application for Epoetin Hospira in the US.
Hospira, a global leader in biosimilars and the world’s leading provider of injectable drugs and infusion technologies, presented two studies at the National Kidney Foundation (NKF) Spring Meeting.
The two presentations were “PK/PD Equivalence of Epoetin Hospira and Epogen Following Single Subcutaneous Doses to Healthy Subjects,” and “Epoetin Hospira and Epogen PK/PD Equivalence Following Multiple Subcutaneous Doses to Healthy Subjects.” Both studies support an evaluation of biosimilarity of its proposed biosimilar, Epoetin Hospira, with the US Food and Drug Administration (FDA) conditionally approved name of Retacrit, compared to the reference product, Amgen’s Epogen (epoetin alfa).
In the US, Epogen is approved to treat anemia caused by chronic kidney disease in patients on dialysis to reduce or avoid the need for red blood cell transfusions.
Both of the studies evaluated the pharmacokinetic (PK) and pharmacodynamic (PD) equivalence of Epoetin Hospira compared to Amgen’s Epogen administered by subcutaneous injection in healthy volunteers. One study tested a single dose of 100 units/kg, and the other evaluated multiple doses of 100 units/kg administered three times per week for a total of four weeks. The studies included measuring the effect of well-established PD clinical markers of reticulocyte count and hemoglobin. These measures were chosen because they are directly reflective of the mechanism of action of epoetin alfa and are known to directly correlate with clinical effects.
“Both studies are consistent with the assessment of biosimilarity between the reference product, Epogen, and the Hospira proposed biosimilar, Epoetin Hospira,” said Stan Bukofzer, MD, corporate vice president and chief medical officer, Hospira. “These studies contribute to the demonstration of biosimilarity and are an integral part of the overall biosimilar development program.”
Hospira, which has agreed to be bought by Pfizer for a value of $17 billion, said that it has already filed a Biologics License Application (BLA) for Epoetin Hospira to the US Food and Drug Administration (FDA), under the new approval pathway created by the Biologics Price Competition and Innovation Act (BPCIA).
Source: Hospira, Inc.
Last updated: 3/27/14; 2:25pm EST


Common problems of sludge treatment- sludge bulking
Source：Jiangsu Envset Time:23 October 2020
When we use the sludge dehydrator for sludge treatment, we will encounter many problems. How should we deal with these problems? Next, we will introduce you to the solution when the sludge expands.
We can control sludge expansion by adjusting the process operation measures. Adjusting and operating process control measures are very effective for sludge expansion caused by improper process conditions.
1.Add clay, hydrated lime, raw sludge or digested sludge at the water inlet of the aeration tank to improve the sedimentation and compactness of activated sludge;
2.Keep the wastewater entering the aeration tank in a fresh state, such as taking pre-aeration measures to make the wastewater in an aerobic state;
3.Strengthen the aeration intensity, increase the DO concentration of the mixed solution, and prevent the mixed solution from being hypoxic or anaerobic;
4.Supply nutrients such as nitrogen and phosphorus to maintain the balance of nutrients such as C, N, P in the mixed solution;
5.Increase the sludge return ratio and reduce the residence time of sludge in the secondary settling tank;
6.Perform pre-aeration to remove acid gas or add alkali to adjust the wastewater to increase the pH value of the influent of the aeration tank;
7.Play the role of the adjustment tank to ensure that the sludge load of the aeration tank is relatively stable;
8.Control the inlet water temperature of the aeration tank;
Add a biological selector in front of the aeration tank (permanent measure). The aerobic biological selector is to perform regenerative aeration before the return sludge enters the aeration tank, reduce the content of viscous substances in the return sludge, make the microorganisms enter the endogenous respiration stage, and improve the ability of the bacteria micelles to take up organic matter and Competitiveness with filamentous microorganisms. In order to enhance the effect of the biological selector, a sufficient amount of nutrients such as nitrogen and phosphorus can be added in the aeration process to improve the activity of the sludge.
Jiangsu Envset provides customers with high-quality sludge dewatering machines. We are familiar with common problems encountered when dealing with sludge. If you have any questions about the solution to sludge bulking, please contact us.
Tag: sludge treatment common problems, sludge bulking, sludge expansion


Broccoli has edible young flowering stems and leaves that can be eaten raw or cooked. The plant produces a central inflorescence, the broccoli head, which can sometimes be followed by smaller flowering shoots.
Please note that due to stock-take and a phenomenal start to the season, the MeadowSweet online shop will not fulfill orders for a few weeks (10 Nov - 20 Nov) . You can still catch me at the Orewa Farmers Market, or you are most welcome to send inquiries on plant availability.
Thank you !
Minette - MeadowSweet Herbs Dismiss


The complement system consists of 30 proteins that interact in a carefully regulated manner to destroy invading bacteria and prevent the deposition of immune complexes in normal tissue. This complex system can be activated by diverse mechanisms proceeding through distinct pathways, yet all converge on a final common pathway in which five proteins assemble into a multimolecular complex, the membrane attack complex (MAC). The MAC inserts into cell membranes to form a functional pore, resulting in ion flux and ultimately osmotic lysis. Immunohistochemical evidence of the MAC decorating neurons in cortical gray matter has been identified in multiple CNS diseases, yet the deleterious consequences, if any, of MAC deposition in the cortex of mammalian brain in vivo are unknown. Zhi-Qi Xiong et al. demonstrate that the sequential infusion of individual proteins of the membrane attack pathway (C5b6, C7, C8, and C9) into the hippocampus of awake, freely moving rats induced both behavioral and electrographic seizures as well as cytotoxicity. The onset of seizures occurred during or shortly after the infusion of C8/C9. Neither seizures nor cytotoxicity resulted from the simultaneous infusion of all five proteins premixed in vitro. The requirement for the sequential infusion of all five proteins together with the temporal relationship of seizure onset to infusions of C8/C9 implies that the MAC was formed in vivo and triggered both seizures and cytotoxicity. Deposition of the complement MAC in cortical gray matter may contribute to epileptic seizures and cell death in diverse diseases of the human brain.
Due to the multiple functions of the MAC, it is no surprise that the membrane attack complex has been implicated in an impressive number of diseases, evident via its detection in diseased tissues or its elevated levels in the blood, and that so many different clinically relevant microorganism have adopted numerous different techniques to escape the destructive action of complement.
Deficiencies of the membrane attack complex / MAC cascade predispose to meningococcal infections, indicating that its cytolytic properties are of particular importance in host defence against Neisseria, for which there appears to be no sufficient back-up. Neutrophils can only provide partial protection, although they can kill meningococci when incubated in terminal complement deficient serum, and this effect increases after vaccination so that this may represent an alternative treatment option in addition to, or instead of, vigilance and antibiotic prophylaxis.
Typically, membrane attack complex / MAC deficient subjects present in adolescence or in young adulthood, and suffer from recurrent meningococcal infections with especially the rarer serogroups. By way of example, the index case of a report in this journal issue by Vazquez-Bermudez et al. was ascertained because of three meningococcal disease episodes in a 15-year-old-boy.
1. Xiong, Z. Q., Qian, W., Suzuki, K., & McNamara, J. O. (2003). Formation of complement membrane attack complex in mammalian cerebral cortex evokes seizures and neurodegeneration. The Journal of neuroscience, 23(3), 955-960. 2. Würzner, R. (2003). Deficiencies of the complement MAC II gene cluster (C6, C7, C9): is subtotal C6 deficiency of particular evolutionary benefit?. Clinical & Experimental Immunology, 133(2), 156-159.


BackgroundAgouti and Extension loci control the relative amount of eumelanin and pheomelanin production in melanocytes that, in turn, affects pigmentation of skin and hair. The Extension locus encodes the melanocortin 1 receptor (MC1R) whose permanent activation, caused by functional mutations, results in black coat colour, whereas other inactivating mutations cause red coat colour in different mammals.ResultsThe whole coding region of the MC1R gene was sequenced in goats of six different breeds showing different coat colours (Girgentana, white cream with usually small red spots in the face; Maltese, white with black cheeks and ears; Derivata di Siria, solid red; Murciano-Granadina, solid black or solid brown; Camosciata delle Alpi, brown with black stripes; Saanen, white; F1 goats and the parental animals). Five single nucleotide polymorphisms (SNPs) were identified: one nonsense mutation (p.Q225X), three missense mutations (p.A81V, p.F250V, and p.C267W), and one silent mutation. The stop codon at position 225 should cause the production of a shorter MC1R protein whose functionality may be altered. These SNPs were investigated in a larger sample of animals belonging to the six breeds. The Girgentana breed was almost fixed for the p.225X allele. However, there was not complete association between the presence of red spots in the face and the presence of this allele in homozygous condition. The same allele was identified in the Derivata di Siria breed. However, its frequency was only 33%, despite the fact that these animals are completely red. The p.267W allele was present in all Murciano-Granadina black goats, whereas it was never identified in the brown ones. Moreover, the same substitution was present in almost all Maltese goats providing evidence of association between this mutation and black coat colour.ConclusionsAccording to the results obtained in the investigated goat breeds, MC1R mutations may determine eumelanic and pheomelanic phenotypes. However, they are probably not the only factors. In particular, the surprising not complete association of the nonsense mutation (p.Q225X) with red coat colour raises a few hypotheses on the determination of pheomelanic phenotypes in goats that should be further investigated.
|Numero di pagine||12|
|Stato di pubblicazione||Published - 2009|


Glycemic Index (GI) and Glycemic Load (GL) are two important things to know about foods we’re consuming as they may play big roles in helping us reduce the risks of getting heart diseases and several types of cancer. Additionally, low GI diets can also be beneficial to prevent diabetes and obesity.
Foods with low GI are usually ones high in dietary fiber. Fiber is important due to its ability to bind large amount of liquid in our digestive tract, making us feel fuller longer. Fiber also triggers the release of leptin, hormone responsible for satiety, and controls the release of ghrelin that causes hunger.
But what are glycemic index and glycemic load exactly?
Glycemic index is a number used to show how fast the carbs we consume can be turned by the body into glucose that serves as one of our energy sources, and how fast it can increase our blood sugar levels. Glycemic index is divided into 3 categories, which are low (<55), medium (56-69), and high (>70). The higher the GI, the faster a food is turned into glucose and the faster it affects the blood sugar levels. This is why people with diabetes are ordered to avoid foods with high glycemic index.
Meanwhile, glycemic load is the number used to accurately show how much carbs get absorbed by our body from all the foods we eat. In one serving of a food, a GL lower than 10 is said to be low, a GL between 11-19 is considered medium, and a GL greater than 20 is considered high. We calculate the GL of a particular food using this following formula:
Glycemic load = (glycemic index x carbohydrate content per portion)/100
Both GI and GL are useful for us to determine which foods may be added to or should be removed from our diets. By knowing the GI, we can see how fast our blood sugar levels can be affected by a certain food. And by calculating the GL, we know how much carbs are absorbed by our body.
However, foods with low glycemic index don’t always mean they can’t affect our blood sugar levels. When consumed excessively, low GI foods will still cause blood sugar spikes. For example, 25 grams of red beans contain 17 grams of carbohydrates, has glycemix index of 20, and a glycemic load of 3,4 which is categorized as low. But when we increase the consumption to 200 grams, the IG will remain the same while the BG will increase to 24, which is said to be high.
Aside from the amount, we should also watch the combination of foods that we consume. Tea and chocolate drink that originally have low IG may turn into high GI beverages if we add sugar to increase the sweetness and enhance the taste. To keep the GI low, and keep the good flavor at the same time, we can use alternative products that we know have low glycemic index and are widely available on the market. Like FiberCreme, high-fiber multi-purpose creamer that we can find easily at stores near us, has glycemic index of 51 which is pretty low, and allows us to conveniently increase our fiber intake. To add sweetness, we can replace our regular sugar with low-calorie sweetener like stevia or monk fruit extract powder.
Foster-Powell, K & Miller, J.B., 1995. International table of Glycemic Index. Am. J. Clin. Nutr. 62: 871S-893S.
Marsono, Y., Wiyono, P., dan Zuheid Noor 2002. Index Glisemik kacang-kacangan. Jurnal Teknologi & Industri Pangan XIII (3): 211-216.
Truswell, A.S. (1992) Glycaemic index of foods. Eur. J. Clin. Nutr. 46 (Suppl;. 2): S91-S101.


