Did NFL doctors and trainers push painkillers on players?

A lawsuit filed against all 32 NFL teams says doctors and trainers abuse the use of powerful painkillers and anti-inflammatory drugs

From: http://www.cbsnews.com/news/did-the-nfl-doctors-and-trainers-push-powerful-painkillers-on-players/

Bone and joint problems associated with diabetes

From: http://www.mayoclinic.com/diseases-conditions/diabetes/in-depth/diabetes/art-20049314

California Dental Association achieves favorable settlement with Delta Dental

The California Dental Association has reached a proposed settlement agreement with Delta Dental of California in its lawsuit against the insurer regarding CDA's claims that Delta breached its contractual commitments with thousands of dentists in the state.

From: http://www.ada.org/en/publications/ada-news/2017-archive/march/california-dental-association-achieves-favorable-settlement-with-delta-dental

Bone and joint problems associated with diabetes

From: http://www.mayoclinic.org/diseases-conditions/diabetes/in-depth/diabetes/art-20049314

Could a 4-day workweek be hazardous to health?

Though the idea of a three-day weekend sounds ideal, compressing work hours may have long-term health effects, researchers say

From: http://www.cbsnews.com/news/could-a-4-day-workweek-be-hazardous-to-health/

GOP leaders say Medicaid expansion rollback would be "very difficult" to move up

The treatment of the Medicaid expansion is opposed from two sides within the GOP

From: http://www.cbsnews.com/news/house-gop-leaders-say-medicaid-expansion-rollback-would-be-very-difficult-to-move-up/

Mayo Clinic Cancer Center Gene Analysis Shared Resource: A Virtual Tour

From: Mayo Clinic http://www.youtube.com/watch?v=NwALnuWm0bM

Mayo Clinic Cancer Center Cytogenetics Core: A Virtual Tour

From: Mayo Clinic http://www.youtube.com/watch?v=QS1sS-IUjPU

Mayo Clinic Cancer Center Proteomics Core: A Virtual Tour

From: Mayo Clinic http://www.youtube.com/watch?v=wVp8WMMQwo0

Glioma Diagnosis & Personalized Medicine

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

Updates, improvements underway for ADA Credentialing Service

ADA members and nonmembers can expect new updates and improvements to the ADA Credentialing Service this summer and fall.

From: http://www.ada.org/en/publications/ada-news/2017-archive/march/updates-improvements-underway-for-ada-credentialing-service

Bone and joint problems associated with diabetes

From: http://www.mayoclinic.com/diseases-conditions/diabetes/in-depth/diabetes/art-20049314

Trump says 2017 “would be a disaster for Obamacare”

The president's remarks come during a meeting with key committee members involved in the GOP health-care plan

From: http://www.cbsnews.com/news/trump-says-2017-would-be-a-disaster-for-obamacare/

Virus linked to heart trouble in some adults

For the first time, doctors have tied Zika infection to dangerous heart problems

From: http://www.cbsnews.com/news/zika-virus-linked-to-heart-trouble-in-some-adults/

6-pound tumor removed from girl's mouth

12-year-old from Africa is smiling again after New York surgeons operated in January

From: http://www.cbsnews.com/news/6-pound-tumor-removed-from-gambia-africa-girls-mouth/

Andy’s Story of Multiple Myeloma

From: Mayo Clinic http://www.youtube.com/watch?v=A4ph1VcH-Tw

Story by Story Episode 13: Colorectal Cancer Genetic Screening and Awareness

From: Mayo Clinic http://www.youtube.com/watch?v=5THk2rZUVSU

ADA Board of Trustees votes to create national dental licensure exam

The ADA took a giant step forward in February to create a national exam to assess a licensure candidate's entry-level clinical knowledge, skills and competency — while averting the potential ethical issues involved in the use of patients for dental licensure examinations.

From: http://www.ada.org/en/publications/ada-news/2017-archive/march/ada-board-of-trustees-votes-to-create-national-dental-licensure-exam

CMS will hold Open Payments call on April 13

The Centers for Medicare & Medicaid Services will hold an informational call from 1:30-3 p.m. ET on April 13 on how to access and use the Open Payments system to review and dispute the accuracy of records submitted by industry.

