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Public universities in Bangladesh arrange admission test to judge the students' merit before the enrollment. Academic results of previous examinations (SSC and HSC) are also considered in the admission procedure. There are some disputes regarding the importance of admission test besides the previous academic records. The universities emphasize on the admission test while the government authorities ponder it as a burden for the students. This study has made an attempt to examine the importance of admission test in selection procedure utilizing a particular year admission test database of Shahjalal University of Science and Technology (SUST). Univariate and bivariate analyses along with regression models were used to analyze the data. The results indicate that students with higher score in both SSC and HSC examinations had higher possibility to be eligible for enrollment. However, a vital proportion of applicants with maximum GPA 5.00 in both examinations did not qualify in merit and waiting position. The results also show association and moderate positive correlation of admission test score with SSC and HSC results. Finally, regression analysis indicates that though the contributions of the SSC and HSC results on admission test scores are significant, the variation in admission test scores is not much explained by the previous records. Such findings recommend arranging admission test, besides academic qualification, to select the eligible applicants for enrollment in public universities.

Background & aimsThere is evidence from clinical studies that compromised intestinal epithelial permeability contributes to the development of nonalcoholic steatohepatitis (NASH), but the exact mechanisms are not clear. Mice with disruption of the gene (F11r) encoding junctional adhesion molecule A (JAM-A) have defects in intestinal epithelial permeability. We used these mice to study how disruption of the intestinal epithelial barrier contributes to NASH.MethodsMale C57BL/6 (control) or F11r(-/-) mice were fed a normal diet or a diet high in saturated fat, fructose, and cholesterol (HFCD) for 8 weeks. Liver and intestinal tissues were collected and analyzed by histology, quantitative reverse-transcription polymerase chain reaction, and flow cytometry. Intestinal epithelial permeability was assessed in mice by measuring permeability to fluorescently labeled dextran. The intestinal microbiota were analyzed using 16S ribosomal RNA sequencing. We also analyzed biopsy specimens from proximal colons of 30 patients with nonalcoholic fatty liver disease (NAFLD) and 19 subjects without NAFLD (controls) undergoing surveillance colonoscopy.ResultsF11r(-/-) mice fed a HFCD, but not a normal diet, developed histologic and pathologic features of severe NASH including steatosis, lobular inflammation, hepatocellular ballooning, and fibrosis, whereas control mice fed a HFCD developed only modest steatosis. Interestingly, there were no differences in body weight, ratio of liver weight:body weight, or glucose homeostasis between control and F11r(-/-) mice fed a HFCD. In these mice, liver injury was associated with significant increases in mucosal inflammation, tight junction disruption, and intestinal epithelial permeability to bacterial endotoxins, compared with control mice or F11r(-/-) mice fed a normal diet. The HFCD led to a significant increase in inflammatory microbial taxa in F11r(-/-) mice, compared with control mice. Administration of oral antibiotics or sequestration of bacterial endotoxins with sevelamer hydrochloride reduced mucosal inflammation and restored normal liver histology in F11r(-/-) mice fed a HFCD. Protein and transcript levels of JAM-A were significantly lower in the intestinal mucosa of patients with NAFLD than without NAFLD; decreased expression of JAM-A correlated with increased mucosal inflammation.ConclusionsMice with defects in intestinal epithelial permeability develop more severe steatohepatitis after a HFCD than control mice, and colon tissues from patients with NAFLD have lower levels of JAM-A and higher levels of inflammation than subjects without NAFLD. These findings indicate that intestinal epithelial barrier function and microbial dysbiosis contribute to the development of NASH. Restoration of intestinal barrier integrity and manipulation of gut microbiota might be developed as therapeutic strategies for patients with NASH.

Aim: This study aimed to identify the predictors of mortality and ICU requirements in hospitalized COVID‐19 Patients with Diabetes. Design: Cross‐sectional study. Methods: It was a retrospective study of patients hospitalized with COVID‐19 infection from October 2020–February 2021 in four hospitals in Sylhet, Bangladesh. Logistic regression analysis was applied to explore the predictors of ICU requirement and in‐hospital mortality. Results: In the whole cohort (n = 500), 11% of patients died and 24% of patients required intensive care unit (ICU) support. Non‐survivors had significantly higher prevalence of lymphopenia, thrombocytopenia and leukocytosis. Significant predictors of in‐hospital mortality were older age, neutrophil count, platelet count and admission peripheral capillary oxygen saturation (SpO2). Older age, ischemic heart disease, WBC count, D‐dimer and admission SpO2 were identified as significant predictors for ICU requirement. Patient or Public Contribution: No. [ABSTRACT FROM AUTHOR]

The ability of the cadherin fragments obtained from Anopheles gambiae to synergize the toxicity of Bacillus thuringiensis subsp. israelensis Cry4Ba against Aedes aegypti larvae is discussed. The fragments are demonstrated to be highly syngergizing and hence are widely used for the purpose.

The fragment containing the three most C-terminal cadherin repeats (CR) from the cadherin of the western corn rootworm has bound toxins and has enhanced Cry3 toxicity to larvae of naturally susceptible species. The region spanning CR8 to CR10 of the WCRW cadherin is cloned and expressed in Escherichia coli and this cadherin fragment has enhanced the toxicities of Bacillus Thuringiensis Cry3Aa and Cry3Bb toxins to Colorado potato beetle (CPB) and rootworms.

