醒脑静注射液对脑缺血再灌注小鼠记忆功能的保护作用

目的：观察醒脑静（XNJI）对脑缺血再灌注后小鼠记忆功能的保护作用。方法：采用暂时性阻断两侧颈总动脉的方法制备小鼠脑缺血再灌注损伤的模型。测试其被动回避能力，脑内抗氧化酶活性及小鼠断头喘气时间，结果：XNJI可延长脑缺血再灌注小鼠的避暗潜伏期，减少错误次数，并提高谷胱甘肽过氧化物酶（GSH-Px)的活性。延长小鼠断头喘气时间。结论：XNJI可明显减轻脑缺血再灌注导致的小鼠学习记忆功能障碍状态。其主要机制可能与抗氧化作用有关。     

Ischemic rat brain extracts induce human marrow stromal cell growth factor production

Intravenous administration of human bone marrow stromal cells (hMSCs) after middle cerebral artery occlusion (MCAo) in rats provides functional benefit. We tested the hypothesis that these functional benefits are derived in part from hMSC production of growth and trophic factors. Quantitative sandwich enzyme‐linked immunosorbent assay (ELISA) of hMSCs cultured with normal and MCAo brain extracts were performed. hMSCs cultured in supernatant derived from ischemic brain extracts increased production of brain‐derived neurotrophic factor (BDNF), nerve growth factor (NGF), vascular endothelial growth factor (VEGF) and hepatocyte growth factor (HGF). These neurotrophins and angiogenic growth factors increased in a post‐ischemia time‐dependent manner. The hMSC capacity to increase expression of growth and trophic factors may be the key to the benefit provided by transplanted hMSCs in the ischemic brain.     

住院脑血管病人主要照顾者负荷

目的 探讨影响住院脑血管病人主要照顾负荷的相关因素。方法采用问卷方式对1997年～2000年60名符合研究对象进行调查。结果脑血管病人的主要照顾中60％为配偶，且年龄较大，知识水平偏低，使其身体、心理、社交方面的负荷增大。同时发现雇用身体及心理压力明显低于家属，但两社交负荷无差异。结论临床护理人员应给予住院病人主要照顾一定的协助及指导，减轻家属的压力，使主要照顾能有效地承担起照顾责任。     

牛磺酸对大鼠缺血心肌Bcl-2和Bax蛋白表达的影响

目的：探讨大鼠心肌缺血损伤与凋亡相关基因bcl-2和bax表达的关系及牛磺酸的影响。方法：结扎大鼠冠状动脉左前降支建立心肌缺血模型。检测心肌线粒体中超氧化物歧化酶（SOD）、Ca^2 -ATPase活性及MDA（丙二醛）含量，用免疫组化法检测Bcl-2和Bax蛋白在心肌中的表达量。结果：结扎冠脉左前降支可致心肌线粒体MDA含量升高，SOD和Ca^2 －ATPase活性下降；缺血心肌Bax蛋白表达呈显著升高；牛磺酸能明显减少缺血心肌线粒体MDA的生成，降低心肌Bax蛋白的表达，增加Bcl-2蛋白的表达。结论：结扎大鼠冠状动脉左前降支导致的心肌缺血损伤与Bcl-2和Bax蛋白的表达有关。     

抑肽酶预处理防护大鼠肝脏缺血再灌注损伤的实验研究

目的 探讨抑肽酶预处理对肝脏缺血再灌注损伤的防护作用。方法 SD大鼠80只，随机分为抑肽酶预处理和生理盐水预处理两组，观察肝脏缺血再灌注损伤引起及抑肽酶预处理的影响。结果 拟肽酶预处理组大鼠缺血再灌注损伤引起的血清谷丙转氨酶（ALT），谷草转氨酶（AST）活性及肝组织丙二醛（MDA）含量变化均显著低于生理盐水预处理组（P＜0．01）；肝细胞形态学异常改变也明显较生理盐水预处理组轻。结论 抑肽酶预处理对大鼠肝脏缺血再灌注损伤有明显的防治作用。     

高温、亚低温对大鼠脑缺血再灌注损伤的作用及其机制研究

目的：研究轻度高温、亚低温对大鼠脑缺血再灌注损伤组织兴奋性氨基酸（EAA）与氧自由基的相互关系及病理损伤程度的影响。方法：60只Wistar大鼠按不同脑温条件随机分为生化组（n=28）和病理组（n=32)，采用改良Nagasawa局灶脑缺血再灌注模型，观察脑缺血再灌注损伤组织谷氨酸（Glu），超氧化物歧化酶（SOD）、丙二醛（MDA）的变化及光镜，电镜下的病理变化。结果：轻度高温明显加重常温脑缺血再灌注损伤组织Glu、MDA的升高（P＜0．01）及SOD的下降（P＜0．05），加重常温脑缺血再灌注组织病理损伤程度，亚低温的作用则相反，结论：轻度高温可能通过同时促进EAA合成，释放和氧自由基生成系统活化，造成大鼠脑缺血再灌注损组织损伤加重；亚低温可能通过同时抑制EAA合成，释放和氧自由基生成系统活化，减轻大鼠脑缺血再灌注组织损伤程度，对大鼠脑缺血再灌注损伤组织起保护作用。     

Is neighbourhood deprivation a risk factor for gestational diabetes mellitus?

