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Monday, February 15, 2016
Teen suicides in affluent Calif. city to be subject of CDC study
From: http://www.cbsnews.com/news/teen-suicides-in-affluent-california-city-to-be-subject-of-cdc-study/
Mayo Clinic Minute: Barbie Gets a Makeover
From: Mayo Clinic http://www.youtube.com/watch?v=RIEDiu-g1hw
Proposed Viagra law would require wife's permission
From: http://www.cbsnews.com/news/kentucky-lawmaker-protests-anti-abortion-advocates-with-viagra-bill/
Popular heartburn drugs linked to risk of dementia
From: http://www.cbsnews.com/news/heartburn-drugs-ppi-prilosec-nexium-prevacid-risk-of-dementia/
Jamaica warns about Zika with catchy reggae PSA
From: http://www.cbsnews.com/news/jamaica-warns-citizens-about-zika-with-reggae-psa/
Classes resume after mystery illness sickened 200 students
From: http://www.cbsnews.com/news/classes-resume-after-mystery-illness-sickened-200-students/
Paralysis syndrome rises along with Zika cases
From: http://www.cbsnews.com/news/guillain-barre-syndrome-paralysis-rises-along-with-zika-cases/
Homeostasis alteration within small intestinal mucosa after acute enteral refeeding in total parenteral nutrition mouse model
Feeding strategies to care for patients who transition from enteral nutrient deprivation while on total parenteral nutrition (TPN) to enteral feedings generally proceed to full enteral nutrition once the gastrointestinal tract recovers; however, an increasing body of literature suggests that a subgroup of patients may actually develop an increased incidence of adverse events, including death. To examine this further, we studied the effects of acute refeeding in a mouse model of TPN. Interestingly, refeeding led to some beneficial effects, including prevention in the decline in intestinal epithelial cell (IEC) proliferation. However, refeeding led to a significant increase in mucosal expression of proinflammatory cytokines, including tumor necrosis factor-α (TNF-α), as well as an upregulation in Toll-like receptor 4 (TLR-4). Refeeding also failed to prevent TPN-associated increases in IEC apoptosis, loss of epithelial barrier function, and failure of the leucine-rich repeat-containing G protein-coupled receptor 5-positive stem cell expression. Transitioning from TPN to enteral feedings led to a partial restoration of the small bowel microbial population. In conclusion, while acute refeeding led to some restoration of normal gastrointestinal physiology, enteral refeeding led to a significant increase in mucosal inflammatory markers and may suggest alternative strategies to enteral refeeding should be considered.
From: Feng, Y., Barrett, M., Hou, Y., Yoon, H. K., Ochi, T., Teitelbaum, D. H. http://ajpgi.physiology.org/cgi/content/abstract/310/4/G273?rss=1
Redefining the functional roles of the gastrointestinal migrating motor complex and motilin in small bacterial overgrowth and hunger signaling
During the fasting state the upper gastrointestinal tract exhibits a specific periodic migrating contraction pattern that is known as the migrating motor complex (MMC). Three different phases can be distinguished during the MMC. Phase III of the MMC is the most active of the three and can start either in the stomach or small intestine. Historically this pattern was designated to be the housekeeper of the gut since disturbances in the pattern were associated with small intestinal bacterial overgrowth; however, its role in the involvement of hunger sensations was already hinted in the beginning of the 20th century by both Cannon (Cannon W, Washburn A. Am J Physiol 29: 441–454, 1912) and Carlson (Carlson A. The Control of Hunger in Health and Disease. Chicago, IL: Univ. of Chicago Press, 1916). The discovery of motilin in 1973 shed more light on the control mechanisms of the MMC. Motilin plasma levels fluctuate together with the phases of the MMC and induce phase III contractions with a gastric onset. Recent research suggests that these motilin-induced phase III contractions signal hunger in healthy subjects and that this system is disturbed in morbidly obese patients. This minireview describes the functions of the MMC in the gut and its regulatory role in controlling hunger sensations.
