The key role of Calpain in COVID-19 as a therapeutic strategy

Inflammopharmacology - COVID-19 is one of the viral diseases that has caused many deaths and financial losses to humans. Using the available information, this virus appears to activate the host...     

Sex and smoking differences in the association between gastroesophageal reflux and risk of esophageal squamous cell carcinoma in a high-incidence area: Golestan Cohort Study

Prior studies have conflicting findings regarding the association between gastroesophageal reflux disease (GERD) and esophageal squamous cell carcinoma (ESCC). We examined this relationship in a prospective cohort in a region of high ESCC incidence. Baseline exposure data were collected from 50 045 individuals using in-person interviews at the time of cohort entry. Participants were followed until they developed cancer, died, or were lost to follow up. Participants with GERD symptoms were categorized into any GERD (heartburn or regurgitation), mixed symptoms, or heartburn alone. Multivariable Cox regression was used to assess the relationship between GERD symptom group and histologically confirmed ESCC. The model was adjusted for known risk factors for GERD and ESCC. 49 559 individuals were included in this study, of which 9005 had GERD symptoms. Over 13.0 years of median follow up, 290 individuals were diagnosed with ESCC. We found no association between any GERD and risk of ESCC (aHR 0.90, 95% CI: 0.66-1.24, P = .54). Similar findings were observed for the GERD symptom subtypes. Significant interactions between any GERD and sex (P = .013) as well as tobacco smoking (P = .028) were observed. In post-hoc analyses, GERD was associated with a decreased risk of ESCC in men (aHR 0.51, 95% CI: 0.27-0.98 P = .04) and in smokers (aHR 0.26, 95% CI: 0.08-0.83 P = .02). While there was little evidence for an overall association between GERD symptoms and ESCC risk, significant interactions with sex and smoking were observed. Men and smokers with GERD symptoms had a lower risk of ESCC development.     

Serum vitamin D status in type 2 diabetic patients from Gaza Strip

ObjectiveTo assess serum vitamin D status and its relations to other biochemical parameters in type 2 diabetic patients from Gaza Strip.Materials and methodsThis case-control study included 58 type 2 diabetic patients as well as 58 non-diabetic controls. Patients and controls were matched for age and gender. Data were obtained from questionnaire interview, and biochemical analysis of blood samples.ResultsSerum vitamin D was significantly lower in diabetic patients compared to non-diabetic controls (25.9 ± 11.0 versus 34.6 ± 13.8 ng/dl, % difference = 28.8%, P < 0.001). The number of patients having vitamin D deficient, insufficient and sufficient were 6 (10.4%), 35 (60.3%) and 17 (29.3%) compared to controls of 3 (5.2%), 16 (27.6%) and 39 (67.2%), respectively (χ² = 14.672, P < 0.001). Serum glucose, glycated hemoglobin (HbA1c), serum alanine aminotransferase (ALT), aspartate aminotransferase (AST) and triglycerides were significantly higher in patients than in controls whereas serum insulin, high density lipoprotein cholesterol (HDL-C) and calcium were significantly lower in patients. Serum vitamin D showed significant negative correlations with HbA1c (r = ? 0.186, P = 0.046), ALT (r = ? 192, P = 0.040) and AST (r = ? 0.188, P = 0.044) whereas significant positive correlations were found with HDL-C (r = 0.188, P = 0.044) and calcium (r = 0.239, P = 0.010).ConclusionThe significant negative and positive correlations of vitamin D with HbA1c and calcium, respectively suggests that vitamin D supplementation would be of potential therapeutic value in clinical settings for controlling of type 2 diabetes and more importantly its complications. However, a well-designed clinical trials are needed to define the contribution of vitamin D status and therapy in the global diabetes problem.     

Interaction of opioid with insulin/IGFs signaling in Alzheimer's disease

Journal of Molecular Neuroscience - Alzheimer's disease is associated with biochemical and histopathological changes characterized by molecular abnormalities. Due to the lack of effective...     

