09/15/15

Tuesday, September 15, 2015

Crying baby: What to do when your newborn cries

From: http://www.mayoclinic.org/healthy-lifestyle/infant-and-toddler-health/in-depth/healthy-baby/art-20043859

Many U.S. kids eat fast food every day

Pizza, burgers and fries are a fattening part of the daily diet for millions of American children, the CDC reports

From: http://www.cbsnews.com/news/many-u-s-kids-eat-fast-food-every-day/

Blood Sugar Highs and Lows

What's the difference between hyperglycemia and hypoglycemia? WebMD Magazine explains.

From: http://www.webmd.com/diabetes/features/blood-sugar-highs-lows?src=RSS_PUBLIC

Diabetes News Roundup

WebMD Magazine has the details on big headlines about diabetes from the first half of 2015.

From: http://www.webmd.com/diabetes/features/diabetes-news-roundup?src=RSS_PUBLIC

Hand Sanitizers Poisoning More Kids

Poison center officials are warning parents and school officials about a troubling trend -- small children becoming intoxicated after drinking alcohol-based hand sanitizer.

From: http://www.webmd.com/children/news/20150915/hand-sanitizers-poisoning-kids?src=RSS_PUBLIC

Have Diabetes? Make a Move

Ready to get fit? It'll help you take charge of your diabetes, burn stress, and make you feel good.

From: http://www.webmd.com/diabetes/features/diabetes-make-move?src=RSS_PUBLIC

Rehab centers to close amid insurance fraud scheme

A federal judge has approved plans to close 18 drug rehab centers run by Narco Freedom, after the organization's founders were busted for alleged insurance fraud

From: http://www.cbsnews.com/videos/rehab-centers-to-close-amid-insurance-fraud-scheme/

Hand sanitizers linked to alcohol poisoning in kids

Some schools are alerted to the risk of children drinking hand sanitizer

From: http://www.cbsnews.com/news/hand-sanitizers-linked-to-alcohol-poisoning-in-kids/

Hip-Fracture Surgery Risk Not Just Due to Age

From: http://www.webmd.com/osteoporosis/news/20150915/hip-fracture-surgery-risk?src=RSS_PUBLIC

FDA Bans Sale of New R.J. Reynolds Cigarettes

From: http://www.webmd.com/smoking-cessation/news/20150915/fda-bans-new-cigarettes?src=RSS_PUBLIC

Vitamin D deficiency linked to cognitive decline

Dr. Kevin Campbell joins Kristine Johnson to discuss vitamin D deficiency in older adults

From: http://www.cbsnews.com/videos/vitamin-d-deficiency-linked-to-cognitive-decline/

Mediterranean diet could cut breast cancer cases

A new study suggests a diet rich in extra virgin olive oil and primarily plant-based foods, such as fruits and vegetables, whole grains, legumes and nuts, could decrease the risk of breast cancer for women between the ages of 60 and 80.

From: http://www.cbsnews.com/videos/mediterranean-diet-could-cut-breast-cancer-cases/

Kids who get more sunlight less likely to need glasses

Researchers say an extra 40 minutes a day of outdoor activity can have a signifcant impact on children's eyesight

From: http://www.cbsnews.com/news/kids-exposed-to-more-sunlight-less-likely-to-need-glasses/

Too Little Vitamin D May Hasten Mental Decline

From: http://www.webmd.com/brain/news/20150915/vitamin-d-mental-decline?src=RSS_PUBLIC

Can More Outside Time Help Kids' Eyesight?

From: http://www.webmd.com/children/news/20150915/children-outdoors-eyesight?src=RSS_PUBLIC

Get Cart-Smart: Tips for Healthy Grocery Shopping

You can eat well with type 2 diabetes when you make smart choices at the grocery store.

From: http://www.webmd.com/diabetes/features/grocery-shopping-diabetes?src=RSS_PUBLIC

Plain Truth: Diabetes Myths Debunked

Diabetes is one of the most common chronic diseases -- and one of the most misunderstood. WebMD Magazine debunks common myths about it.

