Familial aggregation of bone mineral density and bone mineral content in a Chinese population

Familial aggregation of bone mineral density (BMD) and bone mineral content (BMC) has been shown in twin and familial studies, but most sample sizes were small. We here report a large familial aggregation study in a Chinese population. A total of 13,973 siblings aged 25–64 years from 3,882 families were enrolled from Anhui, China. We assessed the whole-body, hip and lumbar spine BMD and BMC by dual-energy X-ray absorptiometry (DXA). Intra-class correlation coefficients of BMD and BMC between siblings varied among different skeletal sites and between different age groups of male sib-pairs and premenopausal and postmenopausal female sib-pairs, with a range of 0.228 to 0.397. The sibling recurrence risk ratio (s) of osteoporosis was 2.6 in our population. We also evaluated the joint association of the BMD values of the first siblings and the second siblings with the risk of low BMD (defined as less than the 10th percentile of the same group population) of their younger siblings. If both the first and second siblings BMDs were in the lowest tertile, the odd ratios (ORs) of low BMD in their subsequent siblings were 8.32 [95% confidence interval (CI) 5.59–12.39)], 8.71 (95% CI 5.74–13.22) and 5.90 (95% CI 3.57–9.76) for total body, total hip and lumbar spine, respectively. This study demonstrates a significant familial aggregation of BMD and BMC in a large sample of rural Chinese adults.     

肺硬化性血管瘤的诊断和外科治疗(附33例报告)

目的探讨肺硬化性血管瘤诊断和外科治疗.方法回顾性分析我院1987～2002年33例(34个肿瘤)肺硬化性血管瘤的临床资料.男6例,女27例.年龄24～57岁,平均41.3岁.症状以痰中带血23例;无症状10例.影像学均表现为孤立性结节,其中5例有新月征.结果术前28例诊断为肺良性肿瘤,其中5例考虑诊断为肺硬化性血管瘤;1例经皮肺穿刺确诊为肺硬化性血管瘤;4例误诊为肺癌.全组均行手术治疗,其中肺叶切除21例,双肺叶切除1例,肺段切除5例,楔形切除4例(其中1例为经胸腔镜双侧同期切除),肿瘤摘除2例.手术时间45 min～3.5 h,平均1.5 h,出血量100～600 ml,平均230 ml.无围术期死亡.33例随访3～10年,平均5.5年,无一例复发.结论对中年女性,痰中带血,影像学表现为孤立性结节,特别是有新月征者,应考虑本症.经皮肺穿刺病理学检查,可使部分患者确诊.手术治疗效果良好.     

石化企业硫化氢中毒防治措施的探讨

通过调查原油情况、生产工艺、现场监测及历年中毒事故,分析石化企业产生硫化氢中毒的基本原因,提示应根据三级预防的原则,综合防治硫化氢中毒。     

Isoflurane postconditioning prevents opening of the mitochondrial permeability transition pore through inhibition of glycogen synthase kinase 3beta

