Is Sertraline Effective At Reducing The Symptoms Of Anxiety In Those Diagnosed With Generalized Anxiety Disorder (GAD)?

OBJECTIVE: The objective of this selective EBM review is to determine whether or not sertraline is effective at reducing the symptoms of anxiety in those diagnosed with generalized anxiety disorder (GAD). STUDY DESIGN: This is a systematic review of three randomized control trials (RCTs) published between 2008 and 2015, all in the English language and published in peer-reviewed journals. DATA SOURCES: Three randomized control trials that study the effects of sertraline for reduction of anxiety symptoms in patients with GAD, obtained using PubMed, CINAHL Plus and Academic Search Premier. OUTCOMES MEASURED: The primary outcome measured in each study was patient-reported reduction in anxiety symptoms and improvement of quality of life. These outcomes were measured using several scales, including the Hamilton Rating Scale for Anxiety, the Pediatric Anxiety Rating Scale, the Children’s Global Assessment Scale, The Clinical Global Impression- Improvement Scale, and the Clinical Global Impressions Severity Scale. RESULTS: Cvjetkovic-Bosnjak et al. found sertraline to be equally effective as pregabalin for the treatment of GAD (Eur Rev Med Pharmacol Sci 2015: 19 (11), 2020-2024). Similarly, Mokhber et al. found sertraline to be equally effective to buspirone in treating GAD (Psychiatry Clin Neurosci: 64: 128-133. doi: 10.1111/j.1440-1819.2009.02055.x). Finally, Walkup et al. found that sertraline and cognitive behavioral therapy either in combination or as monotherapies are effective in treating GAD (NEJM 2008; 359 (26): 2753-2766. doi: 10.1056/NEJMoa0804633). CONCLUSION: The results of this systematic review show that sertraline is effective in treating the symptoms of anxiety in patients with a diagnosis of generalized anxiety disorder. While the results from these studies were promising, additional research with larger, more diverse populations, standardized measurements of outcomes, increased time frame, and further examination of adverse drug reactions and cost-effectiveness are required to determine the true long-term benefit of sertraline as therapy for GAD

Changes in cholesterol kinetics following sugar cane policosanol supplementation: a randomized control trial

<p>Abstract</p> <p>Background</p> <p>Sugar cane policosanols (SCP) have been shown to exert cholesterol-modulating properties in various studies conducted in Cuba by substantially reducing cholesterol synthesis. Independent research examining changes in cholesterol kinetics in response to SCP is limited to few studies, none of which was able to replicate findings of the original research. Moreover, no data are available on the effect of SCP on cholesterol absorption to date. The present study was undertaken to determine effects on cholesterol kinetics, namely synthesis and absorption, within hypercholesterolemic individuals consuming a SCP treatment. Twenty-one otherwise healthy hypercholesterolemic subjects participated in a randomized double-blind crossover study where they received 10 mg/day of policosanols or a placebo incorporated in margarine as an evening snack for a period of 28 days. The last week of the study phase, subjects were given ¹³C labelled cholesterol and deuterated water for the measurement of cholesterol absorption and synthesis respectively. Blood was collected on the first two and last five days of the trial. Cholesterol absorption and synthesis were determined by measuring red cell cholesterol ¹³C and deuterium enrichment, respectively.</p> <p>Results</p> <p>There was no significant change in LDL cholesterol levels as compared to control. In addition, the area under the curve for red cell cholesterol ¹³C enrichment across 96 hours was not significantly different in the SCP group as compared to control. Similarly, no difference was observed in the fractional rate of cholesterol synthesis over the period of 24 hours between the two treatment groups.</p> <p>Conclusion</p> <p>The findings of the present study fail to support previous research concerning efficacy and mechanism of action for policosanols.</p

P-Element Homing Is Facilitated by engrailed Polycomb-Group Response Elements in Drosophila melanogaster

P-element vectors are commonly used to make transgenic Drosophila and generally insert in the genome in a nonselective manner. However, when specific fragments of regulatory DNA from a few Drosophila genes are incorporated into P-transposons, they cause the vectors to be inserted near the gene from which the DNA fragment was derived. This is called P-element homing. We mapped the minimal DNA fragment that could mediate homing to the engrailed/invected region of the genome. A 1.6 kb fragment of engrailed regulatory DNA that contains two Polycomb-group response elements (PREs) was sufficient for homing. We made flies that contain a 1.5kb deletion of engrailed DNA (enΔ1.5) in situ, including the PREs and the majority of the fragment that mediates homing. Remarkably, homing still occurs onto the enΔ1. 5 chromosome. In addition to homing to en, P[en] inserts near Polycomb group target genes at an increased frequency compared to P[EPgy2], a vector used to generate 18,214 insertions for the Drosophila gene disruption project. We suggest that homing is mediated by interactions between multiple proteins bound to the homing fragment and proteins bound to multiple areas of the engrailed/invected chromatin domain. Chromatin structure may also play a role in homing

by M Sprenger Rapid communications HIV and AIDS in the European Union, 2009 4

D Tubin-Delic, on behalf of the outbreak control team Surveillance and outbreak reports Control of a multi-hospital outbreak of KPC-producing Klebsiella pneumonia

Keck-I MOSFIRE spectroscopy of compact star-forming galaxies at z≳\gtrsim2: High velocity dispersions in progenitors of compact quiescent galaxies

