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Vineet Ahuja

Publications and source records attributed to Vineet Ahuja.

5 recordsLinked to original sources

Phylogeny and evolution of SARS-CoV-2 during Delta and Omicron variant waves in India.

SARS-CoV-2 evolution has continued to generate variants, responsible for new pandemic waves locally and globally. Varying disease presentation and severity has been ascribed to inherent variant characteristics and vaccine immunity. This study analyzed genomic data from 305 whole genome sequences from SARS-CoV-2 patients before and through the third wave in India. Delta variant was reported in patients without comorbidity (97%), while Omicron BA.2 was reported in patients with comorbidity (77%). Tissue adaptation studies brought forth higher propensity of Omicron variants to bronchial tissue than lung, contrary to observation in Delta variants from Delhi. Study of codon usage pattern distinguished the prevalent variants, clustering them separately, Omicron BA.2 isolated in February grouped away from December strains, and all BA.2 after December acquired a new mutation S959P in ORF1b (44.3% of BA.2 in the study) indicating ongoing evolution. Loss of critical spike mutations in Omicron BA.2 and gain of immune evasion mutations including G142D, reported in Delta but absent in BA.1, and S371F instead of S371L in BA.1 could explain very brief period of BA.1 in December 2021, followed by complete replacement by BA.2. Higher propensity of Omicron variants to bronchial tissue, probably ensured increased transmission while Omicron BA.2 became the prevalent variant possibly due to evolutionary trade-off. Virus evolution continues to shape the epidemic and its culmination.Communicated by Ramaswamy H. Sarma.

SARS-CoV-2↗

Amebiasis.

Explore the source record for details and available documents.

Humans↗

Presence of white bile associated with lower survival in malignant biliary obstruction.

OBJECTIVE: The chemical composition and clinical significance of white bile in patients with malignant biliary obstruction were evaluated in a prospective study. METHODS: Consecutive patients (January 1996 through December 1997) with inoperable malignant biliary obstruction underwent endoscopic placement of 10F straight, plastic biliary stents. Bile was aspirated during the endoscopic procedure. Patients were divided into 2 groups: those with white and those with yellow bile. The chemical composition of bile was analyzed. Levels of bile acids in the serum and bile (11 samples) were estimated by high-performance thin-layer chromatography. The groups were compared for decremental fall in bilirubin (b value), cholangitis after stent insertion, and survival. RESULTS: Thirty-five patients (15 men, 20 women; mean age 54 years) underwent endoscopic drainage for malignant obstruction (29 hilar, 6 distal bile duct). Eighteen patients had white bile. Refractory jaundice (b > -0.025) was seen in 9 (50%) patients with white bile compared with 3 (17.6%) with yellow bile; mean difference -42.2 (95% CI [-62.4, -22.0]) and -45.7 (95% CI [-72.0, -19.4]), respectively. The bilirubin (0.48 mg/L) and bile acid (15.6 mmol/L) concentrations in white bile were significantly less than bilirubin (42.7 mg/L) and bile acid (61.3 mmol/L) concentrations in yellow bile; mean difference -42.2 (95% CI [-62.4, -22.0]) and mean difference -45.7 (95% CI [-72.0, -19.4]), respectively. Cholangitis developed in 66.6% of patients with white bile compared with 35% of those with yellow bile (OR 3.67: 95% CI [0.74, 19.25]). Kaplan-Meier curves showed that median survival (interquartile range) was shorter in patients with white bile (35 [23-60] versus 77 [35-220] days) (p = 0.004, log rank test), which was significant even after adjusting for potential confounders with Cox proportional hazards regression. CONCLUSION: White bile is largely devoid of bilirubin and bile acids. The presence of white bile was associated with significantly worse survival in patients with malignant biliary obstruction.

Adult↗

Pre and post eradication gastric inflammation in Helicobacter pylori-associated duodenal ulcer.

BACKGROUND: Distribution and nature of gastritis are major determinants of clinical outcome of H. pylori infection. The gastric inflammatory changes associated with this infection in developing countries have not been systematically studied. AIMS: To evaluate the inflammatory changes in gastric antrum and corpus in patients with duodenal ulcer and H. pylori infection, before and after H. pylori eradication therapy. METHODS: Histology and H. pylori density were studied in gastric biopsies obtained from 53 consecutive patients with active duodenal ulcer and H. pylori infection. Biopsies were obtained before and 4 weeks after H. pylori eradication therapy, from the anterior and posterior walls of the antrum and corpus, and were evaluated according to the Sydney system. RESULTS: In the pre-H. py/ori eradication antral biopsies, chronic gastritis, active gastritis, atrophy, intestinal metaplasia (IM) and lymphoid follicles / aggregates were seen in 53 (100%), 49 (92%), 11 (21%), 7 (13%) and 28 (53%) patients, respectively. In the corresponding biopsies from gastric corpus, these changes were seen in 49 (92%), 23 (43%), 2 (4%), 2 (4%) and 8 (15%), respectively. All changes except IM were significantly more frequent and of higher grade in the antrum. The grade of chronic gastritis was significantly higher in antrum than corpus; the frequency of gastritis in the antrum and corpus was similar (100% vs. 92%). H. pylori density was also higher in the antrum and correlated well with the grades of chronic gastritis and activity at both sites. Eradication of H. pylori was achieved in 39 patients (74%), and led to significant decrease in gastritis; no change was seen in patients who did not eradicate the organism. CONCLUSIONS: Antral-predominant chronic gastritis and activity are present in more than 90% of patients with H. pylori infection associated with duodenal ulcer, and the grade of gastritis correlates with the density of the organism. Eradication therapy results in improvement of both chronic gastritis and activity.

2-Pyridinylmethylsulfinylbenzimidazoles↗