From: http://www.webmd.com/diabetes/features/diabetes-myths-truth?src=RSS_PUBLIC

Low vitamin D linked to mental decline, study finds

Older adults with dementia tested lower for vitamin D, but would taking supplements help?

From: http://www.cbsnews.com/news/low-vitamin-d-linked-to-mental-decline-study-finds/

Can you use humor to get through to your kids?

Taking a lighter touch with parenting may get you the results you want, faster. Learn more at WebMD.

From: http://www.webmd.com/parenting/features/when-all-else-fails-parent-with-humor?src=RSS_PUBLIC

Modern Moms Ask for Help

How and why mothers of young children can ask for help.

From: http://www.webmd.com/parenting/features/modern-moms-ask-for-help?src=RSS_PUBLIC

Straight Talk About Diabetes

WebMD Magazine shares tips on how to let friends and family know what kind of help you need when you have diabetes.

From: http://www.webmd.com/diabetes/features/straight_talk_diabetes?src=RSS_PUBLIC

The pH-sensing receptor OGR1 improves barrier function of epithelial cells and inhibits migration in an acidic environment

The pH-sensing receptor ovarian cancer G protein-coupled receptor 1 (OGR1; GPR68) is expressed in the gut. Inflammatory bowel disease is typically associated with a decrease in local pH, which may lead to altered epithelial barrier function and subsequent gastrointestinal repair involving epithelial cell adhesion and migration. As the mechanisms underlying the response to pH changes are not well understood, we have investigated OGR1-mediated, pH-dependent signaling pathways in intestinal epithelial cells. Caco-2 cells stably overexpressing OGR1 were created and validated as tools to study OGR1 signaling. Barrier function, migration, and proliferation were measured using electric cell-substrate impedance-sensing technology. Localization of the tight junction proteins zonula occludens protein 1 and occludin and the rearrangement of cytoskeletal actin were examined by confocal microscopy. Paracellular permeability and protein and gene expression analysis using DNA microarrays were performed on filter-grown Caco-2 monolayers. We report that an acidic pH shift from pH 7.8 to 6.6 improved barrier function and stimulated reorganization of filamentous actin with prominent basal stress fiber formation. Cell migration and proliferation during in vitro wound healing were inhibited. Gene expression analysis revealed significant upregulation of genes related to cytoskeleton remodeling, cell adhesion, and growth factor signaling. We conclude that acidic extracellular pH can have a signaling function and impact the physiology of intestinal epithelial cells. The deconstruction of OGR1-dependent signaling may aid our understanding of mucosal inflammation mechanisms.

From: de Valliere, C., Vidal, S., Clay, I., Jurisic, G., Tcymbarevich, I., Lang, S., Ludwig, M.-G., Okoniewski, M., Eloranta, J. J., Kullak-Ublick, G. A., Wagner, C. A., Rogler, G., Seuwen, K. http://ajpgi.physiology.org/cgi/content/abstract/309/6/G475?rss=1

TAK1 is a key modulator of the profibrogenic phenotype of human ileal myofibroblasts in Crohn's disease

Transforming growth factor (TGF)-β-activated kinase 1 (TAK1) signaling can mediate inflammatory responses as well as tissue remodeling. Intestinal mucosal myofibroblast (IMF) activation drives gut fibrosis in Crohn's disease (CD); however, the molecular pathways involved are largely unknown. Thus we investigated the yet-unknown expression and function of TAK1 in human CD-associated fibrosis. Ileal surgical specimens, ileal biopsies, and IMF isolated from controls and CD patients were analyzed for TAK1 and its active phosphorylated form (pTAK1) by Western blotting, immunohistochemistry, and real-time quantitative PCR. TAK1 pharmacological inhibition and silencing were used to assess its role in collagen and inflammatory cytokine synthesis in IMF. TAK1 and pTAK1 levels increased in ileum specimens from CD patients compared with controls and correlated to tissue fibrosis. Similarly, TAK1 mRNA in ileal biopsies of CD patients correlated with fibrogenic marker expression but not inflammatory cytokines. CD-derived IMF showed higher TAK1 and pTAK1 expression associated with increased collagen1(α)1 mRNA levels compared with control IMF. TGF-β1 promoted pTAK1 nuclear translocation and collagen synthesis. TAK1 inhibition or silencing significantly reduced TGF-β1-stimulated collagen production and normalized the profibrogenic phenotype of CD-derived IMF. Taken together, these data suggest that TAK1 activation and nuclear translocation induce and maintain a fibrogenic phenotype in the IMF. Thus the TAK1 signaling pathway may represent a suitable target to design new, antifibrotic therapies.

