无家可归者多地点结核病传播

地点：2002-2003年，在华盛顿King县，结核病（TB）在多个收容所的人群中大规模爆发。 目的：控制结核病在多个地点的传播。设计：2002年，对收容所病人的接触者进行筛查，作结核菌素皮试（TSTs）和症状回顾。根据这些筛查的结果，确定和优选传播的地点。2003年，对暴露于这些点的队列作彻底的筛查（例如，症状回顾，TST，胸部X线检查[CXR]，痰检和痰培养）。利用PCR为基础的方法对从病人那里分离出来的结核分枝杆菌作基因分型，以快速确认爆发相关病人。 结果：2002-2003年，King县313例确诊的病人中有48例（15％）与爆发相关；通过基因分型，47例培阳病人分离出和爆发相匹配的菌株。3个收容所由于在2002年接纳的病人超过12人，所以人群中TST阳性率（约30％）高于收容所中的一般水平（7％）。用一个痰培养筛查接触者和CXR发现结核病人的敏感度相似（分别为77％和62％）。 结论：一个广泛的资源密集的途径可能有助于控制疾病的传播。这次爆发突显出无家可归者的脆弱性和在城市维持强有力的结核病规划的必要性。     

Detection of penicillin-resistant Streptococcus pneumoniae with commercially available broth microdilution panels.

We compared penicillin MICs obtained with three different commercially available broth microdilution panels (MicroScan, Sensititre, and Pasco) with MICs obtained with reference microdilution panels for 20 well-characterized pneumococci with decreased susceptibilities to penicillin (7 resistant and 13 intermediate). All panels were supplemented with 2 to 5% lysed horse blood (LHB) prepared in-house. Additional supplements included fastidious inoculum broth (FIB) for MicroScan panels and commercially prepared LHB (Difco) for Pasco panels. The percentages of penicillin-resistant strains (MIC 2 micrograms/ml) detected by the different methods follow: MicroScan-FIB, 0; MicroScan-LHB 0; Pasco in-house LHB, 71; and Sensititre-LHB, 100. The percentages of intermediate strains (MIC = 0.1 to 1.0 micrograms/ml) detected by the different methods follow: MicroScan-FIB, 31; MicroScan-LHB 23; Pasco in-house LHB, 46; and Sensititre-LHB, 85. Difco LHB supplement failed to support the growth of 86% of the strains in the Pasco panels. Of the commercially available panels evaluated, only Sensititre, supplemented with LHB prepared in-house could reliably detect penicillin-resistant pneumococci.     

A somatostatin analogue decreases embryonic loss following superovulation in rats by normalizing insulin-like growth factor-I action in the uterus

This study was designed to determine whether the somatostatin analogue, octreotide, could prevent embryonic loss by normalizing increased uterine insulin-like growth factor-I (IGF-I) action related to hyperoestrogenaemia following superovulation. Superovulated immature and oestradiol-17beta-treated adult rats were infused with 100 or 300 microg/ml of octreotide respectively, or injected daily with 1 or 10 microg of octreotide from day 1 to day 3 of pregnancy. On day 3, embryos were collected from the oviducts and uteri. Uterine luminal fluid was subjected to embryo culture. The amounts of uterine IGF-I and IGF binding proteins (IGFBP) were determined by radioimmunoassay and ligand binding assay respectively. Octreotide infusion normalized uterine IGF-I action following superovulatory and oestradiol-17beta treatment, by reducing IGF-I concentrations and increasing IGFBP concentrations. Octreotide infusion increased the number of normal embryos by 2.7-fold and 1.7-fold in superovulated and oestradiol-17beta- treated rats respectively, and reversed the detrimental effects of uterine luminal fluid on embryonic development caused by superovulatory and oestradiol-17beta treatment. Daily injections with octreotide had similar but reduced effects in all parameters examined in both treatment groups. In conclusion, octreotide may reduce embryonic loss, at least in part, by normalizing IGF-I action following superovulation.      

