Do stents ease chest pain?

A new study has grabbed the attention of heart specialists and patients. It questions whether stents really ease chest pain. Dr. Jon LaPook discusses the study.

From: http://www.cbsnews.com/videos/do-stents-ease-chest-pain/

Study questions use of stents for many heart patients

New findings could change cardiovascular care for patients with chest pain or angina, some experts say

From: http://www.cbsnews.com/news/study-questions-artery-opening-heart-stents-angina/

Infectious Diseases A-Z: Leptospirosis in Puerto Rico

From: Mayo Clinic https://www.youtube.com/watch?v=D6qAEEiYA7w

Crackdown on bogus marijuana "cures" for cancer

FDA issued a warning to four companies illegally selling products that claim to prevent, diagnose, treat, or cure cancer without evidence

From: http://www.cbsnews.com/news/fda-marijuana-cannabidiol-cancer-health-claims-crackdown/

Sugary Drinks Could Break Your Heart

If you're a fan of sodas, fruit juices and sugary sports drinks, you're probably not doing your heart any favors.

From: https://www.webmd.com/food-recipes/news/20171102/sugary-drinks-could-break-your-heart?src=RSS_PUBLIC

Are Artery-Opening Stents for Chest Pain Useless?

A new study suggests that the placebo effect of stents in heart patients with chest pain may be far more pronounced than thought.

From: https://www.webmd.com/heart/news/20171102/are-artery-opening-stents-for-chest-pain-useless?src=RSS_PUBLIC

Women’s Wellness: Hormone therapy and Alzheimer’s disease

From: Mayo Clinic https://www.youtube.com/watch?v=tajDIWvPMo8

Mom's Skin Cancer Pic Shoots Around the Web

California mom Kari Cummins didn't think much of it when she first shared pictures of her skin cancer on social media. But one image in particular -- of a large hole in the lower part of her face -- shot around the internet.

From: https://www.webmd.com/features/skin-cancer-carcinoma-melanoma?src=RSS_PUBLIC

The Mayo Clinic's HABIT Healthy Action to Benefit Independence & ThinkingR Progam

From: Mayo Clinic https://www.youtube.com/watch?v=0trSH5JnmIw

Fiber-Rich Diet Boosts Survival From Colon Cancer

Among people treated for non-metastatic colon cancer, every 5 grams of fiber added to their diet reduced their odds of dying by nearly 25 percent, said lead researcher Dr. Andrew Chan. He is an associate professor in the department of medicine at Harvard Medical School.

From: https://www.webmd.com/colorectal-cancer/news/20171102/fiber-rich-diet-boosts-survival-from-colon-cancer?src=RSS_PUBLIC

Are Green Cleaners Better For You??

Green cleaning products market themselves as better for you. Are you getting what you paid for?

From: https://www.webmd.com/asthma/news/20171102/are-green-cleaners-better-for-your-health?src=RSS_PUBLIC

Mayo Clinic Transform 2017 - Session 8: A Personal Perspective: Clay Christensen

From: Mayo Clinic https://www.youtube.com/watch?v=p6vkDm50Bh8

Mayo Clinic Transform 2017 - Closing Comments: Elisabeth Rosenthal, M.D.

From: Mayo Clinic https://www.youtube.com/watch?v=D1ftG9uUDDY

KLF-5 extends its fingers to desmosomes: the next frontier for enteric epithelial research?

From: Israelyan, N., Margolis, K. G. http://ajpgi.physiology.org/cgi/content/full/313/5/G476?rss=1

Krüppel-like factor 5 is essential for maintenance of barrier function in mouse colon