From: Grillo, A. R., Scarpa, M., D'Inca, R., Brun, P., Scarpa, M., Porzionato, A., De Caro, R., Martines, D., Buda, A., Angriman, I., Palu, G., Sturniolo, G. C., Castagliuolo, I. http://ajpgi.physiology.org/cgi/content/abstract/309/6/G443?rss=1

Sodium butyrate stimulates NHE8 expression via its role on activating NHE8 basal promoter activity

Butyrate is a major metabolite in colonic lumen. It is produced from bacterial fermentation of dietary fiber. Butyrate has been shown to stimulate electroneutral sodium absorption through its regulation on sodium/hydrogen exchanger 3 (NHE3). Although NHE8, the newest addition of intestinal NHE family, is involved in sodium absorption in the intestinal tract, whether butyrate modulates NHE8 expression in the intestinal epithelial cells is not known. In the current study, we showed that butyrate treatment strongly induced NHE8 protein and NHE8 mRNA expression in human intestinal epithelial cells. Transfection with the human NHE8 promoter reporter constructs showed that butyrate treatment stimulated reporter gene expression at an amount comparable with its stimulation of NHE8 mRNA expression. Interestingly, a similar result was also observed in human NHE8 promoter transfected cells after trichostatin (TSA) treatment. Gel mobility shift assay identified an enhanced Sp3 protein binding on the human NHE8 basal promoter region upon butyrate stimulation. Furthermore, Sp3 acetylation modification is involved in butyrate-mediated NHE8 activation in Caco-2 cells. Our findings suggest that the mechanism of butyrate action on NHE8 expression involves enhanced Sp3 interaction at the basal promoter region of the human NHE8 gene promoter to activate NHE8 gene transcription. Thus butyrate is involved in intestinal regulation of NHE8 resulting enhanced sodium absorption.

From: Xu, H., McCoy, A., Li, J., Zhao, Y., Ghishan, F. K. http://ajpgi.physiology.org/cgi/content/abstract/309/6/G500?rss=1

Mitophagy, mitochondrial spheroids, and mitochondrial-derived vesicles in alcohol-induced liver injury

From: Williams, J. A., Ding, W.-X. http://ajpgi.physiology.org/cgi/content/full/309/6/G515?rss=1

The gastrin-releasing peptide analog bombesin preserves exocrine and endocrine pancreas morphology and function during parenteral nutrition

Stimulation of digestive organs by enteric peptides is lost during total parental nutrition (PN). Here we examine the role of the enteric peptide bombesin (BBS) in stimulation of the exocrine and endocrine pancreas during PN. BBS protects against exocrine pancreas atrophy and dysfunction caused by PN. BBS also augments circulating insulin levels, suggesting an endocrine pancreas phenotype. While no significant changes in gross endocrine pancreas morphology were observed, pancreatic islets isolated from BBS-treated PN mice showed a significantly enhanced insulin secretion response to the glucagon-like peptide-1 (GLP-1) agonist exendin-4, correlating with enhanced GLP-1 receptor expression. BBS itself had no effect on islet function, as reflected in low expression of BBS receptors in islet samples. Intestinal BBS receptor expression was enhanced in PN with BBS, and circulating active GLP-1 levels were significantly enhanced in BBS-treated PN mice. We hypothesized that BBS preserved islet function indirectly, through the enteroendocrine cell-pancreas axis. We confirmed the ability of BBS to directly stimulate intestinal enteroid cells to express the GLP-1 precursor preproglucagon. In conclusion, BBS preserves the exocrine and endocrine pancreas functions during PN; however, the endocrine stimulation is likely indirect, through the enteroendocrine cell-pancreas axis.