From: http://www.ada.org/en/publications/ada-news/2017-archive/march/cms-will-hold-open-payments-call-on-april-13

Study links pot use to risk of stroke, heart failure

New research raises concerns, but a marijuana advocacy group says the study contradicts previous findings

From: http://www.cbsnews.com/news/pot-marijuana-risk-stroke-heart-failure/

White coat syndrome or white coat logo syndrome? The pitfalls of doctor shopping by “brand”

People often get hung up on brand names—many times in situations where branding is of little significance. For example, some people are willing to pay double the price for a wool coat that is exactly the same in terms of material, style, and outward appearance just because there is a small designer label on the lining that nobody sees. In some cases, the brand-name and no-name wool coats are manufactured in the exact same factory. The consumer had the wool pulled over their eyes in terms of the price markup for identical merchandise. This can also happen when it comes to health care.

Co-pay or co-played?

In terms of cost, co-pays can double or even triple when your doctor is not in network. Even when the physician is in network, if he or she practices at different facilities, the one that does the billing may not be in network. One of my patients told me she was paying a $15 co-pay to see me in one office and $60 co-pay to see me in my other office. Same doctor, same services, but different facility with a different insurance contract. To the surprise of many, these co-pays are determined by administrators, and doctors have little involvement or direct financial benefit from these deals. To calm her frustration, I said, “These co-pays are out of my hands, but I am happy to see you at the location that is most convenient and affordable for you. Please keep in mind that at both locations, puns, political satire, and sarcasm are complimentary services.”

I recall meeting one of my patients for the first time at my practice in Braintree, MA for a headache medicine consultation. After I introduced myself, she said, “It’s nice to meet you. My primary doctor referred me to see you, but I really wanted to be seen at the Graham Headache Center at Brigham & Women’s Hospital (BWH).” I replied, “Well I work there on Tuesdays and Thursdays. If you want, I can take off this white coat, and put on the one with the BWH logo if that will make you more confident in my ability to take care of you.” She smiled and said, “That will not be necessary, Doctor.” I said, “There are many excellent doctors at this practice. Since none of them are currently available, I guess you can get started with me.”

The name game

In addition to cost, there is a misconception that physicians who practice at big name hospitals or hospitials affiliated with medical schools are superior to those in community-based hospitals or private practice. Although physicians in teaching hospitals may be more likely to be involved in research and teaching, that does not necessarily translate to being a better doctor. In addition, being involved in research and teaching can at times limit a physician’s availability in terms of office hours and access outside of the office (refills, questions between visits, etc.).  As such, the community/private physicians can at times provide comparable care with better availability and a more convenient location. Some of the most talented physicians I know are in private practice.

I recall another patient who upon entering my office said, “My husband is a neurologist at Massachusetts General Hospital, and he referred me to see you, which should tell you what he thinks of the reputation of you and the BWH Graham Headache Center.” Given her lofty expectations, I replied, “Well Ms. Smith (not her actual name), I look forward to disappointing you over the next 60 minutes.” Fortunately, I was able to exceed her expectations, and my reputation has somehow remained intact.

The post White coat syndrome or white coat logo syndrome? The pitfalls of doctor shopping by “brand” appeared first on Harvard Health Blog.

From: Paul G. Mathew, MD, FAAN, FAHS http://www.health.harvard.edu/blog/white-coat-syndrome-white-coat-logo-syndrome-pitfalls-doctor-shopping-brand-2017031011278

Hepatocyte-specific PPARA expression exclusively promotes agonist-induced cell proliferation without influence from nonparenchymal cells

