几种常用线粒体基因在多房棘球绦虫虫种鉴定中的应用现状及进展

cox1、nad1等线粒体基因用于多房棘球绦虫虫种鉴定,克服了传统方法耗时、费力的缺点,并能保持较高灵敏性和特异性,还可承受大批量虫种鉴定工作,目前在多房棘球绦虫终宿主及中间宿主的感染筛查中应用广泛,本文通过介绍几种常用线粒体基因的结构特点、进化速度、相关研究结果,阐述研究现状及进展,探讨目前存在的主要问题。     

内蒙古兴安盟地区布鲁氏菌流行株种型鉴定和体外药物敏感性分析

目的 了解内蒙古兴安盟布鲁氏菌流行株的主要种型,分析布鲁氏菌流行株的体外药物敏感性,指导临床治疗。方法 选择内蒙古兴安盟布病发病率较高的旗县和人口密集的旗县,采集临床诊断的布病患者200份血液样本,用全自动血液培养仪培养分离出28株布鲁氏菌,用全自动生化鉴定系统、BCSP31-PCR及传统经典的方法进行种型鉴定,最后用肉汤微量稀释法对其中的25株布鲁氏菌进行13种抗生素的体外药敏试验。结果 28株布鲁氏菌中羊种3型18株(64.29%)和羊种1型10株(35.71%),进行药敏试验的25株菌中,100%菌株对多西环素、庆大霉素、链霉素、四环素均敏感,16%的菌株对利福平、头孢曲松的药物敏感性可能降低,20%的菌株对复方新诺明耐药,100%的菌株对阿奇霉素耐药。结论 内蒙古兴安盟布鲁氏菌流行株主要是羊种3型和羊种1型,目前对一线方案药物较为敏感,在布病的急性期治疗上,宜规范化治疗,首选一线方案药物:多西环素、庆大霉素、链霉素、利福平。     

Interleukin-33 facilitates neutrophil recruitment and bacterial clearance in S. aureus-caused peritonitis

Interleukin (IL)-33, a newly recognized member of IL-1 family of cytokines, plays an important role in polarizing Th2-associated immunity. Recently growing evidence indicates that IL-33 also represents a crucial mediator of antimicrobial infection. In this study, we investigated the effect of IL-33 on antibacterial response using an acute Staphylococcus aureus peritoneal infection model. Our results showed that IL-33 administration induced a rapid bacterial clearance and markedly reduced the S. aureus infection-related mortality. IL-33-treated mice displayed increased neutrophil influx into the focus of infection and higher concentrations of chemokine CXCL2 in the peritoneum than untreated mice. The beneficial effect of IL-33 priming was related to reversal of the S. aureus-induced reduction of CXCR2 expression on the surface of neutrophils. Furthermore, conditioning of neutrophils by IL-33 led to the enhancement of complement receptor 3 expression induced by S. aureus, which in turn facilitates the phagocytosis of opsonized S. aureus. Finally, neutrophils primed by IL-33 upregulated the production of reactive oxygen species and the subsequent killing activity for S. aureus. All together, these findings suggest that IL-33, through regulating multiple steps of neutrophil-mediated bactericidal function, provides a profound effect in host antimicrobial defense response.     

Necrotic cell death induced by delta-aminolevulinic acid in mouse astrocytes. Protective role of melatonin and other antioxidants

Accumulation of delta-aminolevulinic acid (ALA), as it occurs in acute intermittent porphyria (AIP), is the origin of an endogenous source of reactive oxygen species (ROS), which can exert oxidative damage to cell structures. In the present work we examined the ability of different antioxidants to revert ALA-promoted damage, by incubating mouse astrocytes with 1.0 mM ALA for different times (1-4 hr) in the presence of melatonin (2.5 mM), superoxide dismutase (25 units/mL), catalase (200 units/mL) or glutathione (0.5 mM). The defined relative index [(malondialdehyde levels/accumulated ALA) x 100], decreases with incubation time, reaching values of 76% for melatonin and showing that the different antioxidants tested can protect astrocytes against ALA-promoted lipid peroxidation. Concerning porphyrin biosynthesis, no effect was observed with catalase and superoxide dismutase whereas increases of 57 and 87% were obtained with glutathione and melatonin, respectively, indicating that these antioxidants may prevent the oxidation of porphobilinogen deaminase, reactivating so that the AIP genetically reduced enzyme. Here we showed that ALA induces cell death displaying a pattern of necrosis. This pattern was revealed by loss of cell membrane integrity, marked nuclear swelling and double labeling with annexin V and propidium iodide. In addition, no caspase 3-like activity was detected. These findings provide the first experimental evidence of the involvement of ALA-promoted ROS in the damage of proteins related to porphyrin biosynthesis and the induction of necrotic cell death in astrocytes. Interestingly, melatonin decreases the number of enlarged nuclei and shows a protective effect on cellular morphology.     

