In mice fed a diet high in fat and low in fiber, vitamin D and calcium — the so-called Western diet — expression of a series of genes collectively associated with immune and inflammatory responses was altered. The findings show that a Western diet induces oxidative stress and alters immune responses in the colon of mice long before tumors occur. 
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High fat diet increases inflammation in the mouse colon
Rockefeller University has joined more than 50 U.S. research institutions in making information about its clinical research trials available on ResearchMatch, the country’s first registry for recruiting research participants. The secure Web site offers a free and safe way for volunteers to connect with thousands of researchers who are conducting research on a wide range of diseases.
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Rockefeller joins first national research study recruitment registry
Non alcoholic fatty liver disease (NAFLD) represents a spectrum of fatty liver diseases associated with increased risk of type 2 diabetes and cardiovascular disease. The spectrum of fatty liver diseases, comprises simple steatosis, steatosis with inflammation (i.e. non alcoholic steatohepatitis or NASH), fatty liver disease with inflammation and fibrosis (severe NASH) and cirrhosis. The molecular mechanisms contributing to NASH are the subject of considerable investigation, as a better understanding of the pathogenesis of NASH will lead to novel therapies for a condition that hitherto remains difficult to treat. In this edition of the Journal Piquet et al have investigated the effects of hypoxia in the PTEN deficient mouse, a mouse model that develops NAFLD. Piquet et al show that a short period (7 days) of exposure to hypoxia aggravates the NAFLD phenotype, causing changes in the liver that are in keeping with NASH, with increased lipogenesis and inflammation.
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Hypoxia and non alcoholic fatty liver disease
The activity of the vagus nerve is negatively associated with risk factors such as stress and smoking, morbidity, and mortality. In contrast it is also a target of therapeutic intervention. Vagus nerve stimulation is used in depression and epilepsy. Due to its high invasivity and exclusive application to therapy-resistant patients, there is interest in less invasive methods affecting the vagus nerve. Several studies examining acupuncture report beneficial effects on vagal activity. However, findings are inconsistent and applied methods are heterogeneous resulting in difficulties in interpretation. The purpose of the present study was evaluation of the effects of acupuncture on vagal activity in a three-armed randomized trial while controlling several disturbing factors. Fourteen healthy men participated in random order in four examinations: a control condition without intervention, a condition with placebo, manual acupuncture, and electroacupuncture. Acupuncture was conducted on the concha of the ear, as there is neuroanatomical evidence for vagal afferents. Each examination took place once, with a week’s time between examinations. Respiratory sinus arrhythmia adjusted for tidal volume (RSATR) indicating vagal activity was measured continuously. The study was conducted partially blind in accordance with recommendations. After controlling for respiration, condition-specific pain sensation, individual differences in belief of acupuncture effectiveness, and time effects not attributable to the interventions, electroacupuncture but not manual acupuncture was found to have a positive effect on RSATR. The results underline the potential role of auricular electrical stimulation to induce an increase in vagal activity, and it therefore might be used as preventive or adjuvant therapeutic intervention promoting health.
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Effects of auricular electrical stimulation on vagal activity in healthy men: Evidence from a three-armed randomized trial
Dual antiplatelet therapy with aspirin and clopidogrel, a P2Y12 antagonist, is a cornerstone for treatment of patients with stroke, peripheral arterial disease, and acute coronary artery disease followed with or without percutaneous coronary intervention. Giachini and colleagues found that clopidogrel could normalize the increased phenylephrine-induced vascular contraction and impaired acetylcholine-induced vasodilatation in mesenteric arteries from angiotensin II-infused Sprague-Dawley rats. This might develop a new area for clopidogrel application. However, whether clopidogrel can improve the arterial function in patients with hypertension or diabetes, or whether clopidogrel outweighs the beneficial effect aspirin in those patients, remains an open field for future inquiry.
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Clopidogrel application: beyond coronary artery disease
For all the good it does, a liver protein that senses and gets rid of drugs and pollutants from our body has a downside. For the first time, it has been shown that when it is chronically activated, the protein, called PXR, rejiggers how cholesterol is processed in the liver and increases the risk of developing atherosclerosis. The work has direct clinical consequences to patients under long-term treatment of PXR-activating drugs, including several antibiotic and anti-cancer medications — and your daily latte.