Krüppel-like factor 5 (KLF5) is a member of the zinc finger family of transcription factors that regulates homeostasis of the intestinal epithelium. Previous studies suggested an indispensable role of KLF5 in maintaining intestinal barrier function. In the current study, we investigated the mechanisms by which KLF5 regulates colonic barrier function in vivo and in vitro. We used an inducible and a constitutive intestine-specific Klf5 knockout mouse models (Villin-CreER^T2;Klf5^fl/fl designated as Klf5^IND and Villin-Cre;Klf5^fl/fl as Klf5^IS) and studied an inducible KLF5 knockdown in Caco-2 BBe cells using a lentiviral Tet-on system (Caco-2 BBe KLF5IND). Specific knockout of Klf5 in colonic tissues, either inducible or constitutive, resulted in increased intestinal permeability. The phenotype was accompanied by a significant reduction in Dsg2, which encodes desmoglein-2, a desmosomal cadherin, at both mRNA and protein levels. Transmission electron microscopy showed alterations of desmosomal morphology in both KLF5 knockdown Caco-2 BBe cells and Klf5 knockout mouse colonic tissues. Inducible knockdown of KLF5 in Caco-2BBe cells grown on Transwell plates led to impaired barrier function as evidenced by decreased transepithelial electrical resistance and increased paracellular permeability to fluorescein isothiocyanate-4 kDa dextran. Furthermore, DSG2 was significantly decreased in KLF5 knockdown cells, and DSG2 overexpression partially rescued the impaired barrier function caused by KLF5 knockdown. Electron microscopy studies demonstrated altered desmosomal morphology after KLF5 knockdown. In combination with chromatin immunoprecipitation analysis and promoter study, our data show that KLF5 regulates intestinal barrier function by mediating the transcription of DSG2, a gene encoding a major component of desmosome structures.

NEW & NOTEWORTHY The study is original research on the direct function of a Krüppel-like factor on intestinal barrier function, which is commonly exerted by cell junctions, including tight junctions, adherens junctions, and desmosomes. Numerous previous studies were focused on tight junctions and adherens junctions. However, this study provided a new perspective on how the intestinal barrier function is regulated by KLF5 through DSG2, a component of desmosome complexes.

From: Liu, Y., Chidgey, M., Yang, V. W., Bialkowska, A. B. http://ajpgi.physiology.org/cgi/content/abstract/313/5/G478?rss=1

A small population of liver endothelial cells undergoes endothelial-to-mesenchymal transition in response to chronic liver injury

Rising evidence points to endothelial-to-mesenchymal transition (EndMT) as a significant source of the mesenchymal cell population in fibrotic diseases. In this context, we hypothesized that liver endothelial cells undergo EndMT during fibrosis progression. Cirrhosis in mice was induced by CCl₄. A transgenic mouse expressing a red fluorescent protein reporter under the control of Tie2 promoter (Tie2-tdTomato) was used to trace the acquisition of EndMT. Sinusoidal vascular connectivity was evaluated by intravital microscopy and high-resolution three-dimensional confocal microscopy. A modest but significant fraction of liver endothelial cells from both cirrhotic patients and CCl₄-treated Tie2-tdTomato mice acquired an EndMT phenotype characterized by the coexpression of CD31 and α-smooth muscle actin, compared with noncirrhotic livers. Bone morphogenetic protein-7 (BMP-7) inhibited the acquisition of EndMT induced by transforming growth factor-β1 (TGF-β1) treatment in cultured primary mouse liver endothelial cells from control mice. EndMT was also reduced significantly in vivo in cirrhotic Tie2-tdTomato mice treated intraperitoneally with BMP-7 compared with untreated mice (1.9 ± 0.2 vs. 3.8 ± 0.3%, respectively; P < 0.05). The decrease of EndMT in cirrhotic livers correlated with a significant decrease in liver fibrosis (P < 0.05) and an improvement in the vascular disorganization rate (P < 0.05). We demonstrated the acquisition of the EndMT phenotype by a subpopulation of endothelial cells from cirrhotic livers in both animal models and patients. BMP-7 treatment decreases the occurrence of the EndMT phenotype and has a positive impact on the severity of disease by reducing fibrosis and sinusoidal vascular disorganization.

NEW & NOTEWORTHY A subpopulation of liver endothelial cells from cirrhotic patients and mice with liver fibrosis undergoes endothelial-to-mesenchymal transition. Liver endothelial cells from healthy mice could transition into a mesenchymal phenotype in culture in response to TGF-β1 treatment. Fibrotic livers treated chronically with BMP-7 showed lower EndMT acquisition, reduced fibrosis, and improved vascular organization.