From: Pierre, J. F., Neuman, J. C., Brill, A. L., Brar, H. K., Thompson, M. F., Cadena, M. T., Connors, K. M., Busch, R. A., Heneghan, A. F., Cham, C. M., Jones, E. K., Kibbe, C. R., Davis, D. B., Groblewski, G. E., Kudsk, K. A., Kimple, M. E. http://ajpgi.physiology.org/cgi/content/abstract/309/6/G431?rss=1

Mitophagy in steatotic hepatocytes of ethanol-treated wild-type and Parkin knockout mice

From: Eid, N., Ito, Y., Otsuki, Y. http://ajpgi.physiology.org/cgi/content/full/309/6/G513?rss=1

Blocking peripheral serotonin synthesis by telotristat etiprate (LX1032/LX1606) reduces severity of both chemical- and infection-induced intestinal inflammation

Mucosal inflammation is accompanied by an alteration in 5-HT. Intestinal 5-HT synthesis is catalyzed by tryptophan hydroxylase 1 (Tph1) and we have shown that mice deficient in this rate-limiting enzyme have reduced severity of intestinal inflammation in models of chemical-induced experimental colitis. Here, we investigated the effect of blocking peripheral 5-HT synthesis in generation of intestinal inflammation by a using peripheral Tph inhibitor, telotristat etiprate (LX1606), in models of intestinal inflammation. LX1606 was given orally either prophylactically or therapeutically to mice with dextran sulfate sodium (DSS)-induced colitis or with infection with Trichuris muris. Severity of intestinal inflammation was measured by assessment of disease activity scores, histological damage, and MPO and inflammatory cytokine levels. LX1606 significantly reduced intestinal 5-HT levels and delayed onset and severity of DSS-induced acute and chronic colitis. This was associated with decreased MPO and proinflammatory cytokine levels compared with vehicle-treated controls. In the infection-induced inflammation model, treatment with LX1606 enhanced worm expulsion as well as increased IL-10 production and goblet cell numbers. LX1606-treated mice had significantly lower MPO and IL-1β levels compared with controls postinfection. Our results demonstrate that peripheral 5-HT plays an important role in intestinal inflammation and in the generation of immune responses. Pharmacological reduction of peripheral 5-HT may serve as a potential strategy for modulating various intestinal inflammatory disorders.

From: Kim, J. J., Wang, H., Terc, J. D., Zambrowicz, B., Yang, Q. M., Khan, W. I. http://ajpgi.physiology.org/cgi/content/abstract/309/6/G455?rss=1

Rhesus rotavirus VP4 sequence-specific activation of mononuclear cells is associated with cholangiopathy in murine biliary atresia

Biliary atresia (BA), a neonatal obstructive cholangiopathy, remains the most common indication for pediatric liver transplantation in the United States. In the murine model of BA, Rhesus rotavirus (RRV) VP4 surface protein determines biliary duct tropism. In this study, we investigated how VP4 governs induction of murine BA. Newborn mice were injected with 16 strains of rotavirus and observed for clinical symptoms of BA and mortality. Cholangiograms were performed to confirm bile duct obstruction. Livers and bile ducts were harvested 7 days postinfection for virus titers and histology. Flow cytometry assessed mononuclear cell activation in harvested cell populations from the liver. Cytotoxic NK cell activity was determined by the ability of NK cells to kill noninfected cholangiocytes. Of the 16 strains investigated, the 6 with the highest homology to the RRV VP4 (>87%) were capable of infecting bile ducts in vivo. Although the strain Ro1845 replicated to a titer similar to RRV in vivo, it caused no symptoms or mortality. A Ro1845 reassortant containing the RRV VP4 induced all BA symptoms, with a mortality rate of 89%. Flow cytometry revealed that NK cell activation was significantly increased in the disease-inducing strains and these NK cells demonstrated a significantly higher percentage of cytotoxicity against noninfected cholangiocytes. Rotavirus strains with >87% homology to RRV's VP4 were capable of infecting murine bile ducts in vivo. Development of murine BA was mediated by RRV VP4-specific activation of mononuclear cells, independent of viral titers.

