Charlie Sheen expected to announce HIV diagnosis

Former "Two And A Half Men" star Charlie Sheen is expected to announce he is HIV positive in a interview with NBC's Matt Lauer

From: http://www.cbsnews.com/videos/charlie-sheen-expected-to-announce-hiv-diagnosis/

Coffee drinking linked to a longer life

A new study adds to growing evidence that moderate coffee drinking is good for your health

From: http://www.cbsnews.com/news/coffee-drinking-linked-to-a-longer-life/

After Paris attacks, how to talk to kids about terrorism

Children can be traumatized by seeing images of violence; here's what parents need to know to help kids of all ages cope

From: http://www.cbsnews.com/news/paris-attacks-how-to-talk-to-kids-about-terrorism/

Do You Make Good Food Choices?

Have diabetes? Test your holiday food smarts with this quiz from WebMD Magazine.

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

Diabetes and Holiday Stress

Stress can wreak havoc on blood sugar. WebMD Magazine explains how.

From: http://www.webmd.com/diabetes/features/diabetes-holiday-stress?src=RSS_PUBLIC

Coffee Drinkers May Live Longer

Regular java and decaf were linked to survival benefits in study

From: http://www.webmd.com/diet/20151116/coffee-drinkers-may-live-longer?src=RSS_PUBLIC

Rectal Thermometer Remains Gold Standard for This

Better than temperatures taken by mouth or under arm, study says

From: http://www.webmd.com/news/20151116/rectal-thermometer-remains-gold-standard-for-spotting-fever?src=RSS_PUBLIC

How to Overcome Diabetes Burnout

Is your diabetes routine wearing you out? WebMD Magazine offers tips on how to cope.

From: http://www.webmd.com/diabetes/features/diabetes-routine-burnout?src=RSS_PUBLIC

Man Who Lost His Vision Now Helps Others

Thomas Tobin lost his sight to diabetic retinopathy. Now he has a new focus, and he's sharing his inspirational story with WebMD Magazine.

From: http://www.webmd.com/diabetes/features/diabetes-vision-loss?src=RSS_PUBLIC

High-Tech Glasses Instead of Patch for 'Lazy Eye'?

Digital specs were programmed to block vision in good eye every 30 seconds

From: http://www.webmd.com/children/news/20151116/high-tech-glasses-instead-of-eye-patch-for-lazy-eye?src=RSS_PUBLIC

WHO: Antibiotic resistance is a "global health crisis"

A new survey finds widespread misconceptions about antibiotic overuse and resistance

From: http://www.cbsnews.com/news/world-health-organization-study-finds-myths-about-antibiotic-resistance/

Watching Paris news coverage may take toll on viewers

Experts say repeated exposure to violent events through the media can lead to severe psychological distress

From: http://www.cbsnews.com/news/paris-attacks-psychological-effects-of-viewing-media-coverage/

Mayo Clinic Pulmonary Hypertension Center

From: Mayo Clinic http://www.youtube.com/watch?v=WR_MYsYtikg

Laura's Story: Mayo Clinic Pulmonary Hypertension & Vascular Disease Center

From: Mayo Clinic http://www.youtube.com/watch?v=POskT8R_3t4

Failing Sense of Smell May Be Alzheimer's Warning

As the ability to identify odors goes, so does mental ability, researchers say

From: http://www.webmd.com/alzheimers/news/20151116/failing-sense-of-smell-might-be-alzheimers-warning?src=RSS_PUBLIC

USDA Awards $18 Million for 1890 Land-Grant Universities Research, Education and Extension Activities

WASHINGTON, Nov. 16, 2015 — Agriculture Secretary Tom Vilsack today announced 53 grants totaling more than $18 million to support research, teaching, and extension activities at 1890 historically black land-grant colleges and universities through the U.S. Department of Agriculture’s (USDA) National Institute of Food and Agriculture (NIFA).

