Presynaptic opioid kappa-receptor and regulation of the release of Met-enkephalin in the rat brainstem

Opioid kappa-agonists had much more potent inhibitory effects on the high K+-evoked Met-enkephalin release from rat brain slices than did the mu- or delta-agonists. The opioid kappa- antagonist, MR2266 enhanced the evoked release of Met-enkephalin to a greater extent than did mu- or delta-antagonists in vitro and had a potent analgesia in mice in vivo. These findings suggest that the release of Met-enkephalin may be regulated in vitro and in vivo, mainly by presynaptic kappa-receptor-mediated mechanisms.     

Brachydactyly type A3 is caused by a novel 13 bp HOXD13 frameshift deletion in a Chinese family

Brachydactyly type A (BDA) is defined as short middle phalanges of the affected digits and is subdivided into four types (BDA1‐4). To date, the molecular cause is unknown. However, there is some evidence that pathogenic variants of HOXD13 could be associated with BDA3 and BDA4. Here, we report a Chinese autosomal dominant BDA3 pedigree with a novel HOXD13 mutation. The affected individuals presented with an obviously shorter fifth middle phalanx. The radial side of the middle phalanx was shorter than the ulnar side, and the terminal phalanx of the fifth finger inclined radially and formed classical clinodactyly. Interestingly, the index finger was normal. The initial diagnosis was BDA3. However, the distal third and fourth middle phalanges were also slightly affected, resulting in mild radial clinodactyly. Both feet showed shortening of the middle phalanges, which were fused to the distal phalanges of the second to the fifth toes, as reported in BDA4. Therefore, this pedigree had combined BDA3 and atypical BDA4. By direct sequencing, a 13 bp deletion within exon 1 of HOXD13 (NM_000523.4: c.708_720del13; NP_000514.2: p.Gly237fs) was identified. The 13 bp deletion resulted in a frameshift and premature termination of HOXD13. This study provides further evidences that variants in HOXD13 cause BDA3‐BDA4 phenotypes.     

Cortical dendritic pathology in human immunodeficiency virus encephalitis.

Previous neuropathological and morphometric studies of the cerebral cortex of patients with human immunodeficiency virus encephalitis (HIVE) have shown a decrease in the population of large neurons, moderate loss in synaptophysin immunoreactivity, and pathological changes in dendrites. To further characterize and quantify alterations in the dendritic tree of neocortical pyramidal neurons, we performed a modified Golgi impregnation technique on Formalin fixed blocks from the frontal cortex of 5 HIVE cases, 5 human immunodeficiency virus seropositive control cases without encephalitis, and 5 human immunodeficiency virus seronegative controls. Apical dendrites of HIVE cases were dilated, vacuolated, and tortuous with decreased length and branching. Basal and oblique dendrites also showed these alterations, but to a lesser extent. Some dendrites presented lacunae and filopodia consistent with remodeling. Computer aided quantification of HIVE cases showed a 40-60% decrease in spine density throughout the entire length of dendrites. Laser confocal imaging of Golgi impregnated sections displayed aberrant spines in regions of abnormal second order dendritic branches. These observations support the role of primary dendritic damage in HIVE in contrast to other neurodegenerative disorders where the primary pathology is presynaptic.     