From: Walther, A., Mohanty, S. K., Donnelly, B., Coots, A., Lages, C. S., Lobeck, I., Dupree, P., Meller, J., McNeal, M., Sestak, K., Tiao, G. http://ajpgi.physiology.org/cgi/content/abstract/309/6/G466?rss=1

Ranolazine inhibits voltage-gated mechanosensitive sodium channels in human colon circular smooth muscle cells

Human jejunum smooth muscle cells (SMCs) and interstitial cells of Cajal (ICCs) express the SCN5A-encoded voltage-gated, mechanosensitive sodium channel Na_V1.5. Na_V1.5 contributes to small bowel excitability, and Na_V1.5 inhibitor ranolazine produces constipation by an unknown mechanism. We aimed to determine the presence and molecular identity of Na⁺ current in the human colon smooth muscle and to examine the effects of ranolazine on Na⁺ current, mechanosensitivity, and smooth muscle contractility. Inward currents were recorded by whole cell voltage clamp from freshly dissociated human colon SMCs at rest and with shear stress. SCN5A mRNA and Na_V1.5 protein were examined by RT-PCR and Western blots, respectively. Ascending human colon strip contractility was examined in a muscle bath preparation. SCN5A mRNA and Na_V1.5 protein were identified in human colon circular muscle. Freshly dissociated human colon SMCs had Na⁺ currents (–1.36 ± 0.36 pA/pF), shear stress increased Na⁺ peaks by 17.8 ± 1.8% and accelerated the time to peak activation by 0.7 ± 0.3 ms. Ranolazine (50 μM) blocked peak Na⁺ current by 43.2 ± 9.3% and inhibited shear sensitivity by 25.2 ± 3.2%. In human ascending colon strips, ranolazine decreased resting tension (31%), reduced the frequency of spontaneous events (68%), and decreased the response to smooth muscle electrical field stimulation (61%). In conclusion, SCN5A-encoded Na_V1.5 is found in human colonic circular smooth muscle. Ranolazine blocks both peak amplitude and mechanosensitivity of Na⁺ current in human colon SMCs and decreases contractility of human colon muscle strips. Our data provide a likely mechanistic explanation for constipation induced by ranolazine.

From: Neshatian, L., Strege, P. R., Rhee, P.-L., Kraichely, R. E., Mazzone, A., Bernard, C. E., Cima, R. R., Larson, D. W., Dozois, E. J., Kline, C. F., Mohler, P. J., Beyder, A., Farrugia, G. http://ajpgi.physiology.org/cgi/content/abstract/309/6/G506?rss=1

Imaging approach to measuring small bowel motility

From: Camilleri, M. http://ajpgi.physiology.org/cgi/content/full/309/6/G411?rss=1

Classification of functional bowel disorders by objective physiological criteria based on endoluminal image analysis

We have previously developed an original method to evaluate small bowel motor function based on computer vision analysis of endoluminal images obtained by capsule endoscopy. Our aim was to demonstrate intestinal motor abnormalities in patients with functional bowel disorders by endoluminal vision analysis. Patients with functional bowel disorders (n = 205) and healthy subjects (n = 136) ingested the endoscopic capsule (Pillcam-SB2, Given-Imaging) after overnight fast and 45 min after gastric exit of the capsule a liquid meal (300 ml, 1 kcal/ml) was administered. Endoluminal image analysis was performed by computer vision and machine learning techniques to define the normal range and to identify clusters of abnormal function. After training the algorithm, we used 196 patients and 48 healthy subjects, completely naive, as test set. In the test set, 51 patients (26%) were detected outside the normal range (P < 0.001 vs. 3 healthy subjects) and clustered into hypo- and hyperdynamic subgroups compared with healthy subjects. Patients with hypodynamic behavior (n = 38) exhibited less luminal closure sequences (41 ± 2% of the recording time vs. 61 ± 2%; P < 0.001) and more static sequences (38 ± 3 vs. 20 ± 2%; P < 0.001); in contrast, patients with hyperdynamic behavior (n = 13) had an increased proportion of luminal closure sequences (73 ± 4 vs. 61 ± 2%; P = 0.029) and more high-motion sequences (3 ± 1 vs. 0.5 ± 0.1%; P < 0.001). Applying an original methodology, we have developed a novel classification of functional gut disorders based on objective, physiological criteria of small bowel function.