Diabetes is a condition that affects how your body uses sugar for energy. It can cause serious complications, such as damage to your eyes, kidneys, nerves, and heart. The most common type of diabetes is type 2 diabetes, which occurs when your body becomes resistant to insulin, a hormone that helps sugar move from your blood into your cells. Type 2 diabetes can be prevented or delayed by making some lifestyle changes.
Here are some tips on how not to get diabetes in future:
Maintain a healthy weight. Being overweight or obese can increase your risk of diabetes, as excess fat can make your cells more resistant to insulin. Losing even a small amount of weight can improve your blood sugar control and lower your risk of diabetes. Aim for a body mass index (BMI) between 18 and 23, which is considered a healthy range.
Be physically active. Exercise can help you burn calories, lose weight, lower your blood pressure and cholesterol levels, and improve your insulin sensitivity. It can also reduce your stress and boost your mood. Try to get at least 150 minutes of moderate-intensity physical activity per week, such as brisk walking, cycling, swimming, or dancing. You can also do some strength training exercises twice a week to build muscle and bone mass. Muscle tissue uses more glucose than fat tissue, so having more muscle can help lower your blood sugar levels.
Eat a balanced diet. Choose foods that are low in added sugars and refined carbohydrates, such as white rice, soda, candy, white bread, and pasta. These foods can spike your blood sugar and insulin levels, which can increase your risk of diabetes. Instead, opt for foods that are high in fiber, such as non-starchy vegetables, whole fruits, brown rice, and millets. Fiber helps slow down the absorption of sugar and keep your blood sugar stable. Also, include lean proteins, such as fish, eggs, chicken, and beans, and healthy fats, such as sesame oil, almonds, nuts, and seeds. These foods can help you feel full and satisfied without raising your blood sugar too much.
Quit smoking. Smoking can damage your blood vessels and increase your risk of heart disease and stroke. It can also make your cells more resistant to insulin, which can lead to higher blood sugar levels. If you smoke, talk to your doctor about ways to quit. There are many options available, such as nicotine patches, gums, lozenges, inhalers, or medications. You can also join a support group or use online resources to help you quit.
Limit alcohol intake. Alcohol can interfere with your blood sugar control and increase your risk of liver problems. It can also add extra calories and carbs to your diet, which can lead to weight gain. If you drink alcohol, do so in moderation and only with food. The recommended limit is one drink per day for women and two drinks per day for men.
Get enough sleep. Lack of sleep can affect your hormones and metabolism, which can increase your appetite and cravings for sugary and fatty foods. It can also impair your insulin sensitivity and raise your cortisol levels, which can lead to higher blood sugar levels. Aim for at least seven hours of quality sleep per night. To improve your sleep hygiene, avoid caffeine and alcohol before bedtime, keep your bedroom dark and cool, turn off electronic devices at least an hour before bed, and stick to a regular sleep schedule.
By following these tips, you can lower your risk of developing diabetes and improve your overall health and well-being.
Dr. Karuturi Subrahmanyam, MD, FRCP (London), FACP (USA)
Internal Medicine Specialist
Phone : 85000 23456


Our wild plants and flowers support all other wildlife, and as they are disappearing from our countryside, so are the birds and pollinators and other creatures that depend upon them.
Many of us are keen to restore meadows, but Plantlife, the conservation charity, cautions against immediately reaching for the seed packet or seed bomb. The challenge is to conserve species while maintaining their essential 'wildness’.
Restoring a meadow can take years, and you will need to take a hay crop in the late summer and ideally have livestock grazing in the autumn and over winter. But if you want to create a wildflower meadow in your garden, you just need an open, sunny space.
If you have an existing lawn, this could be a good starting point. Have a close look at it – it may already be home to wild flowers that mowing has prevented from flowering. The easiest thing to do is to allow the area you have allocated to grow one summer and see what comes up.
If you discover some attractive species that you would like to keep, simply weed out the more aggressive perennial weeds, such as nettles, and add wildflower plugs or seed.
STARTING FROM SCRATCH
1 Remove the topsoil
An ideal time to do this is in July. Wild flowers thrive on nutrient-poor soil, so remove your turf and five centimetres of topsoil. You will need a strong spade and lots of energy, but it is worth it. Not only will this reduce nutrient levels, it is a good opportunity to get rid of weed roots. Once you have removed the topsoil, rake over the ground until you have a fine tilth.
2 Remove the competition
Leave the area for three to four weeks. It is likely that a spread of garden “weeds” may appear, so to ensure the wildflower seed will have a good start, weeding may be needed.
3 Sowing the seed
Do this towards the end of August. You only need one or two teaspoonfuls of seed per square metre, which should be sown on a day with no wind. Buy from a local supplier that provides seed from native British plants, as this will ensure that your flowers will grow happily and be suitable for local wildlife.
4 Adding annuals
Cornfield flower seeds, such as poppies and cornflowers, will give you brilliant colour in the first year while the perennial meadow plants are getting established. They can also help to smother any unwanted “weeds”. Make sure you have some Yellow Rattle seed (see varieties, right), a pretty wild flower in its own right, as this semi-parasitic plant will limit the growth of competing grasses.
5 Mowing is the key
Mow your meadow area at the end of winter to remove any old growth before spring. Then leave it untouched through spring and summer, to allow your wild flowers to grow to their full height. When the flowers are no longer looking their best and have set seed in late summer, give it a thorough mow. Remove the cuttings, otherwise you may be adding unwanted nutrients.
FROM LAWN TO MEADOW
1 Good lawn, bad lawn
The older and “weedier” your lawn, the better. If your lawn is like a bowling green, with fertile soil and no weeds, try to lower the nutrients in the soil by mowing regularly and removing the cuttings. It will take a year or two to get it down to the right nutrient level for wild flowers to thrive.
2 Adding wild flowers
Step 1 will create the right habitat for your plants. You can then add a selection of pot-grown wild flowers or seed. If you prefer seed, cut your lawn very short in the autumn and scarify it with a rake, creating patches of bare soil onto which you can scatter your seed. However, a more successful way is to grow your plants from seed in pots. Sow the seed in autumn and leave the pots outside over winter, as many wild flowers need a cold spell before they can germinate.
Transplant your seedlings into individual pots when they have three or four leaves and concentrate the growth on getting healthy roots by cutting off any flower stems. You can then plant them out into your lawn in the spring.
3 Keep up the mowing
See step 5, above
For more information: Plant Life


Some genetic diseases are caused by a single fault in a 3 billion letter, DNA sequence. With more of our genetic sequence now understood, should we be editing those genes that don’t work properly, or even using this knowledge to eradicate pest populations? Gene editing tools such as CRISPR hold potential to do these things but, what is it and should we be getting excited just yet?
CRISPR (pronounced ‘crisper’) stands for: Clustered Regularly Interspaced Short Palindromic Repeats. Hold on. This is a controversial gene editing tool and was unveiled in 2013, and posed the ability to eradicate diseases such as Huntington’s and Cystic Fibrosis, where the genetic problem had been identified. It also held the potential for ‘designer babies’, providing the opportunity for parents to choose more beneficial or wanted genes for their offspring. This is mainly why the general public objected to it. Many researchers however, were looking at CRISPR’s potential to remove faulty genes and even it’s application in pest control. So how does it work?
A gene editing tool provides the ability to edit an organism’s DNA. DNA is made up of bases (A,T,C,G), and a group of bases make a gene. One gene can be made from anywhere between 100 – 2 million bases. The really hard bit is knowing what part of the sequence of bases causes the fault. Once this is discovered, a gene editing tool can remove, alter or add to the sequence of bases, correcting the problem. CRISPR uses an enzyme (i.e. nature’s catalysts) called Cas9 to target and chop up the DNA sequence where the fault lies. Chopping the sequence will ‘turn off’ the gene and stop the expression which that particular gene codes for. You can also use this method to add in more bases where they are missing and causing disease as a result. Once the change has been made, in theory, this change will be passed to subsequent cells when they divide and grow. What are some applications?
The obvious target would be diseases caused by genetic mutations or lack required genes. One such target could be cancer. At the start of this year (2018), CancerResearchUK published a blog post about the use of CRISPR against cancer cells. Not all cancers are caused by a genetic fault but some are and as a result, are a target for CRISPR research. If it were known which genes caused cancer directly, people could be tested in early life and have this detrimental gene removed. In theory. Tests have been conducted using CRISPR on embryos to successfully remove heart disease causing genes, and make them resistant to HIV. (It should be noted that these embryos were never implanted into a woman, and were not kept for more than 14 days). CRISPR tests on embryos are granted for those which are not to be grown to full term, a HUGE change in ethical law would be required to test further into embryonic growth.
A study was conducted for the first time in mammals to see if researchers could eliminate pests. CRISPR could be used to ensure certain detrimental genetic mutations are passed to offspring, meaning that after only 2 generations the species could be eradicated. An example of this use could be in the elimination of mosquitoes which carry malaria. The idea is not to introduce an entirely new gene but instead, to use those which naturally occur and cause eventual death or infertility. This technique has been tested on mice at the University of California, but the results were hit and miss, not providing a consistent result each time. Please note, the researchers did not give the mice detrimental genes, instead they gave them ones which would express only white fur, to determine if the method would work. The team found that only female mutated mice were able to pass on the new gene to the offspring, and even then it was only a 73% success rate.
The use of CRISPR has seemingly no known bounds. In 2014, CRISPR was used to cure a disease in an adult mammal. Since then, CRISPR has been used to modify genetic material in human embryos, eliminate HIV in mice, and even improve agriculture. However, there is still far to go. Last month, two studies were published in the journal NATURE Medicine, identifying problems with the CRISPR process. They had seen that cells edited with CRISPR were missing key anti-cancer mechanisms, obviously increasing the risk of cancer for those cells. Another paper in NATURE Biotechnology, highlighted issues still to overcome, mentioning that we do not yet know the full effects when we change DNA in gene editing. Preventing the removal of, or damage to ‘good’ DNA, is still to be completely investigated. Therefore, the technology holds potential to be amazing and change the lives of many people with genetic disorders. However, there is still far to go and MUCH more research required before CRISPR can be used as a genetic treatment strategy.


