Saturday, April 1, 2017
Personalized therapy for multiple sclerosis (MS)
From: http://www.mayoclinic.com/diseases-conditions/multiple-sclerosis/in-depth/personalized-therapy-for-multiple-sclerosis/art-20095758
Personalized therapy for multiple sclerosis (MS)
From: http://www.mayoclinic.org/diseases-conditions/multiple-sclerosis/in-depth/personalized-therapy-for-multiple-sclerosis/art-20095758
Global EpiPen Recall Now Includes U.S.
The recall was triggered by a defective part, manufacturer Mylan says
From: http://www.webmd.com/allergies/news/20170401/epipen-us-recall?src=RSS_PUBLIC
Personalized therapy for multiple sclerosis (MS)
From: http://www.mayoclinic.com/diseases-conditions/multiple-sclerosis/in-depth/personalized-therapy-for-multiple-sclerosis/art-20095758
Selfies could help diagnose rare genetic disease
In a study, facial recognition software determines who suffers from a condition that's typically hard to pinpoint
From: http://www.cbsnews.com/news/digeorge-syndrome-a-rare-genetic-disease-could-be-diagnosed-with-selfies/
From: http://www.cbsnews.com/news/digeorge-syndrome-a-rare-genetic-disease-could-be-diagnosed-with-selfies/
Doctors say patient surveys help fuel opioid epidemic
Two million Americans are hooked on pain pills, and overdoses kill more people than gun homicides
From: http://www.cbsnews.com/news/opioid-epidemic-doctors-say-hospital-patient-satisfaction-survey-fuel-dependence/
From: http://www.cbsnews.com/news/opioid-epidemic-doctors-say-hospital-patient-satisfaction-survey-fuel-dependence/
Personalized therapy for multiple sclerosis (MS)
From: http://www.mayoclinic.org/diseases-conditions/multiple-sclerosis/in-depth/personalized-therapy-for-multiple-sclerosis/art-20095758
Molecular mechanism(s) involved in differential expression of vitamin C transporters along the intestinal tract
Mammalian cells utilize two transporters for the uptake of ascorbic acid (AA), Na+-dependent vitamin C transporter SVCT-1 and SVCT-2. In the intestine, these transporters are involved in AA absorption and are expressed at the apical and basolateral membrane domains of the polarized epithelia, respectively. Little is known about the differential expression of these two transporters along the anterior-posterior axis of the intestinal tract and the molecular mechanism(s) that dictate this pattern of expression. We used mouse and human intestinal cDNAs to address these issues. The results showed a significantly lower rate of carrier-mediated AA uptake by mouse colon than jejunum. This was associated with a significantly lower level of expression of SVCT-1 and SVCT-2 at the protein, mRNA, and heterogeneous nuclear RNA (hnRNA) levels in the colon than the jejunum, implying the involvement of transcriptional mechanism(s). Similarly, expression levels of SVCT-1 and SVCT-2 mRNA and hnRNA were significantly lower in human colon. We also examined the levels of expression of hepatocyte nuclear factor 1α and specificity protein 1, which drive transcription of the Slc23a1 and Slc23a2 promoters, respectively, and found them to be markedly lower in the colon. Furthermore, significantly lower levels of the activating markers for histone (H3) modifications [H3 trimethylation of lysine 4 (H3K4me3) and H3 triacetylation of lysine 9 (H3K9ac)] were observed in the Slc23a1 and Slc23a2 promoters in the colon. These findings show, for the first time, that SVCT-1 and SVCT-2 are differentially expressed along the intestinal tract and that this pattern of expression is, at least in part, mediated via transcriptional/epigenetic mechanisms.
NEW & NOTEWORTHY Our findings show, for the first time, that transporters of the water-soluble vitamin ascorbic acid (i.e., the vitamin C transporters SVCT-1 and SVCT-2) are differentially expressed along the length of the intestinal tract and that the pattern of expression is mediated, at least in part, by transcriptional and epigenetic mechanism(s) affecting both Slc23a1 and Slc23a2 genes.
From: Subramanian, V. S., Srinivasan, P., Wildman, A. J., Marchant, J. S., Said, H. M. http://ajpgi.physiology.org/cgi/content/abstract/312/4/G340?rss=1
Gut microbiota differs between children with Inflammatory Bowel Disease and healthy siblings in taxonomic and functional composition: a metagenomic analysis
Current treatment for pediatric inflammatory bowel disease (IBD) patients is often ineffective, with serious side effects. Manipulating the gut microbiota via fecal microbiota transplantation (FMT) is an emerging treatment approach but remains controversial. We aimed to assess the composition of the fecal microbiome through a comparison of pediatric IBD patients to their healthy siblings, evaluating risks and prospects for FMT in this setting. A case-control (sibling) study was conducted analyzing fecal samples of six children with Crohn’s disease (CD), six children with ulcerative colitis (UC) and 12 healthy siblings by metagenomic sequencing. In addition, lifetime antibiotic intake was retrospectively determined. Species richness and diversity were significantly reduced in UC patients compared with control [Mann-Whitney U-test false discovery rate (MWU FDR) = 0.011]. In UC, bacteria positively influencing gut homeostasis, e.g., Eubacterium rectale and Faecalibacterium prausnitzii, were significantly reduced in abundance (MWU FDR = 0.05). Known pathobionts like Escherichia coli were enriched in UC patients (MWU FDR = 0.084). Moreover, E. coli abundance correlated positively with that of several virulence genes (SCC > 0.65, FDR < 0.1). A shift toward antibiotic-resistant taxa in both IBD groups distinguished them from controls [MWU Benjamini-Hochberg-Yekutieli procedure (BY) FDR = 0.062 in UC, MWU BY FDR = 0.019 in CD). The collected results confirm a microbial dysbiosis in pediatric UC, and to a lesser extent in CD patients, replicating associations found previously using different methods. Taken together, these observations suggest microbiotal remodeling therapy from family donors, at least for children with UC, as a viable option.
