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排序方式: 共有1587条查询结果,搜索用时 15 毫秒
1.
Sina Dami 《World Journal of Clinical Cases》2022,10(26):9207-9218
The coronavirus disease 2019 (COVID-19) has currently caused the mortality of millions of people around the world. Aside from the direct mortality from the COVID-19, the indirect effects of the pandemic have also led to an increase in the mortality rate of other non-COVID patients. Evidence indicates that novel COVID-19 pandemic has caused an inflation in acute cardiovascular mortality, which did not relate to COVID-19 infection. It has in fact increased the risk of death in cardiovascular disease (CVD) patients. For this purpose, it is dramatically inevitable to monitor CVD patients’ vital signs and to detect abnormal events before the occurrence of any critical conditions resulted in death. Internet of things (IoT) and health monitoring sensors have improved the medical care systems by enabling latency-sensitive surveillance and computing of large amounts of patients’ data. The major challenge being faced currently in this problem is its limited scalability and late detection of cardiovascular events in IoT-based computing environments. To this end, this paper proposes a novel framework to early detection of cardiovascular events based on a deep learning architecture in IoT environments. Experimental results showed that the proposed method was able to detect cardiovascular events with better performance (95.30% average sensitivity and 95.94% mean prediction values). 相似文献
2.
Sina Alexander Debbie M Nathan Melvyn G Korman 《Clinical gastroenterology and hepatology》2006,4(5):661; author reply 661-661; author reply 662
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C. Wood B. Sina C. G. Webster D. Kurgansky C. B. Drachenberg E. A. Reedy 《Journal of cutaneous pathology》1992,19(2):128-133
A 57-year-old woman with cutaneous mastocytosis of 23 years duration developed a hyperpigmented abdominal plaque composed of confluent indurated papules that enlarged for a period of 1 year to 12 x 8 cm. Biopsy showed dermal infiltration by closely packed spindle-shaped mast cells, fibroblasts, collagen, and scattered lymphocytes, predominantly T-suppressor cells. Electron microscopy showed close contact between mast cells, fibroblasts, and lymphocytes. Piecemeal mast cell degranulation and extrusion of mast cell granules was seen, with rare mast cell granules in fibroblasts, and collagen fibers in peripheral and perinuclear endoplasmic reticulum of mast cells. the term Fibrous mastocytoma is suggested for this tumor-like dermal fibrosis, possibly induced by lymphokines. 相似文献
7.
Protection against bacterial superantigen staphylococcal enterotoxin B by passive vaccination 总被引:3,自引:0,他引:3
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We investigated the ability of two overlapping fragments of staphylococcal enterotoxin B (SEB), which encompass the whole toxin, to induce protection and also examined if passive transfer of chicken anti-SEB antibodies raised against the holotoxin could protect rhesus monkeys against aerosolized SEB. Although both fragments of SEB were highly immunogenic, the fragments failed to protect mice whether they were injected separately or injected together. Passive transfer of antibody generated in chickens (immunoglobulin Y [IgY]) against the whole toxin suppressed cytokine responses and was protective in mice. All rhesus monkeys treated with the IgY specific for SEB up to 4 h after challenge survived lethal SEB aerosol exposure. These findings suggest that large fragments of SEB may not be ideal for productive vaccination, but passive transfer of SEB-specific antibodies protects nonhuman primates against lethal aerosol challenge. Thus, antibodies raised in chickens against the holotoxin may have potential therapeutic value within a therapeutic window of opportunity after SEB encounter. 相似文献
8.