Effect of atropine on the bronchial response of asthmatic subjects to the inhalation of ultrasonically nebulized distilled water

To determine whether atropine provides protection against the bronchoconstriction that develops in asthmatic subjects after inhalation of ultrasonically nebulized distilled water, we exposed six asthmatic patients to this stimulus with and without pretreatment with atropine (0.04 mg/kg). The mean FEV1 decreased from 3.32 to 2.39 L (-28%) without and from 3.49 to 3.18 L (-9%) with atropine. This protective effect was statistically significant (p less than 0.05), suggesting that cholinergic pathways are involved in the obstructive response to the inhalation of ultrasonically nebulized distilled water.     

Activation of invariant NK T cells protects against experimental rheumatoid arthritis by an IL-10-dependent pathway

Invariant natural killer T (iNKT) cells are a unique lymphocyte subtype implicated in the regulation of autoimmunity and a good source of protective Th2 cytokines. Agonist alpha-galactosylceramide (alpha-GalCer) of iNKT cells exert a therapeutical effect in type 1 diabetes. We investigated whether iNKT activation with alpha-GalCer was protective in collagen-induced arthritis (CIA) in DBA/1 mice, a standard model of rheumatoid arthritis. Here, we have shown that in vivo iNKT cell function was altered in DBA/1 mice since stimulation with alpha-GalCer led to decreased IL-4 and IFN-gamma levels in sera, as compared with C57BL/6 mice. alpha-GalCer induced a clear-cut diminution of clinical and histological arthritides. An anti-IL-10 receptor antibody abrogated the protective effect of alpha-GalCer, suggesting a key role for IL-10 in the protection against CIA by activated iNKT cells. Confirming these data, disease protection conferred by alpha-GalCer correlated with the ability of LN CD4+ cells to secrete larger amounts of IL-10. These findings suggest that in CIA susceptibility to autoimmunity is associated with dysfunctions of iNKT cells. Our demonstration that iNKT cell activation by alpha-GalCer remains efficient in CIA-prone DBA/1 mice to provide protective IL-10 suggests that this could be used therapeutically to treat autoimmune arthritis.     

Experimental pneumococcal meningitis: impaired clearance of bacteria from the blood due to increased apoptosis in the spleen in Bcl-2-deficient mice

Necrotic and apoptotic neuronal cell death can be found in pneumococcal meningitis. We investigated the role of Bcl-2 as an antiapoptotic gene product in pneumococcal meningitis using Bcl-2 knockout (Bcl-2(-/-)) mice. By using a model of pneumococcal meningitis induced by intracerebral infection, Bcl-2-deficient mice and control littermates were assessed by clinical score and a tight rope test at 0, 12, 24, 32, and 36 h after infection. Then mice were sacrificed, the bacterial titers in blood, spleen, and cerebellar homogenates were determined, and the brain and spleen were evaluated histologically. The Bcl-2-deficient mice developed more severe clinical illness, and there were significant differences in the clinical score at 24, 32, and 36 h and in the tight rope test at 12 and 32 h. The bacterial titers in the blood were greater in Bcl-2-deficient mice than in the controls (7.46 +/- 1.93 log CFU/ml versus 5.16 +/- 0.96 log CFU/ml [mean +/- standard deviation]; P < 0.01). Neuronal damage was most prominent in the hippocampal formation, but there were no significant differences between groups. In situ tailing revealed only a few apoptotic neurons in the brain. In the spleen, however, there were significantly more apoptotic leukocytes in Bcl-2-deficient mice than in controls (5,148 +/- 3,406 leukocytes/mm2 versus 1,070 +/- 395 leukocytes/mm2; P < 0.005). Bcl-2 appears to counteract sepsis-induced apoptosis of splenic lymphocytes, thereby enhancing clearance of bacteria from the blood.     

Health-related quality of life following percutaneous coronary intervention during the COVID-19 pandemic

Quality of Life Research - During the COVID-19 pandemic, widespread public health measures were implemented to control community transmission. The association between these measures and...