Vitamin D Is Necessary for Murine Gastric Epithelial Homeostasis

Unlike other organs, the importance of VD in a normal stomach is unknown. This study focuses on understanding the physiological role of vitamin D in gastric epithelial homeostasis. C57BL/6J mice were divided into three groups that were either fed a standard diet and kept in normal light/dark cycles (SDL), fed a standard diet but kept in the dark (SDD) or fed a vitamin D-deficient diet and kept in the dark (VDD). After 3 months, sera were collected to measure vitamin D levels by LC-MS/MS, gastric tissues were collected for immunohistochemical and gene expression analyses and gastric contents were collected to measure acid levels. The VDD group showed a significant decrease in the acid-secreting parietal cell-specific genes Atp4a and Atp4b when compared with the controls. This reduction was associated with an increased expression of an antral gastrin hormone. VDD gastric tissues also showed a high proliferation rate compared with SDL and SDD using an anti-BrdU antibody. This study indicates the requirement for normal vitamin D levels for proper parietal cell functions.

Draft Genome Sequences of Three Amino Acid-Secreting Lactococcus lactis Strains

Three Lactococcus lactis strains with the ability to secrete various amino acids (leucine, isoleucine, methionine, valine, glutamic acid, and histidine) were sequenced in order to identify the mechanisms involved in the secretion. Amino acids contribute to flavor formation; therefore, bacterial strains with this ability are relevant for the food industry.

Evaluation of efficacy and safety of Gas-O-Fast (Ajwain) in Amalpitta

Modern era’s, changing lifestyle along with changing food habits and depending upon one’s body constitution Amlapitta is one of the most common symptom (disease) seen in the society. Amlapitta is very distressing due to its chronic, relapsing and remittent nature. ‘Hurry’, ‘Worry’, and ‘Curry’ are the three main reasons for the disease. The industrialization, stress due to work, lack of exercise and faulty food habits leads to disturbance of Agni or metabolism which leads to many disorders, Amlapitta is one of them. Acidity refers to set of symptoms caused by an imbalance between the acid secreting mechanism of stomach and the protective mechanisms of gastric mucosa that ensure their safety. When due to some reason, there is excess production of acid by acid secreting glands of stomach, it results in condition known as Acidity. Acidity tends to have a much higher incidence in highly emotional and nervous individuals. Faulty lifestyle undoubtedly has a much higher role in this disease. Non-steroidal Anti Inflammatory Drugs (NSAID’s) also predispose to gastric acidity. Prolonged acidity is responsible for symptoms like Dyspepsia, Heartburn and if not taken care of, the erosion of the lining of stomach or intestines result with the formation of Ulcers. Current research proposal is small step to explore evidence based therapeutic potential of Ayurvedic herbal formulation. Present short term clinical trial was designed to evaluate efficacy of Gas-O-Fast (Ajwain), when used in a dose of 3 sachet /day in volunteers. Drug was given to the patients of dyspepsia for 30 days. It is evident that improvement in symptoms of Amalpitta (Non ulcer dyspepsia) was statistically highly significant without any side effects/ toxic effects of formulation.Â

Unique Cellular Lineage Composition of the First Gland of the Mouse Gastric Corpus

The glandular stomach has two major zones: the acid secreting corpus and the gastrin cell–containing antrum. Nevertheless, a single gland lies at the transition between the forestomach and corpus in the mouse stomach. We have sought to define the lineages that make up this gland unit at the squamocolumnar junction. The first gland in mice showed a notable absence of characteristic corpus lineages, including parietal cells and chief cells. In contrast, the gland showed strong staining of Griffonia simplicifolia-II (GSII)-lectin-positive mucous cells at the bases of glands, which were also positive for CD44 variant 9 and Clusterin. Prominent numbers of doublecortin-like kinase 1 (DCLK1) positive tuft cells were present in the first gland. The first gland contained Lgr5-expressing putative progenitor cells, and a large proportion of the cells were positive for Sox2. The cells of the first gland stained strongly for MUC4 and EpCAM, but both were absent in the normal corpus mucosa. The present studies indicate that the first gland in the corpus represents a unique anatomic entity. The presence of a concentration of progenitor cells and sensory tuft cells in this gland suggests that it may represent a source of reserve reparative cells for adapting to severe mucosal damage.

Approach to the patient with renal tubular acidosis

The renal tubular acidoses are a collection of syndromes characterized by defective urinary acidification. These syndromes have classically caused some confusion, and many opine that the widely used numerical system (type 1, 2) should be abandoned. We consider distal renal tubular acidosis and proximal renal tubular acidosis separately, and briefly cover hypoaldosteronism. Distal (Type 1) renal tubular acidosis is a syndrome of hypokalaemia, metabolic acidosis, kidney stones, nephrocalcinosis, and osteomalacia or rickets. It is caused by failure of the acid secreting α‎‎‎-intercalated cells in the distal nephron. Proximal (Type 2) renal tubular acidosis is a syndrome of metabolic acidosis that is almost always accompanied by the Fanconi syndrome of glycosuria, phosphaturia, uricosuria, aminoaciduria, and low-molecular-weight proteinuria. It is caused by a failure of bicarbonate reabsorption by the proximal tubular cells. Type 3 or mixed renal tubular acidosis, as originally described, has vanished (or was originally incompletely described). It is sometimes used to describe a mutation of carbonic anhydrase II, which causes both proximal and distal renal tubular acidosis, as well as cerebral calcification and osteopetrosis. Type 4 or hypoaldosteronism is a syndrome of hyperkalaemia and mild metabolic acidosis. It is due to a lack of aldosterone or resistance to its action.