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Scientists reveal a new mechanism that increases atherosclerosis in mice
New research shows how an antiviral protein, tetherin, lashes newborn viral particles to infected cells, slowing the spread of infection. Understanding how this immune system defense works against HIV, Ebola and other deadly viruses could lead to better antiviral therapies.
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Immune system uses a “leash” to restrict HIV’s spread
Nutrition and growth rate during early life can influence later health and lifespan. We previously demonstrated that low birth weight resulting from maternal protein restriction during pregnancy followed by catch-up growth in rodents was associated with shortened lifespan whereas protein restriction and slow growth during lactation increased lifespan. The underlying mechanisms by which these differences arise are unknown. Here we report that maternal protein restriction in mice influences thymic growth in early adult life. Offspring of dams fed a low protein diet during lactation (PLP offspring) showed significant thymic growth from 21 days to 12 weeks of age whereas this was not observed in control mice or offspring of dams fed a low protein diet during pregnancy (recuperated offspring). PCNA and SIRT1 protein levels at 21 days of age were significantly higher in thymus from both PLP (P < 0.001 and P < 0.05 respectively) and recuperated mice (P < 0.001 and P < 0.01 respectively) compared to controls. At 12 weeks PLP maintained a higher SIRT1 level whereas PCNA was decreased in thymus from recuperated offspring. This suggests that mitotic activity was initially enhanced in thymus of both PLP and recuperated offspring but remained sustained into adulthood only in PLP mice. The differential mitotic activity in thymus of PLP and recuperated animals appeared to be influenced by changes in sex hormone concentrations and expression of p53, p16, the androgen receptor, IL-7 and the IL-7 receptor. The differential thymic growth may contribute to the regulation of longevity by maternal diet.
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Early life nutrition influences thymic growth in male mice that may be related to the regulation of longevity
Modern life disrupts our natural sleep cycles with shift-work, jet lag and ubiquitous electric lighting, among other things. New research in mice suggests that the resulting disturbance of nature’s circadian rhythms could have major effects on the body and brain, from a slowing of metabolism to impaired thinking and poor impulse control.
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Disrupting sleep causes problems for the body and brain
Inhibition or blockade of hepatic stellate cells (HSCs), the main matrix producing cells involved in would healing response, represents an attractive strategy for the treatment of liver fibrosis. In vitro studies have shown that activation of the AMP-activated protein kinase (AMPK), a key player in the regulation of cellular energy homeostasis, inhibits proliferation of myofibroblasts derived from HSC. If AMPK is a true regulator of fibrogenesis then defective AMPK activity would enhance fibrogenesis and hepatic fibrosis. To test this, in vitro studies were performed on mouse primary HSCs treated or not with AMPK activator AICAR or isolated from mice lacking the AMPKα1 catalytic subunit (AMPKα1-/-) or their littermates (AMPKα1+/+). Liver fibrosis was induced in vivo in AMPKα1-/- and +/+ mice by repeated injections of CCl4. During culture activation of HSC, AMPK protein and activity significantly increased and regulatory AMPKγ3 mRNA was specifically up-regulated. Stimulation of AMPK activity by AICAR inhibited HSC proliferation, as expected, as well as collagen-α1 expression. Importantly, AMPKα1 deletion inhibited proliferation of HSC, but not fibrogenesis in vivo. Moreover, AMPKα1 deletion was not associated with enhanced carbon tetrachloride-induced fibrosis in vivo. Our data demonstrate that HSC trans-differentiation is associated with increased AMPK activity that could relate to the stabilization of AMPK complex by the γ3 subunits. Activation of AMPK in HSC inhibits in vitro fibrogenesis. By contrast low AMPK activity does not prevent HSC activation in vitro nor in vivo fibrosis.
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The development of hepatic fibrosis occurs normally in AMPK deficient mice
The 2009 Pearl Meister Greengard Prize recognizes Suzanne Cory, a world-renowned geneticist and pioneering scientific leader. The first woman to serve as director of Australia’s prestigious Walter and Eliza Hall Institute, she has been an influential force in shaping science policy in her nation.