From: http://www.usda.gov/wps/portal/usda/usdahome?contentid=2015/11/0313.xml&contentidonly=true

UCL Tear and Tommy John Surgery: What You Need to Know

For a major-league pitcher like Matt Harvey, a torn elbow tendon means Tommy John surgery and a long stint in rehab.What's it like when a regular guy gets this injury? Will you need surgery? What happens in rehab?

From: http://www.webmd.com/men/features/ucl-tear-recovery?src=RSS_PUBLIC

Firefighter gets most extensive face transplant ever

Extraordinary surgery gives donor's face to a volunteer firefighter who was badly burned in 2001

From: http://www.cbsnews.com/news/firefighter-gets-most-extensive-face-transplant-ever/

Interstitial Lung Disease and Lung Transplant: What Patients Need to Know

From: Mayo Clinic http://www.youtube.com/watch?v=kspzJlE0fko

Interactive Webinar: What Patients and Donors Need to Know About Living-Donor Kidney Transplant

From: Mayo Clinic http://www.youtube.com/watch?v=7mLsUVfrLsU

Insight into Endoscopic Balloon Dilatation for Crohn’s Disease - IBD in the News

From: Mayo Clinic http://www.youtube.com/watch?v=GjPKR2UpGzQ

This May Signal Higher Testicular Cancer Odds

Abnormally low sperm count tied to greater risk, study suggests

From: http://www.webmd.com/men/news/20151116/male-infertility-might-signal-higher-odds-of-testicular-cancer?src=RSS_PUBLIC

Teens, Parents Share E-Cig Concerns, Poll Finds

Both groups want tighter controls on devices' use, health warnings on packaging

From: http://teens.webmd.com/news/20151116/teens-parents-share-e-cigarette-concerns-poll-finds?src=RSS_PUBLIC

Chronic high-fat feeding increases GIP and GLP-1 secretion without altering body weight

The incretin hormones, glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide-1 (GLP-1), enhance postprandial insulin secretion, promote adipogenesis, and regulate gastrointestinal motility and food intake. To date, a consensus on how the incretin response is altered in obesity is lacking. We investigated the effects of chronic high-fat (HF) feeding on incretin secretion in the lymph fistula rat model. Male Sprague-Dawley rats (8 wk) were provided a semipurified AIN93M HF or low-fat (LF) diet ad libitum for 3 or 13 wk; a HF pair-fed (HF-PF) group was included as a control during the 3-wk feeding trial. Energy intake, body weight, and body composition were regularly monitored. At the culmination of the feeding period, an intestinal lymphatic duct cannula and duodenal infusion tube were installed. All animals were challenged with a 3-ml Ensure bolus (3.125 kcal/animal) to measure lymphatic incretin secretion. Despite a significantly higher energy intake, both the 3-wk and 13-wk HF-fed animals did not have an increase in body weight and only a slight increase in body fat compared with LF-fed rats. Following the duodenal Ensure challenge, the 3-wk and 13-wk HF-fed rats had significantly greater lymphatic GIP and GLP-1 secretion than the LF-fed animals. Additionally, the HF-PF group displayed a secretion profile similar to the HF-fed animals for GIP but a similar pattern to the LF-fed animals for GLP-1. The HF-PF data suggest that the increased GIP secretion is driven by the greater percentage of fat intake, whereas the increased GLP-1 secretion is driven by the excess caloric intake.

From: Wang, F., Yoder, S. M., Yang, Q., Kohan, A. B., Kindel, T. L., Wang, J., Tso, P. http://ajpgi.physiology.org/cgi/content/abstract/309/10/G807?rss=1

Effects of nerve growth factor antagonist K252a on peritoneal mast cell degranulation: implications for rat postoperative ileus