正常人周围神经内膜中的纤维性长间距体及神经束膜细胞的超微结构

本文报道在电镜下观察了正常人腹壁神经小分支的神经束膜细胞的超微结构,并在神经内膜间质中发现了纤维性长间距体(FLS)。 1.2～5层神经束膜细胞紧密地包绕着神经束。束膜细胞呈扁平样排列,胞质内有丰富的微丝和吞饮小泡,基膜明显而连续。紧贴其外的和神经内膜中的成纤维细胞均无基膜。两相贴的束膜细胞之间可见缝管连接和丰富的桥粒,也可见胶原纤维。神经内膜间质中胶原原纤维细,有FLS体存在;而束膜外侧的胶原原纤维较粗,未见FLS体。 2.多数FLS体与无髓神经纤维的Schwann细胞基膜相连,个别处周围为一般胶原原纤维,未见基膜;有髓神经纤维的Schwann细胞处未见FLS体。纵切面上,多数FLS体呈纺锤状,大小不等,其长轴与相邻胶原原纤维的长轴平行,有时可见两者相互延续移行。偶见FLS体呈桥样架于两Schwann细胞之间,FLS体的暗带与两侧Schwann细胞的基膜相延续。还见2～3个FLS体并为一体,但横纹错开。FLS体的斜断面近似长方形,也呈横纹样结构,与纵断面没有很大区别。FLS体的横纹周期长约133nm,暗带约53nm,主要由电子较密的颗粒状物构成;明带约80nm,由方向大致相同的微丝网构成;横纹周期中无细横纹存在。本文并对神经束膜细胞可能的作用、FLS体与基膜的关系、FLS体的横纹周期问题进行了讨论。     

Physics-Driven CFD Modeling of Complex Anatomical Cardiovascular Flows—A TCPC Case Study

Recent developments in medical image acquisition combined with the latest advancements in numerical methods for solving the Navier-Stokes equations have created unprecedented opportunities for developing simple and reliable computational fluid dynamics (CFD) tools for meeting patient-specific surgical planning objectives. However, for CFD to reach its full potential and gain the trust and confidence of medical practitioners, physics-driven numerical modeling is required. This study reports on the experience gained from an ongoing integrated CFD modeling effort aimed at developing an advanced numerical simulation tool capable of accurately predicting flow characteristics in an anatomically correct total cavopulmonary connection (TCPC). An anatomical intra-atrial TCPC model is reconstructed from a stack of magnetic resonance (MR) images acquired in vivo. An exact replica of the computational geometry was built using transparent rapid prototyping. Following the same approach as in earlier studies on idealized models, flow structures, pressure drops, and energy losses were assessed both numerically and experimentally, then compared. Numerical studies were performed with both a first-order accurate commercial software and a recently developed, second-order accurate, in-house flow solver. The commercial CFD model could, with reasonable accuracy, capture global flow quantities of interest such as control volume power losses and pressure drops and time-averaged flow patterns. However, for steady inflow conditions, both flow visualization experiments and particle image velocimetry (PIV) measurements revealed unsteady, complex, and highly 3D flow structures, which could not be captured by this numerical model with the available computational resources and additional modeling efforts that are described. Preliminary time-accurate computations with the in-house flow solver were shown to capture for the first time these complex flow features and yielded solutions in good agreement with the experimental observations. Flow fields obtained were similar for the studied total cardiac output range (1–3 l/min); however hydrodynamic power loss increased dramatically with increasing cardiac output, suggesting significant energy demand at exercise conditions. The simulation of cardiovascular flows poses a formidable challenge to even the most advanced CFD tools currently available. A successful prediction requires a two-pronged, physics-based approach, which integrates high-resolution CFD tools and high-resolution laboratory measurements.     

中国健康人两项血液流变学参考值与海拔高度的关系

为制定中国健康成年男性血沉参考值(温氏法)和中老年女性红细胞压积参考值(温氏法)的统一标准提供科学依据,本文研究了中国226个单位测定的22707例健康成年男性的血沉参考值(温氏法)和312个单位测定的15608例健康中老年女性的红细胞压积参考值(温氏法),并对其与海拔高度的关系进行了研究,发现随着海拔高度的逐渐增大,健康成年男性血沉参考值(温氏法)在逐渐的减小,而健康中老年女性红细胞压积参考值(温氏法)在逐渐的增大,相关性都很显著。用回归分析的方法推导出了二个一元回归方程。如果知道了中国某地的海拔高度,就可以用这二个回归方程,估算这个地区的健康成年男性血沉参考值(温氏法)和健康中老年女性红细胞压积参考值(温氏法)。     