hace1 Influences zebrafish cardiac development via ROS‐dependent mechanisms

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Ionoregulatory and oxidative stress issues associated with the evolution of air-breathing

Aquatic areas frequently face hypoxic conditions. In order to get sufficient oxygen to support aerobic metabolism, a number of freshwater fish resort to aerial respiration to supplement gill respiration especially in situations with reduced oxygen availability in the water. In many species a concomitant reduction in gill surface area or in gill perfusion reduces possible loss of aerially acquired oxygen to the water at the gills, but it also compromises the ion regulatory capacity of gill tissue. In consequence, the reduced gill contact area with water requires appropriate compensation to maintain ion and acid-base homeostasis, often with important ramifications for other organs. Associated modifications in the structure and function of the gills themselves, the skin, the gut, the kidney, and the physiology of water exchange and ion-linked acid-base regulation are discussed. In air-breathing fish, the gut may gain particular importance for the uptake of ions. In addition, tissues frequently exposed to environmental air encounter much higher oxygen partial pressures than typically observed in fish tissues. Physostomous fish using the swimbladder for aerial respiration, for example, will encounter aerial oxygen partial pressure at the swimbladder epithelium when frequently gulping air in hypoxic water. Hyperoxic conditions or rapid changes in oxygen partial pressures result in an increase in the production of reactive oxygen species (ROS). Accordingly, in air-breathing fish, strategies of ionoregulation may be greatly modified, and the ROS defense capacity of air-exposed tissues is improved.     

Serodiagnosis of tuberculosis and leprosy by enzyme immunoassay

Objective: To evaluate the use of serodiagnosis for tuberculosis and leprosy using mycobacterial antigen 38 kDa, with kits from Omega laboratories, to detect IgG by enzyme immunoassay (EIA).
Method: The study population consisted of 58 patients with evidence of tuberculous infection (culture of Mycobacterium tuberculosis complex or microscopic evidence), of whom 23 had pulmonary and 35 had extrapulmonary disease. There were six subjects who had recently been treated for tuberculosis, 11 patients on treatment for leprosy and 137 patients suspected of having tuberculosis on clinical or radiologic grounds (without laboratory evidence). A control group comprised 35 healthy individuals or patients suffering from diseases other than tuberculosis.
Results: The tests showed that there was a significant difference in antibody levels between the patients with active pulmonary disease, extrapulmonary tuberculosis and leprosy in comparison with the control group ( p <0.001). The sensitivities of the two tests together for proven pulmonary tuberculosis were 100% and 95.7% at 1.0–1.5 and >1.6 EIA cut-off points respectively, while the specificities were 88.5% and 100% at the same cut-off points. The sensitivities for extrapulmonary tuberculosis were 71.4% and only 51.4% at 1.0–1.5 and >1.6 EIA cut-off points. The test was positive in 30 (21.9%) of the 137 suspected patients, while 43 (31.4%) had an equivocal result and the remaining 64 (47.7%) suspects were definitely negative. There was again a significant difference in positivity rates between suspects and the control group.
Conclusions: Omega IgG test is useful in the serodiagnosis of active pulmonary tuberculosis and leprosy, but less sensitive in extrapulmonary disease, particularly in children. Equivocal results may only add to the evidence of tuberculosis in early or minimal disease.     

铁死亡在肝脏疾病中的作用与机制研究进展

[摘要]?铁死亡是近年发现的一种非凋亡形式的程序性细胞死亡方式,其中心环节是铁代谢紊乱导致的胞内脂质过氧化与氧化应激失调。机体内部铁转运系统以及组织细胞的抗氧化系统抑制了铁死亡并维持了生理状态的铁稳态。目前,在多种肝脏疾病中均发现了以脂质过氧化物和活性氧的堆积为特征的铁死亡现象,而铁死亡抑制剂可以有效地抑制铁死亡所致的肝脏损伤。因此,调控铁死亡的发生、发展成为一种新的肝脏疾病潜在治疗策略。本文综述了铁死亡的发生机制以及各种肝脏疾病中铁死亡的研究进展,为探索肝脏疾病的新型治疗方法提供理论基础。