Stabilization of mast cell (MC) degranulation has been proposed to prevent postoperative ileus (POI). Nerve growth factor (NGF) mediates MC degranulation. The aim of the study was to evaluate whether NGF receptor antagonist K252a acts as a MC stabilizer in vitro and in vivo model of POI. Peritoneal mast cells (PMCs) were obtained from Sprague-Dawley rats and were incubated with K252a and exposed to NGF or Compound 48/80 (C48/80). MC degranulation was assessed by β-hexosaminidase assay. POI was induced in rats by intestinal manipulation (IM). Rats were pretreated with K252a (100 μg/kg sc) 20 min prior to POI induction. At 20 min after IM, release of rat mast cell protease 6 (RMCP-6) was evaluated in peritoneal lavage. At 24 h, intestinal transit (IT) and gastric emptying (GE) were evaluated. Ileal inflammation was assessed by myeloperoxidase (MPO) activity, expression of IL-6, NGF, TrkA, RMCP-2 and 6, and MC density within the full-thickness ileum. C48/80 and NGF evoked degranulation of PMCs in a dose-dependent manner. K252a prevented NGF-evoked, but not C48/80-evoked, MC degranulation. IM evoked the release of peritoneal RMCP-6 and subsequently delayed IT and GE. IM increased MPO activity and expression of IL-6. In IM rats, K252a prevented upregulation of IL-6 expression and reduced TrkA. IT, GE, and inflammation were not affected by K252a. K252a inhibited NGF-evoked degranulation of PMCs in vitro. In vivo, K252a decreased IL-6 and PMC degranulation. This may be of relevance for the development of new therapeutic targets for POI.

From: Berdun, S., Rychter, J., Vergara, P. http://ajpgi.physiology.org/cgi/content/abstract/309/10/G801?rss=1

The p66Shc protein controls redox signaling and oxidation-dependent DNA damage in human liver cells

The p66^Shc protein mediates oxidative stress-related injury in multiple tissues. Steatohepatitis is characterized by enhanced oxidative stress-mediated cell damage. The role of p66^Shc in redox signaling was investigated in human liver cells and alcoholic steatohepatitis. HepG2 cells with overexpression of wild-type or mutant p66^Shc, with Ser³⁶ replacement by Ala, were obtained through infection with recombinant adenoviruses. Reactive oxygen species and oxidation-dependent DNA damage were assessed by measuring dihydroethidium oxidation and 8-hydroxy-2'-deoxyguanosine accumulation into DNA, respectively. mRNA and protein levels of signaling intermediates were evaluated in HepG2 cells and liver biopsies from control and alcoholic steatohepatitis subjects. Exposure to H₂O₂ increased reactive oxygen species and phosphorylation of p66^Shc on Ser³⁶ in HepG2 cells. Overexpression of p66^Shc promoted reactive oxygen species synthesis and oxidation-dependent DNA damage, which were further enhanced by H₂O₂. p66^Shc activation also resulted in increased Erk-1/2, Akt, and FoxO3a phosphorylation. Blocking of Erk-1/2 activation inhibited p66^Shc phosphorylation on Ser³⁶. Increased p66^Shc expression was associated with reduced mRNA levels of antioxidant molecules, such as NF-E2-related factor 2 and its target genes. In contrast, overexpression of the phosphorylation defective p66^Shc Ala³⁶ mutant inhibited p66^Shc signaling, enhanced antioxidant genes, and suppressed reactive oxygen species and oxidation-dependent DNA damage. Increased p66^Shc protein levels and Akt phosphorylation were observed in liver biopsies from alcoholic steatohepatitis compared with control subjects. In human alcoholic steatohepatitis, increased hepatocyte p66^Shc protein levels may enhance susceptibility to DNA damage by oxidative stress by promoting reactive oxygen species synthesis and repressing antioxidant pathways.

From: Perrini, S., Tortosa, F., Natalicchio, A., Pacelli, C., Cignarelli, A., Palmieri, V. O., Caccioppoli, C., De Stefano, F., Porro, S., Leonardini, A., Ficarella, R., De Fazio, M., Cocco, T., Puglisi, F., Laviola, L., Palasciano, G., Giorgino, F. http://ajpgi.physiology.org/cgi/content/abstract/309/10/G826?rss=1

Mesenchymal stromal cell therapy in liver disease: opportunities and lessons to be learnt?