From: Ribera, J., Pauta, M., Melgar-Lesmes, P., Cordoba, B., Bosch, A., Calvo, M., Rodrigo-Torres, D., Sancho-Bru, P., Mira, A., Jimenez, W., Morales-Ruiz, M. http://ajpgi.physiology.org/cgi/content/abstract/313/5/G492?rss=1

Effects of NK1 receptors on gastric motor functions and satiation in healthy humans: results from a controlled trial with the NK1 antagonist aprepitant

Aprepitant, an NK1 receptor antagonist, is approved for the treatment of chemotherapy-induced or postoperative emesis by blocking NK1 receptors in the brain stem vomiting center. The effects of NK1 receptors on gastric functions and postprandial symptoms in humans are unclear; a single, crossover study did not show a significant effect of aprepitant on gastrointestinal transit. Our aim was to compare, in a randomized, double-blind, placebo-controlled, parallel-group study (12 healthy volunteers per group), the effects of aprepitant vs. placebo on gastric emptying of solids (by scintigraphy) with a 320-kcal meal, gastric volumes (GVs; fasting and accommodation by single photon emission-computed tomography ), satiation [maximum tolerated volume (MTV)], and symptoms after a dyspeptogenic meal of Ensure. Aprepitant (125 mg on day 1, followed by 80 mg on days 2–5) or placebo, one tablet daily, was administered for 5 consecutive days. Statistical analysis was by unpaired rank sum test, adjusted for sex difference and body mass index. To assess treatment effects on symptoms, we incorporated MTV in the model. Aprepitant increased fasting, postprandial, and accommodation GV and tended to increase volume to fullness and MTV by ~200 kcal. However, aprepitant increased aggregate symptoms, nausea, and pain scores after ingestion the MTV of Ensure. There was no significant effect of aprepitant on gastric half-emptying time of solids. We conclude that NK1 receptors are involved in the control of GV and in determining postprandial satiation and symptoms. Further studies of the pharmacodynamics and therapeutic role of NK1 receptor antagonists in patients with gastroparesis and dyspepsia are warranted.

NEW & NOTEWORTHY Aprepitant increases fasting, postprandial, and accommodation gastric volumes. Aprepitant increases volume to fullness and maximum tolerated volume during a nutrient drink test. NK1 receptors are involved in the control of gastric volume and in determining postprandial satiation and symptoms.

From: Jacob, D., Busciglio, I., Burton, D., Halawi, H., Oduyebo, I., Rhoten, D., Ryks, M., Harmsen, W. S., Camilleri, M. http://ajpgi.physiology.org/cgi/content/abstract/313/5/G505?rss=1

Hamp1 mRNA and plasma hepcidin levels are influenced by sex and strain but do not predict tissue iron levels in inbred mice

Iron homeostasis is tightly regulated, and the peptide hormone hepcidin is considered to be a principal regulator of iron metabolism. Previous studies in a limited number of mouse strains found equivocal sex- and strain-dependent differences in mRNA and serum levels of hepcidin and reported conflicting data on the relationship between hepcidin (Hamp1) mRNA levels and iron status. Our aim was to clarify the relationships between strain, sex, and hepcidin expression by examining multiple tissues and the effects of different dietary conditions in multiple inbred strains. Two studies were done: first, Hamp1 mRNA, liver iron, and plasma diferric transferrin levels were measured in 14 inbred strains on a control diet; and second, Hamp1 mRNA and plasma hepcidin levels in both sexes and iron levels in the heart, kidneys, liver, pancreas, and spleen in males were measured in nine inbred/recombinant inbred strains raised on an iron-sufficient or high-iron diet. Both sex and strain have a significant effect on both hepcidin mRNA (primarily a sex effect) and plasma hepcidin levels (primarily a strain effect). However, liver iron and diferric transferrin levels are not predictors of Hamp1 mRNA levels in mice fed iron-sufficient or high-iron diets, nor are the Hamp1 mRNA and plasma hepcidin levels good predictors of tissue iron levels, at least in males. We also measured plasma erythroferrone, performed RNA-sequencing analysis of liver samples from six inbred strains fed the iron-sufficient, low-iron, or high-iron diets, and explored differences in gene expression between the strains with the highest and lowest hepcidin levels.