NEW & NOTEWORTHY In this sibling study, prior reports of microbial dysbiosis in IBD patients from 16S rRNA sequencing was verified using deep shotgun sequencing and augmented with insights into the abundance of bacterial virulence genes and bacterial antibiotic resistance determinants, seen against the background of data on the specific antibiotic intake of each of the study participants. The observed dysbiosis, which distinguishes patients from siblings, highlights such siblings as potential donors for microbiotal remodeling therapy in IBD.
From: Knoll, R. L., Forslund, K., Kultima, J. R., Meyer, C. U., Kullmer, U., Sunagawa, S., Bork, P., Gehring, S. http://ajpgi.physiology.org/cgi/content/abstract/312/4/G327?rss=1
Personalized therapy for multiple sclerosis (MS)
From: http://www.mayoclinic.com/diseases-conditions/multiple-sclerosis/in-depth/personalized-therapy-for-multiple-sclerosis/art-20095758
Eat better, live longer
Follow me on Twitter @RobShmerling
We’ve all heard it before: to be as healthy as you can be, choose a healthy diet. And while that’s easier said than done, the impact of improving your diet may be large. That’s according to a recent study that estimated the impact of dietary modifications on premature cardiovascular deaths in this country. The verdict? More than 400,000 deaths each year could be prevented with dietary improvement.
Exactly how should you improve your diet?
Just what does “improving your diet” mean? Limiting unhealthy foods is a good start. Fewer French fries, less salt, and a little less ice cream are all good ideas and make sense. But this new report, and several expert guidelines, suggest that it’s not only what you don’t eat. What you do eat matters, too. It’s also important to eat more healthy foods.
In this study, researchers analyzed patient surveys between 1990 and 2012, food availability data from the Food and Agriculture Organization of the United Nations, and data on cardiovascular deaths in 2015. They estimated that the biggest contributors to the premature cardiovascular deaths of more than 220,000 men and about 190,000 women were due to
- high consumption of salt and trans fat (a particularly unhealthy form of unsaturated fat commonly found in processed foods as “partially hydrogenated oils”)
- low consumption of nuts, seeds, vegetables, and whole grains.
And here’s why it matters: Cardiovascular disease is the #1 cause of death in the U. S.
Cardiovascular disease accounts for an estimated 787,000 deaths each year. And dietary factors can affect one’s risk of cardiovascular disease because
- obesity increases the risk of type 2 diabetes, and both obesity and diabetes are risk factors for cardiovascular disease
- high blood pressure (hypertension) is more common among those with high salt intake and obesity
- diet affects cholesterol levels
- research suggests that not eating enough fruits, vegetables, and fiber may increase risk.
Ever started a new diet?
It’s easy to make recommendations about improving dietary choices. Making long-lasting change is hard. Willpower and commitment is often not enough. Just ask anyone who has been frustrated by repeated and unsuccessful efforts to lose weight, lower blood pressure, or lower cholesterol by starting a new diet.
The pervasiveness of unhealthy diets and the epidemic of obesity in this country have led to the suggestion that we should approach this as a public health problem that might be improved by taxing unhealthy foods and subsidizing healthier options. Another new study looked at the impact of this approach. In fact, in places where unhealthy foods were taxed or where healthy foods became less expensive through subsidies, diets tended to improve. Of course, that raises the question of how much government agencies or others should be involved in swaying consumers’ dietary choices. But from a public health perspective, the data seem clear: if you want to encourage healthier eating, one approach is through the pocketbook.
And, finally…
If you’re not sure what constitutes a healthy diet, it might be because there is no one diet that’s best for everyone. However, there a number of dietary guidelines worth considering, including:
- The Mediterranean Diet
- Choose My Plate from the USDA
- the Healthy Eating Plate from the Harvard School of Public Health and Harvard Medical School.
Talk to your doctor about your diet. Depending on your overall health and current diet, it might be a good idea to meet with a nutritionist. The goal is to come up with a healthy diet you can stick with. It may not be easy, but a change that could prevent more than 400,000 deaths per year is a change worth making. After all, one of those prevented deaths could be yours.
The post Eat better, live longer appeared first on Harvard Health Blog.
From: Robert H. Shmerling, MD http://www.health.harvard.edu/blog/eat-better-live-longer-2017033111493
Personalized therapy for multiple sclerosis (MS)
From: http://www.mayoclinic.org/diseases-conditions/multiple-sclerosis/in-depth/personalized-therapy-for-multiple-sclerosis/art-20095758
Stress management
From: http://www.mayoclinic.com/healthy-lifestyle/stress-management/basics/stress-basics/hlv-20049495
Bed rest during pregnancy: Get the facts
From: http://www.mayoclinic.com/healthy-lifestyle/pregnancy-week-by-week/in-depth/pregnancy/art-20048007
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