AIMS: To assess the relationship between neighbourhood deprivation and the rate of gestational diabetes mellitus (GDM) using routinely collected data from a clinical information system, in Plymouth, UK. METHODS: Between 1 January 1996 and 31 December 1997, 3933 women residing within the Plymouth Primary Care Trust (PCT) were screened for GDM using indices of neighbourhood deprivation and prevalence of GDM. Areas (n = 43) were classified according to the Townsend index, measuring material deprivation. Pregnant women with and without GDM were compared. RESULTS: The prevalence of GDM was 1.7%[95%, confidence interval (CI) 1.20, 2.11]. The prevalence of GDM ranged from 1.05% (95% CI 0.60, 1.70) in the most deprived to 2.10% (95%, CI 1.34, 3.13), in the least deprived neighbourhood. Crude rates decreased by 50%[relative prevalence (RP) (95% CI) 0.50 (0.27, 0.94); P = 0.06] amongst those living in the most-deprived compared with those living in the least-deprived areas. Using a stepwise binary logistic regression model, older age at delivery significantly increased the risk of developing GDM. [RP (95%, CI) 1.09, (1.04, 1.13)]. Townsend deprivation score had no significant independent association with GDM when other covariates were considered. CONCLUSION: These data suggest that the neighbourhood context in which women live has no impact on the risk of GDM. Diabet.     

Prevalence of diabetic peripheral neuropathy and relation to glycemic control therapies at baseline in the BARI 2D cohort

Abstract   We evaluated the associations between glycemic therapies and prevalence of diabetic peripheral neuropathy (DPN) at baseline among participants in the Bypass Angioplasty Revascularization Investigation 2 Diabetes (BARI 2D) trial on medical and revascularization therapies for coronary artery disease (CAD) and on insulin-sensitizing vs. insulin-providing treatments for diabetes. A total of 2,368 patients with type 2 diabetes and CAD was evaluated. DPN was defined as clinical examination score >2 using the Michigan Neuropathy Screening Instrument (MNSI). DPN odds ratios across different groups of glycemic therapy were evaluated by multiple logistic regression adjusted for multiple covariates including age, sex, hemoglobin A1c (HbA1c), and diabetes duration. Fifty-one percent of BARI 2D subjects with valid baseline characteristics and MNSI scores had DPN. After adjusting for all variables, use of insulin was significantly associated with DPN (OR = 1.57, 95% CI: 1.15–2.13). Patients on sulfonylurea (SU) or combination of SU/metformin (Met)/thiazolidinediones (TZD) had marginally higher rates of DPN than the Met/TZD group. This cross-sectional study in a cohort of patients with type 2 diabetes and CAD showed association of insulin use with higher DPN prevalence, independent of disease duration, glycemic control, and other characteristics. The causality between a glycemic control strategy and DPN cannot be evaluated in this cross-sectional study, but continued assessment of DPN and randomized therapies in BARI 2D trial may provide further explanations on the development of DPN.     

Prior diabetes mellitus is associated with increased morbidity in cystic fibrosis patients undergoing bilateral lung transplantation: an ‘orphan’ area? A retrospective case–control study

Background: The aim of this study was to determine whether pre-existing diabetes mellitus increases the risk of rejection, infection and/or death in cystic fibrosis patients undergoing bilateral sequential single-lung transplantation.
Methods: A retrospective audit of 25 consecutive patients with cystic fibrosis who underwent bilateral sequential single-lung transplantation between 1 January 2003 and 31 December 2005 at a tertiary referral hospital was carried out.
Results: Although 32% patients had diabetes diagnosed before lung transplantation, 92% had random blood glucose levels ≥11.1 mmol/L requiring insulin during admission. Patients with pre-existing diabetes had increased infection-related (3.9 vs 1.2, P = 0.01) and putative rejection-related (1.4 vs 0.5, P = 0.04) hospital admissions post-transplantation compared with those without diabetes pre-transplant. During the period of observation, four of eight patients with a prior diagnosis of diabetes died compared with none of 17 patients without prior diabetes ( P = 0.0055).
Conclusion: Almost all cystic fibrosis patients develop hyperglycaemia after lung transplantation, but patients with prior diabetes have more complication-related admissions to hospital and a higher mortality rate.     

Ischemia independent lesion evolution during focal stroke in rats

Lesion evolution during focal cerebral ischemia may depend on flow restrictions or on accumulation of toxic mediators within the infarct and expansion of these factors to the periinfarct region. So far, the precise contribution of flow dependent versus spreading-mediated impairment of viable periinfarct tissue has not been determined. Therefore, we measured lesion expansion, flow restrictions and glutamate distribution on serial brain sections at different time points after experimental focal ischemia.Permanent focal ischemia was induced by occlusion of the right middle cerebral artery in male rats and the flow reduction was subsequently measured at 1, 12 and 24 h using iodo[¹⁴C]antipyrine autoradiography. Additionally, the necrotic volume was determined on serial brain sections and the glutamate content was measured in tissue samples from adjacent microdissections.Twelve hours after focal ischemia no noteworthy viable areas with blood flow restrictions of 20-40 ml 100 g^− 1 min^− 1 existed but at 24 h the necrotic tissue exceeded the hemodynamically compromised region by 40 ± 21 mm³ (24%). Furthermore, at 12 and 24 h the glutamate content was elevated in areas surrounding the infarct.Relevant flow restrictions are detectable only during early stages of infarct maturation, whereas the propagation of secondary factors may be the predominant mechanism for delayed infarct evolution.