End-stage liver disease is responsible for 30,000 deaths per year in the United States alone, and it is continuing to increase every year. With liver transplantation the only curative treatment currently available, new therapies are in great demand. Mesenchymal stem cells (MSC) offer an opportunity to both treat liver inflammatory damage, as well as reverse some of the changes that occur following chronic liver injury. With the ability to regulate both the innate and adaptive immune system, as well as both inhibit and promote apoptosis of effector inflammatory cells, there are numerous therapeutic opportunities for MSC in acute and chronic liver disease. This article critically appraises the potential therapeutic roles of MSC in liver disease, as well as the barriers to their adoption into clinical practice.

From: Owen, A., Newsome, P. N. http://ajpgi.physiology.org/cgi/content/abstract/309/10/G791?rss=1

PACAP intraperitoneal treatment suppresses appetite and food intake via PAC1 receptor in mice by inhibiting ghrelin and increasing GLP-1 and leptin

Pituitary adenylate cyclase-activating peptide (PACAP) is expressed within the gastroenteric system, where it has profound physiological effects. PACAP was shown to regulate food intake and thermogenesis centrally; however, PACAP peripheral regulation of appetite and feeding behavior is unknown. Therefore, we studied PACAP's effect on appetite and food intake control by analyzing feeding behavior and metabolic hormones in PAC1-deficient (PAC1–/–) and age-matched wild-type (WT) mice intraperitoneally injected with PACAP_1–38 or PACAP_1–27 before the dark phase of feeding. Food intake and feeding behavior were analyzed using the BioDAQ system. Active ghrelin, glucagon-like peptide-1 (GLP-1), leptin, peptide YY, pancreatic polypeptide, and insulin were measured following PACAP_1–38 administration in fasted WT mice. PACAP_1–38/PACAP_1–27 injected into WT mice significantly decreased in a dose-dependent manner cumulative food intake and reduced bout and meal feeding parameters. Conversely, PACAP_1–38 injected into PAC1–/– mice failed to significantly change food intake. Importantly, PACAP_1–38 reduced plasma levels of active ghrelin compared with vehicle in WT mice. In PAC1–/– mice, fasting levels of active ghrelin, GLP-1, insulin, and leptin and postprandial levels of active ghrelin and insulin were significantly altered compared with levels in WT mice. Therefore, PAC1 is a novel regulator of appetite/satiety. PACAP_1–38/PACAP_1–27 significantly reduced appetite and food intake through PAC1. In PAC1–/– mice, the regulation of anorexigenic/orexigenic hormones was abolished, whereas active ghrelin remained elevated even postprandially. PACAP significantly reduced active ghrelin in fasting conditions. These results establish a role for PACAP via PAC1 in the peripheral regulation of appetite/satiety and suggest future studies to explore a therapeutic use of PACAP or PAC1 agonists for obesity treatment.

From: Vu, J. P., Goyal, D., Luong, L., Oh, S., Sandhu, R., Norris, J., Parsons, W., Pisegna, J. R., Germano, P. M. http://ajpgi.physiology.org/cgi/content/abstract/309/10/G816?rss=1

Bilirubin prevents acute DSS-induced colitis by inhibiting leukocyte infiltration and suppressing upregulation of inducible nitric oxide synthase