From: Malagelada, C., Drozdzal, M., Segui, S., Mendez, S., Vitria, J., Radeva, P., Santos, J., Accarino, A., Malagelada, J.-R., Azpiroz, F. http://ajpgi.physiology.org/cgi/content/abstract/309/6/G413?rss=1

Suppression of fibrogenic signaling in hepatic stellate cells by Twist1-dependent microRNA-214 expression: Role of exosomes in horizontal transfer of Twist1

A hallmark of liver fibrosis is the activation of hepatic stellate cells (HSC), which results in their production of fibrotic molecules, a process that is largely regulated by connective tissue growth factor (CCN2). CCN2 is increasingly expressed during HSC activation because of diminished expression of microRNA-214 (miR-214), a product of dynamin 3 opposite strand (DNM3os) that directly suppresses CCN2 mRNA. We show that an E-box in the miR-214 promoter binds the basic helix-loop-helix transcription factor, Twist1, which drives miR-214 expression and results in CCN2 suppression. Twist1 expression was suppressed in HSC of fibrotic livers or in cultured HSC undergoing activation in vitro or after treatment with ethanol. Furthermore, Twist1 decreasingly interacted with DNM3os as HSC underwent activation in vitro. Nanovesicular exosomes secreted by quiescent but not activated HSC contained high levels of Twist1, thus reflecting the suppression of cellular Twist1 during HSC activation. Exosomal Twist1 was intercellularly shuttled between HSC and stimulated expression of miR-214 in the recipient cells, causing expression of CCN2 and its downstream effectors to be suppressed. Additionally, the miR-214 E-box in HSC was also regulated by hepatocyte-derived exosomes, showing that functional transfer of exosomal Twist1 occurs between different cell types. Finally, the levels of Twist1, miR-214, or CCN2 in circulating exosomes from fibrotic mice reflected fibrosis-induced changes in the liver itself, highlighting the potential utility of these and other constituents in serum exosomes as novel circulating biomarkers for liver fibrosis. These findings reveal a unique function for cellular or exosomal Twist1 in CCN2-dependent fibrogenesis.

From: Chen, L., Chen, R., Kemper, S., Charrier, A., Brigstock, D. R. http://ajpgi.physiology.org/cgi/content/abstract/309/6/G491?rss=1

bak deletion stimulates gastric epithelial proliferation and enhances Helicobacter felis-induced gastric atrophy and dysplasia in mice

Helicobacter infection causes a chronic superficial gastritis that in some cases progresses via atrophic gastritis to adenocarcinoma. Proapoptotic bak has been shown to regulate radiation-induced apoptosis in the stomach and colon and also susceptibility to colorectal carcinogenesis in vivo. Therefore we investigated the gastric mucosal pathology following H. felis infection in bak-null mice at 6 or 48 wk postinfection. Primary gastric gland culture from bak-null mice was also used to assess the effects of bak deletion on IFN--, TNF-α-, or IL-1β-induced apoptosis. bak-null gastric corpus glands were longer, had increased epithelial Ki-67 expression, and contained fewer parietal and enteroendocrine cells compared with the wild type (wt). In wt mice, bak was expressed at the luminal surface of gastric corpus glands, and this increased 2 wk post-H. felis infection. Apoptotic cell numbers were decreased in bak-null corpus 6 and 48 wk following infection and in primary gland cultures following cytokine administration. Increased gastric epithelial Ki-67 labeling index was observed in C57BL/6 mice after H. felis infection, whereas no such increase was detected in bak-null mice. More severe gastric atrophy was observed in bak-null compared with C57BL/6 mice 6 and 48 wk postinfection, and 76% of bak-null compared with 25% of C57BL/6 mice showed evidence of gastric dysplasia following long-term infection. Collectively, bak therefore regulates gastric epithelial cell apoptosis, proliferation, differentiation, mucosal thickness, and susceptibility to gastric atrophy and dysplasia following H. felis infection.