Peroxisome proliferator-activated receptor-α (PPARA) is a nuclear transcription factor and key mediator of systemic lipid metabolism. Prolonged activation in rodents causes hepatocyte proliferation and hepatocellular carcinoma. Little is known about the contribution of nonparenchymal cells (NPCs) to PPARA-mediated cell proliferation. NPC contribution to PPARA agonist-induced hepatomegaly was assessed in hepatocyte (Ppara^Hep)- and macrophage (Ppara^Mac)-specific Ppara null mice. Mice were treated with the agonist Wy-14643 for 14 days, and response of conditional null mice was compared with conventional knockout mice (Ppara^–/–). Wy-14643 treatment caused weight loss and severe hepatomegaly in wild-type and Ppara^Mac mice, and histological analysis revealed characteristic hepatocyte swelling; Ppara^Hep and Ppara^–/– mice were protected from these effects. Ppara^Mac serum chemistries, as well as aspartate aminotransferase and alanine aminotransferase levels, matched wild-type mice. Agonist-treated Ppara^Hep mice had elevated serum cholesterol, phospholipids, and triglycerides when compared with Ppara^–/– mice, indicating a possible role for extrahepatic PPARA in regulating circulating lipid levels. BrdU labeling confirmed increased cell proliferation only in wild-type and Ppara^Mac mice. Macrophage PPARA disruption did not impact agonist-induced upregulation of lipid metabolism, cell proliferation, or DNA damage and repair-related gene expression, whereas gene expression was repressed in Ppara^Hep mice. Interestingly, downregulation of inflammatory cytokines IL-15 and IL-18 was dependent on macrophage PPARA. Cell type-specific regulation of target genes was confirmed in primary hepatocytes and Kupffer cells. These studies conclusively show that cell proliferation is mediated exclusively by PPARA activation in hepatocytes and that Kupffer cell PPARA has an important role in mediating the anti-inflammatory effects of PPARA agonists.

From: Brocker, C. N., Yue, J., Kim, D., Qu, A., Bonzo, J. A., Gonzalez, F. J. http://ajpgi.physiology.org/cgi/content/abstract/312/3/G283?rss=1

Inhibition of sphingosine 1-phosphate signaling ameliorates murine nonalcoholic steatohepatitis

Nonalcoholic steatohepatitis (NASH) is a lipotoxic disorder, wherein proinflammatory lipids, such as ceramide and its derivative sphingosine 1-phosphate (S1P), contribute to macrophage-associated liver inflammation. For example, we have previously demonstrated a role for S1P in steatotic hepatocyte-derived S1P-enriched extracellular vesicles in macrophage chemotaxis in vitro. Therefore, we hypothesized that FTY720, an S1P antagonist, would ameliorate NASH by inhibiting proinflammatory monocyte chemotaxis. To test our hypothesis, NASH was established in C57BL/6 male mice by feeding a diet high in fructose, saturated fat, and cholesterol for 22 wk. Then mice received daily intraperitoneal injections of FTY720 for 2 wk before analysis of liver injury, inflammation, and fibrosis. FTY720-treated mice with NASH demonstrated improved liver histology with a significant reduction in hepatocyte ballooning and inflammatory foci. Hepatomegaly was reversed, and liver triglycerides were reduced following FTY720 administration to mice with NASH. Correspondingly, serum ALT levels, hepatic inflammatory macrophage accumulation, and the expression of Ly6C in recruited myeloid cells was reduced in FTY720-treated mice. Hepatic collagen accumulation and expression of α-smooth muscle actin were significantly lowered as well. Body composition, energy consumption and utilization, and hepatic sphingolipid composition remained unchanged following FTY720 administration. FTY720 ameliorates murine nonalcoholic steatohepatitis. Reduction in liver injury and inflammation is associated with a reduction in hepatic macrophage accumulation, likely due to dampened recruitment of circulating myeloid cells into the liver. Nonalcoholic steatohepatitis may be a novel indication for the therapeutic use of FTY720.

NEW & NOTEWORTHY There are no approved pharmacologic therapies for nonalcoholic steatohepatitis (NASH), the leading cause of chronic liver disease worldwide. This study describes the use of FTY720, a novel small molecule, for the amelioration of NASH in a mouse model. We demonstrate that 2-wk administration of FTY720 to mice with NASH led to a reduction in liver injury, inflammation, and fibrosis. These data provide a preclinical rationale for studying this drug in human NASH.