Images and screenshots
Screenshots and other example images:
MDFF with symmetry restraints
- Kwok-Yan Chan
- Leonardo G. Trabuco
- Eduard Schreiner
- Klaus Schulten
(hint: click '+' to add more items)
Fitted a homology model (based on the closed state structure) into the map provided (which is in open state) by the molecular dynamics flexible fitting method. Fittings were done in solvent and here we first let the water and ions equilibrate by constraining the protein, and next we let the side chains equilibrate as well and finally performed the fitting. Symmetry restraints were used to maintain the symmetry.
Chiral errors and cis-peptide bonds in the starting structure were corrected by 2 VMD plugins, Chirality and Cispeptide, and restraints were used to prevent such errors during the fitting.
open-fitted.pdb - Fitting without symmetry restraints
open-symmetry.pdb - Fitting with symmetry restraints
Submitted PDB Models:


Sleep disorders in seniors are more than just a nuisance. The results of a recent study (published in the American Heart Association’s journal Stroke) show that a decrease in the amount or quality of sleep that a senior enjoys can dramatically increase their risk of hardening of the arteries in the brain, This, in turn, can lead to stroke.
The study examined the cases of over 300 patients who lived to the age of 90 and who had undergone at least a full week-long sleep study. When researchers correlated the data they found that individuals with poor sleep patterns (with or without a diagnosed sleep disorders in seniors studied) were much more likely to have suffered at least one stroke than those who enjoyed normal sleep patterns.
In fact, 61% of those with poor sleep patterns had moderate to severe damage to the blood vessels in the brain. That made the at risk group 21% more likely to have blood vessel damage than those who regularly slept through the night.
Sleep Disorders in Seniors Aren’t “Part of Getting Older”
Many of us believe that as we age less sleep is normal. We’ve all heard stories from older individuals who say they only sleep a few hours per night and get by fine the next day. However, no matter what your aging loved one says, their body still needs as much sleep as it did when they were in their 20s.
Sleep allows the body to rest and reset. It’s during our sleeping hours when the majority of the healing process occurs and sleep is essential for both mental and physical health. People who suffer sleep deprivation are at much higher risk for:
High Blood Pressure
Memory and Cognitive Impairment
Obesity (and all the health issues associated with it)


Research may show how poverty shapes the brain
TheGlobeandMail.com – news/national
Published Saturday, Jan. 01, 2011. Anne Mcilroy
Studying “orchid children” could also provide new insight into how poverty shapes the brain.
Preliminary evidence suggests poor children may be more likely to be highly sensitive to their environments, but scientists don’t yet know why this may be the case.
A possible answer is epigenetics, or the way the environment – everything from stress to smoking – can affect the activity of genes.
The genetic code itself is not altered by stress, but studies with laboratory animals have shown the activity of some genes can be affected. The result can be either an increase or decrease in the production of stress hormones or various neurotransmitters that play a key role in the brain.
Tom Boyce and his colleagues at the University of British Columbia are running a series of sophisticated tests to assess whether the stress of living in poverty alters the activity of genes involved in brain development and function.
“We are looking at the DNA involved in neuroregulation, the development of the brain, the control of emotion and so on,” Dr. Boyce says.
< http://www.theglobeandmail.com/news/national/research-may-show-how-poverty-shapes-the-brain/article1855099/ >
TheGlobeandMail.com – news/national/parenting – How to raise an ‘orchid child’ to blossom
Published Friday, Dec. 31, 2010. Last updated Saturday, Jan. 01, 2011. Anne Mcilroy
A brown van with a small laboratory in the back pulls up at Connie Low’s home in Vancouver and a research assistant welcomes the nine-year-old inside. Soon, she is playing a frustrating computer game while machines monitor changes in her heart rate and breathing and assess other signs of stress.
Inside the house, a second member of the research team interviews Connie’s father about his daughter’s health and major events in her life, as well as her temperament and behaviour. How does she react to change or conflict? Does she get upset when her clothes are wet or the bath water is too hot? Is she observant? Do the tags on her clothes bug her?
The questions and tests are designed to identify “orchid children,” the 15 to 20 per cent of youngsters who are highly sensitive to their environments and very reactive to stress. This makes them more vulnerable to health and behaviour problems if they live in stressful conditions, preliminary studies have found. But with careful attention and nurturing, they can thrive and excel.
It is a new theory, a revolution in thinking that recasts genetic vulnerabilities as potential strengths. The University of British Columbia’s Tom Boyce, Anthony Herdman and their colleagues want to learn what is different about the genes and brains of orchid children, as well as the factors in their lives that help them do well. Are mentors, for example, important? What about feeling like being part of a school community or playing a sport?
One day, the work could lead to new screening tools, programs or teaching approaches designed to spot orchid children and help them bloom.
So far, the scientists have assessed 200 eight- to 10-year-old volunteers from a wide range of socioeconomic backgrounds. They plan to do 200 more by the end of the school year.
They collect DNA samples and measure each child’s response to stress. Connie is asked to prepare and deliver a five-minute speech about herself, both good things and bad, and to imagine she is speaking to her class rather than to research assistants and technicians. The research assistant also asks her to count backwards, by 3, from 200.
“There will be some who aren’t responsive at all, some who are exceedingly responsive and a whole bunch in the middle,” says Dr. Boyce, who is also part of B.C’s Child & Family Research Institute.
The exceedingly responsive ones are the orchid children.
The children are also asked to perform a number of tasks designed to allow researchers to learn about their brains. The video game, called flanker fish, is used to assess how well they can focus their attention. Some of the children, although not Connie, are asked to perform other tasks on the computer while a machine measures the electrical activity of their brains.
Dr. Boyce and his colleagues are focused on children, but American psychologist Elaine Aron studies adults who were very likely orchid children in their youth.
She started the work two decades ago when she asked for student volunteers who were introverted and easily overwhelmed by stimulation, like being in a noisy place.
She found these individuals, up 15 to 20 per cent of the population, had much in common: They startled easily, were sensitive to pain, deeply moved by art and sensitive to bright lights, strong smells and coarse fabrics.
Since then, Dr. Aron, who works at Stony Brook University in New York, has written a number of books about highly sensitive people.
She now calls the trait sensory-processing sensitivity and says something similar is found in other animals, including fruit flies, dogs, cats and horses. Individuals with it are more likely to watch and observe a situation before plunging in.
< http://www.theglobeandmail.com/news/national/how-to-raise-an-orchid-child-to-blossom/article1854895/ >


- Which variation is subject to natural selection?
- How do Diploidy and balancing selection preserve genetic variation?
- What is the difference between balancing and stabilizing selection?
- What are 3 types of natural selection?
- What are the 4 types of selection?
- Is balancing selection natural selection?
- Does balancing selection maintain genetic variation?
- What decreases genetic variation?
- Does directional selection reduce genetic variation?
- How does selection affect genetic variation?
- What is an example of balancing selection?
- What are the 3 types of genetic variation?
- Does natural selection increase or decrease genetic variation?
- What are examples of disruptive selection?
- What is positive selection in genetics?
Which variation is subject to natural selection?
Four conditions are needed for natural selection to occur: reproduction, heredity, variation in fitness or organisms, variation in individual characters among members of the population.
If they are met, natural selection automatically results..
How do Diploidy and balancing selection preserve genetic variation?
How does diploidy act to maintain genetic variation? In order to be subject to natural selection, an allele must have an expressed phenotype. In diploid (or polyploid) species, recessive alleles can be maintained, even if they are deleterious, because the phenotype is not expressed in heterozygotes.
What is the difference between balancing and stabilizing selection?
The key difference between stabilizing and balancing selection is that stabilizing selection is a type of natural selection which favours average phenotypes in a population while balancing selection is the maintenance of multiple alleles of a gene within a population in order to enhance genetic diversity.
What are 3 types of natural selection?
Directional selection, stabilizing selection and disruptive selection are three types of natural selection.
What are the 4 types of selection?
19.3B: Stabilizing, Directional, and Diversifying SelectionStabilizing Selection.Directional Selection.Diversifying (or Disruptive) Selection.Comparing Types of Natural Selection.
Is balancing selection natural selection?
Balancing selection means that two alleles are maintained in the population because of natural selection. … This means that the fitness of an individual with two different versions of the allele is higher than the fitness of an individual with two copies of one of the alleles.
Does balancing selection maintain genetic variation?
Balancing selection, on the other hand, brings the favored allele to an intermediate equilibrium, where it is maintained as a genetic polymorphism that potentially increases the variability in the genomic region nearby the selected locus.
What decreases genetic variation?
Sources of Decreased Variation Mutation, recombination, and gene flow all act to increase the amount of variation in the genotypes of a given population. There are also forces at work that act to decrease this variability.
Does directional selection reduce genetic variation?
Directional selection has no effect on the amount of genetic variation in a population.
How does selection affect genetic variation?
Because natural selection acts directly only on phenotypes, more genetic variation within a population usually enables more phenotypic variation. Some new alleles increase an organism’s ability to survive and reproduce, which then ensures the survival of the allele in the population.
What is an example of balancing selection?
A well-studied case is that of sickle cell anemia in humans, a hereditary disease that damages red blood cells. … This is an example of balancing selection between the fierce selection against homozygous sickle-cell sufferers, and the selection against the standard HgbA homozygotes by malaria.
What are the 3 types of genetic variation?
For a given population, there are three sources of variation: mutation, recombination, and immigration of genes.
Does natural selection increase or decrease genetic variation?
Natural selection can decrease the genetic variation in populations of organisms by selecting for or against a specific gene or gene combination (leading to directional selection). … Selection can also prevent speciation by homogenizing the population genetic structure across all locations.
What are examples of disruptive selection?
Disruptive Selection Examples: ColorPeppered moths: One of the most studied examples of disruptive selection is the case of London’s peppered moths. … Oysters: Light- and dark-colored oysters could also have a camouflage advantage as opposed to their medium-colored relatives.More items…•
What is positive selection in genetics?
Positive selection is the process by which new advantageous genetic variants sweep a population. Though positive selection, also known as Darwinian selection, is the main mechanism that Darwin envisioned as giving rise to evolution, specific molecular genetic examples are very difficult to detect.