NEW & NOTEWORTHY Both sex and strain have a significant effect on both hepcidin mRNA (primarily a sex effect) and plasma hepcidin levels (primarily a strain effect). Liver iron and diferric transferrin levels are not predictors of Hamp1 mRNA levels in mice, nor are the Hamp1 mRNA and plasma hepcidin levels good predictors of tissue iron levels, at least in males.

From: McLachlan, S., Page, K. E., Lee, S.-M., Loguinov, A., Valore, E., Hui, S. T., Jung, G., Zhou, J., Lusis, A. J., Fuqua, B., Ganz, T., Nemeth, E., Vulpe, C. D. http://ajpgi.physiology.org/cgi/content/abstract/313/5/G511?rss=1

Roles of autophagy and metabolism in pancreatic cancer cell adaptation to environmental challenges

Pancreatic ductal adenocarcinoma (PDAC) displays extensive and poorly vascularized desmoplastic stromal reaction, and therefore, pancreatic cancer (PaCa) cells are confronted with nutrient deprivation and hypoxia. Here, we investigate the roles of autophagy and metabolism in PaCa cell adaptation to environmental stresses, amino acid (AA) depletion, and hypoxia. It is known that in healthy cells, basal autophagy is at a low level, but it is greatly activated by environmental stresses. By contrast, we find that in PaCa cells, basal autophagic activity is relatively high, but AA depletion and hypoxia activate autophagy only weakly or not at all, due to their failure to inhibit mechanistic target of rapamycin. Basal, but not stress-induced, autophagy is necessary for PaCa cell proliferation, and AA supply is even more critical to maintain PaCa cell growth. To gain insight into the underlying mechanisms, we analyzed the effects of autophagy inhibition and AA depletion on PaCa cell metabolism. PaCa cells display mixed oxidative/glycolytic metabolism, with oxidative phosphorylation (OXPHOS) predominant. Both autophagy inhibition and AA depletion dramatically decreased OXPHOS; furthermore, pharmacologic inhibitors of OXPHOS suppressed PaCa cell proliferation. The data indicate that the maintenance of OXPHOS is a key mechanism through which autophagy and AA supply support PaCa cell growth. We find that the expression of oncogenic activation mutation in GTPase Kras markedly promotes basal autophagy and stimulates OXPHOS through an autophagy-dependent mechanism. The results suggest that approaches aimed to suppress OXPHOS, particularly through limiting AA supply, could be beneficial in treating PDAC.

NEW & NOTEWORTHY Cancer cells in the highly desmoplastic pancreatic ductal adenocarcinoma confront nutrient [i.e., amino acids (AA)] deprivation and hypoxia, but how pancreatic cancer (PaCa) cells adapt to these conditions is poorly understood. This study provides evidence that the maintenance of mitochondrial function, in particular, oxidative phosphorylation (OXPHOS), is a key mechanism that supports PaCa cell growth, both in normal conditions and under the environmental stresses. OXPHOS in PaCa cells critically depends on autophagy and AA supply. Furthermore, the oncogenic activation mutation in GTPase Kras upregulates OXPHOS through an autophagy-dependent mechanism.

From: Maertin, S., Elperin, J. M., Lotshaw, E., Sendler, M., Speakman, S. D., Takakura, K., Reicher, B. M., Mareninova, O. A., Grippo, P. J., Mayerle, J., Lerch, M. M., Gukovskaya, A. S. http://ajpgi.physiology.org/cgi/content/abstract/313/5/G524?rss=1

Mayo Clinic Transform 2017 - Session 7: Closing the Gap: Gianrico Farrugia, M.D.

From: Mayo Clinic https://www.youtube.com/watch?v=AivYLGg7JnQ

Mayo Clinic Transform 2017 - Session 7: Closing the Gap: Danielle Ofri, M.D., Ph.D.

From: Mayo Clinic https://www.youtube.com/watch?v=_ZCoOckImRQ

Mayo Clinic Transform 2017 - Session 7: Closing the Gap: Laura Adams

From: Mayo Clinic https://www.youtube.com/watch?v=kWAx34ldCYo

Mayo Clinic Transform 2017 - Session 7: Closing the Gap: Doug Wood, M.D.