From: Mauer, A. S., Hirsova, P., Maiers, J. L., Shah, V. H., Malhi, H. http://ajpgi.physiology.org/cgi/content/abstract/312/3/G300?rss=1

RCAD/BiP pathway is necessary for the proper synthesis of digestive enzymes and secretory function of the exocrine pancreas

Alcoholism causes an imbalance of endoplasmic reticulum (ER) homeostasis in pancreatic acini. In those cells, the ER is involved in the synthesis and folding of pancreatic enzymes. Ubiquitin-fold modifier 1 (Ufm1) is part of a novel ubiquitin-like modification system involved in maintaining ER homeostasis. Among the components of the Ufm1 system, Regulator of C53 and DDRGK1 (RCAD) has recently been identified as a Ufm1-specific E3 ligase that promotes ufmylation of DDRGK1, an RCAD-interacting protein. We determined the importance of RCAD in the proper synthesis and secretion of pancreatic enzymes using mice with genetically deleted RCAD. The pancreas of RCAD-deficient mice was of normal size and histology. Using quantitative PCR and Western blotting, we found that amylase was upregulated in pancreas organs from RCAD-knockout (KO) mice. Constitutive amylase secretion was much higher in isolated pancreatic acini from RCAD KO mice, whereas CCK-stimulated amylase secretion was disturbed. RCAD deficiency caused a downregulation in expression of ER chaperone BiP, which affected ER homeostasis and activated both apoptosis and trypsin. We also found that both RCAD and DDRGK1 transcript levels were upregulated in pancreatic acini from alcohol-preferring rats. Elevated expression of RCAD and DDRGK1 was associated with increased ER stress and UPR activation. Because of the lack of BiP expression, caspase 3 and trypsin activation we enhanced in RCAD-deficient pancreatic acini upon treatment with ethanol and CCK. In conclusion, the RCAD/BiP pathway is required for proper synthesis and secretion of pancreatic enzymes. In alcoholism, increased levels of components of the Ufm1 system could prevent the deleterious effects of alcohol in the pancreas by regulating BiP levels.

NEW & NOTEWORTHY RCAD/BiP pathway is required for the proper synthesis and secretion of amylase from pancreatic acini, as well as for the maintenance of the ER homeostasis. In alcoholism, the exocrine pancreas could increase the levels of components of the Ufm1 system to protect itself from alcohol's deleterious effects by regulating the expression of ER chaperone BiP.

From: Miller, C., Cai, Y., Patton, T., Graves, S. H., Li, H., Sabbatini, M. E. http://ajpgi.physiology.org/cgi/content/abstract/312/3/G314?rss=1

Enteric glia cells are critical to limiting the intestinal inflammatory response after injury

Vagal nerve stimulation (VNS) has been shown to limit intestinal inflammation following injury; however, a direct connection between vagal terminals and resident intestinal immune cells has yet to be identified. We have previously shown that enteric glia cell (EGC) expression is increased after injury through a vagal-mediated pathway to help restore gut barrier function. We hypothesize that EGCs modulate immune cell recruitment following injury and relay vagal anti-inflammatory signals to resident immune cells in the gut. EGCs were selectively ablated from an isolated segment of distal bowel with topical application of benzalkonium chloride (BAC) in male mice. Three days following BAC application, mice were subjected to an ischemia-reperfusion injury (I/R) by superior mesenteric artery occlusion for 30 min. VNS was performed in a separate cohort of animals. EGC⁺ and EGC^– segments were compared utilizing histology, flow cytometry, immunohistochemistry, and intestinal permeability. VNS significantly reduced immune cell recruitment after I/R injury in EGC⁺ segments with cell percentages similar to sham. VNS failed to limit immune cell recruitment in EGC^– segments. Histologic evidence of gut injury was diminished with VNS application in EGC⁺ segments, whereas EGC^– segments showed features of more severe injury. Intestinal permeability increased following I/R injury in both EGC⁺ and EGC^– segments. Permeability was significantly lower after VNS application compared with injury alone in EGC⁺ segments only (95.1 ± 30.0 vs. 217.6 ± 21.7 μg/ml, P < 0.05). Therefore, EGC ablation uncouples the protective effects of VNS, suggesting that vagal-mediated signals are translated to effector cells through EGCs.

NEW & NOTEWORTHY Intestinal inflammation is initiated by local immune cell activation and epithelial barrier breakdown, resulting in the production of proinflammatory mediators with subsequent leukocyte recruitment. Vagal nerve stimulation (VNS) has been shown to limit intestinal inflammation following injury; however, direct connection between vagal terminals and resident intestinal immune cells has yet to be identified. Here, we demonstrate that intact enteric glia cells are required to transmit the gut anti-inflammatory effects of VNS.