Programmed death-1 (PD-1) was proven to deliver an inhibitory sign following binding to its ligands PD-L1 (B7-H1) or PD-L2 (B7-DC). cells and PD-L2-expressing Compact disc14+B monocytes. In chosen SLE sufferers and normal topics useful research of PD-1/ PD-1 ligands pathway in the creation of cytokines by activated PBMC was analyzed. Blockages of PD-1 or PD-1 ligands significantly increased the creation of IL-2 IFN-and IL-10 the amplitude Rabbit Polyclonal to Cyclin D3 (phospho-Thr283). of boost roughly ranged in one to 3 x. There have been no significant distinctions of the improving results on cytokine creation by blockage of PD-1/PDL pathway between SLE sufferers and normal topics. The study signifies that we now have no intrinsically faulty appearance and function of PD-1 and PD-1 ligands on PBMC in sufferers with SLE. 1 Launch Programmed loss of life-1 (PD-1) is certainly a novel person in CD28 family members. PD-1 was proven to deliver a poor indication after binding to either of its two ligands PD-L1 (B7-H1) or PD-L2 (B7-DC) in immune system responses [1-4]. On the other hand PD-1 and its own ligands have already been reported to try out an important function in the etiopathogenesis of murine autoimmune illnesses. Spontaneous autoimmune illnesses including lupus-like glomerulonephritis joint disease and fatal autoimmune dilated cardiomyopathy created in PD-1 deficient mice of different genetic backgrounds [5-7]. In addition blockade of PD-1/PD-L pathway could exaggerate or accelerate the development of autoimmune diseases such as diabetes in prediabetic NOD mice and experimental autoimmune encephalitis [8 9 Recently up-regulated manifestation of PD-1 molecule and/or its ligands was shown in human diseases including rheumatoid arthritis (RA) and inflammatory colitis indicating that PD-1 and PD-1 ligands were actively participating in the pathogenetic process in human being autoimmune diseases [10 11 Systemic lupus erythematosus (SLE) is definitely a prototype of human being systemic autoimmune disease characterized by dysregulated activation of both T and B lymphocytes and development of many autoantibodies. Accordingly PD-1 and PD-1 ligands may play a critical part in the pathogenesis of SLE. The present study thus aimed to investigate the manifestation and function of PD-1 and its two Talarozole ligands on peripheral mononuclear cells (PBMCs) in individuals with SLE. 2 Individuals and Methods 2.1 Individuals Twenty-eight individuals Talarozole who fulfilled at least 4 criteria for the analysis of SLE collection from the American College of Rheumatology  were enrolled in the study. They include 26 females and 2 males. All enrolled individuals were not taking corticosteroid and immunosuppressant providers for more than 4 weeks prior to the study. 26 young healthy females were utilized being a control group. Their peripheral blood was drawn and PBMC were isolated for flowcytometric analysis and in vitro culture immediately. 2.2 Measurement of PD-1 and PD-1 Ligands Appearance by Flowcytometry Flowcytometry with dual staining was performed using fluorescece-conjugatd MAbs including FITC-conjugated anti-CD3 anti-CD19 and anti-CD14 (BD Biosciences Sna Diego Talarozole CA USA) and PE-conjugated anti-PD-1 anti-PDL1 and anti-PDL2 (MIH clones e Bioscience Sna Diego CA USA). Quickly PBMC were ready from clean heparinized bloodstream using Ficoll-Hypaque thickness gradient parting and altered to 5 × 106 cells/mL. 2 hundred microliters of cell suspension system had been incubated with 20 < concurrently .001) and PD-1-expressing Compact disc19+B cells (5.11 ± 3.91% versus 2.14 ± 1.67% < .005). Relating to PD-1 ligands SLE sufferers had even more PD-L1-expressing Compact disc19+B cells (20.59 ± 10.24% versus 13.21 ± 1.67% < .005) and PD-L2-expressing Compact disc14+monocytes (84.78 ± 12.82% versus 72.12 ± 26.92% < .005) than normal controls. Despite somewhat elevated frequencies of PD-1 and PD-1 ligands appearance in a few cell populations from SLE sufferers the indicate fluorescence intensities of PD-1 and PD-1 ligands appearance over the positive cells weren't considerably different between sufferers with SLE and regular controls (data not really shown). The full total result shows that the expression of PD-1/PD-1 ligands had not been impaired in human SLE. 3.2 Ramifications of Blocking PD-1/PD-1 Ligands Pathway on Cytokines Creation by Stimulated PBMC In Vitro Cytokines are believed to play a significant function in the pathogenesis of SLE. We hence made to investigate the useful ramifications of preventing PD-1 or PD-1 ligands over the creation of varied cytokines made by in vitro cultured PBMC. The cytokines analyzed in the analysis included Th1-produced cytokines (IL-2 and IFN-production was more Talarozole powerful in SLE. The differences didn't Nevertheless.


Purpose The goal of this study was to judge the result of aldose reductase (AR) inhibition on Posterior capsular opacification (PCO) using pig eye capsular bag super model tiffany livingston. of pig eyes capsular luggage, residual cells on both anterior and posterior capsule demonstrated vigorous development. Treatment with AR inhibitors considerably prevented the zoom lens epithelial cell development in capsular luggage and appearance of -SMA, -crystallin and ICAM-1. HLEC demonstrated a dose-dependent response to b-FGF, proliferation at lower Oxymatrine (Matrine N-oxide) ( 20 ng/ml) and differentiation/transdifferentiation at higher ( 50 ng/ml) concentrations. Inhibition of AR also avoided the b-FGF -induced activation of ERK1/2, JNK and NF-B in HLEC. Conclusions Our outcomes claim that AR is necessary for zoom lens epithelial cell development and differentiation/transdifferentiation in the capsular luggage indicating that inhibition of AR is actually a potential healing target in preventing PCO. aswell for 10 min at 4C. Aliquots from the lysates filled with equal quantity of proteins (40 g) had been separated on 10% SDS-polyacrylamide gels and used in polyvinylidene difluoride membranes (Immobilon; Millipore, Bedford, MA). The membranes had been after that incubated in preventing solution filled with 5% wt/vol dried out fat-free dairy and 0.1% vol/vol Tween-20 in tris-buffered saline. Subsequently, the membranes had been incubated with antibodies against CSMA, -crystallin, ICAM-1, phospho-p38, phospho-ERK1/2, phospho-SAPK/JNK, and total-p38, -ERK1/2 and CSAPK/JNK. The membranes had been cleaned and probed using the particular HRP- conjugated supplementary antibodies (SouthernBiotech, Birmingham, AL) and visualized by chemiluminescence (Pierce biotechnology, Rockford, IL). All blots had been probed with GAPDH or -actin being a launching control and proteins band intensities had been dependant on densitometric analysis through the use of Kodak Image place 2000R. Electrophoretic Flexibility Change Goat polyclonal to IgG (H+L) Assay (EMSA) The HLEC had been pretreated with or without AR inhibitors for 24 h in serum free of charge medium, accompanied by treatment with b-FGF (50 ng/ml) for extra 1 h. The nuclear ingredients were ready as defined previously.26 The Consensus oligonucleotides for NF-B transcription factors were 5-end labeled using T4 polynucleotide kinase. EMSA was performed as defined previous.26 The specificity from the assay was examined by competition with an excessive amount of unlabeled oligonucleotide and supershift assays with antibodies to p65. NF-B-Dependent Secretory Alkaline Phosphatase (SEAP) Appearance Assay To examine NF-B promoter activity in HLEC in response to b-FGF treatment, cells (1105 cells/well) had been plated in 24-well dish. The cells had been starved for 16 h in 0.5% FBS medium without or with AR inhibitors and transfected with pNF-B-SEAP2-construct and pTAL-SEAP control plasmid (Clontech, USA) using Lipofectamine plus (Invitrogen, Carlsbad, CA) transfection reagent following suppliers instructions. After 6 h of trasnfection, cells had been activated with b-FGF (50 ng/ml) for 48 h. The cell tradition media were gathered and centrifuged Oxymatrine (Matrine N-oxide) at 5000 rpm Oxymatrine (Matrine N-oxide) and supernatants had been kept at ?80C. The moderate was thawed and useful for chemiluminescent secretory alkaline phosphatase (SEAP) assay using Great EscAPeTM SEAP reporter assay program according to process essentially as referred to by the product manufacturer, (BD Biosciences, Palo Alto, CA) utilizing a 96-well chemiluminescence dish reader. All of the recommended controls by producers were found in the assay. RNA disturbance ablation of AR HLEC had been cultivated to 60% confluence in DMEM supplemented with 20% FBS in 6-well dish. The cells had been incubated with OptiMEM moderate comprising the AR-siRNA (AATCGGTGTCTCCAACTTCAA) or scrambled siRNA (AAAATCTCCCTAAAT CATACA; control) to your final focus of 100 nM as well as the RNAiFectTM transfection reagent (Qiagen) as referred to by us previous.38 Briefly, for every well, 2 g AR siRNA was diluted in serum-free moderate to give one last level of 100 l and incubated with 6 l RNAiFect? for 15 min at space temp. The transfection blend was put into the particular wells, each comprising 1900 l full moderate (20% fetal bovine serum), and incubated for 24 h. After 24 h, the moderate was changed with clean DMEM.


CBD treats for dogs have gained popularity as pet owners seek natural remedies to improve their furry friends’ well-being. Cannabidiol (CBD), a non-psychoactive compound derived from the cannabis plant, cbd treats for dogs has shown promising benefits for various health issues in dogs, making it a popular choice for holistic pet care.
One of the primary reasons pet owners turn to cbd treats for dogs is to alleviate anxiety and stress in their dogs. Dogs, like humans, can experience anxiety due to various factors such as separation, loud noises, or changes in their environment. CBD interacts with the endocannabinoid system in dogs, helping to regulate mood and reduce stress levels. Many pet owners have reported positive results, with their dogs exhibiting calmer behavior after incorporating CBD treats into their routine.
Another significant application of CBD treats for dogs is in managing pain and inflammation. Aging dogs or those suffering from conditions like arthritis may experience discomfort and reduced mobility. CBD has anti-inflammatory properties that can help alleviate pain by targeting the source of inflammation. This makes it a natural alternative to traditional pain medications, which may have potential side effects.
CBD treats may also have a positive impact on dogs with epilepsy or seizures. Some studies suggest that CBD can help reduce the frequency and severity of seizures in dogs with epilepsy. While more research is needed to fully understand the mechanisms behind this, anecdotal evidence from pet owners suggests that CBD treats can be a valuable addition to the treatment plan for dogs with seizure disorders.
Skin conditions, such as allergies or dermatitis, are common in dogs and can cause discomfort and itching. CBD’s anti-inflammatory and immune-modulating properties may provide relief for dogs with skin issues. Pet owners have reported improvements in their dogs’ coat condition and a reduction in itching after incorporating CBD treats into their pets’ diet.
It’s crucial for pet owners to choose high-quality CBD treats specifically designed for dogs. These treats should be free from THC, the psychoactive compound found in cannabis, as it can be harmful to dogs. Additionally, proper dosing is essential, and consulting with a veterinarian before introducing CBD treats is advisable, especially if the dog is on other medications.
CBD treats for dogs offer a natural and holistic approach to supporting their overall well-being. Whether managing anxiety, alleviating pain, or addressing specific health issues, many pet owners have found CBD treats to be a valuable addition to their dogs’ daily routine. As with any supplement, it’s essential to prioritize the health and safety of the furry companions by choosing reputable products and consulting with a veterinarian when in doubt.