From: Deloose, E., Tack, J. http://ajpgi.physiology.org/cgi/content/abstract/310/4/G228?rss=1
An organotypic slice model for ex vivo study of neural, immune, and microbial interactions of mouse intestine
Organotypic tissue slices provide seminatural, three-dimensional microenvironments for use in ex vivo study of specific organs and have advanced investigative capabilities compared with isolated cell cultures. Several characteristics of the gastrointestinal tract have made in vitro models for studying the intestine challenging, such as maintaining the intricate structure of microvilli, the intrinsic enteric nervous system, Peyer's patches, the microbiome, and the active contraction of gut muscles. In the present study, an organotypic intestinal slice model was developed that allows for functional investigation across regions of the intestine. Intestinal tissue slices were maintained ex vivo for several days in a physiologically relevant environment that preserved normal enterocyte structure, intact and proliferating crypt cells, submucosal organization, and muscle wall composure. Cell death was measured by a membrane-impermeable DNA binding indicator, ethidium homodimer, and less than 5% of cells were labeled in all regions of the villi and crypt epithelia at 24 h ex vivo. This tissue slice model demonstrated intact myenteric and submucosal neuronal plexuses and functional interstitial cells of Cajal to the extent that nonstimulated, segmental contractions occurred for up to 48 h ex vivo. To detect changes in physiological responses, slices were also assessed for segmental contractions in the presence and absence of antibiotic treatment, which resulted in slices with lesser or greater amounts of commensal bacteria, respectively. Segmental contractions were significantly greater in slices without antibiotics and increased native microbiota. This model renders mechanisms of neuroimmune-microbiome interactions in a complex gut environment available to direct observation and controlled perturbation.
From: Schwerdtfeger, L. A., Ryan, E. P., Tobet, S. A. http://ajpgi.physiology.org/cgi/content/abstract/310/4/G240?rss=1
Pathophysiological roles of proteases in gastrointestinal disease
Gastrointestinal diseases, such as irritable bowel syndrome, inflammatory bowel disease, and colorectal cancer, affect a large proportion of the population and are associated with many unpleasant symptoms. Although the causes of these diseases remain largely unknown, there is increasing evidence to suggest that dysregulated protease activity may be a contributing factor. Proteases are enzymes that cleave other proteins, and their activity is normally very tightly regulated. During disease, however, the balance between proteases and their inhibitors is often shifted, leading to altered spatial and temporal control of substrate cleavage. Evaluating protease levels in normal physiology and disease has relied heavily on the use of chemical tools. Although these tools have greatly advanced the field, they are not without caveats. This review provides an introduction to these tools, their application in the gut, and a summary of the current knowledge on the contribution of protease activity to gastrointestinal disease.
From: Edgington-Mitchell, L. E. http://ajpgi.physiology.org/cgi/content/abstract/310/4/G234?rss=1
Conditional (intestinal-specific) knockout of the riboflavin transporter-3 (RFVT-3) impairs riboflavin absorption
Riboflavin (RF) is indispensable for normal cell metabolism, proliferation, and growth. The RFVT-3 protein (product of the Slc52a3 gene) is expressed in the gut with the expression being restricted to the apical membrane domain of the polarized intestinal epithelial cells. The relative contribution of RFVT-3 to total carrier-mediated RF uptake in the native intestine, however, is not clear. We addressed this issue in the current investigation using a conditional (intestinal-specific) RFVT-3 knockout (cKO) mouse model developed by the Cre/Lox approach. All RFVT-3 cKO mice were found to be RF deficient and showed a significant growth and development retardation; also, nearly two-thirds of them died prematurely between the age of 6 and 12 wk. In vivo (intestinal and colonic loops) and in vitro (native isolated intestinal epithelial cells) uptake studies showed a severe inhibition in carrier-mediated RF uptake in the cKO mice compared with control littermates. We also observed a significant increase in the level of expression of oxidative stress-responsive genes in the intestine of the cKO mice compared with control littermates. Supplementation of the RFVT-3 cKO mice with pharmacological doses of RF led to a complete correction of the growth retardation and to normalization in the level of expression of the oxidative stress-responsive genes in the gut. These results show, for the first time, that the RFVT-3 system is the main transporter involved in carrier-mediated RF uptake in the native mouse small and large intestine, and that its dysfunction impairs normal RF body homeostasis.
