Intestinal uptake of nutrients in normal and malnourished animals infected with Giardia lamblia

The effect of malnutrition on the uptake of nutrients was studied in Swiss albino mice infected with Giardia lamblia. The moderate deficiency (8% protein-deficient diet) was observed to enhance the uptake of nutrients like glucose and alanine, whereas in severely malnourished (3% protein-deficient diet) animals the uptake was significantly decreased (p less than 0.001). G. lamblia infection in mice decreased the uptake of nutrients and this recovered slightly with the recovery of infection. The combined effect of moderate protein deficiency and infection lowered the enhanced uptake observed in moderately malnourished animals to a significant level (p less than 0.001). In severely malnourished animals, infection with G. lamblia showed further deleterious effects on the uptake of nutrients.     

Familial leucine-sensitive hypoglycemia of infancy due to a dominant mutation of the beta-cell sulfonylurea receptor

Familial leucine-sensitive hypoglycemia of infancy was described in 1956 as a condition in which symptomatic hypoglycemia was provoked by protein meals or the amino acid, leucine. The purpose of this study was to determine the genetic basis for hypoglycemia in a family diagnosed with leucine-sensitive hypoglycemia in 1960. Recently diagnosed family members showed a dominantly transmitted pattern of diazoxide-responsive hyperinsulinism (HI). However, they did not fit the characteristics of HI caused by glutamate dehydrogenase gene mutations, previously felt to explain leucine-sensitive hypoglycemia. Islet function was examined using acute insulin response (AIR) tests to calcium, leucine, glucose, and tolbutamide as well as oral protein tolerance tests. Five of five affected family members showed an abnormal positive calcium AIR, and two of five showed a positive leucine AIR. Protein-induced hypoglycemia was demonstrated in five of six affected subjects. Mutation analysis of four known HI genes (sulfonylurea receptor 1, Kir6.2, glutamate dehydrogenase, and glucokinase) in family members identified an R1353H missense mutation in exon 33 of SUR1. (86)Rb(+) efflux and electrophysiological studies of R1353H SUR1 coexpressed with wild-type Kir6.2 in COSm6 cells demonstrated partially impaired ATP-dependent potassium channel function. Leucine-sensitive hypoglycemia in this family was found to result from a dominantly expressed SUR1 mutation.     

Functional Uncoupling NMDAR NR2A Subunit from PSD-95 in the Prefrontal Cortex: Effects on Behavioral Dysfunction and Parvalbumin Loss after Early-Life Stress

Exposure to early-life stress increases vulnerability to psychiatric disorders, including depression, schizophrenia, and anxiety. Growing evidence implicates aberrant development of the prefrontal cortex (PFC) in the effects of early-life stress, which often emerge in adolescence or young adulthood. Specifically, early-life stress in the form of maternal separation (MS) in rodents has been shown to decrease parvalbumin (PVB)-positive interneurons in the adolescent PFC; however, the mechanism underpinning behavioral dysfunction and PVB loss is not yet known. We recently reported that MS causes overexpression of the NMDA subunit NR2A in the PFC of adolescent rats. Elevated PFC NR2A is also found in developmental models of schizophrenia and is correlated with behavioral deficits, acting largely through its association with the postsynaptic protein PSD-95. In addition, adolescent maturation of PVB-positive interneurons relies on NR2A-driven NMDA activity. Therefore, it is possible that the NR2A/PSD-95 signaling complex has a role in adolescent MS effects. Here, we aimed to determine whether a discrete manipulation of PFC NR2A could prevent MS effects on PFC-controlled behaviors, including cognition, anxiety, and novelty-induced hyperlocomotion, as well as PVB loss in adolescence. We intracranially infused the NR2A-specific blocking peptide TAT2A in order to uncouple NR2A from PSD-95 in the early-adolescent PFC, without antagonizing the NMDA receptor. We demonstrated that MS rats treated with TAT2A during early adolescence were protected from MS-induced PVB loss and exhibited less anxious behavior than those infused with control peptide. These data implicate NR2A-related N-methyl-D-aspartate receptor development in adolescent behavioral and neural consequences of early-life stress.     

Extremely low HDL and residual cardiovascular risk—a case report

International Journal of Diabetes in Developing Countries - Extremely low high-density lipoprotein cholesterol (HDL-C) is defined as levels below 20 mg/dL. Association between extremely low HDL-C...     