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High fructose corn syrup (HFCS) is corn syrup whose glucose has been converted to fructose. It is an artificial sugar made from corn syrup. Glucose is easily transported and utilized by every cell in your body. It’s also the predominant fuel source for high-intensity exercise and various processes. Your body metabolizes fructose differently than glucose, and consuming too much fructose can lead to health problems. It is a common sweetener in sodas and fruit-flavored drinks. As use of high-fructose corn syrup has increased, so have levels of obesity and related health problems.
High-fructose corn syrup is a sugar-based sweetener, used in processed foods and drinks in the United States. Like regular sugar, it consists of the simple sugars glucose and fructose.
It’s important to note that the detrimental effects of fructose in added sugar, including HFCS, should not be equated with the fructose in fruit. The conversion produces sweetness of desired types. The material is used in many breads, cereal, sodas, yogurt, and breakfast bars. In contrast, the fructose from high fructose corn syrup or table sugar needs to be converted into glucose, glycogen (stored carbs), or fat by the liver before it can be used as fuel.
To create HFCS, manufacturers add enzymes to corn syrup that convert some of the glucose to fructose. HFCS is derived from corn starch. Fructose is the type of sugar present in fruit and is very sweet. When corn starch is broken down into individual glucose molecules, the end product is corn syrup, which is essentially 100% glucose. The amount of fructose in HFCS varies, but the most common varieties contain either 42% or 55%. HFCS is ‘high’ in fructose compared to the pure glucose that is in corn syrup. Research has consistently shown links between the consumption of HFCS and obesity, metabolic dysregulation, and similar health issues.
High fructose corn syrup was first introduced during the late 1950s. The fructose in HFCS can cause health issues if eaten in excessive amounts. The material did not come to the United States until the late 1970s into the 1980s. It is a sweetener that manufacturers make from corn starch. As with other sugars, it can cause tooth decay, obesity, and metabolic syndrome when a person consumes it in large quantities.
High fructose corn syrup has been linked to obesity, diabetes and certain other health matters. Like regular table sugar, HFCS is a rich source of fructose. In the past few decades, the intake of fructose and HFCS has increased significantly. It’s difficult to consume excessive amounts of fructose from whole fruits, which are healthy and safe in sensible amounts. Due to its fructose content, it has been heavily criticized for its potential negative health effects. Many people claim that it’s even more harmful than other sugar-based sweeteners.


2012 Seven Things to tell your friends about GMO (Fact Sheet)
In the 1990s, GMOs took off in the US without public debate and today they’re in most processed foods — making Americans the world’s GMO guinea pigs. Now, peer-reviewed and other authoritative studies reveal that: 1. GMOs HAVE NEVER UNDERGONE STANDARD TESTING OR REGULATION FOR HUMAN SAFETY. And now that they’re in 70 percent of processed foods it’s extremely difficult for scientists to isolate their health risks. 2. BUT WE KNOW THAT GMOs HAVE PROVEN HARMFUL IN ANIMAL STUDIES. A 2009 review of 19 studies found mammals fed GM corn or soy developed “liver and kidney problems” that could mark the “onset of chronic diseases.” In a new 2-year study, rats fed GM corn developed 2-3 times more tumors and they appeared much earlier than those fed non-GM corn. Among scientists, both defenders and critics underscore that we need more long-term studies. 3. AND THE MOST WIDELY USED GMOs ARE PAIRED WITH AN HERBICIDE LINKED TO SERIOUS REPRODUCTIVE PROBLEMS AND DISEASE. GM crops – Roundup Ready soy & corn – are treated with the herbicide glyphosate. A physicians’ study found people exposed to glyphosate had increased risk of miscarriages, birth defects, cancer, and neurological problems in children. Neurologists report that herbicides, especially glyphosate, “have been recognized as the main environmental factor associated with ... Parkinson’s disease.” 4. THE CONSEQUENCES OF GMO TECHNOLOGY ARE UNPREDICTABLE. Inserting a single gene can result in multiple, unintended DNA changes and mutations. “Unintended effects are common in all cases where GE [genetic engineering] techniques are used,” warn scientists. One such environmental consequence—genetic contamination of other plants—is already documented. Note that unlike food, once released into the environment, seeds can’t be “recalled”! 5. GMO MAKERS INTIMIDATE AND SILENCE FARMERS AND SCIENTISTS. GMO corporations use patents and intellectual property rights to sue farmers, block research, and threaten investigators. “For a decade,” protested Scientific American editors in 2009, GMO companies “have explicitly forbidden the use of the seeds for any independent research” so “it is impossible to verify that genetically modified crops perform as advertised.” 6. GMOs UNDERMINE OUR FOOD SECURITY. Because three GMO companies – Monsanto, DuPont, and Syngenta – control 70% of the global seed market, GMOs reinforce monopoly power over our food. GMO seeds are costly and must be purchased every year, so they worsen farmers’ indebtedness, dependency, and vulnerability to hunger. 7. GMOs AREN’T NEEDED IN THE FIRST PLACE, SO WHY WOULD WE TAKE ON THESE RISKS AND HARMS? Studies show that safe, sustainable farming practices applied worldwide could increase our food supply as much as 50 percent. And keep in mind that the world’s already producing 2,800 calories for every person on earth every day — more than enough. And that’s just with what’s left over: Half the world’s grain goes not to people but to feed, fuel and other purposes. Plus, one-third of all food. So the urgent question isn’t about “more” anyway. It is, How can all of the world’s people gain the power to secure healthy food? And a good start is knowing what’s in our food.
1. Source for GMOs in 70% processed foods: California Department of Food and Agriculture, “A Food Foresight Analysis of Agricultural Biotechnology: A Report to the Legislature,” Jan. 1, 2003. www.cdfa.ca.gov/files/pdf/ag_biotech_report_03.pdf. Source for safety testing: Freese, W. & Schubert, D., “Safety testing and regulation of genetically engineered foods,” Biotechnol Genet Eng Rev, 2004: 299-324. www.saveourseeds.org/downloads/schubert_safety_reg_us_11_2004.pdf. 2. Source for GM corn study: Séralini, G.-E., et al., “Long term toxicity of Roundup herbicide and a Roundup-tolerant genetically modified maize,” Food and Chemical Toxicity, http://dx.doi.org/10.1016/j.fct.2012.08.005. Source 19 GM corn and soy studies: Séralini G.-E. et al., “Genetically modified crops safety assessments: Present limits and possible improvements,” Environmental Sciences Europe, 2011; 23(10). www.enveurope.com/content/23/1/10 3. Sources for miscarriages, birth defects, cancer: Report from the 1st NATIONAL MEETING OF PHYSICIANS IN THE CROP-SPRAYED TOWNS, Faculty of Medical Sciences, National U. of Cordoba. Aug 2010, University Campus, Cordoba Coordinators: Dr. Medardo Ávila Vazquez, Prof. Dr. Carlos Nota. www.permaculturenews.org/files/INGLES-Report-from-the-1st-National-Meeti.... Source for link to Parkinson’s Disease: Gui, Y. et al., “Glyphosate induced cell death through apoptotic and autophagic mechanisms,” Neurotoxicol Teratol. March 27, 2012; 34: 344-349. http://www.sciencedirect.com/science/article/pii/S0892036212000438 4. Source for unpredictability: Wilson, A.K. et al., “Transformation-induced mutations in transgenic plants: Analysis and biosafety implications,” Biotechnol Genet Eng Rev, 2006; 23: 209–238. www.somloquesembrem.org/img_editor/file/Wilson%2006%20BGER.pdf. Source for 1st quote: Freese, W. & Schubert, D., “Safety Testing and Regulation of Genetically Engineered Foods,” Biotechnology and Genetic Engineering Reviews, Nov 2004; Vol. 21. www.intercept.co.uk/gb/not.asp?id=RS6HS3O6S6ROTD&rec=oui&pos=0&referer=%.... Source for genetic contamination: Quist, D. & Chapela, I., “Transgenic DNA introgressed into traditional maize landraces in Oaxaca, Mexico,” Nature, Nov 29, 2001; 414: 541-543. http://www.nature.com/nature/journal/v414/n6863/full/414541a.html. Source for 2nd quote: Cummings, C. H., “Trespass: Genetic Engineering as the Final Conquest,” WorldWatch Institute, World Watch Magazine, Jan/Feb 2005: 18(1), http://www.worldwatch.org/node/568 5. Waltz, E. “Under wraps – Are the crop industry’s strong-arm tactics and close-fisted attitude to sharing seeds holding back independent research and undermining public acceptance of transgenic crops?” Nat Biotechnol, Oct 2009; 27(10): 880–882. www.nature.com/nbt/journal/v27/n10/abs/nbt1009-880.html. See also: Center for Food Safety. “Monsanto vs. US farmers: Nov. 2007 Update.” Washington, DC & San Francisco, CA. Nov. 2007. www.centerforfoodsafety.org/pubs/Monsanto%20November%202007%20update.pdf. For Scientific American editors: The Editors, “Do Seed Companies Control GM Crop Research?” Scientific American, Aug 13, 2009. www.scientificamerican.com/article.cfm?id=do-seed-companies-control-gm-c.... 6. Source for Monsanto 90% statistic: Marie-Monique Robin, “The World According to Monsanto: pollution, corruption and the control of our food supply,” The New Press, 2010, http://thenewpress.com/index.php?option=com_title&task=view_title&metapr.... And: Center for Food Safety, “Monsanto vs. US Farmers,” 2005: www.centerforfoodsafety.org/pubs/CFSMOnsantovsFarmerReport1.13.05.pdf Source for GMO monopoly statistic: GRAIN, “Global agribusiness: two decades of plunder,” July 13, 2010. www.grain.org/article/entries/4055-global-agribusiness-two-decades-of-pl.... Source for GMO impacts on farmers: FAO, “Weighing the GMO arguments: against,” FAO Newsroom, 2003. www.fao.org/english/newsroom/focus/2003/gmo8.htm. 7. Source for producing plenty: Badgley, C. et al., “Organic Agriculture and the Global Food Supply,” Renewable Agriculture and Food Systems, 22 (2007): 86-108. http://journals.cambridge.org/action/displayAbstract?fromPage=online&aid.... Source for calories: FAOSTAT, Food Balance Sheets, Commodity Balances, 2009, faostat.fao.org/site/368/DesktopDefault.aspx?PageID=368#ancor Grain statistic calculated from: FAO, “Crop Prospects and Food Situation,” Oct. 2007, No. 5, Table 2 ftp://ftp.fao.org/docrep/fao/010/ah873e/ah873e00.pdf Source for food wasted: FAO, “Global Food Losses and Food Waste,” Rome: 2011, http://www.fao.org/docrep/014/mb060e/mb060e00.pdf [verified 4/17/14]


