重型颅脑损伤患者亚低温治疗的临床研究

Objective To compare the prognoses of patients with severe brain injury receiving mild hypothermia and normothermia interventions and evaluate the brain protective effect of mild hypothermia. Methods Seventy-six patients with severe head injury (Glaseow Coma Score≤8) were divided into mild hypothermia group (36 cases) and normothermia group (40 cases). The patients in the normothermia group were managed with measures for reducing the intracranial pressure and controlling the hemorrhage and gastric acid, with also administration of neurotrophic treatment and nutritional support. In addition to these conventional interventions, the patients in mild hypothermia group received mild hypothermia treatment administered using a water blanket to reduce the core body temperature and brain temperature to 32-34℃, which was maintained for 3-14 days as needed. Results The patients receiving mild hypothermia therapy had significantly improved prognosis in comparison with those in normothermia group (P<0.05). Conclusion Mild hypothermia treatment has brain protective effect and improves the prognosis of patients with severe brain injury.     

重型颅脑损伤患者亚低温治疗的临床研究

Objective To compare the prognoses of patients with severe brain injury receiving mild hypothermia and normothermia interventions and evaluate the brain protective effect of mild hypothermia. Methods Seventy-six patients with severe head injury (Glaseow Coma Score≤8) were divided into mild hypothermia group (36 cases) and normothermia group (40 cases). The patients in the normothermia group were managed with measures for reducing the intracranial pressure and controlling the hemorrhage and gastric acid, with also administration of neurotrophic treatment and nutritional support. In addition to these conventional interventions, the patients in mild hypothermia group received mild hypothermia treatment administered using a water blanket to reduce the core body temperature and brain temperature to 32-34℃, which was maintained for 3-14 days as needed. Results The patients receiving mild hypothermia therapy had significantly improved prognosis in comparison with those in normothermia group (P<0.05). Conclusion Mild hypothermia treatment has brain protective effect and improves the prognosis of patients with severe brain injury.     

重型颅脑损伤患者亚低温治疗的临床研究

Objective To compare the prognoses of patients with severe brain injury receiving mild hypothermia and normothermia interventions and evaluate the brain protective effect of mild hypothermia. Methods Seventy-six patients with severe head injury (Glaseow Coma Score≤8) were divided into mild hypothermia group (36 cases) and normothermia group (40 cases). The patients in the normothermia group were managed with measures for reducing the intracranial pressure and controlling the hemorrhage and gastric acid, with also administration of neurotrophic treatment and nutritional support. In addition to these conventional interventions, the patients in mild hypothermia group received mild hypothermia treatment administered using a water blanket to reduce the core body temperature and brain temperature to 32-34℃, which was maintained for 3-14 days as needed. Results The patients receiving mild hypothermia therapy had significantly improved prognosis in comparison with those in normothermia group (P<0.05). Conclusion Mild hypothermia treatment has brain protective effect and improves the prognosis of patients with severe brain injury.     

重型颅脑损伤患者亚低温治疗的临床研究

Objective To compare the prognoses of patients with severe brain injury receiving mild hypothermia and normothermia interventions and evaluate the brain protective effect of mild hypothermia. Methods Seventy-six patients with severe head injury (Glaseow Coma Score≤8) were divided into mild hypothermia group (36 cases) and normothermia group (40 cases). The patients in the normothermia group were managed with measures for reducing the intracranial pressure and controlling the hemorrhage and gastric acid, with also administration of neurotrophic treatment and nutritional support. In addition to these conventional interventions, the patients in mild hypothermia group received mild hypothermia treatment administered using a water blanket to reduce the core body temperature and brain temperature to 32-34℃, which was maintained for 3-14 days as needed. Results The patients receiving mild hypothermia therapy had significantly improved prognosis in comparison with those in normothermia group (P<0.05). Conclusion Mild hypothermia treatment has brain protective effect and improves the prognosis of patients with severe brain injury.     