Liver fibrosis is a growing global health problem characterized by excess deposition of fibrillar collagen, and activation of hepatic stellate cells (HSCs). Adiponectin is known to possess anti-fibrotic properties; however a high physiological concentration and multiple forms circulating in blood prohibit clinical use. Recently, an adiponectin-like small synthetic peptide agonist (ADP355: H-DAsn-Ile-Pro-Nva-Leu-Tyr-DSer-Phe-Ala-DSer-NH2) was synthesized for the treatment of murine breast cancer. The present study was designed to evaluate the efficacy of ADP355 as an anti-fibrotic agent in the in vivo carbon tetrachloride (CCl4)-induced liver fibrosis model. Liver fibrosis was induced in eight-week old male C57BL/6J mice by CCl4-gavage every other day for four weeks before injection of a nanoparticle-conjugated with ADP355 (nano-ADP355). Control gold nanoparticles and nano-ADP355 were administered by intraperitoneal injection for two weeks along with CCl4-gavage. All mice were sacrificed after 6 weeks, and serum and liver tissue were collected for biochemical, histopathologic and molecular analyses. Biochemical studies suggested ADP355 treatment attenuates liver fibrosis, determined by reduction of serum aspartate aminotransferase (AST), alanine aminotransferase ALT) and hydroxyproline. Histopathology revealed chronic CCl4-treatment results in significant fibrosis, while ADP355 treatment induced significantly reversed fibrosis. Key markers for fibrogenesis–α-smooth muscle actin (α-SMA), transforming growth factor-beta1 (TGF-β1), connective tissue growth factor (CTGF), and the tissue inhibitor of metalloproteinase I (TIMP1) were also markedly attenuated. Conversely, liver lysates from ADP355 treated mice increased phosphorylation of both endothelial nitric oxide synthase (eNOS) and AMPK while AKT phosphorylation was diminished. These findings suggest ADP355 is a potent anti-fibrotic agent that can be an effective intervention against liver fibrosis. [ABSTRACT FROM AUTHOR]

The Cry proteins produced by Bacillus thuringiensis (Bt) are the most widely used biopesticides effective against a range of crop pests and disease vectors. Like chemical pesticides, development of resistance is the primary threat to the long-term efficacy of Bt toxins. Recently discovered cadherin-based Bt Cry synergists showed the potential to augment resistance management by improving efficacy of Cry toxins. However, the mode of action of Bt Cry synergists is thus far unclear. Here we elucidate the mechanism of cadherin-based Cry toxin synergism utilizing two cadherin peptides, Spodopterafrugiperda Cad (SfCad) and Manduca sexta Cad (MsCad), which differentially enhance CrylFa toxicity to Spodopterafrugiperda neonates. We show that differential SfCadand MsCad-mediated protection of CrylFa toxin in the Spodopterafrugiperda midgut correlates with differential Cryl Fa toxicity enhancement. Both peptides exhibited high affinity for CrylFa toxin and an increased rate of CrylFa-induced pore formation in S. frugiperda. However, only SfCad bound the S. frugiperda brush border membrane vesicle and more effectively prolonged the stability of CrylFa toxin in the gut, explaining higher CrylFa enhancement by this peptide. This study shows that cadherin fragments may enhance B. thuringiensis toxicity by at least two different mechanisms or a combination thereof: (i) protection of Cry toxin from protease degradation in the insect midgut and (ii) enhancement of pore-forming ability of Cry toxin. [ABSTRACT FROM AUTHOR]

Persistent hepatotropic viral infections are a common etiologic agent of chronic liver disease. Unresolved infection can be attributed to nonfunctional intrahepatic CD8+ T-cell responses. In light of dampened CD8 + T-cell responses, liver disease often manifests systemically as immunoglobulin (Ig)-related syndromes due to aberrant B-cell functions. These two opposing yet coexisting phenomena implicate the potential of altered CD4 + T-cell help. Elevated CD4 + forkhead box P3-positive (Foxp3+) T cells were evident in both human liver disease and a mouse model of chemically induced liver injury despite marked activation and spontaneous IgG production by intrahepatic B cells. While this population suppressed CD8 + T-cell responses, aberrant B-cell activities were maintained due to expression of CD40 ligand on a subset of CD4 + Foxp3+ T cells. In vivo blockade of CD40 ligand attenuated B-cell abnormalities in a mouse model of liver injury. A phenotypically similar population of CD4 + Foxp3+, CD40 ligand-positive T cells was found in diseased livers explanted from patients with chronic hepatitis C infection. This population was absent in nondiseased liver tissues and peripheral blood., Conclusion: Liver disease elicits alterations in the intrahepatic CD4 + T-cell compartment that suppress T-cell immunity while concomitantly promoting aberrant IgG mediated manifestations. (Hepatology 2017;65:661-677)., Competing Interests: The authors have no conflicts of interest to disclose., (© 2016 by the American Association for the Study of Liver Diseases.)