From: Subramanian, V. S., Lambrecht, N., Lytle, C., Said, H. M. http://ajpgi.physiology.org/cgi/content/abstract/310/4/G285?rss=1
Role of TGF-{beta} signaling in differentiation of mesothelial cells to vitamin A-poor hepatic stellate cells in liver fibrosis
Mesothelial cells (MCs) form a single layer of the mesothelium and cover the liver surface. A previous study demonstrated that, upon liver injury, MCs migrate inward from the liver surface and give rise to hepatic stellate cells (HSCs) in biliary fibrosis induced by bile duct ligation (BDL) or myofibroblasts in CCl4-induced fibrosis. The present study analyzed the role of transforming growth factor-β (TGF-β) signaling in mesothelial-mesenchymal transition (MMT) and the fate of MCs during liver fibrosis and its regression. Deletion of TGF-β type II receptor (Tgfbr2) gene in cultured MCs suppressed TGF-β-mediated myofibroblastic conversion. Conditional deletion of Tgfbr2 gene in MCs reduced the differentiation of MCs to HSCs and myofibroblasts in the BDL and CCl4 models, respectively, indicating that the direct TGF-β signaling in MCs is responsible to MMT. After BDL and CCl4 treatment, MC-derived HSCs and myofibroblasts were distributed near the liver surface and the thickness of collagen was increased in Glisson's capsule beneath the liver surface. Fluorescence-activated cell sorting analysis revealed that MC-derived HSCs and myofibroblasts store little vitamin A lipids and have fibrogenic phenotype in the fibrotic livers. MCs contributed to 1.4 and 2.0% of activated HSCs in the BDL and CCl4 models, respectively. During regression of CCl4-induced fibrosis, 20% of MC-derived myofibroblasts survived in the liver and deactivated to vitamin A-poor HSCs. Our data indicate that MCs participate in capsular fibrosis by supplying vitamin A-poor HSCs during a process of liver fibrosis and regression.
From: Li, Y., Lua, I., French, S. W., Asahina, K. http://ajpgi.physiology.org/cgi/content/abstract/310/4/G262?rss=1
Central apelin mediates stress-induced gastrointestinal motor dysfunction in rats
Apelin, an endogenous ligand for APJ receptor, has been reported to be upregulated in paraventricular nucleus (PVN) following stress. Central apelin is known to stimulate release of corticotropin-releasing factor (CRF) via APJ receptor. We tested the hypothesis that stress-induced gastrointestinal (GI) dysfunction is mediated by central apelin. We also assessed the effect of exogenous apelin on GI motility under nonstressed (NS) conditions in conscious rats. Prior to solid gastric emptying (GE) and colon transit (CT) measurements, APJ receptor antagonist F13A was centrally administered under NS conditions and following acute stress (AS), chronic homotypic stress (CHS), and chronic heterotypic stress (CHeS). Plasma corticosterone was assayed. Strain gage transducers were implanted on serosal surfaces of antrum and distal colon to record postprandial motility. Stress exposure induced coexpression of c-Fos and apelin in hypothalamic PVN. Enhanced hypothalamic apelin and CRF levels in microdialysates were detected following AS and CHeS, which were negatively and positively correlated with GE and CT, respectively. Central F13A administration abolished delayed GE and accelerated CT induced by AS and CHeS. Central apelin-13 administration increased the plasma corticosterone and inhibited GE and CT by attenuating antral and colonic contractions. The inhibitory effect elicited by apelin-13 was abolished by central pretreatment of CRF antagonist CRF9–41 in antrum, but not in distal colon. Central endogenous apelin mediates stress-induced changes in gastric and colonic motor functions through APJ receptor. The inhibitory effects of central exogenous apelin-13 on GI motility appear to be partly CRF dependent. Apelin-13 inhibits colon motor functions through a CRF-independent pathway.