From: Langness, S., Kojima, M., Coimbra, R., Eliceiri, B. P., Costantini, T. W. http://ajpgi.physiology.org/cgi/content/abstract/312/3/G274?rss=1

PKC{beta}: Expanding role in hepatic adaptation of cholesterol homeostasis to dietary fat/cholesterol

Cholesterol homeostasis relies on an intricate network of cellular processes whose deregulation in response to Western type high-fat/cholesterol diets can lead to several life-threatening pathologies. Significant advances have been made in resolving the molecular identity and regulatory function of transcription factors sensitive to fat, cholesterol, or bile acids, but whether body senses the presence of both fat and cholesterol simultaneously is not known. Assessing the impact of a high-fat/cholesterol load, rather than an individual component alone, on cholesterol homeostasis is more physiologically relevant because Western diets deliver both fat and cholesterol at the same time. Moreover, dietary fat and dietary cholesterol are reported to act synergistically to impair liver cholesterol homeostasis. A key insight into the role of protein kinase C-β (PKCβ) in hepatic adaptation to high-fat/cholesterol diets was gained recently through the use of knockout mice. The emerging evidence indicates that PKCβ is an important regulator of cholesterol homeostasis that ensures normal adaptation to high-fat/cholesterol intake. Consistent with this function, high-fat/cholesterol diets induce PKCβ expression and signaling in the intestine and liver, while systemic PKCβ deficiency promotes accumulation of cholesterol in the liver and bile. PKCβ disruption results in profound dysregulation of hepatic cholesterol and bile homeostasis and imparts sensitivity to cholesterol gallstone formation. The available results support involvement of a two-pronged mechanism by which intestine and liver PKCβ signaling converge on liver ERK1/2 to dictate diet-induced cholesterol and bile acid homeostasis. Collectively, PKCβ is an integrator of dietary fat/cholesterol signal and mediates changes to cholesterol homeostasis.

From: Mehta, D., Mehta, K. D. http://ajpgi.physiology.org/cgi/content/abstract/312/3/G266?rss=1

Gastrointestinal immune and microbiome changes during parenteral nutrition

Parenteral nutrition (PN) is a lifesaving therapy that provides intravenous nutrition support to patients who cannot, or should not, feed via the gastrointestinal (GI) tract. Unfortunately, PN also carries certain risks related to infection and metabolic complications compared with enteral nutrition. In this review, an overview of PN and GI immune and microbiome changes is provided. PN impacts the gut-associated lymphoid tissue functions, especially adaptive immune cells, changes the intestinal epithelium and chemical secretions, and significantly alters the intestinal microbiome. Collectively, these changes functionally result in increased susceptibility to infectious and injurious challenge. Since PN remains necessary in large numbers of patients, the search to improve outcomes by stimulating GI immune function during PN remains of interest. This review closes by describing recent advances in using enteric nervous system neuropeptides or microbially derived products during PN, which may improve GI parameters by maintaining immunity and physiology.

From: Pierre, J. F. http://ajpgi.physiology.org/cgi/content/abstract/312/3/G246?rss=1

CRISPR/Cas 9 genome editing and its applications in organoids

Organoids are three-dimensional (3D) structures derived from adult or embryonic stem cells that maintain many structural and functional features of their respective organ. Recently, genome editing based on the bacterial defense mechanism CRISPR/Cas9 has emerged as an easily applicable and reliable laboratory tool. Combining organoids and CRISPR/Cas9 creates exciting new opportunities to study organ development and human disease in vitro. The potential applications of CRISPR in organoids are only beginning to be explored.

From: Driehuis, E., Clevers, H. http://ajpgi.physiology.org/cgi/content/abstract/312/3/G257?rss=1

Bone and joint problems associated with diabetes

From: http://www.mayoclinic.org/diseases-conditions/diabetes/in-depth/diabetes/art-20049314

Bone and joint problems associated with diabetes

From: http://www.mayoclinic.com/diseases-conditions/diabetes/in-depth/diabetes/art-20049314