Bilirubin is thought to exert anti-inflammatory effects by inhibiting vascular cell adhesion molecule-1 (VCAM-1)-dependent leukocyte migration and by suppressing the expression of inducible nitric oxide synthase (iNOS). As VCAM-1 and iNOS are important mediators of tissue injury in the dextran sodium sulfate (DSS) murine model of inflammatory colitis, we examined whether bilirubin prevents colonic injury in DSS-treated mice. Male C57BL/6 mice were administered 2.5% DSS in the drinking water for 7 days, while simultaneously receiving intraperitoneal injections of bilirubin (30 mg/kg) or potassium phosphate vehicle. Disease activity was monitored, peripheral blood counts and serum nitrate levels were determined, and intestinal specimens were analyzed for histological injury, leukocyte infiltration, and iNOS expression. The effect of bilirubin on IL-5 production by HSB-2 cells and on Jurkat cell transendothelial migration also was determined. DSS-treated mice that simultaneously received bilirubin lost less body weight, had lower serum nitrate levels, and exhibited reduced disease severity than vehicle-treated animals. Concordantly, histopathological analyses revealed that bilirubin-treated mice manifested significantly less colonic injury, including reduced infiltration of eosinophils, lymphocytes, and monocytes, and diminished iNOS expression. Bilirubin administration also was associated with decreased eosinophil and monocyte infiltration into the small intestine, with a corresponding increase in peripheral blood eosinophilia. Bilirubin prevented Jurkat migration but did not alter IL-5 production. In conclusion, bilirubin prevents DSS-induced colitis by inhibiting the migration of leukocytes across the vascular endothelium and by suppressing iNOS expression.

From: Zucker, S. D., Vogel, M. E., Kindel, T. L., Smith, D. L. H., Idelman, G., Avissar, U., Kakarlapudi, G., Masnovi, M. E. http://ajpgi.physiology.org/cgi/content/abstract/309/10/G841?rss=1

FDA Finalizes New Food Safety Rules

Farms, importers will be responsible for preventing outbreaks of foodborne illness

From: http://www.webmd.com/food-recipes/food-poisoning/20151113/fda-finalizes-new-food-safety-rules?src=RSS_PUBLIC

Best Practices: Subarachnoid Hemorrhage from Ruptured Brain Aneurysm

From: Mayo Clinic http://www.youtube.com/watch?v=a86y04dqma8

Nutritional psychiatry: Your brain on food

Think about it. Your brain is always “on.” It takes care of your thoughts and movements, your breathing and heartbeat, your senses — it works hard 24/7, even while you’re asleep. This means your brain requires a constant supply of fuel. That “fuel” comes from the foods you eat — and what’s in that fuel makes all the difference. Put simply, what you eat directly affects the structure and function of your brain and, ultimately, your mood.

Like an expensive car, your brain functions best when it gets only premium fuel. Eating high-quality foods that contain lots of vitamins, minerals, and antioxidants nourishes the brain and protects it from oxidative stress — the “waste” (free radicals) produced when the body uses oxygen, which can damage cells.

Unfortunately, just like an expensive car, your brain can be damaged if you ingest anything other than premium fuel. If substances from “low-premium” fuel (such as what you get from processed or refined foods) get to the brain, it has little ability to get rid of them. Diets high in refined sugars, for example, are harmful to the brain. In addition to worsening your body’s regulation of insulin, they also promote inflammation and oxidative stress. Multiple studies have found a correlation between a diet high in refined sugars and impaired brain function — and even a worsening of symptoms of mood disorders, such as depression.

It makes sense. If your brain is deprived of good-quality nutrition, or if free radicals or damaging inflammatory cells are circulating within the brain’s enclosed space, further contributing to brain tissue injury, consequences are to be expected. What’s interesting is that for many years, the medical field did not fully acknowledge the connection between mood and food.

Today, fortunately, the burgeoning field of nutritional psychiatry is finding there are many consequences and correlations between not only what you eat, how you feel, and how you ultimately behave, but also the kinds of bacteria that live in your gut.

How the foods you eat affect how you feel

Serotonin is a neurotransmitter that helps regulate sleep and appetite, mediate moods, and inhibit pain. Since about 95% of your serotonin is produced in your gastrointestinal tract, and your gastrointestinal tract is lined with a hundred million nerve cells, or neurons, it makes sense that the inner workings of your digestive system don’t just help you digest food, but also guide your emotions. What’s more, the function of these neurons — and the production of neurotransmitters like serotonin — is highly influenced by the billions of “good” bacteria that make up your intestinal microbiome. These bacteria play an essential role in your health. They protect the lining of your intestines and ensure they provide a strong barrier against toxins and “bad” bacteria; they limit inflammation; they improve how well you absorb nutrients from your food; and they activate neural pathways that travel directly between the gut and the brain.

