猫脑震荡与脑损伤的实验性研究

了解轻型颅脑损伤和脑震荡的脑组织病理形态学及生理功能的变化情况。以流体液压冲击法及胶锤打击的方式 ,分别造成闭合性脑外伤及脑震荡的动物模型。结果显示 :较大的钝性外力可造成脑组织明显的病理形态学改变和脑电、心电等生理功能的持续性改变 ,即脑损伤 ;较小的钝力则只能造成动物意识的一过性丧失 ( 3 0min以内 )及脑电、心电的可复性变化 ,脑组织光镜下病理形态学改变不明显。区别脑震荡与轻型脑损伤应以有无明显的病理形态学改变为“界” ,以脑电、心电、意识障碍等改变是否可复为“度”来划分脑震荡与脑损伤     

Hypoglycemic brain damage

Hypoglycemia was long considered to kill neurons by depriving them of glucose. We now know that hypoglycemia kills neurons actively from without, rather than by starvation from within. Hypoglycemia only causes neuronal death when the EEG becomes flat. This usually occurs after glucose levels have fallen below 1 mM (18 mg/dl) for some period, depending on body glycogen reserves. At the time that abrupt brain energy failure occurs, the excitatory amino acid aspartate is massively released into the limited brain extracellular space and floods the excitatory amino acid receptors located on neuronal dendrites. Calcium fluxes occur and membrane breaks in the cell lead rapidly to neuronal necrosis. Significant neuronal necrosis occurs after 30 min of electrocerebral silence. Other neurochemical changes include energy depletion to roughly 25% of control, phospholipase and other enzyme activation, tissue alkalosis and a tendency for all cellular redox systems to shift towards oxidation. The neurochemistry of hypoglycemia thus differs markedly from ischemia. Hypoglycemia often differs from ischemia in its neuropathologic distribution, a phenomenon applicable in forensic practice. The border-zone distribution of global ischemia is not seen, necrosis of the dentate gyrus of the hippocampus can occur and a predilection for the superficial layers of the cortex is sometimes seen. Cerebellum and brainstem are universally spared in hypoglycemic brain damage. Hypoglycemia constitutes a unique metabolic brain insult.     

Detection of diphenhydramine in autolytic brain tissue in poison-induced brain death syndrome

A case of accidental monointoxication caused by diphenhydramine is reported. Having taken 12 dragées of Neo-Emedyl (50 mg diphenhydramine), an 18-month-old girl showed the following symptoms: generalized erythema, dyspnoea, vomiting, hyperpyrexia, tremor, convulsions, coma, respiratory arrest and absence of reflexes. Computed tomography (CT) suggested a massive cerebral oedema. Her electroencephalogram was abnormally diffused at first; later on, it flattened significantly and became isoelectric between the 14th day and the final stoppage of circulation (after 5 weeks). Autopsy revealed total necrosis of the brain, with the venous cerebral blood vessels being thrombosed (the morphological basis for dissociated cerebral death). In autolysed brain tissue, diphenhydramine was detected at a concentration of 30 ng/g by GC/MS (gas chromatography, mass spectrometry); the concentration of the substance was less than 10 ng/g in the liver. The relatively high concentration in the brain was due to the previous blocking of the circulation. Cerebral death syndrome caused by intoxication offers the chance of detecting measurable amounts of the unchanged drug in autolysed brain tissue.     

大鼠脑外伤后溶酶体酶Cathepsin—B和D的表达

目的研究大鼠脑外伤后溶酶体酶cathepsin-B和-D是否被激活及其不同时段表达变化,阐述其与凋亡执行因子caspase-3表达的关系,并探讨对脑外伤诊断及形成时间的意义。方法采用自由落体打击法建立脑外伤动物模型,并对模型及对照样本进行免疫荧光、双标和激光共聚焦检测,结果用SPSS10.0软件处理。结果脑外伤后1hcathepsin-B表达即增加,4～8d达高峰,脑外伤后32d仍处于高表达水平;cathepsin-D的表达于脑外伤后12h增加,4～8d达高峰,32d的表达仍然高于12h的表达水平。脑外伤初期,cathepsin-B和-D阳性细胞与caspase-3阳性细胞重叠较少,脑外伤后6h开始增加,32d仍然有很多阳性细胞重叠。结论脑外伤后cathepsin-B和-D被激活,其激活在脑外伤早期可能抑制细胞凋亡执行因子caspase-3的激活,之后(6h后)则与caspase-3起协同作用,共同促进细胞死亡;cathepsin-B和-D表达的时程变化对于脑外伤的法医学诊断和中晚期的时间推断有参考意义。     

Aspects of brain death

The different aspects of brain death are discussed. It is pointed out that the diagnosis of poisoning as the cause of brain death can be checked by toxicological examination of brain tissue and of blood in the sinus of the dura mater, since the metabolism in the brain and sinus blood is markedly reduced while drugs and toxic substances continue to be broken down in the other organs. Particular importance attaches to this difference in the case of crimes of violence creating conditions that predispose to brain death when the significance of a further violent act, e.g. stabbing with resultant haemorrhage, has to be assessed. The simple vital reaction of bleeding does not of itself constitute proof in such a situation, unless it is possible to say with a good degree of certainty that brain death did not occur at the moment when the victim was stabbed. It may, however, be possible to state that brain death that could have been caused by violence has not yet occurred if complex vital reactions, such as inflammation of a wound, are seen.     

