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排序方式: 共有2596条查询结果,搜索用时 15 毫秒
81.
Samantha S.Y. Lee David A. Mackey Gareth Lingham Julie M. Crewe Michael D. Richards Fred K. Chen Jason Charng Fletcher Ng Ian Flitcroft James J. Loughman Augusto Azuara‐Blanco Nicola S. Logan Christopher J. Hammond Audrey Chia Tan Tai Truong Antony Clark 《Clinical & experimental ophthalmology》2020,48(5):569-579
82.
Phan TG Amesbury M Gardam S Crosbie J Hasbold J Hodgkin PD Basten A Brink R 《The Journal of experimental medicine》2003,197(7):845-860
In both humans and animals, immunoglobulin (Ig)G autoantibodies are less frequent but more pathogenic than IgM autoantibodies, suggesting that controls over Ig isotype switching are required to reinforce B cell self-tolerance. We have used gene targeting to produce mice in which hen egg lysozyme (HEL)-specific B cells can switch to all Ig isotypes (SWHEL mice). When crossed with soluble HEL transgenic (Tg) mice, self-reactive SWHEL B cells became anergic. However, in contrast to anergic B cells from the original nonswitching anti-HEL x soluble HEL double Tg model, self-reactive SWHEL B cells also displayed an immature phenotype, reduced lifespan, and exclusion from the splenic follicle. These differences were not related to their ability to Ig class switch, but instead to competition with non-HEL-binding B cells generated by VH gene replacement in SWHEL mice. When activated in vitro with B cell receptor (BCR)-independent stimuli such as anti-CD40 monoclonal antibody plus interleukin 4 or lipopolysaccharide (LPS), anergic SWHEL double Tg B cells proliferated and produced IgG anti-HEL antibodies as efficiently as naive HEL-binding B cells from SWHEL Ig Tg mice. These results demonstrate that no intrinsic constraints to isotype switching exist in anergic self-reactive B cells. Instead, production of IgG autoantibodies is prevented by separate controls that reduce the likelihood of anergic B cells encountering BCR-independent stimuli. That bacteria-derived LPS could circumvent these controls may explain the well-known association between autoantibody-mediated diseases and episodes of systemic infection. 相似文献
83.
Antony George Attokaran FRACP FCICM Mahesh Ramanan MMed FCICM Lisa Hunt MBBS Kavita Chandra MBBS Rajbir Sandha FACEM Stacey Watts RN BN GC Balasubramanian Venkatesh MD FCICM FAHMS 《Emergency medicine Australasia : EMA》2023,35(4):657-663
Objective
To test the hypothesis that fluid resuscitation in the ED with plasmalyte-148 (PL) compared with 0.9% sodium chloride (SC) would result in a lower proportion of patients with diabetic ketoacidosis (DKA) requiring intensive care unit (ICU) admission.Methods
We performed a prespecified nested cohort study at two hospitals within a cluster, crossover, open label, randomised, controlled trial comparing the effects of PL versus SC as fluid therapy for patients who presented to the ED with DKA. All patients presenting within a fixed recruitment period were included. The primary outcome was the proportion of patients admitted to ICU.Results
Eighty-four patients were enrolled (SC n = 38, PL n = 46). The SC group had a lower median pH on admission (SC: 7.09 [interquartile range (IQR) 7.01–7.21], PL: 7.17 [IQR 6.99–7.26]). The median volume of intravenous fluids administered in ED was 2150 mL (IQR 2000–3200 mL; SC) and 2200 mL (IQR 2000–3450; PL); respectively. A higher proportion of patients in the SC group, 19 (50%), was admitted to ICU compared with PL group, 18 (39.1%); however, after adjustment for pH at presentation and diabetes type in a multivariable logistic regression model, the PL group did not have a significantly different rate of ICU admission compared with the SC group (odds ratio for ICU admission 0.73, 95% confidence interval 0.13–3.97, P = 0.71).Conclusion
Patients with DKA treated with PL compared with SC in the EDs had similar rates of requiring ICU admission. 相似文献84.
Ambrish Singh Salman Hussain Benny Antony 《Diabetes & Metabolic Syndrome: Clinical Research & Reviews》2021,15(3):813-822
BackgroundNon-alcoholic fatty liver disease (NAFLD) patients represent a vulnerable population that may be susceptible to more severe COVID-19. Moreover, not only the underlying NAFLD may influence the progression of COVID-19, but the COVID-19 may affect the clinical course of NAFLD as well. However, comprehensive evidence on clinical outcomes in patients with NAFLD is not well characterized.ObjectivesTo systematically review and meta-analysis the evidence on clinical outcomes in NAFLD patients with COVID-19.MethodsMEDLINE, EMBASE, and Cochrane Central were searched from inception through November 2020. Epidemiological studies assessing the clinical outcomes in COVID-19 patients with NAFLD were included. Newcastle-Ottawa Scale (NOS) was used to assess study quality. Generic inverse variance method using RevMan was used to determine the pooled estimates using the random-effects model.ResultsFourteen studies consisting of 1851 NAFLD patients, were included. Significant heterogeneity was observed among the studies, and studies were of moderate to high quality [mean, (range):8 (6, 8)]. For NAFLD patients, the adjusted odds ratio (aOR) for the severe COVID-19 was 2.60 (95%CI:2.24–3.02; p < 0.001) (studies,n:8), aOR for admission to ICU due to COVID-19 was 1.66 (95%CI:1.26–2.20; p < 0.001) (studies,n:2), and aOR for mortality for was 1.01 (95%CI:0.65–1.58; p = 0.96) (studies,n:2).ConclusionsAn increased risk of severe COVID-19 infection and admission to ICU due to COVID-19 with no difference in mortality was observed between NAFLD and non-NAFLD patients. Future studies should include the mortality outcome to conclusively elucidate the impact of NAFLD in patients with COVID-19. 相似文献
85.