Studies have shown that when people take probiotics (supplements containing the good bacteria), their anxiety levels, perception of stress, and mental outlook improve, compared with people who did not take probiotics. Other studies have compared “traditional” diets, like the Mediterranean diet and the traditional Japanese diet, to a typical “Western” diet and have shown that the risk of depression is 25% to 35% lower in those who eat a traditional diet. Scientists account for this difference because these traditional diets tend to be high in vegetables, fruits, unprocessed grains, and fish and seafood, and to contain only modest amounts of lean meats and dairy. They are also void of processed and refined foods and sugars, which are staples of the “Western” dietary pattern. In addition, many of these unprocessed foods are fermented, and therefore act as natural probiotics. Fermentation uses bacteria and yeast to convert sugar in food to carbon dioxide, alcohol, and lactic acid. It is used to protect food from spoiling and can add a pleasant taste and texture.

This may sound implausible to you, but the notion that good bacteria not only influence what your gut digests and absorbs, but that they also affect the degree of inflammation throughout your body, as well as your mood and energy level, is gaining traction among researchers. The results so far have been quite amazing.

What does this mean for you?

Start paying attention to how eating different foods makes you feel — not just in the moment, but the next day. Try eating a “clean” diet for two to three weeks — that means cutting out all processed foods and sugar. Add fermented foods like kimchi, miso, sauerkraut, pickles, or kombucha. You also might want to try going dairy-free — and some people even feel that they feel better when their diets are grain-free. See how you feel. Then slowly introduce foods back into your diet, one by one, and see how you feel.

When my patients “go clean,” they cannot believe how much better they feel both physically and emotionally, and how much worse they then feel when they reintroduce the foods that are known to enhance inflammation. Give it a try!

Related Posts:

• Extra protein is a decent dietary choice, but don’t…
• Switching to a fiber-rich diet may lower colon cancer risk…
• Going gluten-free just because? Here’s what you need…
• Fish oil: friend or foe?
• Infection, autoimmune disease linked to depression

The post Nutritional psychiatry: Your brain on food appeared first on Harvard Health Blog.

From: Eva Selhub MD http://www.health.harvard.edu/blog/nutritional-psychiatry-your-brain-on-food-201511168626

The most common causes of eye injuries in the U.S.

Thousands of eye injuries occur in ways you might not expect, and the cost of treating them has risen sharply

From: http://www.cbsnews.com/news/the-most-common-causes-of-eye-injuries-in-the-u-s/

Drug Lucentis May Fight Diabetic Eye Disease

Government-funded study finds injected medicine beats laser therapy for form of retinopathy

From: http://www.webmd.com/diabetes/news/20151113/drug-lucentis-may-fight-diabetic-eye-disease?src=RSS_PUBLIC

WHO: Misconceptions about antibiotics and resistance

A look at 12 countries reveals widespread misconceptions about antibiotic resistance, calling it “a global health crisis”

From: http://www.cbsnews.com/videos/who-misconceptions-about-antibiotics-and-resistance/

WHO multi-country survey reveals widespread public misunderstanding about antibiotic resistance

As WHO ramps up its fight against antibiotic resistance, a new multi-country survey shows people are confused about this major threat to public health and do not understand how to prevent it from growing.

Antibiotic resistance happens when bacteria change and become resistant to the antibiotics used to treat the infections they cause. Over-use and misuse of antibiotics increase the development of resistant bacteria, and this survey points out some of the practices, gaps in understanding and misconceptions which contribute to this phenomenon.

From: http://www.who.int/entity/mediacentre/news/releases/2015/antibiotic-resistance/en/index.html

Antibiotics in animal feed can harm children, doctors warn

Pediatricians say antibiotic-resistant infections are especially tough to treat in kids with cancer, serious illnesses

From: http://www.cbsnews.com/news/antibiotics-animal-feed-harm-children-american-academy-of-pediatrics/