G蛋白β3亚单位基因C825T多态性与PTCA支架内再狭窄

目的 探讨G蛋白β3亚单位基因C825T多态性与PTCA支架植入后再狭窄之间的相关性。方法 采用多聚酶联反应结合限制性内切酶片断长度多态性分析方法(PCR-RFLP)检测50例经PTCA支架植入术后半年内发生再狭窄的患者和85例经PTCA支架植入在半年内未发生再狭窄的患者之间G蛋白β3亚单位基因C825T多态性。结果 再狭窄组G蛋白β3亚单位基因型频率(CC 14％、CT 54％、TT 32％),等位基因频率(C 41％、T 59％)与未狭窄组G蛋白β3亚单位基因型频率(CC31.8％、CT 44.7％、TT 23.5％),等位基因频率(C 54.2％、T 45.8％)比较统计学上有差异。结论 G蛋白β3亚单位基因C825T多态性可能与PTCA支架内再狭窄有关。     

微创DHS内固定与传统DHS内固定治疗老年股骨粗隆间骨折比较研究

目的:对微创动力髋螺钉(dynamic hip screw,DHS)内固定和传统DHS内固定治疗老年股骨粗隆间骨折的效果进行比较.方法:将91例老年股骨粗隆间骨折患者随机分为两组,传统组46例采用传统方式置入内固定物治疗,微创组45例采用微创方式置入内固定物.对两组手术创伤大小、术后并发症、骨折愈合及功能恢复情况进行比较.主要通过考察手术切口长度、出血量、输血量、血红蛋白下降幅度、术后术区肢体肿胀情况、血沉变化等来反映手术创伤大小.结果:两组手术创伤差异有统计学意义,传统组大于微创组(P＜0.05).微创组有2例复位不良,传统组有3例复位不良,两组均无深部血肿发生.传统组围手术期死亡2例,其余患者均顺利出院,获12～30个月随访,平均17.1个月.两组各有1例在随访期间死于其它内科疾病,其余骨折均获愈合.术后平均骨折愈合时间微创组3.6个月,传统组3.8个月.术后1年髋关节功能优良率微创组84.1%,传统组79.1%,两组差异无统计学意义(P＞0.05).结论:微创DHS内固定治疗老年股骨隆间骨折,手术创伤小,有利于围手术期恢复和髋关节功能康复.     

两种兔源内毒素结合蛋白的分离、纯化及其体外生物学活性的对比研究

目的　从烧伤合并内毒素血症致多器官损害家兔血清中分离纯化内毒素结合蛋白 ,并初步对比研究它们的生物学活性。方法　兔血清蛋白质通过二步离子交换层析 (Bio Rex 70Resin、Mono Q)及凝胶过滤分离纯化 ,并经流式细胞分析实验、绵羊红细胞凝聚实验、氨基末端氨基酸残基测序等方法鉴定 ,再将所获蛋白质作用于体外培养的人单核细胞 (U937) ,观测其分泌TNFα等细胞因子的生物效应。结果　获得两种具有促进内毒素 (LPS)与外周血单核细胞 (PBMC)结合的蛋白质 ,其中一种相对分子质量为 6 0× 10 4 ,其N端 10个氨基酸序列为TNPGLITRIT ,证实为兔内毒素结合蛋白 (LBP) ;另一种蛋白质相对分子质量为 4 8× 10 4 ,其N端 10个氨基酸序列为GSQGTFTSEE ,与NCBI蛋白质库中的氨基酸序列进行比较 ,未发现相同序列 ,命名为p48。结论　p48与LBP具有相似的生物学功能 ,p48的生物学活性稍弱于LBP。提示体内除LBP外 ,p48也同样起着介导LPS的毒性作用。这可能是近年国外研究中阻断LBP的活性后 ,机体毒性反应并无明显减轻的原因之一。