Neural coding of action in three dimensions: Task- and time-invariant reference frames for visuospatial and motor-related activity in parietal area V6A

Goal-directed movements involve a series of neural computations that compare the sensory representations of goal location and effector position, and transform these into motor commands. Neurons in posterior parietal cortex (PPC) control several effectors (e.g., eye, hand, foot) and encode goal location in a variety of spatial coordinate systems, including those anchored to gaze direction, and to the positions of the head, shoulder, or hand. However, there is little evidence on whether reference frames depend also on the effector and/or type of motor response. We addressed this issue in macaque PPC area V6A, where previous reports using a fixate-to-reach in depth task, from different starting arm positions, indicated that most units use mixed body/hand-centered coordinates. Here, we applied singular value decomposition and gradient analyses to characterize the reference frames in V6A while the animals, instead of arm reaching, performed a nonspatial motor response (hand lift). We found that most neurons used mixed body/hand coordinates, instead of “pure” body-, or hand-centered coordinates. During the task progress the effect of hand position on activity became stronger compared to target location. Activity consistent with body-centered coding was present only in a subset of neurons active early in the task. Applying the same analyses to a population of V6A neurons recorded during the fixate-to-reach task yielded similar results. These findings suggest that V6A neurons use consistent reference frames between spatial and nonspatial motor responses, a functional property that may allow the integration of spatial awareness and movement control.     

Controlled Growth of Polyamide Films atop Homogenous and Heterogeneous Hydrogels Using Gel–Liquid Interfacial Polymerization

Controlled growth of crosslinked polyamide (PA) thin films is demonstrated at the interface of a monomer‐soaked hydrogel and an organic solution of the complementary monomer. Termed gel–liquid interfacial polymerization (GLIP), the resulting PA films are measured to be chemically and mechanically analogous to the active layer in thin film composite (TFC) membranes. PA thin films are prepared using the GLIP process on both a morphologically homogeneous hydrogel prepared from poly(2‐hydroxyethylmethacrylate) and a phase‐separated, heterogeneous hydrogel prepared from poly(acrylamide). Two monomer systems are examined: trimesoyl chloride (TMC) reacting with m‐phenylene diamine (MPD) and TMC reacting with piperazine (PIP). Unlike the self‐limiting growth behavior in TFC membrane fabrication, diffusion‐limited, continuous growth of the PA films is observed, where both the thickness and roughness of the PA layers increase with reaction time. A key morphological difference is found between the two monomer systems using the GLIP process; TMC/MPD produces a ridge‐and‐valley surface morphology whereas TMC/PIP produces nodule/granular structures. The GLIP process represents a unique opportunity to not only explore the pore characteristics (size, spacing, and continuity) on the resulting structure and morphology of the interfacially polymerized thin films, but also a method to modify the surface of (or encapsulate) hydrogels.     

Atherogenic consequence of antiepileptic drugs: a study of intima-media thickness

We intended to evaluate the carotid intima-media thickness (CA-IMT) as a surrogate factor for atherogenesis in epileptic patients on enzyme inducer (EI) antiepileptic drugs (AEDs) or valproate (VA). The study included 71 patients with epilepsy (37 females) aged 27.7 ± 8.1 and 71 age- and sex-matched non-epileptic subjects. Patients with history of at least 2 years antiepileptic treatment were enrolled. Subjects with known history of cardiovascular risk factors were not included. Thirty-eight patients (21 females) were treated with EI medications and 33 (16 females) with VA. CA-IMTs were measured by a single sonography system in all participants. CA-IMT values were compared between patients with epilepsy and the controls and within the patients with epilepsy on VA or EI medications. Duration of epilepsy was 10.1 ± 7.1 years. Patients were treated with their current AED for 6.9 ± 4.8 years. The CA-IMT of patients with epilepsy was higher than non-epileptic control subjects on either left (0.502 ± 0.079 vs. 0.470 ± 0.073 mm; p = 0.012) or right side (0.524 ± 0.078 vs. 0.458 ± 0.068 mm; p < 0.001). Patients on VA were younger than those receiving EI medications (25.8 ± 7.1 vs. 29.4 ± 8.7 years). Age adjusted CA-IMT values of patients on VA did not differ from the values of patients receiving EI medications. Duration of drug administration did not correlate with CA-IMT values. Patients with epilepsy on AEDs are at higher risk for atherogenesis. In the population of this study the increased risk of atherogenesis was not attributable to the administered AED or duration of treatment.