An Analytical Study on the Damage to School Buildings by the 2015 Nepal Earthquake and Damage Level-Based Reconstruction Experience

The 2015 Nepal Earthquake (Mw7.8) affected more than 9000 schools in the country. Damage distribution in the 14 most-affected administrative districts shows that the construction practices were an important determent for the level of damage extended. The use of improper construction materials, lack of construction supervision, and non-compliance with the existing building codes during design and construction probably contributed to severe damage to most of the school buildings. Based on the damage analysis data and experience of the rebuilding process after the 2015 Nepal Earthquake, this paper highlights the steps to be considered during a rebuilding plan for school buildings after an earthquake disaster. Preliminary damage assessment results show that in the most-affected districts, about 86% of schools (locations) were affected by the earthquake and about one million students were out of their schools for a long time. The damage survey data indicate that about 30% of classrooms collapsed, about 13% of classrooms sustained major damage, and about 17% of classrooms sustained minor damage within the most-affected 14 districts. This damage report is largely based on the secondary data provided by the concerned government authorities. Such evidence of loss and damage in earthquake disasters provides an opportunity to learn lessons for future preparedness and to encounter disaster challenges. This work shares an experience on the rebuilding process of damaged schools and classrooms. It is expected that the experience reported in this paper will help in better planning of the seismic safety of school buildings in Nepal as well as in other similar seismically active regions. Most papers related to the 2015 Nepal Earthquake focus on overall building damage, but this paper addresses the issues of school buildings. As a case report, this paper probably lacks scientific originality, but the presentation of the damage data and the rebuilding process are the original work of the authors

A comparison of techniques to address the frequency of Helicobacter pylori positive dyspeptic patient

Abstract Objectives The study was aimed to compare the diagnostic techniques, for the detection of Helicobacter pylori infection, available in low-income countries, where molecular testing is not available or inaccessible to anyone. Results Of total enrolled patient, with the mean age of 41.4 ± 13.33 years, 24 (14 female; 10 male) were diagnosed to have been infected. The diagnosis was established based upon the gold standard test [either two of three tests: Rapid Urease Test (RUT), culture and histological examinations]. Of clinical presentation, the epigastric pain (75%) was the commonest; nevertheless, the endoscopic findings had shown an equivocal specificity since the larger percentile (58.3%) reported as normal findings, in a presumed dyspepsia. Based on the premise—with calculated sensitivity, specificity, and predictive values; the accuracy order observed as histology > RUT > serology > stool antigen test, in H. pylori detection from the clinical samples. The accuracy order of the diagnostic test may vary depending upon the laboratory settings and study population. Therefore, in reference to low-income countries, the clinicians must resort any available positive test so that the supporting positive rudiments would be an ancillary in augmenting the diagnostic accuracy

Interferon alpha inhibits antigen-specific production of proinflammatory cytokines and enhances antigen-specific transforming growth factor beta production in antigen-induced arthritis