Antibody tests to determine if a person has had a past infection of COVID-19 may be wrong up to half of the time, according to the CDC.
"I don't think we should be making any decisions using those antibody tests," said Dr. Sanjay Gupta.
Dr. Gupta says a lot of the antibody tests initially put out were not good. The FDA has since put out a policy requiring antibody test makers to submit emergency authorization requests, along with proof the tests work.
"False positives is the worst kind of results because you think if I've got the antibodies, I'm good to go -- you're not and so the tests aren't good enough right now," said Dr. Gupta.
The CDC says health officials or healthcare providers using antibody tests need to use the most accurate tests they can find and might need to test people twice.
"Also we still don't know the exact meaning of what the antibodies are going to provide in terms of how long people would be protected as a result of these antibodies how strong these antibodies will be," explained Dr. Gupta. "It's likely they'll have some protection but we just don't know the extent of it yet."


The first divers visiting Alor have written enthusiastically about the dive sites being full of schools of fish and sharks (there is even dive site called Sharks Galore see No 12). Nowadays you come here more for the beautifully covered walls and the interesting critters you find in the muck here. In 2015 I spend 2 weeks in Alor and we didn’t see many sharks except while snorkelling in front of our resort in Kepa, but I took loads of photos of the smaller critters there, among them some nudibranch species I hadn’t seen in my over 20 years of diving except in books! So I think it is still well worth to come here, just enjoy the spectacular walls and the weird critters!
Alor Island, situated in the east of Indonesia (Nusa Tenggara) has become more and more accessible with flights from Denpasar / Jakarta to Kupang and daily flight on to Alor. Alor can also be reached by ferries either from Kupang (Timor) or overland from Maumere (Flores) through Lembata and Pantar. There are 4 dive centers in Alor and Pantar and also liveaboards stopping in the area.
Between the islands of Alor and Pantar lies the strait of Pantar (Selat Pantar). Here the water coming from the Pacific in the north is flowing through this strait to the Indian Ocean in the south. This big “river” in the ocean is called the Indonesian Throughflow (see dive conditions in Komodo or southern Bali, where the situation is similiar) and the Pantar strait is one of the few gaps in the long chain of islands reaching from Sumatra to Timor where it can flow through, mostly from north to south. The smaller islands of Pura, Kepa, Ternate and Buaya lie smack in the middle of the strait and where the strait narrows the currents can be quite fierce. At some places the currents are so strong, that boats get turned sideways and have to really fight to reach places up current.
Water temperatures are around 27 degrees, but especially in the south it can get quite cold – we had 23 degrees at some of the dive sites. Cold water is upwelling from the very deep parts north of Alor and then hitting the southern shores. This also means that sunfish (Mola mola) and Thresher sharks come up from the deep to get cleaned. Sometimes very strange animals appear from the depth (see Lophiodes fimbriatus (video), a deep sea anglerfish). The bay is somewhat protected, so there are often large pods of dolphins and whales travelling through.
Want to know more about how to assess accurately the rate of current? Click here.
1. Kal's Dream (Pulau Kepa) - 2. The Bullet - 3. Tri-Top - 4. Mucky Mosque - 5. Pertamina Pier - 6. Dive Logs - 7. The Mini Wall - 8. No Man's Land - 9. The Cathedral (Motolang) - 10. Hari Lalong - 11. School's Out - 12. Sharks Galore - 13. Clown Valley (Apuri) - 14. Malal - 15. Slab City - 16. The Boardroom (Tangaban) - 17. Smart's Lament (Abila Wall) - 18. Coconut Grove (Teluk Limraning) - 19. Sea Apple Slopes - 20. Bama - 21. Pan Abang - 22. The Arch - 23. Babylon - 24. Coral Cliffs - 25. The Edge (Umapura) - 26. Crocodile Rock - 27. Peter's Prize - 28. Half Moon Bay - 29. Cave Point - 30. Nite Delight - 31. The Patch - 32. Fault Line
A) La P’tite Kepa Divers (www.alor-diving.com) based on Kepa Island close to Alor
B) Alor Dive (www.alor-dive.com) based in Kalabahi
C) Alami Alor Dive Resort (www.alamialor.com) based in the Bay of Kalabahi
D) Eco Dive Resort Alor (www.alor-divers.com) based on northern Pantar
Dive Alor Dive (www.divealor.com) based in Kupang (Timor)
Some of the dive operators are closed in winter. And - since internet connections are difficult fast answers to mails are not always possible....!
1. Kal's Dream (Batu Kepa): You dive on two underwater pinnacles (top = 7m and 2m) lying northwest of Kepa island. The currents coming from the north hit these rocks smack on, so most of the time it is too wild to dive here. Sometimes the currents also shift and what was a nice dive turns into an up and down, left and right tugging experience!
On my first trip to Alor in 2002 with a liveaboard this dive site was supposed to be the ne plus ultra with large fish, sharks and rays. Actually at the start of our first dive it seemed like great things were to come - we saw a group of barracudas, then a whitetip shark and a large marble ray. When these animals disappeared, there was nothing more to report. Nearly no medium sized fish, just Anthias over corals and current. We waited and waited, but nothing large showed. On our second dive not even a single large fish showed up. The most adventurous thing was actually surfacing among the up and down currents where one of my dive buddies came up with 20 bars left, because he was swept down to a considerable depth before he was able to surface.
Coming back in 2015 I dived with Cedric from La P’tite Kepa. He knows the divesite inside out and he checked out the dive conditions on the site over several days. So when we actually dived there, the currents had calmed down for most of the dive, though they switched and picked up somewhat towards the end. We even managed to first dive around the deeper pinnacle and also follow part of the spur going out to a corner where there were lots of fish gathering and then leisurely swim over to the other pinnacle and finish our dive there. We saw a large dogtooth tuna, three large Napoleon wrasses, two of the fighting with each other, some trevallies and sweetlips. The pinnacles are nicely covered, though corals are low lying because they are exposed to the currents. Interesting were also some Coral Crouchers (Caracanthus maculatus) and several Yellow-spotted Scorpionfishes (Sebastapistes cyanostigma) packed tightly between the branches of an Acropora coral. Still a spectacular dive site, but only dive there, if the conditions are right!
This narrow and steep bay looks like a finger pointing to the east and it nearly separates Alor kechil (small Alor) from Alor besar (big Alor). The bay is quite long and deep with some pearl farms and fishing rafts close to the shore. The terrain is very rugged with Kalabahi situated where Alor kechil and Alor besar are joined together - the only flat area...
4. Mucky Mosque dive sites: Along the northern coast of Kalabahi bay are several muck dive sites. These dive sites are also good for night dives. You find everything you want, from Rhinopias scorpionfishes to leaffishes, ghostpipefishes (Halimeda, Ornate and Robust) to frogfishes, seahorses and dragonets as well as crabs, shrimps and a lot of different nudibranchs. Often long ropes covered with hydroids and small corals come down from the shore – a good place to look for frogfishes perching there. On one of my dives a big black Giant frogfish was actually swimming away from one of these ropes and trying to perch on my (black) camera housing instead. When I moved away (I wanted to take photos of the frogfish swimming!) it decided on the next dark place which was one of my dive buddies. It made straight for him as if attacking him and ended up sitting on his chest, face to face with him! Probably thought he was a nice black sponge……
5. Pertamina Pier and 6. Dive Logs: Further up towards Kalabahi close to the Pertamina Pier is another nice muck dive site – lots of sand but with many interesting animals living on it. I found a fingered dragonet, two Ambon scorpionfishes, juvenile batfishes and lots of squat lobsters, some on featherstars, some on sponges and a nice selection of slugs and nudis. My dive guide told me, you also find the Wonderpus (Wonderpus photogenicus) and Mimic Octopus (Thaumoctopus mimicus) here. On the other side of the bay (Dive Logs) there is an area with mangroves which is also very interesting for muck diving. Here you can find Randall's goby, the metallic goby, waspfishes and also Rhinopias and other interesting scorpionfishes.
9. The Cathedral (Motolang): I really liked this dive site! Above water there is a steep rock wall descending into the sea, so underwater there are huge jumbled rocks and boulders and a steep wall covered with lots of hard and soft corals and sponges. We saw Barbiganti seahorses, a Potohi Seahorse (in the Halimeda algae), a bluering octopus and two different species of frogfish. There is a swim through with a cave at about 25 meters and we were lucky and found a huge tawny nurseshark (Nebrius ferrugineus) lying in the cave there.
10. Hari Lalong: A really beautiful dive site with huge rocks lying side by side with many narrow spaces in between to swim through. There was a hidden comet fish, mandarin fishes and a large morey eel which was gaping at us. Good for a slow drift dive with a gentle slope at the end, covered with soft corals and plenty of small fish. You finish the dive leisurely following a small group of Barracudas in the shallow and taking a close look at the huge coral blocks covered with glassfishes.
12. Sharks Galore: Our dive started in the dive site called Sharks Galore but the sharks must have all been on vacations because we didn't see a single one. The underwater landscape is quite nice and like in other dive sites along the eastern coast of Pura there were a lot of anemones. Coming out of the water our dive guide laughed and said he had just thought of a new name for this dive site - “Sharks No More”.
13. Clown Valley (Apuri): This dive site is astonishing, because every surface is covered in sea anemones. Nearly all of the anemones I believe are Bulb-tentacle Sea Anemone (Entacmaea quadricolor) mostly with Clarks Anemonefishes (Amphiprion clarkii) and a few with Tomato Anemonefish (Amphiprion frenatus) in them. Considering how many anemones there are – I calculate there must be millions - there are only relatively few anemone fishes living in them. I often saw them flitting from one anemone to the next when I approached, so they seemed to change their host frequently. Apart from the anemones we saw also some sea apples (see Sea Apples Slope No 19) and – what a nice surprise – two yellow Miamira miamira nudibranchs in the shallow. While surfacing we also noticed bubbles coming out from the ground – a testimony to the volcanic nature of Pura Island.
14. Malal: This is another dive site where the entire area is covered with thousands of anemones. Just for that it is well worth to go there, it is a sight seen only in very few places. The reason for this abundance of sea anemones is unclear. Apart from the anemones we were lucky to find a Wobbegon shark (Orectolobus leptolineatus), a smaller species than Wobbegon sharks in Papua and with only a few tassels.
Pura island is a small volcano cone island, the extinct volcano is 1015m high with a heavy forested crater. Pura being an extinct volcano there are several dive sites where there are air bubbles coming out from the ground, mostly in the shallow sandy areas.
16. The Boardroom (Tangaban): A muck dive site with low coral cover on a slope. My dive guide found two pegasus sea moths, a pair of robust ghostpipefishes and a large Kentrodoris rubescens nudibranch which in my opinion looks just like a poodle without legs....!
17. Smart’s Lament (Abila Wall): A nice wall with lots of small crannies, covered with soft corals, black coral bushes and hydroids. Halfway on the wall there is a huge Elephant Ear sponge, perhaps 3 meters wide, like a vertical barrier. Lots of yellow cup corals, so if there is some current it must look really beautiful with the tentacles out. During our dive the current picked up and we had schools of fusiliers and hunting jackfishes.
18. Coconut Grove (Teluk Limraning): You descend on dark volcanic sand mixed with small coral boulders covered with soft corals and hydroids. Doesn’t look like much but to my amazement our dive guide Bram found three Weedy Scorpionfishes (Rhinopias frondosa) in reddish-brown-yellow colours and with a lot of skin flaps. Every time I took a photo and looked away to adjust my camera settings and looked again I found it hard to find the scopionfish again, it was so well camouflaged! They seemed to disappear among the algae and soft coral, even imitating the jerky movements of algae in a swell.
I think we were lucky to find so many Rhinopias since they also seem to move around, so sometimes you might find them on one dive site, then at the on one next over…
See also my text about Rhinopias – are Rhinopias frondosa and Rhinopias eschmeyeri the same species?
I only visited the dive sites on the east coast of Pantar close to Pura island. The southern part of Pantar is dominated by Gunung Sirung (862m), an active stratovolcano which errupted last in 2012. You can hike up to the crater rim from nearby village Kakamauta. There is large suphurous crater lake and active steam vents inside the caldera. A small natural harbour, Beangabang Bay, lies in the southeast of the volcano (not on the map) with three dive sites (Hot Property, Ribbon Eel Run and The Lava Flow), all of them on black sand with lots of critters. The water here is generally colder.
19. Sea Apple Slopes: The further south you go the colder it gets but like in the Komodo islands but this also means some special animals are living here. This is a good place to find the rare filter-feeding sea cucumbers called sea apple (Pseudocolochirus violaceus). This sea cucumber is round like a football and of a bright red and purple colour with white or yellow stripes. Long colourful tentacles grab small plankton animals from the water and transfer them to the mouth opening on top of the sea cucumber. Small yellow sea cucumbers (Colochirus robustus) are also found here, some clinging in large numbers to the underside of the brownish leaflike sponges (Phyllospongia sp) found here.
20. Bama: After a boat ride from Kepa with sightings of bottlenose and Fraser dolphins we dived on this nice slope on the east side of Pantar. The strait narrows so there is sometimes quite some current on this dive site. The whole dive site is just covered with fish – anthias, butterflyfishes, triggerfishes, surgeonfishes, damselfishes. Out in the blue lots of Long jawed Mackerels (Rastrelliger kanagurta) were swimming in a tightly bunched school, feeding on plankton with their mouths opening simultaneously and schools of fusiliers were passing by. When we came to the wall the current started to pick up and we were swept alongside. Our guide found nudis, flatworms and in one of the black coral bushes a longnose hawkfish. I spent a lot of time looking into the blue, though, because there were groups of bluefin trevallies (Caranx melampygus) out hunting. Deeper down I even saw a Napoleon wrasse, but my computer told me – too deep for you….
21. Pan Abang: This is one of several dive site lying close to the Eco Dive Resort in northern Pantar. It is a good muck dive site where you can see interesting critters like Wunderpus, Mimic octopus, Rhinopias, ghostpipefishes, spearing mantis shrimp, frogfish, devil fish, pegasus and Coleman shrimps. You dive on sand interspaced with some corals.
22. The Arch: This place is very beautiful! On the wall huge underwater cervices form a large arch at about 20 to 30 meter. Very healthy coral cover with whip corals and gorgonians. On some of the over 3 meter long whip corals you might find the rare Wire Coral Shrimp (Pontonides ankeri). I also saw some interesting animals in the upper part of the reef such as the marble dragonet, some special filefish and nudibranchs such as Jorunna funebris. Some dive sites have very impressive topography like big walls, arches, chimneys, cracks and overhangs, this is one of them!
23. Babylon: Our dive guide who likes Bob Marley was trying to sing underwater to live up to the Caribbean name of this dive site while I was looking for nudibranchs and found 6 different species of them - Alor is always quite a good place for nudies. This is a nice dive site with some interesting overhangs at 30 meters.
24. Coral Cliffs: A steep wall with a lot of whip corals, some 3 to 4 meter long. Nice dive but not so spectacular.
25. The Edge (Umapura): For this wall dive it is well worth coming all the way to Ternate. When you perch on top the wall seems to go down and down and then disappear! There are overhangs and small crevices everywhere, sponges, black coral bushes and large corals cover everything. We had a leisurely dive along the wall, shining our lights into all the holes and crannies and just having a great time. And as a highlight, already on our way back and during the safety stop our guide Bram found a white frogfish perching on some blue sponges under an overhang! We spent our safety stop watching it luring and yawning in between.
29. Cave Point: A nice easy dive on a wall riddled with small caves between 20 and 35 meter. The wall is nicely covered with corals and sponges and we found a lot of nudibranchs and had a nice long swim with a banded sea krait (Laticauda colubrina).
I did several night dives, mainly on some of the muck dive sites in Kalabahi Bay and I really recommend that you include som, while you are staying in Alor since they were all truely spectacular!! On each we saw a great many nudibranchs, with several species I didn’t know before (Ceratosoma moloch, several Marionia species,Pleurobranchaea brockii, Phestilla melanobranchia and more), although I dive since 20 years. Then cuttlefishes and octopuses, shrimps and crabs, stargazers, stonefishes, pegasus sea moths, ghostpipefishes, frogfishes (a black frogfish at night, luring…..) and much more…!
The dive operators also offer night diving, mostly close to the resort in sheltered bays. Try places like Nite Delight No 30, The Mini Wall No 7 or some of the muck dive sites (4. Mucky Mosque, 5. Pertamina Pier and 6. Dive Logs) I described above.
Description of dive sites
- Dive safety in South East Asia -
judge the currents
Bali - Borneo and Kalimantan - Burma and Thailand - Malaysia (east coast) - Manado, Lembeh and Siau islands - Nusa Tenggara (Lombok, Sumbawa, Komodo, Flores, Alor) - Moluccas (Ambon, Banda, Halmahera) - Palawan (Sangat, Tubbataha) - Sulawesi - Sulawesi central - Visayas (Bohol, Cebu, Negros, Siquijor)
Print version reports
Alor - Bali east - Bali north - Bali south - Bangka - Bohol - Borneo overview - Bunaken - Burma - Cebu - Flores - Gorontalo - Kalimantan - Komodo - Lankayan - Lembeh - Leyte - Lombok - Malaysia (east coast) - Manado - Moluccas - Negros - Palawan - Sabah and Sarawak - Sangat - Siau - Sipadan-Mabul - Siquijor - Sulawesi central - Sulawesi south - Sulawesi southeast - Togian and Banggai islands - Wallacea
Print version maps
Alor - Ambon - Apo - Bali
- Bohol - Borneo
- Burma - Gorontalo
- Kalimantan - Komodo
- Lankayan - Lembeh
- Leyte - Lombok
- Malaysia (east coast) - Manado
- Palawan (Tubbataha) - Sangat
- Siau - Sipadan-Mabul
- Siquijor - Sulawesi
south - Togians
|Grundsätze zur Berichterstattung über Tauchgebiete
. Copyright Teresa Zubi (write to me)