Role of baicalin as a potential therapeutic agent in hepatobiliary and gastrointestinal disorders: A review

Baicalin is a natural bioactive compound derived from Scutellaria baicalensis, which is extensively used in traditional Chinese medicine. A literature survey demonstrated the broad spectrum of health benefits of baicalin such as antioxidant, anticancer, anti-inflammatory, antimicrobial, cardio-protective, hepatoprotective, renal protective, and neuroprotective properties. Baicalin is hydrolyzed to its metabolite baicalein by the action of gut microbiota, which is further reconverted to baicalin via phase 2 metabolism in the liver. Many studies have suggested that baicalin exhibits therapeutic potential against several types of hepatic disorders including hepatic fibrosis, xenobiotic-induced liver injury, fatty liver disease, viral hepatitis, cholestasis, ulcerative colitis, hepatocellular and colorectal cancer. During in vitro and in vivo examinations, it has been observed that baicalin showed a protective role against liver and gut-associated abnormalities by modifying several signaling pathways such as nuclear factor-kappa B, transforming growth factor beta 1/SMAD3, sirtuin 1, p38/mitogen-activated protein kinase/Janus kinase, and calcium/calmodulin-dependent protein kinase kinaseβ/adenosine monophosphate-activated protein kinase/acetyl-coenzyme A carboxylase pathways. Furthermore, baicalin also regulates the expression of fibrotic genes such as smooth muscle actin, connective tissue growth factor, β-catenin, and inflammatory cytokines such as interferon gamma, interleukin-6 (IL-6), tumor necrosis factor-alpha, and IL-1β, and attenuates the production of apoptotic proteins such as caspase-3, caspase-9 and B-cell lymphoma 2. However, due to its low solubility and poor bioavailability, widespread therapeutic applications of baicalin still remain a challenge. This review summarized the hepatic and gastrointestinal protective attributes of baicalin with an emphasis on the molecular mechanisms that regulate the interaction of baicalin with the gut microbiota.     

Interaction of Thrombin with Human Platelets

The first step in thrombin-induced aggregation of blood platelets is binding of thrombin to specific receptors on the platelet membrane. Elucidation of the nature of this receptor in human platelets was attempted using radioactively labelled thrombin. In disc gel electrophoresis an extract of thrombin-treated platelets showed one peak of radioactivity near the origin. Gel filtration of the platelet extract through Sephadex G-200 showed mainly one protein peak at the void volume which contained radioactivity. After column fractionation the final isolate reacted with antiserum to thrombosthenin but did not react with antiserum to serum, fibrinogen or soluble platelet proteins. Gel electrophoresis of the reduced isolate in the presence of sodium dodecyl sulphate showed a pattern similar to thrombosthenin. To explore the possibility that thrombosthenin might be the receptor of thrombin, attempts were made to complex the receptro sites with thrombosthenin antibody or its univalent fragment. It was observed that complexing these receptors potentiates, rather than inhibits, platelet aggregation by thrombin or by adenosine diphosphate. Univalent fragment of antibody to albumin failed to cause this potentiation. Thus, blocking of the thrombosthenin sites is necessary for sensitization of platelets.     

Adrenal steroid responses to ACTH in glucocorticoid-suppressible aldosteronism

To investigate adrenal responses to adrenocorticotrophin (ACTH), we infused graded doses of ACTH (1.25 to 20.0 mIU/30 minutes) in normal subjects, patients with low-renin essential hypertension (LREH), primary aldosteronism (PA), and glucocorticoid-suppressible hyperaldosteronism (GSH). Plasma aldosterone, cortisol, corticosterone, and 18-hydroxycorticosterone were measured. The results revealed a greater increase in the plasma aldosterone and 18-hydroxycorticosterone levels evoked by ACTH in the GSH group than in any other group, which suggested enhanced responsiveness of the aldosterone-producing cells to ACTH and a probable adrenal abnormality.     

Meningoencephalitis associated with COVID-19: a systematic review

Journal of NeuroVirology - With the growing number of COVID-19 cases in recent times. significant set of patients with extra pulmonary symptoms has been reported worldwide. Here we venture out to...