Roy CJ Warfield KL Welcher BC Gonzales RF Larsen T Hanson J David CS Krakauer T Bavari S 《Infection and immunity》2005,73(4):2452-2460
Staphylococcal enterotoxins (SEs) belong to a large group of bacterial exotoxins that cause severe immunopathologies, especially when delivered as an aerosol. SEs elicit the release of lethal amounts of cytokines by binding to major histocompatibility complex (MHC) class II and cross-linking susceptible T-cell receptors. Efforts to develop effective therapeutic strategies to protect against SEs delivered as an aerosol have been hampered by the lack of small animal models that consistently emulate human responses to these toxins. Here, we report that human leukocyte antigen-DQ8 (HLA-DQ8) transgenic (Tg) mice, but not littermate controls, succumbed to lethal shock induced by SEB aerosols without potentiation. Substantial amounts of perivascular edema and inflammatory infiltrates were noted in the lungs of Tg mice, similar to the pathology observed in nonhuman primates exposed by aerosol to SEB. Furthermore, the observed pathologies and lethal shock correlated with an upsurge in proinflammatory cytokine mRNA gene expression in the lungs and spleens, as well as with marked increases in the levels of proinflammatory circulating cytokines in the Tg mice. Unlike the case for littermate controls, telemetric evaluation showed significant hypothermia in Tg mice exposed to lethal doses of SEB. Taken together, these results show that this murine model will allow for the examination of therapeutics and vaccines developed specifically against SEB aerosol exposure and possibly other bacterial superantigens in the context of human MHC class II receptors. 相似文献
9.
Analysis of cell type-specific responses mediated by the type IV secretion system of Helicobacter pylori
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Helicobacter pylori persistently infects the human stomach and can cause gastritis, gastric ulceration, and gastric cancer. The type IV secretion system (TFSS) of virulent H. pylori strains translocates the CagA protein, inducing the dephosphorylation of host cell proteins and leading to changes in the morphology or shape of AGS gastric epithelial cells. Furthermore, the TFSS is involved in the induction of proinflammatory cytokines. While the H. pylori genes required for TFSS function have been investigated systematically, little is known about possible host cell factors involved. We infected 19 different mammalian cell lines individually with H. pylori and analyzed CagA translocation, dephosphorylation of host cell proteins, chemokine secretion (interleukin-8 and macrophage inflammatory protein 2), and changes in cellular phenotypes. Our results demonstrate that not only bacterial but also host cell factors determine the cellular response to infection. The identification of such unknown host cell factors will add to our understanding of host-pathogen interactions and might help in the development of new therapeutic strategies. 相似文献
10.
Reddy MV Storer RD Laws GM Armstrong MJ Barnum JE Gara JP McKnight CG Skopek TR Sina JF DeLuca JG Galloway SM 《Environmental and molecular mutagenesis》2002,40(1):1-17
3-Methylindole (3MI), melatonin (Mel), serotonin (Ser), and tryptamine (Tryp) were evaluated in vitro for their potential to induce DNA adducts, DNA strand breaks, chromosomal aberrations (Abs), inhibition of DNA synthesis, and mutations. All compounds produced DNA adducts in calf thymus DNA in the presence of rat liver S9. In cultured rat hepatocytes, all produced DNA adducts but none induced DNA strand breaks. In Chinese hamster ovary cells, 3MI and Mel produced DNA adducts, Abs, and inhibition of DNA synthesis with and without S9, except that Mel without S9 did not form adducts. Ser formed DNA adducts, was an equivocal Abs inducer, and suppressed DNA synthesis. Tryp induced neither adducts nor Abs, but did suppress DNA synthesis with S9. Ser and Tryp were less cytotoxic than 3MI and Mel. Mel, Ser, and Tryp failed to induce mutations in Salmonella and E. coli strains with or without S9. 3MI and Mel produced DNA adducts but not mutations in Salmonella TA100 with S9. 3MI and its metabolite indole 3-carbinol also did not induce mutations in a shuttle vector system in human cells. The lack of correlation between DNA adducts and other genotoxicity endpoints for these indole compounds may be due to the higher sensitivity of the (32)P-postlabeling adduct assay or it may indicate that the indole-DNA adducts per se are not mutagenic and are not able to induce strand breaks or alkali-labile lesions. The indole-induced Abs may result from cytotoxicity and suppression of DNA synthesis with minimal if any contribution from DNA adducts. 相似文献