Accumulation of low density lipoprotein associated cholesterol in calcifying vesicle fractions correlates with intimal thickening in thoracic aortas of juvenile rabbits fed a supplemental cholesterol diet

Background  

It has been shown that calcifying vesicles play an important role in aortic calcification and that cholesterol content in the isolated vesicle fraction is increased when rabbits are fed supplemental cholesterol diets. Whether lipoprotein-associated cholesterols and other lipids are also increased in the vesicle fraction and whether the increase correlates with atherosclerosis remain unknown.     

The impact of HIV-1 co-infection on long-term mortality in patients with hepatitis C: a population-based cohort study

Objective

To investigate the impact of HIV co‐infection on mortality in patients infected with hepatitis C virus (HCV).

Methods

From a nationwide Danish database of HCV‐infected patients, we identified individuals diagnosed with HCV subsequent to an HIV diagnosis. For each co‐infected patient, four control HCV patients without HIV were matched on age, gender and year of HCV diagnosis. Data on comorbidity, drug abuse, alcoholism and date of death were extracted from two healthcare databases. We constructed Kaplan–Meier curves and used Cox regression analyses to estimate mortality rate ratios (MRRs), controlling for comorbidity.

Results

We identified 483 HCV–HIV co‐infected and 1932 HCV mono‐infected patients, yielding 2192 and 9894 person‐years of observation with 129 and 271 deaths, respectively. The 5‐year probability of survival was 0.74 [95% confidence interval (CI) 0.69–0.80] for HCV–HIV co‐infected patients and 0.87 (95% CI 0.85–0.89) for HCV mono‐infected patients. Co‐infection was associated with substantially increased mortality (MRR 2.1, 95% CI 1.7–2.6). However, prior to the first observed decrease in CD4 counts to below 300 cells/μL, HIV infection did not increase mortality in HCV‐infected patients (MRR 0.9, 95% CI 0.5–1.50).

Conclusions

HIV infection has a substantial impact on mortality among HCV‐infected individuals, mainly because of HIV‐induced immunodeficiency.     

原发性脑室出血20例临床分析

1临床资料 1992-01／2004-01原发性脑室出血20（男13．女7）例,年龄27～75岁．平均63．5岁．临床表现：高血压病史12例,头痛20例,呕吐16例,意识障碍（嗜睡～深昏迷）20例（GCS评分8～12分6例、6～8分3例、6分以下11例）,血压增高者16例,瞳孔光反射消失或迟钝者14例,颈项强直者17例,体温升高者16例;脑血管造影检查：全脑室系统积血10例,部分脑室积血10例,其中四脑室积血并明显扩张6例．     

Dysfunction of endothelial and smooth muscle cells in small arteries of a mouse model of Marfan syndrome

Background and purpose:

Marfan syndrome, a connective tissue disorder caused by mutations in FBN1 encoding fibrillin-1, results in life-threatening complications in the aorta, but little is known about its effects in resistance vasculature.

Experimental approach:

Second-order mesenteric arteries from mice at 3, 6 and 10 months of age (n= 30) heterozygous for the Fbn1 allele encoding a cysteine substitution (Fbn1^C1039G/+) were compared with those from age-matched control littermates.

Key results:

Stress–strain curves indicated that arterial stiffness was increased at 6 and 10 months of age in Marfan vessels. Isometric force measurement revealed that contraction in response to potassium (60 mM)-induced membrane depolarization was decreased by at least 28% in Marfan vessels at all ages, while phenylephrine (3 µM)-induced contraction was reduced by at least 40% from 6 months. Acetylcholine-induced relaxation in Marfan vessels was reduced to 70% and 45% of control values, respectively, at 6 and 10 months. Sensitivity to sodium nitroprusside was reduced at 6 months (pEC₅₀= 5.64 ± 0.11, control pEC₅₀= 7.34 ± 0.04) and 10 months (pEC₅₀= 5.99 ± 0.07, control pEC₅₀= 6.99 ± 0.14). Pretreatment with N_ω-Nitro-L-arginine methyl ester (200 µM) had no effect on acetylcholine-induced relaxation in Marfan vessels, but reduced vasorelaxation in control vessels to 57% of control values. Addition of indomethacin (10 µM) and catalase (1000 U·mL⁻¹) further inhibited vasorelaxation in Marfan vessels to a greater degree compared with control vessels.

Conclusions and implications:

Pathogenesis of Marfan syndrome in resistance-sized arteries increases stiffness and impairs vasomotor function.     

神经干细胞移植治疗损伤脊髓的实验研究

目的 探讨异体胚胎神经干细胞(neural stem cell，NSC：)移植修复治疗损伤脊髓的疗效。方法 由胚胎SD鼠大脑海马区脑组织培养出NSC，经传代、5-溴脱氧尿嘧啶(BrdU)标记后植入按Allen法制成的SD鼠的损伤脊髓内，术后观察鼠的行为改变、斜板试验及改良运动功能Tarlov评分评价功能恢复；体感诱发电位(SEP)和磁刺激运动诱发电位(MEP)监测脊髓感觉及运动电位传递；光镜及电镜观察植入区组织结构；以示踪剂麦胚凝集素。辣根过氧化物酶(WGA-HRP)显色观察轴突的生长及功能恢复；以免疫组化方法检测神经胶质原纤维酸性蛋白(GFAP)和饱和硫蛋白(S100)阳性细胞。结果 NSC在损伤脊髓中能成活并分化为神经元及神经胶质细胞，有轴突形成，分化倾向于神经元，能迁移1cm距离。WGA—HRF，能被运输到挫伤以外区域，运动电位能传递到损伤区远端，行为学观察受试组优于对照组。结果 异体胚胎NSC能在损伤区替代受损的神经元及神经胶质细胞，形成神经轴突联系，使损伤的脊髓功能得到一定程度的恢复。