Introduction: Interferon alpha (IFN-α) has a complex role in autoimmunity, in that it may both enhance and prevent inflammation. We have previously shown that the presence of IFN-α at sensitization protects against subsequent antigen-triggered arthritis. To understand this tolerogenic mechanism, we performed a descriptive, hypothesis-generating study of cellular and humoral responses associated with IFN-α-mediated protection against arthritis.Methods: Arthritis was evaluated at day 28 in mice given a subcutaneous injection of methylated bovine serum albumin (mBSA), together with Freund adjuvant and 0 to 5,000 U IFN-α at days 1 and 7, followed by intraarticular injection of mBSA alone at day 21. The effect of IFN-α on mBSA-specific IgG1, IgG2a, IgG2b, IgA, and IgE was evaluated by enzyme-linked immunosorbent assay (ELISA). Cytokines in circulation and in ex vivo cultures on mBSA restimulation was evaluated with ELISA and Luminex, and the identity of cytokine-producing cells by fluorescence-activated cell sorting (FACS) analysis.Results: Administration of IFN-α protected mice from arthritis in a dose-dependent manner but had no effect on antigen-specific antibody levels. However, IFN-α did inhibit the initial increase of IL-6, IL-10, IL-12, and TNF, and the recall response induced by intraarticular mBSA challenge of IL-1β, IL-10, IL-12, TNF, IFN-γ, and IL-17 in serum. IFN-α decreased both macrophage and CD4+ T cell-derived IFN-γ production, whereas IL-17 was decreased only in CD4+ T cells. Ex vivo, in mBSA-restimulated spleen and lymph node cell cultures, the inhibitory effect of in vivo administration of IFN-α on proinflammatory cytokine production was clearly apparent, but had a time limit. An earlier macrophage-derived, and stronger activation of the antiinflammatory cytokine transforming growth factor beta (TGF-β) was observed in IFN-α-treated animals, combined with an increase in CD4+ T cells producing TGF-β when arthritis was triggered by mBSA (day 21). Presence of IFN-α at immunizations also prevented the reduction in TGF-β production, which was induced by the intraarticular mBSA injection triggering arthritis in control animals.Conclusions: Administration of IFN-α has a profound effect on the cellular response to mBSA plus adjuvant, but does not affect antigen-specific Ig production. By including IFN-α at immunizations, spleen and lymph node cells inhibit their repertoire of antigen-induced proinflammatory cytokines while enhancing antiinflammatory TGF-β production, first in macrophages, and later also in CD4+ T cells. On intraarticular antigen challenge, this antiinflammatory state is reenforced, manifested as inhibition of proinflammatory recall responses and preservation of TGF-β levels. This may explain why IFN-α protects against antigen-induced arthritis. © 2013 Chalise et al.; licensee BioMed Central Ltd

Влияние способа шлифования на величину остаточных напряжений закаленных сталей 14Х2Н3М и 20ХН3МА

Introduction: Interferon alpha (IFN-α) has a complex role in autoimmunity, in that it may both enhance and prevent inflammation. We have previously shown that the presence of IFN-α at sensitization protects against subsequent antigen-triggered arthritis. To understand this tolerogenic mechanism, we performed a descriptive, hypothesis-generating study of cellular and humoral responses associated with IFN-α-mediated protection against arthritis.Methods: Arthritis was evaluated at day 28 in mice given a subcutaneous injection of methylated bovine serum albumin (mBSA), together with Freund adjuvant and 0 to 5,000 U IFN-α at days 1 and 7, followed by intraarticular injection of mBSA alone at day 21. The effect of IFN-α on mBSA-specific IgG1, IgG2a, IgG2b, IgA, and IgE was evaluated by enzyme-linked immunosorbent assay (ELISA). Cytokines in circulation and in ex vivo cultures on mBSA restimulation was evaluated with ELISA and Luminex, and the identity of cytokine-producing cells by fluorescence-activated cell sorting (FACS) analysis.Results: Administration of IFN-α protected mice from arthritis in a dose-dependent manner but had no effect on antigen-specific antibody levels. However, IFN-α did inhibit the initial increase of IL-6, IL-10, IL-12, and TNF, and the recall response induced by intraarticular mBSA challenge of IL-1β, IL-10, IL-12, TNF, IFN-γ, and IL-17 in serum. IFN-α decreased both macrophage and CD4+ T cell-derived IFN-γ production, whereas IL-17 was decreased only in CD4+ T cells. Ex vivo, in mBSA-restimulated spleen and lymph node cell cultures, the inhibitory effect of in vivo administration of IFN-α on proinflammatory cytokine production was clearly apparent, but had a time limit. An earlier macrophage-derived, and stronger activation of the antiinflammatory cytokine transforming growth factor beta (TGF-β) was observed in IFN-α-treated animals, combined with an increase in CD4+ T cells producing TGF-β when arthritis was triggered by mBSA (day 21). Presence of IFN-α at immunizations also prevented the reduction in TGF-β production, which was induced by the intraarticular mBSA injection triggering arthritis in control animals.Conclusions: Administration of IFN-α has a profound effect on the cellular response to mBSA plus adjuvant, but does not affect antigen-specific Ig production. By including IFN-α at immunizations, spleen and lymph node cells inhibit their repertoire of antigen-induced proinflammatory cytokines while enhancing antiinflammatory TGF-β production, first in macrophages, and later also in CD4+ T cells. On intraarticular antigen challenge, this antiinflammatory state is reenforced, manifested as inhibition of proinflammatory recall responses and preservation of TGF-β levels. This may explain why IFN-α protects against antigen-induced arthritis. © 2013 Chalise et al.; licensee BioMed Central Ltd