BACKGROUND: Postischemic administration of volatile anesthetics activates reperfusion injury salvage kinases and decreases myocardial damage. However, the mechanisms underlying anesthetic postconditioning are unclear. METHODS: Isolated perfused rat hearts were exposed to 40 min of ischemia followed by 1 h of reperfusion. Anesthetic postconditioning was induced by 15 min of 2.1 vol% isoflurane (1.5 minimum alveolar concentration) administered at the onset of reperfusion. In some experiments, atractyloside (10 microm), a mitochondrial permeability transition pore (mPTP) opener, and LY294002 (15 microm), a phosphatidylinositol 3-kinase inhibitor, were coadministered with isoflurane. Western blot analysis was used to determine phosphorylation of protein kinase B/Akt and its downstream target glycogen synthase kinase 3beta after 15 min of reperfusion. Myocardial tissue content of nicotinamide adenine dinucleotide served as a marker for mPTP opening. Accumulation of MitoTracker Red 580 (Molecular Probes, Invitrogen, Basel, Switzerland) was used to visualize mitochondrial function. RESULTS: Anesthetic postconditioning significantly improved functional recovery and decreased infarct size (36 +/- 1% in unprotected hearts vs. 3 +/- 2% in anesthetic postconditioning; P < 0.05). Isoflurane-mediated protection was abolished by atractyloside and LY294002. LY294002 inhibited isoflurane-induced phosphorylation of protein kinase B/Akt and glycogen synthase kinase 3beta and opened mPTP as determined by nicotinamide adenine dinucleotide measurements. Atractyloside, a direct opener of the mPTP, did not inhibit phosphorylation of protein kinase B/Akt and glycogen synthase kinase 3beta by isoflurane but reversed isoflurane-mediated cytoprotection. Microscopy showed accumulation of the mitochondrial tracker in isoflurane-protected functional mitochondria but no staining in mitochondria of unprotected hearts. CONCLUSIONS: Anesthetic postconditioning by isoflurane effectively protects against reperfusion damage by preventing opening of the mPTP through inhibition of glycogen synthase kinase 3beta.     

Opposing effects of isoflurane and sevoflurane on neurogenic pulmonary edema development in an animal model

BACKGROUND: The current study was undertaken to investigate the effects of pretreatment with isoflurane and sevoflurane on the development of neurogenic pulmonary edema in an animal model. METHODS: Rats were exposed to room air (control), 1.5% isoflurane, or 2.5% sevoflurane for 4 h. They were then anesthetized with intraperitoneal injections of pentobarbital sodium, and fibrinogen and thrombin were injected into the cisterna magna to induce neurogenic pulmonary edema. RESULTS: Consecutive injections of fibrinogen and thrombin caused increases in blood pressure, with the peak values obtained in the isoflurane and sevoflurane groups being lower than the control values. The incidence of significant neurogenic pulmonary edema was 58%, 100%, and 8% in the control, isoflurane, and sevoflurane groups, respectively. The lung water ratio, an index of severity of edema, was 4.86 +/- 0.78, 6.15 +/- 0.64, and 4.40 +/- 0.32 in the control, isoflurane, and sevoflurane groups, respectively. Furthermore, immunohistochemical staining for vascular endothelial growth factor demonstrated an increase of expression in the rat lungs exposed to isoflurane. Treatment with an anti-vascular endothelial growth factor antibody during exposure to isoflurane completely inhibited the effect of isoflurane to promote neurogenic pulmonary edema in this model. CONCLUSION: Exposure to 1.5% isoflurane enhances the development of neurogenic pulmonary edema development in this animal model, most likely via release of vascular endothelial growth factor from bronchial epithelial cells, an effect not observed with sevoflurane.     

Effects of D3.49A,R3.50A,and A6.34E mutations on ligand binding and activation of the cannabinoid-2 (CB2) receptor

In several G protein-coupled receptors (GPCRs), the Asp-Arg-Tyr (DRY) motif at the bottom of third transmembrane domain and the amino acid at position 6.34 in the sixth transmembrane domain have been shown to play important roles in signal transduction. In this study, we propose that in the cannabinoid-2 (CB2) receptor, R3.50 in the DRY motif may be crucial for interacting with G proteins, and D3.49 and A6.34 may be important for constraining the receptor in an inactive conformation. To test our hypothesis, R3.50A, D3.49A, and A6.34E mutations of the human CB2 receptor were made by site-directed mutagenesis. These mutant receptors were stably transfected into human embryonic 293 cells, and their ligand binding and signal transduction properties were analyzed. Similar to other GPCRs, R3.50 of the CB2 receptor is crucial for signal transduction. Unlike other GPCRs, D3.49 and A6.34 of the CB2 receptor do not seem to be important for keeping the receptor in an inactive state. Furthermore, D3.49A and A6.34E mutations abolished ligand binding, and all three mutations abolished constitutive activity of the wild-type CB2 receptor.