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2009 Pearl Meister Greengard Prize goes to pioneering geneticist
In preparing to divide, mother and daughter cells use different gears and levers to regulate their genes. A collaboration between two geneticists and their labs now reveals that this difference in gene expression ultimately affects the protein CLN3, the levels of which certify whether a cell is ready to commit to another grueling round of cell division. The work sets a new compass point for studying how cell division may go awry in different types of cancer.
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Checkered history of mother and daughter cells explains cell cycle differences
A panel of distinguished scientists and editors have named postdoc Max Heiman a finalist for the Eppendorf & Science Prize for Neurobiology.
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Rockefeller postdoc named finalist for Eppendorf & Science Prize for Neurobiology
Leg crossing increases arterial pressure and combats symptomatic orthostatic hypotension in patients with sympathetic failure. This study compared the central and cerebrovascular effects of leg crossing in patients with sympathetic failure and healthy controls. We addressed the relationship between middle cerebral artery blood velocity (MCA Vmean, TCD), frontal lobe oxygenation (oxyhemoglobin (O2Hb) and mean arterial pressure (MAP), cardiac output (CO) and total peripheral resistance (TPR) in 6 patients (aged 37 to 67 years; 3 women) and age- and gender-matched controls during leg crossing. In the patients, leg crossing increased MAP from 58 (42-79) to 72 (52-89) vs. 84 (70-95) to 90 (74-94) mmHg in the controls. MCA Vmean increased from 55 (38-77) to 63 (45-80) and from 56 (46-77) to 64 (46-80) cm.s-1, respectively (p<0.05) with a larger rise in O2Hb (1.12 (0.52-3.27)) in the patients vs. the controls (0.83 (-0.11-2.04) µmol.l-1)). In the control subjects CO increased 11% (p<0.05) with no change in TPR. By contrast, in the patients CO increased 9% (p<0.05) but also TPR increased by 13% (p<0.05).
In conclusion, leg crossing improves cerebral perfusion and oxygenation both in patients with sympathetic failure and in healthy subjects. However, in healthy subjects cerebral perfusion and oxygenation improve by a rise in CO without significant changes in TPR or MAP, whereas in patients with sympathetic failure cerebral perfusion and oxygenation improve through a rise in MAP due to increments in both CO and TPR.
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Central and cerebrovascular effects of leg crossing in humans with sympathetic failure
Background/Aim. The metabolic disorders that predispose patients to non-alcoholic steatohepatitis (NASH) include insulin resistance and obesity. Repeated hypoxic events, such as occur in obstructive sleep apnoea syndrome have been designated as a risk factor in the progression of liver disease in such patients, but the mechanism is unclear, in particular the role of hypoxia. Therefore we studied the influence of hypoxia on the development and progression of steatohepatitis in an experimental mouse model. Methods. Mice with hepatocellular specific deficiency in the Phosphatase and Tensin Homolog (PTEN) gene, a tumour suppressor, were exposed to a 10% O2 (hypoxic) or 21% O2 (control) atmosphere for 7 days. Hematocrit, AST, glucose, triglycerides and insulin tolerance were measured in blood. Histological lesions were quantified. Expression of genes involved in lipogenesis, mitochondrial β-oxidation, as well as Foxo1, hepcidin, and CYP2E1 were analyzed by quantitative PCR. Results. The hematocrit increased (60±3% vs 50±2%, (p<0.01) and the ratio of liver weight/body weight increased (4.7±0.3% vs 5.4±0.2%, p<0.01) in the hypoxic animals. Steatosis was more pronounced (p<0.01) and the NASH Activity Score (NAS) score (8.3±2.4 vs 2.3±10.7, p<0.01) serum AST, triglycerides and glucose were higher in hypoxic mice. Insulin sensitivity decreased in hypoxic mice relative to controls. The expression of the lipogenic genes, SREBP-1c, PPARγ, ACC1 and ACC2 increased significantly in mice exposed to hypoxia, whereas mitochondria β-oxidation genes (PPARα, CPT1) decreased significantly. Conclusion. The findings demonstrate that hypoxia alone aggravates and accelerates the progression of NASH by upregulating the expression of lipogenic genes, by down-regulating genes involved in lipid metabolism and by decreasing insulin sensitivity.
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Hypoxia aggravates nonalcoholic steatohepatitis in mice lacking hepatocellular PTEN
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