A recently published article in Equine Veterinary Education (EVE) was titled “Epidemiology of exertional heat illness in Thoroughbred racehorses in temperate eastern Australia: The role of extrinsic (environmental) factors in disease causation.” It was authored by Margaret Brownlow, BVSc, MVSc: Dip Vet Anaes, MNurs, MPubHealth, MMed (BMRI), MANZCVs, Racing Australia, Sydney, New South Wales, Australia; and J. X. Mizzi, Department of Regulation, Welfare and Biosecurity Policy, The Hong Kong Jockey Club, Sha Tin Racecourse, Hong Kong, Sha Tin, China.
“A simple epidemiological model of disease causation is proposed for exertional heat illness (EHI) in Thoroughbred racehorses. The agent of disease causation that must be present for the condition to occur is strenuous exercise, producing substantial quantities of metabolic heat. This is stored during racing but must be dissipated rapidly in the post-race period to prevent core body temperature rising to a critical level and causing the clinical manifestations of EHI. Environmental factors are next in the epidemiological triad, and it is a common misconception that these are the direct cause of EHI. In fact, environmental conditions enable EHI by either diminishing the evaporative capacity of the environment or promoting internal heat gain. This article deals with the specific effects of the four thermal elements, separately and in combination, on individual thermo-effector mechanisms. The final component in the epidemiological triad is individual host factors. A critical premise of epidemiology is that conditions such as EHI may not occur randomly in a population but may be more likely to occur in some individuals due to the presence of certain factors that predispose them to the condition. For the purpose of assessing risk, it is not feasible to examine the balance between metabolic heat production and the intrinsic and extrinsic factors, which collectively determine each individual’s heat stress response. Therefore, the measurement of environmental factors remains the only practical way of obtaining a credible risk assessment for EHI, so that effective countermeasures can be instigated and the welfare of our racehorses ensured.”
Read the entire open access article on the Wiley Online Library from BEVA here.