From: Mayo Clinic https://www.youtube.com/watch?v=fxpmNCjUQUo

Hundreds of Marine recruits sickened by E. coli

More than 200 recruits are undergoing treatment for virulent stomach bug

From: http://www.cbsnews.com/news/hundreds-of-marine-corps-recruits-sickened-by-e-coli-outbreak/

Mayo Clinic Transform 2017 - Session 4: Forces That Can't Be Ignored: Bon Ku, M.D.

From: Mayo Clinic https://www.youtube.com/watch?v=q0WX9iugL-g

Recall: Kidde Fire Extinguishers

The federal government has recalled more than 37.8 million Kidde fire extinguishers with plastic handles. One death has been reported.

From: https://www.webmd.com/a-to-z-guides/news/20171102/recall-kidde-fire-extinguishers?src=RSS_PUBLIC

Mayo Clinic Transform 2017 - Session 4: Forces That Can't Be Ignored: Thompson Aderinkomi

From: Mayo Clinic https://www.youtube.com/watch?v=ujdaf7hEd94

Mayo Clinic Minute: Fall back with daylight saving time

From: Mayo Clinic https://www.youtube.com/watch?v=syAylpNknuM

Mayo Clinic Transform 2017 - Session 4: Forces That Can't Be Ignored: Kathryn Perera

From: Mayo Clinic https://www.youtube.com/watch?v=0JwXlu5gR-o

Mayo Clinic Transform 2017 - Session 4: Forces That Can't Be Ignored: Peter Bach, M.D.

From: Mayo Clinic https://www.youtube.com/watch?v=eUAEWFl2y0Y

Mayo Clinic Transform 2017- Session 3: Case Study CODE-X: Andrew Danielsen

From: Mayo Clinic https://www.youtube.com/watch?v=MhysvH8RO78

Mayo Clinic Transform 2017 - Session 3: Case Study CODE-X: Robert Fassett, M.D.

From: Mayo Clinic https://www.youtube.com/watch?v=gWhbuWgp2iE

Mayo Clinic Transform 2017 - Session 3: Case Study CODE-X: Joseph Dudas

From: Mayo Clinic https://www.youtube.com/watch?v=w4G3jMFDy7M

Mayo Clinic Transform 2017 - Session 3: Case Study CODE-X: Lisa Kottschade

From: Mayo Clinic https://www.youtube.com/watch?v=UBP5TOG3hkY

Mayo Clinic Transform 2017 - Session 3: Case Study CODE-X: Svetomir Markovic, M.D., Ph.D.

From: Mayo Clinic https://www.youtube.com/watch?v=YVs2CAkAz-I

Mayo Clinic Transform 2017 - Session 2: Overcoming Inertia: Darshak Sanghavi, M.D.

From: Mayo Clinic https://www.youtube.com/watch?v=fpgmMztgPVk

Mayo Clinic Transform 2017 - Session 2: Overcoming Inertia: Scott Wallace

From: Mayo Clinic https://www.youtube.com/watch?v=JIKIhyngmYM

Mayo Clinic Transform 2017 - Session 2: Overcoming Inertia: Elizabeth Teisberg, Ph.D.

From: Mayo Clinic https://www.youtube.com/watch?v=n6kzXP6P4fk

Mayo Clinic Transform 2017 - Session 2: Overcoming Inertia: Andrea Walsh

From: Mayo Clinic https://www.youtube.com/watch?v=sAnRVFTXRYE

Mayo Clinic Transform 2017 - Session 1: Mind the Gap: Christian Pean, M.D.

From: Mayo Clinic https://www.youtube.com/watch?v=gwUvjmCO540

Can You Trust the Labels on Your Supplements?

More than half of the herbal and dietary supplements analyzed by researchers contained ingredients that differed from the list on their labels.

From: https://www.webmd.com/vitamins-and-supplements/news/20171102/can-you-trust-the-labels-on-your-supplements?src=RSS_PUBLIC

Gene Therapy, New Drug Fight Rare Disease in Kids

Two innovative new therapies for spinal muscular atrophy (SMA) type 1 have proven highly effective in clinical trials, researchers report.