From: Duckworth, C. A., Abuderman, A. A., Burkitt, M. D., Williams, J. M., O'Reilly, L. A., Pritchard, D. M. http://ajpgi.physiology.org/cgi/content/abstract/309/6/G420?rss=1

Couples With Different Parenting Styles Can Learn to Agree

Parents can learn how to compromise or stand their ground when parenting conflicts arise.

From: http://www.webmd.com/parenting/features/when-parenting-styles-clash?src=RSS_PUBLIC

How Does Food Affect Your Blood Sugar?

How Does Food Affect Your Blood Sugar? Test your diabetes smarts with this WebMD Magazine quiz.

From: http://www.webmd.com/diabetes/features/food-blood-sugar-diabetes?src=RSS_PUBLIC

Get the flu vaccine, reduce your risk of death

Last year was a lousy year for the flu vaccine. Hospitalizations for flu hit a nine-year high, and the vaccine prevented flu in only 23% of all recipients, compared with 50% to 60% of recipients in prior years.

Why does the flu vaccine work well in some winters and not others? The flu vaccine primes the immune system to attack two proteins on the surface of the influenza A virus, hemagglutinin (H) and neuraminidase (N). Different flu strains have different combinations of these proteins — for example, the strains targeted by recent flu vaccines are H3N2 and H1N1.

Unfortunately, the influenza virus is microbiology’s answer to Miley Cyrus: it can change enough in just one year to become completely unrecognizable. The H and N proteins are genetic chameleons that undergo constant transformation. This process is called antigenic drift, and it regularly flummoxes vaccine makers, public health experts, and your immune system.

Developing the new flu vaccines

Most flu vaccine in the United States is made from chicken eggs, using production methods that date back to 1945. This cumbersome technique requires 6-8 months of lead time to produce enough vaccine for the upcoming flu season. Every February, the World Health Organization and the Food and Drug Administration (FDA) make their best guess as to which flu strains should be covered by next winter’s vaccine, based on a review of circulating flu viruses from over 100 countries. But a lot can change in 8 months, especially with influenza. This past year, the “drifted” H3N2 influenza strain didn’t match up with the vaccine strain, explaining the vaccine’s poor performance.

Can researchers build a better flu vaccine? They probably already have. The FDA has approved two alternatives to traditional egg-based vaccines. One of these, Flucelvax, uses influenza virus grown in kidney cells that were originally obtained from a single cocker spaniel in 1958. The other one, FluBlok, is made by tricking insect cells into pumping out large amounts of hemagglutinin, which is then purified and used in the vaccine. These methods might sound outlandish, but they seem to be safe and effective.

These newer vaccines have several advantages:

They are safe for patients with egg allergies. Because most flu vaccine is made from eggs, many people with egg allergies can’t receive the traditional flu shot.

They don’t require a massive supply of chicken eggs, and could still be made even if a bird flu epidemic wiped out chicken flocks.

They need less manufacturing time than egg-based vaccines, meaning vaccine production could be ramped up quickly in case of a flu pandemic. This also might give the FDA more time to make their decision on which flu strains should go into the vaccine, reducing the risk of a vaccine–flu mismatch like last year’s.

Scientists are also working on a universal flu vaccine, one that might not need to be changed every year. This vaccine takes advantage of the fact that the H protein has two parts: a head region, which is the part that changes rapidly, and a stem region, which stays more or less the same. Small studies of vaccines using chunks of the stem have shown promising results in animals. Trials of these vaccines are just beginning in humans.

How the flu vaccine reduces your risk

The CDC recommends that all American adults get a flu vaccine every year. Even though the current vaccine is not perfect, there are many good reasons for you to get it. The vaccine does reduce your chance of getting the flu, especially when it matches up well with dominant flu strains.

