Storage Capacity of Extremely Diluted Hopfield Model

The storage capacity of the extremely diluted Hopfield Model is studied by using Monte Carlo techniques. In this work, instead of diluting the synapses according to a given distribution, the dilution of the synapses is obtained systematically by retaining only the synapses with dominant contributions. It is observed that by using the prescribed dilution method the critical storage capacity of the system increases with decreasing number of synapses per neuron reaching almost the value obtained from mean-field calculations. It is also shown that the increase of the storage capacity of the diluted system depends on the storage capacity of the fully connected Hopfield Model and the fraction of the diluted synapses.Comment: Latex, 14 pages, 4 eps figure

Less is more: Design of a highly stable disulfide-deleted mutant of analgesic cyclic alpha-conotoxin Vc1.1

Cyclic alpha-conotoxin Vc1.1 (cVc1.1) is an orally active peptide with analgesic activity in rat models of neuropathic pain. It has two disulfide bonds, which can have three different connectivities, one of which is the native and active form. In this study we used computational modeling and nuclear magnetic resonance to design a disulfide-deleted mutant of cVc1.1, [C2H,C8F]cVc1.1, which has a larger hydrophobic core than cVc1.1 and, potentially, additional surface salt bridge interactions. The new variant, hcVc1.1, has similar structure and serum stability to cVc1.1 and is highly stable at a wide range of pH and temperatures. Remarkably, hcVc1.1 also has similar selectivity to cVc1.1, as it inhibited recombinant human alpha9alpha10 nicotinic acetylcholine receptor-mediated currents with an IC50 of 13μM and rat N-type (Cav2.2) and recombinant human Cav2.3 calcium channels via GABAB receptor activation, with an IC50 of ~900pM. Compared to cVc1.1, the potency of hcVc1.1 is reduced three-fold at both analgesic targets, whereas previous attempts to replace Vc1.1 disulfide bonds by non-reducible dicarba linkages resulted in at least 30-fold decreased activity. Because it has only one disulfide bond, hcVc1.1 is not subject to disulfide bond shuffling and does not form multiple isomers during peptide synthesis

Hawberry (Crataegus monogyna Jaqc.) extracts inhibit lipid oxidation and improve consumer liking of ready-to-eat (RTE) pork patties

The objective of this work was to study the effectiveness of extracts from hawberry (Crataegus monogyna Jacq.) to inhibit lipid oxidation and odor deterioration during processing of ready-to-eat (RTE) pork patties subjected to roasting (180 °C/16 min), chilling (10 days/+3 °C) and reheating in microwave (600 mW/1 min). Acetone extracts of hawberry were chosen based on their total phenolic content (1281.1 ± 84.8 mg gallic acid equivalent (GAE)/100 g fruit) and in vitro antiradical activity (DPPH) (53.33 ± 15.40 g equivalent Trolox per g of fruits). Pork patties treated with increasing concentrations of hawberry extract, 200 and 800 ppm GAE (T2 and T8, respectively) and a control group (T0) of samples, were analyzed for TBARS, volatile carbonyls and odor liking in a consumer test. Hawberry extracts significantly improved the oxidative stability of cooked pork patties keeping TBARS and hexanal counts at basal levels during the whole process. The addition of hawberry phenolic-rich extracts significantly improved the degree of consumer satisfaction regarding the odor of patties. In conclusion, the hawberry extract displayed potential usage as an ingredient with antioxidant properties for the manufacture of high-quality RTE meat products. © 2017, Association of Food Scientists & Technologists (India)