Pathogenesis of pleural infection 总被引:2,自引:0,他引:2
The pleura responds to the presence of infecting organisms with a vigorous inflammatory response associated with an exudation of white blood cells and proteins. The development and outcome of pleural infections is a function of a balance between the virulence of the invading microorganism and the immune reaction involving professional immune cells as well as the pleural mesothelial cells. Most commonly, pleural infection occurs after invasion through the lung parenchyma and a breach in the viscera pleura resulting in the formation of a parapneumonic process. Upon infection, the microorganisms are recognized by the pleural mesothelial cell, which remains the first line of defence. Pleural responses to infection include those of innate immunity as well as adaptive or acquired immunity. Innate and acquired immune responses are closely linked. In this review, we discuss the different virulence factors that allow microorganisms to infect the pleura and the role of the pleural mesothelial cells in bridging the innate and acquired immune responses. 相似文献
86.
No association between apolipoprotein E or N‐Acetyltransferase 2 gene polymorphisms and age‐related hearing loss
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87.
S. Matthijs Boekholdt G. Kees Hovingh Samia Mora Benoit J. Arsenault Pierre Amarenco Terje R. Pedersen John C. LaRosa David D. Waters David A. DeMicco R. John Simes Antony C. Keech David Colquhoun Graham A. Hitman D. John Betteridge Michael B. Clearfield John R. Downs Helen M. Colhoun Antonio M. Gotto Jr. Paul M. Ridker Scott M. Grundy John J.P. Kastelein 《Journal of the American College of Cardiology》2014
Background
Levels of atherogenic lipoproteins achieved with statin therapy are highly variable, but the consequence of this variability for cardiovascular disease risk is not well-documented.Objectives
The aim of this meta-analysis was to evaluate: 1) the interindividual variability of reductions in low-density lipoprotein cholesterol (LDL-C), non–high-density lipoprotein cholesterol (non-HDL-C), or apolipoprotein B (apoB) levels achieved with statin therapy; 2) the proportion of patients not reaching guideline-recommended lipid levels on high-dose statin therapy; and 3) the association between very low levels of atherogenic lipoproteins achieved with statin therapy and cardiovascular disease risk.Methods
This meta-analysis used individual patient data from 8 randomized controlled statin trials, in which conventional lipids and apolipoproteins were determined in all study participants at baseline and at 1-year follow-up.Results
Among 38,153 patients allocated to statin therapy, a total of 6,286 major cardiovascular events occurred in 5,387 study participants during follow-up. There was large interindividual variability in the reductions of LDL-C, non-HDL-C, and apoB achieved with a fixed statin dose. More than 40% of trial participants assigned to high-dose statin therapy did not reach an LDL-C target <70 mg/dl. Compared with patients who achieved an LDL-C >175 mg/dl, those who reached an LDL-C 75 to <100 mg/dl, 50 to <75 mg/dl, and <50 mg/dl had adjusted hazard ratios for major cardiovascular events of 0.56 (95% confidence interval [CI]: 0.46 to 0.67), 0.51 (95% CI: 0.42 to 0.62), and 0.44 (95% CI: 0.35 to 0.55), respectively. Similar associations were observed for non-HDL-C and apoB.Conclusions
The reductions of LDL-C, non-HDL-C, and apoB levels achieved with statin therapy displayed large interindividual variation. Among trial participants treated with high-dose statin therapy, >40% did not reach an LDL-C target <70 mg/dl. Patients who achieve very low LDL-C levels have a lower risk for major cardiovascular events than do those achieving moderately low levels. 相似文献88.
Hannah X Chu Hyun Ah Kim Seyoung Lee Jeffrey P Moore Christopher T Chan Antony Vinh Mathias Gelderblom Thiruma V Arumugam Brad RS Broughton Grant R Drummond Christopher G Sobey 《Journal of cerebral blood flow and metabolism》2014,34(3):450-459
We tested whether significant leukocyte infiltration occurs in a mouse model of permanent cerebral ischemia. C57BL6/J male mice underwent either permanent (3 or 24 hours) or transient (1 or 2 hours+22- to 23-hour reperfusion) middle cerebral artery occlusion (MCAO). Using flow cytometry, we observed ∼15,000 leukocytes (CD45+high cells) in the ischemic hemisphere as early as 3 hours after permanent MCAO (pMCAO), comprising ∼40% lymphoid cells and ∼60% myeloid cells. Neutrophils were the predominant cell type entering the brain, and were increased to ∼5,000 as early as 3 hours after pMCAO. Several cell types (monocytes, macrophages, B lymphocytes, CD8+ T lymphocytes, and natural killer cells) were also increased at 3 hours to levels sustained for 24 hours, whereas others (CD4+ T cells, natural killer T cells, and dendritic cells) were unchanged at 3 hours, but were increased by 24 hours after pMCAO. Immunohistochemical analysis revealed that leukocytes typically had entered and widely dispersed throughout the parenchyma of the infarct within 3 hours. Moreover, compared with pMCAO, there were ∼50% fewer infiltrating leukocytes at 24 hours after transient MCAO (tMCAO), independent of infarct size. Microglial cell numbers were bilaterally increased in both models. These findings indicate that a profound infiltration of inflammatory cells occurs in the brain early after focal ischemia, especially without reperfusion. 相似文献
89.
90.