From: Bülbül, M., Izgüt-Uysal, V. N., Sinen, O., Birsen, I., Tanrıöver, G. http://ajpgi.physiology.org/cgi/content/abstract/310/4/G249?rss=1
Biological modeling of mucus to modulate mucus barriers
A recent study using a transgenic mouse, whose intestinal mucus contains a molecule made of 12 copies of a domain found in many gelling mucins, demonstrates that it is possible to strengthen mucus properties in situ, leading to promising new treatment strategies in diseases in which the mucosal barrier is impaired.
From: Desseyn, J.-L., Gouyer, V., Gottrand, F. http://ajpgi.physiology.org/cgi/content/abstract/310/4/G225?rss=1
American smiles
From: http://www.ada.org/en/publications/ada-news/2016-archive/february/american-smiles
PBHS offers secure email
From: http://www.ada.org/en/publications/ada-news/2016-archive/february/pbhs-offers-secure-email
Innovation highlights 2016 President-Elect’s Conference
From: http://www.ada.org/en/publications/ada-news/2016-archive/february/innovation-highlights-2016-president-elects-conference
Applications due March 11 for Allied Dental Student Scholarships
From: http://www.ada.org/en/publications/ada-news/2016-archive/february/applications-due-march-11-for-allied-dental-student-scholarships
ADA policy on patient use in board examinations
From: http://www.ada.org/en/publications/ada-news/2016-archive/february/ada-policy-on-patient-use-in-board-examinations
Spread smiles for FDI World Oral Health Day
From: http://www.ada.org/en/publications/ada-news/2016-archive/february/spread-smiles-for-fdi-world-oral-health-day
Using patients in board exams under debate in Iowa
From: http://www.ada.org/en/publications/ada-news/2016-archive/february/using-patients-in-board-exams-under-debate-in-iowa
Just the Facts -February 15
From: http://www.ada.org/en/publications/ada-news/2016-archive/february/just-the-facts-february-15
ADA Foundation recognizes dental school programs serving the underserved
From: http://www.ada.org/en/publications/ada-news/2016-archive/february/ada-foundation-recognizes-dental-school-programs-serving-the-underserved
Honoring dental assistants
From: http://www.ada.org/en/publications/ada-news/2016-archive/february/honoring-dental-assistants
April summit to detail smokeless tobacco dangers
From: http://www.ada.org/en/publications/ada-news/2016-archive/february/april-summit-to-detail-smokeless-tobacco-dangers
Dental spending remains stagnant
From: http://www.ada.org/en/publications/ada-news/2016-archive/february/dental-spending-remains-stagnant
Report: Dentists can help reduce ER visits for nontraumatic dental issues
From: http://www.ada.org/en/publications/ada-news/2016-archive/february/report-dentists-can-help-reduce-er-visits-for-nontraumatic-dental-issues
Dentists share addiction struggles
From: http://www.ada.org/en/publications/ada-news/2016-archive/february/dentists-share-addiction-struggles
Track scams geographically
From: http://www.ada.org/en/publications/ada-news/2016-archive/february/track-scams-geographically
Snapshots of American Dentistry February 15
From: http://www.ada.org/en/publications/ada-news/2016-archive/february/snapshots-of-american-dentistry-february-15
Council to hear proposed revisions on sedation and anesthesia guidelines
From: http://www.ada.org/en/publications/ada-news/2016-archive/february/council-to-hear-proposed-revisions-on-sedation-and-anesthesia-guidelines
Speech Disorder Called Apraxia can Progress to Neurodegenerative Disease: Dr Joseph Duffy
From: Mayo Clinic http://www.youtube.com/watch?v=e76LRrUKRWk
Stress raising your blood pressure? Take a deep breath
Stress is rampant, and high blood pressure (what doctors call hypertension) is on the rise. So it’s no wonder patients often ask if stress is causing their hypertension. We have no proof that stress alone can cause persistently elevated blood pressure. (Part of the reason is that high-quality studies quantifying stress are difficult to conduct.) But stress can certainly raise blood pressure, sometimes impressively. And stress reduction can lower blood pressure, frequently improving overall well-being. Deep, slow breathing is the oldest and best-known technique to decrease stress.