From: https://www.webmd.com/children/news/20171101/gene-therapy-new-drug-fight-rare-disease-in-kids?src=RSS_PUBLIC

Americans Are Stressed, and Politics Is To Blame

The survey of more than 3,400 adults, conducted in August, found that 59 percent of respondents said they consider this the lowest point in American history that they can remember.

From: https://www.webmd.com/balance/stress-management/news/20171101/americans-are-stressed-and-politics-is-to-blame?src=RSS_PUBLIC

Mayo Clinic - Session 1: Mind the Gap: James Weinstein, D.O.

From: Mayo Clinic https://www.youtube.com/watch?v=-0pveUqILJg

Mayo Clinic - Session 1: Mind the Gap: Andy Slavitt

From: Mayo Clinic https://www.youtube.com/watch?v=5eqy94HId7I

Mayo Clinic - Opening Comments: Elisabeth Rosenthal, M.D.

From: Mayo Clinic https://www.youtube.com/watch?v=Yhi6YYx7Pnk

Addiction, the opioid crisis, and family pain

In 2015, the opioid crisis was escalating to emergency-level proportions, claiming as many lives as car accidents. As the daughter of a longtime drug addict, the current burgeoning opioid epidemic managed to be both familiar and strange to me at the same time. My mother developed her addictions during the height of drug epidemics that occurred in New York City in the mid-1980s. The timeframe also marked the infancy of the AIDS crisis and the height of Reagan-era “Just Say No” programs. Back then, addiction was treated and viewed more as a crime than a disease, supposedly committed by scoundrels and misfits. The theory held that respectable people did not associate with addicts, much less share their homes and their blood with them.

The intense societal shaming and criminalization of her addictions led to more resistance by my mother to seek the treatment she needed, until she eventually stopped trying to quit altogether. The stigmatization of her disease impacted me profoundly as a child — almost as much as the regular abuses I endured from her due to her addictive behavior. Whether it was being the regular target of smacking, lying, spitting, stealing, or vicious name-calling, it stung all the more because society made me feel complicit by relation. I had no healthy outlet to vent my escalating outrage at my own victimization, at an age when I was too young to properly process or even fully understand what was happening. I learned to stay silent, to repress my feelings, and to isolate myself, so as not to mistakenly disclose our family secret and be swept away into the foster care system, potentially separated forever from my younger brother.

Nowadays, when I see the constant commercials and articles offering support and compassion to those suffering from opioid addiction, I am struck by ambivalence. While I feel both heartened and relieved that addiction is finally being treated as a disease for which such supports can exist, I am also embittered that it did not happen when I needed it. I am angry that the shift in dialogue around addiction — and the companion funding being offered for programs that stress rehabilitation over incarceration for those afflicted — is likely due to the demographic differences in race, class, and regional areas impacted by this epidemic as opposed to the epidemic that claimed my mother. My family was poor, undereducated, and hailed from a low-income inner-city neighborhood where most residents were not white. Thus, we were ignored.

As noted by the National Survey on Drug Use and Health, 75% of all opioid misuse starts with people using medication that wasn’t prescribed for them. Furthermore, 90% of all addictions begin either in adolescence or early adulthood, while most of those who misuse opioids already have a prior history of abusing alcohol and other drugs. In my mother’s case, she began experimenting with cocaine first before jumping to injecting heroin in her mid-twenties; there was no prescription medication involved. My uncle (who was also my godfather) died of an overdose of Xanax (which is a benzodiazepine, not an opioid) after mixing it with too much alcohol. My brother became addicted to my mother’s prescription Dilaudid (a class of opioid) while she was in the late stages of terminal cancer; this occurred in his mid-twenties, after he had struggled for more than a decade with alcoholism.

I personally decided to opt out of using opioids for long-term management of my own pain symptoms because I did not want to risk becoming addicted, considering my own substantial family history and potential genetic predisposition to the disease. However, I understand my decision is a personal one and not something I can or should expect of other people who live with chronic pain. For some patients, long-term opioid treatment can provide adequate pain relief without detracting from their quality of life, but for others it can do more harm over time.

When I hear of people with pain being shamed and stigmatized for trying to fill prescriptions for medications many of them have been using responsibly for years and even decades, it reminds me of the same shame that was thrust onto my mother and family, while we were also deprived of comprehensive and humane treatment for, and even genuine acknowledgement of, our disease. I hope the medical field will work to adopt more nuanced and individualized approaches to treating both pain and addiction that do not cater to one demographic at the expense of the other.