We present Keck-I MOSFIRE near-infrared spectroscopy for a sample of 13 compact star-forming galaxies (SFGs) at redshift $2\leq z \leq2.5$ with star formation rates of SFR$\sim$100M$_{\odot}$ y$^{-1}$ and masses of log(M/M$_{\odot}$)$\sim10.8$. Their high integrated gas velocity dispersions of $\sigma_{\rm{int}}$=230$^{+40}_{-30}$ km s$^{-1}$, as measured from emission lines of H$_{\alpha}$ and [OIII], and the resultant M$_{\star}-\sigma_{\rm{int}}$ relation and M$_{\star}$$-$M$_{\rm{dyn}}$ all match well to those of compact quiescent galaxies at $z\sim2$, as measured from stellar absorption lines. Since log(M$_{\star}$/M$_{\rm{dyn}}$)$=-0.06\pm0.2$ dex, these compact SFGs appear to be dynamically relaxed and more evolved, i.e., more depleted in gas and dark matter ($<$13$^{+17}_{-13}$\%) than their non-compact SFG counterparts at the same epoch. Without infusion of external gas, depletion timescales are short, less than $\sim$300 Myr. This discovery adds another link to our new dynamical chain of evidence that compact SFGs at $z\gtrsim2$ are already losing gas to become the immediate progenitors of compact quiescent galaxies by $z\sim2$.Comment: 12 pages, 7 figures, submitted to Ap

Homocysteine metabolism pathway is involved in the control of glucose homeostasis: a cystathionine beta synthase deficiency study in mouse

Cystathionine beta synthase (CBS) catalyzes the first step of the transsulfuration pathway from homocysteine to cystathionine, and its deficiency leads to hyperhomocysteinemia (HHcy) in humans and rodents. To date, scarce information is available about the HHcy effect on insulin secretion, and the link between CBS activity and the setting of type 2 diabetes is still unknown. We aimed to decipher the consequences of an inborn defect in CBS on glucose homeostasis in mice. We used a mouse model heterozygous for CBS (CBS+/-) that presented a mild HHcy. Other groups were supplemented with methionine in drinking water to increase the mild to intermediate HHcy, and were submitted to a high-fat diet (HFD). We measured the food intake, body weight gain, body composition, glucose homeostasis, plasma homocysteine level, and CBS activity. We evidenced a defect in the stimulated insulin secretion in CBS+/- mice with mild and intermediate HHcy, while mice with intermediate HHcy under HFD presented an improvement in insulin sensitivity that compensated for the decreased insulin secretion and permitted them to maintain a glucose tolerance similar to the CBS+/+ mice. Islets isolated from CBS+/- mice maintained their ability to respond to the elevated glucose levels, and we showed that a lower parasympathetic tone could, at least in part, be responsible for the insulin secretion defect. Our results emphasize the important role of Hcy metabolic enzymes in insulin secretion and overall glucose homeostasis

A contemporaneous infrared flash from a long gamma-ray burst: an echo from the central engine

The explosion that results in a cosmic gamma-ray burst (GRB) is thought to produce emission from two physical processes -- the activity of the central engine gives rise to the high-energy emission of the burst through internal shocking and the subsequent interaction of the flow with the external environment produces long-wavelength afterglow. While afterglow observations continue to refine our understanding of GRB progenitors and relativistic shocks, gamma-ray observations alone have not yielded a clear picture of the origin of the prompt emission nor details of the central engine. Only one concurrent visible-light transient has been found and was associated with emission from an external shock. Here we report the discovery of infrared (IR) emission contemporaneous with a GRB, beginning 7.2 minutes after the onset of GRB 041219a. Our robotic telescope acquired 21 images during the active phase of the burst, yielding the earliest multi-colour observations of any long-wavelength emission associated with a GRB. Analysis of an initial IR pulse suggests an origin consistent with internal shocks. This opens a new possibility to study the central engine of GRBs with ground-based observations at long wavelengths.Comment: Accepted to Nature on March 1, 2005. 9 pages, 4 figures, nature12.cls and nature1.cls files included. This paper is under press embargo until print publicatio

Inhibition of Y1 receptor signaling improves islet transplant outcome

Failure to secrete sufficient quantities of insulin is a pathological feature of type-1 and type-2 diabetes, and also reduces the success of islet cell transplantation. Here we demonstrate that Y1 receptor signaling inhibits insulin release in β-cells, and show that this can be pharmacologically exploited to boost insulin secretion. Transplanting islets with Y1 receptor deficiency accelerates the normalization of hyperglycemia in chemically induced diabetic recipient mice, which can also be achieved by short-term pharmacological blockade of Y1 receptors in transplanted mouse and human islets. Furthermore, treatment of non-obese diabetic mice with a Y1 receptor antagonist delays the onset of diabetes. Mechanistically, Y1 receptor signaling inhibits the production of cAMP in islets, which via CREB mediated pathways results in the down-regulation of several key enzymes in glycolysis and ATP production. Thus, manipulating Y1 receptor signaling in β-cells offers a unique therapeutic opportunity for correcting insulin deficiency as it occurs in the pathological state of type-1 diabetes as well as during islet transplantation.Islet transplantation is considered one of the potential treatments for T1DM but limited islet survival and their impaired function pose limitations to this approach. Here Loh et al. show that the Y1 receptor is expressed in β- cells and inhibition of its signalling, both genetic and pharmacological, improves mouse and human islet function.info:eu-repo/semantics/publishe