The benefits of flu vaccine are particularly impressive in older adults. If you are 65 or older, it lowers your risk of death by 48%. One reason for this lowered risk is that getting the flu increases your risk of developing bacterial pneumonia, which is responsible for many hospitalizations and deaths. But this is not the only reason.

Inflammation is bad for your body, and increases your risk of heart attack or stroke. If you’ve ever had full-blown flu, and you remember how feverish, achy, and miserable you felt, you know that influenza is great at filling your body with inflammation. So, as you might expect, another benefit of the flu vaccine is that it reduces your risk of heart attack and stroke.

Most adults, including me, receive the flu shot made from chicken eggs. If you have an egg allergy, you should get Flucelvak or FluBlok instead. If you are between ages 2 and 49, you are eligible for the intranasal vaccine, which is inhaled rather than injected. Because this vaccine contains live virus, it should be avoided if you are pregnant, have a weak immune system, or are around other people with weak immune systems. The intranasal vaccine may also cause wheezing, so you should avoid it if you are asthmatic.

The post Get the flu vaccine, reduce your risk of death appeared first on Harvard Health Blog.

From: John Ross, MD, FIDSA http://www.health.harvard.edu/blog/get-the-flu-vaccine-reduce-your-risk-of-death-201509158274

Type 2 Diabetes Control and Preventing Dementia

From: http://www.webmd.com/diabetes/news/20150915/type2-diabetes-dementia?src=RSS_PUBLIC

Mom's shocking viral photo shows "reality of addiction"

Photo of children by their father's open casket illustrates "the cold hard truth ... heroin kills"

From: http://www.cbsnews.com/news/moms-shocking-facebook-instagram-photo-reality-of-addiction/

USDA, DOI, and OMB Urge Congress to Fix the Fire Budget

WASHINGTON, Sept. 15, 2015 - On the heels of a notification Monday from USDA to Congress of the need to transfer an additional $250 million to cover wildfire suppression costs for the remainder of the year, Department of Agriculture Secretary Tom Vilsack, Department of the Interior Secretary Sally Jewell, and the White House Office of Management and Budget Director Shaun Donovan sent a joint letter to Congress requesting they act to change the way the nation pays for wildfire costs so that we can continue to adequately invest in forest and rangeland restoration, and make lands less vulnerable to catastrophic wildfire and more resilient.

From: http://www.usda.gov/wps/portal/usda/usdahome?contentid=2015/09/0254.xml&contentidonly=true

Rethink Your Diabetes 'Don't' List

Think sweets and alcohol are off limits when you have diabetes? Think again! WebMD Magazine explains why.

From: http://www.webmd.com/diabetes/features/rethink-diabetes-list?src=RSS_PUBLIC

Feeding Picky Eaters: Mealtime Strategies, Picky Eater Causes, and More

WebMD offers strategies for dealing with your little picky eater. Discover reasons why kids disregard healthy foods and find tips for helping them widen the variety of foods they will eat.

From: http://www.webmd.com/parenting/features/feeding-a-picky-eater?src=RSS_PUBLIC

'How I Took Control of My Diabetes'

Small, manageable goals were the key for this WebMD Community Member.

From: http://www.webmd.com/diabetes/features/took-control-diabetes?src=RSS_PUBLIC

Panel backs aspirin for heart health in some adults

Government task force says daily low-dose aspirin may also reduce risk of colon cancer, but there are serious risks to consider

From: http://www.cbsnews.com/news/aspirin-heart-health-cancer-prevention/

USDA Awards $20.5 Million to Advance the Next Generation of Natural Resources Conservation

WASHINGTON, Sept. 15, 2015 - U.S. Department of Agriculture Secretary Tom Vilsack today announced the award of $20.5 million through its Conservation Innovation Grants (CIG) program for 45 projects that will develop and advance the conservation of natural resources.

From: http://www.usda.gov/wps/portal/usda/usdahome?contentid=2015/09/0253.xml&contentidonly=true

Tuesday, September 15, 2015

Developing the new flu vaccines

How the flu vaccine reduces your risk

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