The post Addiction, the opioid crisis, and family pain appeared first on Harvard Health Blog.

From: Laura Kiesel https://www.health.harvard.edu/blog/addiction-the-opioid-crisis-and-family-pain-2017110212664

Americans Are Stressed, and Politics Is To Blame

The survey of more than 3,400 adults, conducted in August, found that 59 percent of respondents said they consider this the lowest point in American history that they can remember.

From: https://www.webmd.com/a-to-z-guides/news/20171101/americans-are-stressed-and-politics-is-to-blame?src=RSS_PUBLIC

FDA Warns Firms Over Claims Marijuana Cures Cancer

Warning letters have been sent to four companies for claiming that their marijuana-derived products treat or cure cancer, the U.S. Food and Drug Administration says.

From: https://www.webmd.com/cancer/news/20171101/fda-warns-firms-over-claims-marijuana-cures-cancer?src=RSS_PUBLIC

Fire extinguisher recall: 37.8 million at risk of malfunctioning

The federal government is launching a massive recall of 37.8 million Kidde fire extinguishers. The Consumer Product Safety Commission says 142 models might not work during an emergency. Kris Van Cleave reports.

From: http://www.cbsnews.com/videos/fire-extinguisher-recall-37-8-million-at-risk-of-malfunctioning/

Chuck Norris says MRI chemical poisoned his wife

Action star takes on medical device manufacturers in a lawsuit alleging a chemical used in MRI imaging scans poisoned his wife

From: http://www.cbsnews.com/news/chuck-norris-says-mri-chemical-poisoned-his-wife/

Ramachandra R. Sista, M.D.: Pulmonologist - Mayo Clinic

From: Mayo Clinic https://www.youtube.com/watch?v=TkZiQuDm5ZQ

New Clinical Trial for Ebstein’s Anomaly

From: Mayo Clinic https://www.youtube.com/watch?v=IqRDNttlFF0

Mayo Clinic Minute: Why early detection of Alzheimer’s disease matters

From: Mayo Clinic https://www.youtube.com/watch?v=FSC0mlZWUFU

Leucine Transamination Is Lower in Middle-Aged Compared with Younger Adults [Nutrient Physiology, Metabolism, and Nutrient-Nutrient Interactions]

Background: Insulin and age affect leucine (and protein) kinetics in vivo. However, to our knowledge, leucine transamination and the effects of insulin have not been studied in participants of different ages.

Objective: The aims of the study were to measure whole-body leucine deamination to α-ketoisocaproate (KIC) and KIC reamination to leucine in middle-aged and younger healthy adults, both in the postabsorptive state and after hyperinsulinemia.

Methods: Younger (mean ± SE age: 26 ± 2 y) and middle-aged (54 ± 3 y) healthy men and women were enrolled. Isotope dilution methods with 2 independent leucine and KIC tracers, a dual isotope model and the euglycemic, hyperinsulinemic clamp technique, were used.

Results: Leucine deamination [expressed as μmol/(kg x min)] was consistently greater than KIC reamination. In middle-aged adults, postabsorptive leucine deamination (0.77 ± 0.05), reamination (0.49 ± 0.04), and net deamination (0.28 ± 0.04) were ~30% lower than in the younger group (deamination: 1.12 ± 0.07; reamination: 0.70 ± 0.09; net deamination: 0.42 ± 0.04) (P < 0.002, P < 0.05, and P < 0.015, respectively). After the hyperinsulinemic clamp, plasma leucine and KIC concentrations were reduced by ~50% in both groups. Deamination and reamination also were suppressed by ~40–50% in both groups (P < 0.001); however, they remained lower [–35% (P = 0.02) and –25% (P = 0.036), respectively] in the middle-aged than in the younger participants. The leucine rate of appearance and its suppression by insulin were similar in the middle-aged and in the younger subjects. By using both the basal and the clamp data, deamination was directly correlated with the plasma leucine concentration (r = 0.61, P < 0.0025) and reamination to that of plasma KIC (r = 0.79, P < 0.00002). Expressing the data relative to lean body mass did not substantially alter the results.