The relationship between stress and blood pressure Blood pressure regulation is highly dynamic, responding to many interacting factors, ranging from alcohol and sodium intake to sleep and hormone levels. Stress is a key player, with all sorts of stressors (on the job, at home, in the classroom) contributing to a rise in blood pressure. Stress revs up the autonomic nervous system. This system oversees processes generally not under conscious control, including blood pressure and heart rate, but also more mundane functions like sweating and flushing. The hormone adrenaline is a fundamental part of its response.
For much of human evolution, increased nervous system activity has been protective, preparing us to “fight or flight” in a crisis. But today this response is rarely needed, and can even be maladaptive. Most people exhibit some instinctive reactivity: for example, if you’ve ever heard a police siren while driving, you probably noticed a jump in heart rate. There is tremendous variability in how people respond to stress, however. Many people have a highly reactive system. Their nerves and stress hormones can fire in low-pressure situations, like waiting in line or losing a button — and this isn’t always associated with a noticeable feeling of anxiety. Sometimes the nervous system even responds to worried thoughts alone.
Getting a handle on the stress response
Luckily, you can manage that stress response. Common prescriptions include exercise, laughter, and a good night’s sleep. We can also interrupt the acute response to stress by reconditioning our reactions to its triggers.
Simply taking a deep breath is one way to start. A focus on breathing lies at the core of various relaxation techniques. Yogis have incorporated slow breathing as part of meditation practices for centuries, and in the 1970s, the medical world formalized this connection when Dr. Herbert Benson first described the “relaxation response.”
Many of us recognize the value of “taking a deep breath” in everyday situations. Doctors often ask patients to breathe deeply before getting their blood pressure taken, for example, and mindful people may take a deep breath before responding to an insult. But it is also helpful to incorporate deep breathing in a daily routine, especially for “type A” or stress-prone personalities, with an added benefit on blood pressure.
How to get started with deep breathing
One beginner method is called equal breathing, based on inhaling through the nose for a count of four, and exhaling for a count of four. With time, this cycle can be prolonged to counts of eight in, eight out. Another method, called guided visualization, encourages users to hold on to mental images of a peaceful place as they breathe deeply.
There is only one non-drug treatment approved for hypertension by the FDA — a device called RESPeRATE. It uses musical tones to guide deep abdominal breathing. Its goal is to reduce the number of breaths to under 10 per minute, and to prolong each exhalation. Clinical trials have shown that daily RESPeRATE use lowered blood pressure, sometimes as much as a blood pressure pill would have. This lowering effect also lasted long after each session. Instead of a RESPeRATE device, you can always use one of several free mobile apps that teach deep breathing.
Deep breathing shouldn’t replace blood pressure medications, but it can be a helpful supplement. Its advantages are obvious: it is free, portable, and healthful. The only cost is time — ideally, 10 to 15 minutes daily. Adding guided breathing to your routine is a great way to lower your blood pressure while helping you handle the ever-growing stresses of modern life.
Related Post:
The post Stress raising your blood pressure? Take a deep breath appeared first on Harvard Health Blog.
From: Naomi Fisher, MD http://www.health.harvard.edu/blog/stress-raising-your-blood-pressure-take-a-deep-breath-201602159168
Study finds potential biomarkers for bipolar disorders
From: http://www.mayoclinic.org/medical-professionals/clinical-updates/psychiatry-psychology/study-finds-potential-biomarkers-for-bipolar-disorders