Management of Sigmoid Volvulus Avoiding Sigmoid Resection

Acute sigmoid volvulus is typically caused by an excessively mobile and redundant segment of colon with a stretched mesenteric pedicle. When this segment twists on its pedicle, the result can be obstruction, ischemia and perforation. A healthy, 18-year-old Caucasian woman presented to the emergency department complaining of cramping abdominal pain, distention, constipation and obstipation for the last 72 h, accompanied by nausea, vomiting and abdominal tenderness. The patient had tympanitic percussion tones and no bowel sounds. She was diagnosed with acute sigmoid volvulus. Although urgent resective surgery seems to be the appropriate treatment for those who present with acute abdominal pain, intestinal perforation or ischemic necrosis of the intestinal mucosa, the first therapeutic choice for clinically stable patients in good general condition is considered, by many institutions, to be endoscopic decompression. Controversy exists on the decision of the time, the type of definitive treatment, the strategy and the most appropriate surgical technique, especially for teenagers for whom sigmoid resection can be avoided

Are citations from clinical trials evidence of higher impact research? An analysis of ClinicalTrials.gov

An important way in which medical research can translate into improved health outcomes is by motivating or influencing clinical trials that eventually lead to changes in clinical practice. Citations from clinical trials records to academic research may therefore serve as an early warning of the likely future influence of the cited articles. This paper partially assesses this hypothesis by testing whether prior articles referenced in ClinicalTrials.gov records are more highly cited than average for the publishing journal. The results from four high profile general medical journals support the hypothesis, although there may not be a cause-and effect relationship. Nevertheless, it is reasonable for researchers to use citations to their work from clinical trials records as partial evidence of the possible long-term impact of their research

Acute kidney injury biomarkers: renal angina and the need for a renal troponin I

Acute kidney injury (AKI) in hospitalized patients is independently associated with increased morbidity and mortality in pediatric and adult populations. Continued reliance on serum creatinine and urine output to diagnose AKI has resulted in our inability to provide successful therapeutic and supportive interventions to prevent and mitigate AKI and its effects. Research efforts over the last decade have focused on the discovery and validation of novel urinary biomarkers to detect AKI prior to a change in kidney function and to aid in the differential diagnosis of AKI. The aim of this article is to review the AKI biomarker literature with a focus on the context in which they should serve to add to the clinical context facing physicians caring for patients with, or at-risk for, AKI. The optimal and appropriate utilization of AKI biomarkers will only be realized by understanding their characteristics and placing reasonable expectations on their performance in the clinical arena

Archaeology, Architecture, and the Postcolonial Critique

Peer reviewe

IL-6-Mediated Activation of Stat3α Prevents Trauma/Hemorrhagic Shock-Induced Liver Inflammation

Trauma complicated by hemorrhagic shock (T/HS) is the leading cause of morbidity and mortality in the United States for individuals under the age of 44 years. Initial survivors are susceptible to developing multiple organ failure (MOF), which is thought to be caused, at least in part, by excessive or maladaptive activation of inflammatory pathways. We previously demonstrated in rodents that T/HS results in liver injury that can be prevented by IL-6 administration at the start of resuscitation; however, the contribution of the severity of HS to the extent of liver injury, whether or not resuscitation is required, and the mechanism(s) for the IL-6 protective effect have not been reported. In the experiments described here, we demonstrated that the extent of liver inflammation induced by T/HS depends on the duration of hypotension and requires resuscitation. We established that IL-6 administration at the start of resuscitation is capable of completely reversing liver inflammation and is associated with increased Stat3 activation. Global assessment of the livers showed that the main effect of IL-6 was to normalize the T/HS-induced inflammation transcriptome. Pharmacological inhibition of Stat3 activity within the liver blocked the ability of IL-6 to prevent liver inflammation and to normalize the T/HS-induced liver inflammation transcriptome. Genetic deletion of a Stat3β, a naturally occurring, dominant-negative isoform of the Stat3, attenuated T/HS-induced liver inflammation, confirming a role for Stat3, especially Stat3α, in preventing T/HS-mediated liver inflammation. Thus, T/HS-induced liver inflammation depends on the duration of hypotension and requires resuscitation; IL-6 administration at the start of resuscitation reverses T/HS-induced liver inflammation, through activation of Stat3α, which normalized the T/HS-induced liver inflammation transcriptome