Immunohistochemical research on brain stem injury: expression of heat shock protein 70 in rat brain after traumatic brain stem injury

The aim of this study was to determine the expression of heat shock protein 70 (HSP70) as molecular chaperones, following traumatic brain stem injury(TBSI). The expression of HSP70 was detected in respective brain regions of rats 1 h, 3 h, 6 h, 12 h, 24 h after brain stem stabbing wound. Numerous HSP70 immunoreactivity positive blood vessel endothelioid and glia cells were found in cerebral, cerebellar cortex and hippocampus after 1 h, with H.E stain unchanged. In the area near the focal of brain stem injury, HSP70 immunoreactivity positive neurons increased significantly after 1 h of injury, reaching the highest level after 3 h, much higher than in other areas. HSP70 immunoreactivity positive cells still existed after 24 h of injury. It was suggested that TBSI cause the defectiveness of protein structure in brain, and induce HSP70 proteolysis of denature protein including misfolding or aggregate. TBSI can be diagnosed regionally by the increasing of HSP70 immunoreactivity positive neurons in the focal of brain stems.     

脑外伤后的星形胶质细胞反应

本文对脑外伤后星形胶质细胞反应进行综述 ,包括星形胶质细胞结构和功能的新认识 ,脑外伤后星形胶质细胞反应的研究模型、检测技术 ,及其在脑外伤后一系列形态学及代谢变化。强调了脑外伤后星形胶质细胞数目、形态和细胞因子表达变化的时间规律性 ,并对其在脑外伤法医学鉴定中的意义做出展望。     

脑外伤后的星形胶质细胞反应

本文对脑外伤后星形胶质细胞反应进行综述，包括星形胶质细胞结构和功能的新认识，脑外伤后星形胶质细胞反应的研究模型、检测技术，及其在脑外伤后一系列形态学及代谢变化。强调了脑外伤后星形胶质细胞数目、形态和细胞因子表达变化的时间规律性，并对其在脑外伤法医学鉴定中的意义做出展望。     

创伤性脑损伤与细胞凋亡

综述了创伤性脑损伤后神经细胞凋亡发生的证据、特点及其可能的分子机制。研究资料表明:创伤性脑损伤后存在有细胞凋亡,它与坏死的时序空间分布不同,创伤性脑损伤后的神经细胞凋亡可通过多种不同的途径发生,受多种基因的调控。同时,本文还探讨了创伤性脑损伤后神经细胞凋亡的研究在法医学方面的应用。     

脑损伤与半胱天冬酶

脑损伤(brain injury)后脑组织发生的一系列病理、生理和生化改变,由许多基因、细胞因子参与调节并影响着损伤程度的转归。CED基因家族中的半胱天冬酶(cystein-dependent aspartate-specific protease,caspase)与脑损伤后细胞死亡有关,控制着引起细胞死亡的不同层面。细胞凋亡(Apoptosis)参与了神经细胞损伤的发病机制。     

The SEM observation of brain tissues and vascular corrosion cast of closed diffuse brain injuries

The morphologic changes of the closed injured brain of rats were observed by SEM. The rats either died immediately after conclusive injuries or were killed after 5 minutes to 5 days after injuries. The main changes were as follows: the diffuse disorder, twist, wave-like distortion and break of neuron fibers; axonal swelling; formation of axonal retraction balls; stripping and denotation of myelin sheath The ball-like swelling of neuron, break of neuron membrane and vascular wall, and microthrombus formations were also observed. These damages worsened with prolongation of surviving time of the rats. The axonal retraction ball appeared 8 hours after the injury and was approximately 3-5 cm in diameter, and developed to 7-8 cm after 3-5 days. It is observed that frontal lobe, cerebellum and brain stem were severely damaged.     

大鼠脑损伤后慢性病程中CaM与nNOS的免疫组化研究

探索脑损伤后存活一段时间死亡者脑损伤诊断指标。利用液压冲击装置 ,造成大鼠实验性闭合性脑损伤 ;并用抗 Ca M与 n NOS抗体 ,对鼠脑伤后 3d、1、3、4、8周脑内 Ca M与 n NOS的变化规律进行研究。Ca M与 n NOS染色结果显示 :伤侧鼠脑皮质阳性细胞数、阳性细胞平均灰度、海马平均灰度均较对照组有显著下降 ,在 1周时有回升 ,3、4、8周时有不同的反应。说明通过检测 Ca M与 n NOS的免疫反应性来判断脑损伤的程度和损伤时间有一定的可行性和应用前景     

Postmortem decrease in brain temperature.

The postmortem decrease in central brain temperature in a small number of forensic cases is presented. Each case shows a simple exponential fall during the time of the measurements. The data reported by Brinkmann et al. (1978), when plotted in semilogarithmic coordinate system, also show--after an initial "plateau" of about 2 h--a strictly one-term exponential temperature fall for several hours post mortem. The curve of brain temperature fall allows conclusions about the time of death without considering clothing, body stature, and weight. The interval temperature measurements which are required may be obtained on the spot, and the calculations needed are very simple. The method, therefore, seems preferable to those depending on rectal temperature measurements.