Supplementary Materialssupplemental document. then evaluated within a subcutaneous PCa xenograft model (Computer3) by small-animal Family pet imaging and bio-distribution research. Outcomes NODAGA-RM1 and NODAGA-AMBA could be synthesized and radiolabeled with 64Cu and 18F-AlF successfully. 64Cu- and 18F-AlF-labeled NODAGA-RM1 confirmed excellent serum balance and tumor-imaging properties in the in vitro balance assays and in vivo imaging research. 64Cu-NODAGA-RM1 exhibited tumor uptake beliefs of 3.3 0.38, 3.0 0.76, and 3.5 1.0 percentage injected dosage per gram of tissues (%ID/g) at 0.5, 1.5, and 4 h after injection, respectively. 18F-AlF-NODAGA-RM1 exhibited tumor uptake beliefs of 4.6 1.5, 4.0 0.87, and 3.9 0.48 %ID/g at 0.5, 1, and 2 Gefitinib kinase inhibitor h, respectively. Bottom line The high-stability, effective tumor uptake and optimum pharmacokinetic properties high light 18F-AlF-NODAGA-RM1 being a probe with great potential and scientific application for your pet imaging of prostate tumor. QMA SepPak Light cartridge (Waters) set with 18F (1.1 GBq [30 mCi]) was washed with 2.5 mL of metal-free water. The 18F was eluted through the cartridge with 400 L of 0 then.4 M KHCO3, that 200-L fractions had been taken. The pH of the answer was adjusted to 4 with metal-free glacial acetic acid. AlCl3 (2 mM, 3 L) in 0.1 M sodium acetate buffer (pH 4) and 10 L of peptide (1 mg/mL in dimethyl sulfoxide) were then added to the reaction solution sequentially. The reaction mixtures were incubated at 100C for 15 min. The labeled peptides were then purified by semipre-parative HPLC. The fractions made up of the desired products were collected and rotary-evaporated to remove the solvent. The products were reconstituted in phosphate-buffered saline and exceeded through a 0.22-m Millipore filter into sterile vials for the subsequent in vitro and in vivo experiments. Cell-Binding Assays The cell-binding assay was performed similarly as previously reported (19,35). The detailed procedures are included in the supplemental file. Mouse Serum Stability The in vitro stability of the PET probes was evaluated by incubation with mouse serum (1 mL) at 37C. The solutions were filtered using a NanoSep 10 K centrifuge (Pall Corp.) to isolate low-molecular-weight radiocomplexes. The samples were analyzed by the radio-HPLC, and the percentages of intact PET probe were determined by quantifying the peaks corresponding with the intact probe and degradation products. Small-Animal PET Imaging The animal procedures were performed according to a protocol approved by the Stanford University Institutional Animal Care and Use Committee. The establishment of the PC3 tumor mice Rabbit Polyclonal to AKAP10 model and the procedure for small-animal PET are shown in the supplemental file. The PC3 xenograftCbearing mice were injected with approximately 1.85 MBq (50 Ci) of either 64Cu-NODAGA-RM1 or 64Cu-NODAGA-AMBA via the tail vein (= 4 for each group). At the indicated occasions Gefitinib kinase inhibitor after injection (0.5, 1.5, and 4 h), the mice Gefitinib kinase inhibitor were anesthetized with isoflurane (5% for induction and 2% for maintenance in 100% O2) using a knock-down box. Five-minute static scans were then obtained. The PC3 xenograftCbearing mice were injected with 0.37 MBq (10 Ci) of either 18F-AlF-NODAGA-RM1 or 18F-AlF-NODAGA-AMBA probe via the tail vein (= 5 for each group). Blocking studies were performed via tail vein injection of the 18F probe with cold AMBA (10 mg/kg of body weight) (= 5). At 0.5, 1, and 2 h after injection, the small-animal PET images were obtained. The small-animal PET images were reconstructed using the 2-dimensional ordered-subsets expectation maximization algorithm. No background correction was performed. The regions of interest (ROIs; 5 pixels for coronal and transaxial slices) were designated over the tumor on decay-corrected whole-body coronal images. The maximum counts per pixel per minute were obtained from the ROIs and converted to counts per milliliter per minute using a calibration constant. On Gefitinib kinase inhibitor the basis of an assumed tissue density of 1 1 g/mL, the ROIs were converted to counts per gram per min. The image ROICderived percentage of the injected radioactive doses per gram of tissue (%ID/g) values had been dependant on dividing matters per gram each and every minute by injected dosage. No attenuation modification was performed. Pet Biodistribution Research The Computer3 xenograftCbearing nude mice (= 4 for every group) had been injected with around 1.85 MBq (50 Ci) of 64Cu-AlF-NODAGA-RM1 via the tail vein and sacrificed at 2 and 24 h after injection. The tumor and regular tissue appealing had been weighed and taken out, and their degrees of radioactivity had been measured utilizing a -counter-top. The uptake of radioactivity in the tumor and regular tissues was portrayed as %Identification/g. Similarly, Computer3 xenograftCbearing nude mice (= 5 for every group) had been injected with around 0.37 MBq (10 Ci) of 18F-AlF-NODAGA-RM1 via the tail vein and sacrificed at 2 h after shot. The 18F-AlF-NODAGA-RM1 preventing research was performed by coinjection from the probe using the AMBA peptide (10 mg/kg of.


PCR Covid Testing in Austin: Nasal and Saliva Options
Austin Rapid Test has a variety of Covid test types available for our customers, and can administer each of them from the safety and convenience of your home or office. Some tests have different names used for the same or similar tests, so it can all be very confusing when researching the type of Covid test you need or where in Austin you can find a specific type of Covid test.
This page is dedicated to one of the diagnostic tests we provide: the polymerase chain reaction ("PCR") test.
A diagnostic test can show if you have an active coronavirus infection. Currently there are two types of diagnostic tests – molecular tests, such as PCR tests, that detect the virus’s genetic material, and antigen tests that detect specific proteins from the virus.
"Molecular Tests" are also known by other names/terms such as viral tests, nucleic acid amplification tests (NAAT), RNA tests, and PCR tests. In fact, the PCR Test is a type of NAAT test.
Different Types of PCR tests
Yes, there are different types of PCR tests, though most websites don't necessarily differentiate them and simply call them all "PCR" tests. With said, there is the standard PCR, RT-PCR, Hot Start PCR, qPCR, and RT-qPCR.
At Austin Rapid Test, we offer the RT-PCR Covid test and our nurses can administer the test by either a nasal swab or by collecting your saliva.
Like our Nasal swab PCR test, the Saliva Covid test needs to be sent to a lab for processing. Right now, it is sent to a specialty lab slightly further than our nasal PCR test lab, so it occasionally takes a little longer to get results back for the saliva covid tests.
Our partner lab has guaranteed a turnaround time on Saliva Covid tests of 72 hours, though they tend to get us the results faster than that. Our nasal PCR test results are often returned in less than 24 hours but are guaranteed to be provided in no more than 48 hours.
Is the Accuracy of the Nasal Swab PCR Covid Test Higher than it is with the Saliva PCR Covid Test?
Since the early days of the pandemic, clinicians and researchers have been looking for alternatives to nasopharyngeal swabs due to the discomfort that many people experience with this specimen collection method.
An accurate identification of respiratory viruses is critically affected by the source of clinical specimens. While several studies on up to 15 common respiratory viruses suggest that the use of nasopharyngeal swabs provides a higher sensitivity than that of nasopharyngeal washings or oropharyngeal swabs, this is not necessarily the case for SARS-CoV-2, as the infectivity and the predilection for transmission may differ significantly between viruses.
Currently, the available data comparing the sensitivity for SARS-CoV-2 detection using nasal, pharyngeal, or oral swab are very limited. One study from a Chinese group examined 213 hospitalized SARS-CoV-2 patients with a total of 205 oropharyngeal and 490 nasopharyngeal swabs at various time points of disease course. They found that nasopharyngeal swabs have overall higher positive rates (53.6%-73.3%) than oropharyngeal (throat) swabs (11.1%-61.3%), regardless of whether the patients were in mild or severe disease conditions.
Since saliva is easily collected and clinically informative for disease detection, the consideration that maximizes the benefit of using saliva as a diagnostic fluid deserves more attention. Researchers found that the agreement between the saliva and swab administered through the mouth was 93%, and that sensitivity was 96.7%. The swab administered through the nose and saliva had a result agreement of 97.7%, with sensitivity of 94.1%.
This is a rapidly moving research topic and the current evidence is not peer-reviewed and, therefore, is still far from leading to a solid conclusion. In other words, it is still too early to fully determine if the accuracy of Saliva PCR tests and Nasopharyngeal PCR tests is significantly different.
As always, determining which test is best and most appropriate for any individual is a decision best made with the guidance of your healthcare provider.


Make a difference for the lake you love! Join a Shedd Great Lakes Action Day to spend a day outdoors, cleaning local beaches, lakes and forest preserves. You’ll help animals from frogs to fishes and have fun doing it!
Protecting our Great Lakes and other local waters
Together, we all can take actions to protect the Great Lakes from the threats of pollution, invasive species and loss of wetland and shoreline habitats. Our team of policy experts works closely with elected officials and conservation partners to advocate for science-based solutions to our lakes' problems.
Our field biologists and other conservation experts recruit teams of citizen scientists—like you!—to assist with short- and long-term projects, from collecting and documenting beach litter to restoring coastal and wetlands habitats. These collaborations are improving our Great Lakes "neighborhood" for wildlife and people alike.
Get involved in a Great Lakes Action Day activity near you!
Community workdays and locations
for individuals and families
We hosts beach cleanups at sites along the Lake Michigan shoreline through the Alliance for the Great Lakes Adopt-a-Beach™ program. Volunteers work in teams, combing the beach for litter and recording data on their findings to support effective coastal management.
Habitat and wildlife monitoring
To measure the impact of our work on local wildlife, participants can strap on waders to assess water quality in local streams and monitor threatened and endangered plant species.
Invasive plant removal
Make a positive difference for local wildlife, from frogs to migratory birds, by taking action to prevent the spread of harmful ecological invaders. Participants will learn about natural habitats near Chicago as well as the impact of invasive plant and animal species.
Amphibian habitat restoration
Blue-spotted salamanders and chorus frogs are among the native amphibians in our local woodlands and wetlands. We work with the Forest Preserves of Cook County to restore local amphibian habitats, a project that combines land-management expertise with a deep knowledge of amphibians' needs.
Age and Requirements
All ages. Individuals, families and groups up to 100 people can be accommodated.
What to Bring
Reusable water bottles, snacks and sunscreen, and weather-appropriate outdoor clothing and shoes
- Beach cleanup
- Habitat and wildlife monitoring
- Invasive plant removal
- Habitat restoration
What to Know
• All events are weather-dependent.
• Transportation is available for select school and youth groups.
• Participant waivers are required.
Corporate group GLAD opportunities are reserved for current corporate partners. Email to learn more.


To figure out these counterintuitive findings, the researchers conducted an experiment in a hotel room. They rounded up some lizards, gave them a perch, and used a leaf blower to the effects of high winds. They set up a net to catch any lizards that lost their grip. As the artificial wind blew, the lizards so the perch took most of the air flow. But their hind legs would stick out, and if those limbs stuck out too far, they acted as sails. “Eventually those back legs were blown off the perch, and the lizards were just holding on with their front two legs. And they could only hold on like that for so long as the wind speed further and further, until eventually they were blown off the perch and into the So shorter back legs gave a advantage. A trait that might be passed on to the next lizard generation.Answer (score 79+):
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