Conclusions: Leucine deamination and reamination are lower in middle-aged than in younger adults, both in the postabsorptive and in the insulin-stimulated state. In middle age, a decreased net leucine transamination may represent a mechanism to spare this essential amino acid.

From: Tessari, P. http://jn.nutrition.org/cgi/content/short/147/11/2025?rss=1

Whole-Grain Starch and Fiber Composition Modifies Ileal Flow of Nutrients and Nutrient Availability in the Hindgut, Shifting Fecal Microbial Profiles in Pigs [Nutrient Physiology, Metabolism, and Nutrient-Nutrient Interactions]

Background: Changes in whole-grain chemical composition can affect the site of nutrient digestion, which may alter substrate availability and gut microbiota composition.

Objective: This study elucidated the function of whole-grain fermentable fiber composition on ileal substrate flow, hindgut substrate availability, and subsequent gut microbial profiles in pigs.

Methods: Five whole grains—1) high-fermentability, high–β-glucan hull-less barley (HFB); 2) high-fermentability, high-amylose hull-less barley (HFA); 3) moderate-fermentability hull-less barley (MFB); 4) low-fermentability hulled barley (LFB); or 5) low-fermentability hard red spring wheat (LFW)—were included at 800 g/kg into diets fed to ileal-cannulated growing pigs for 9 d in a 6 (periods) x 5 (diets) Youden square. Digesta were analyzed for nutrient flow and microbial composition via 16S ribosomal RNA gene sequencing.

Results: The consumption of fermentable whole grains, HFB, and HFA increased (P < 0.05) ileal starch flow by 69% and dry matter flow by 37% compared with LFB and LFW intakes. The consumption of HFB and HFA increased (P < 0.05) fecal Firmicutes phylum abundance by 26% and 21% compared with LFB intake and increased (P < 0.05) fecal Dialister genus abundance, on average, by 98% compared with LFB and LFW intakes. Fecal Sharpea and Ruminococcus genera abundances increased (P < 0.05) with HFB intake compared with LFB and LFW intakes. In contrast, the consumption of LFB increased (P < 0.05) fecal Bacteroidetes phylum abundance by 43% compared with MFB intake. Ileal starch flow and fecal Firmicutes abundance were positively correlated and determined by using principal components analysis.

Conclusions: Increasing dietary fermentable fiber from whole grains can increase ileal substrate flow and hindgut substrate availability, shifting the fecal microbiota toward Firmicutes phylum members. Thus, digesta substrate flow is important to shape gut microbial profiles in pigs, which indicates that the manipulation of substrate flow should be considered as a tool to modulate gut microbiota composition.

From: Fouhse, J. M., Gänzle, M. G., Beattie, A. D., Vasanthan, T., Zijlstra, R. T. http://jn.nutrition.org/cgi/content/short/147/11/2031?rss=1

#DearDiabetes: Martha Clark

Dear Diabetes,

You moved in 42 years ago… unexpectedly, uninvited and unwelcome… like a high-maintenance relative who requires my constant attention.

At first they told me to be patient… that they knew how to get you to leave… a cure is close, they said… be patient, they said… it will be soon, they said. But you wouldn’t budge; you just had to have it your way. You took some getting used to, and I have learned to be patient.

Let’s face it, our relationship has been up and down… I’ve often resented you, tried to ignore you, resisted you and eventually embraced you. Somewhere along the way I accepted that you are here to stay. So, like many who are in lifelong relationships, I’ve chosen our song… one that captures the truth about our relationship… Willie Nelson’s “Always on My Mind.”

You come with me everywhere I go—intruding on my social life and limiting my flexibility. You’re Always on My Mind.

To be fair, you’ve taught me a lot… discipline, managing risks, empathy for others and patience with myself.

But seriously, feel free to leave anytime. Anytime. Really.

In the meantime, I will continue to thrive and will do what I can to help others do the same. That’s my sweet revenge!

Thinking of You Always,

Martha Clark, MBA
Interim Chief Executive Officer, American Diabetes Association

From: American Diabetes Association http://diabetesstopshere.org/2017/11/01/deardiabetes-martha-clark/