重型颅脑损伤患者亚低温治疗的临床研究

Objective To compare the prognoses of patients with severe brain injury receiving mild hypothermia and normothermia interventions and evaluate the brain protective effect of mild hypothermia. Methods Seventy-six patients with severe head injury (Glaseow Coma Score≤8) were divided into mild hypothermia group (36 cases) and normothermia group (40 cases). The patients in the normothermia group were managed with measures for reducing the intracranial pressure and controlling the hemorrhage and gastric acid, with also administration of neurotrophic treatment and nutritional support. In addition to these conventional interventions, the patients in mild hypothermia group received mild hypothermia treatment administered using a water blanket to reduce the core body temperature and brain temperature to 32-34℃, which was maintained for 3-14 days as needed. Results The patients receiving mild hypothermia therapy had significantly improved prognosis in comparison with those in normothermia group (P<0.05). Conclusion Mild hypothermia treatment has brain protective effect and improves the prognosis of patients with severe brain injury.     

重型颅脑损伤患者亚低温治疗的临床研究

Objective To compare the prognoses of patients with severe brain injury receiving mild hypothermia and normothermia interventions and evaluate the brain protective effect of mild hypothermia. Methods Seventy-six patients with severe head injury (Glaseow Coma Score≤8) were divided into mild hypothermia group (36 cases) and normothermia group (40 cases). The patients in the normothermia group were managed with measures for reducing the intracranial pressure and controlling the hemorrhage and gastric acid, with also administration of neurotrophic treatment and nutritional support. In addition to these conventional interventions, the patients in mild hypothermia group received mild hypothermia treatment administered using a water blanket to reduce the core body temperature and brain temperature to 32-34℃, which was maintained for 3-14 days as needed. Results The patients receiving mild hypothermia therapy had significantly improved prognosis in comparison with those in normothermia group (P<0.05). Conclusion Mild hypothermia treatment has brain protective effect and improves the prognosis of patients with severe brain injury.     

重型颅脑损伤患者亚低温治疗的临床研究

Objective To compare the prognoses of patients with severe brain injury receiving mild hypothermia and normothermia interventions and evaluate the brain protective effect of mild hypothermia. Methods Seventy-six patients with severe head injury (Glaseow Coma Score≤8) were divided into mild hypothermia group (36 cases) and normothermia group (40 cases). The patients in the normothermia group were managed with measures for reducing the intracranial pressure and controlling the hemorrhage and gastric acid, with also administration of neurotrophic treatment and nutritional support. In addition to these conventional interventions, the patients in mild hypothermia group received mild hypothermia treatment administered using a water blanket to reduce the core body temperature and brain temperature to 32-34℃, which was maintained for 3-14 days as needed. Results The patients receiving mild hypothermia therapy had significantly improved prognosis in comparison with those in normothermia group (P<0.05). Conclusion Mild hypothermia treatment has brain protective effect and improves the prognosis of patients with severe brain injury.     

Mild hypothermia for treatment of diffuse axonal injury: a quantitative analysis of diffusion tensor imaging简

Fractional anisotropy values in diffusion tensor imaging can quantitatively reflect the consistency of nerve fibers after brain damage, where higher values generally indicate less damage to nerve fibers. Therefore, we hypothesized that diffusion tensor imaging could be used to evaluate the effect of mild hypothermia on diffuse axonal injury. A total of 102 patients with diffuse axonal injury were randomly divided into two groups: normothermic and mild hypothermic treatment groups. Patient's modified Rankin scale scores 2 months after mild hypothermia were significantly lower than those for the normothermia group. The difference in average fractional anisotropy value for each region of interest before and after mild hypothermia was 1.32–1.36 times higher than the value in the normothermia group. Quantitative assessment of diffusion tensor imaging indicates that mild hypothermia therapy may be beneficial for patients with diffuse axonal injury.     

亚低温对重型颅脑创伤患者血清抗脑抗体含量的影响

目的 研究重型颅脑创伤(sTBI)后患者血清抗脑抗体(ABAb)浓度变化及亚低温治疗对血清ABAb浓度的影响,探讨亚低温脑保护机制.方法 选择80例sTBI住院患者,随机分成常温治疗(NT)组和亚低温治疗(HT)组各40例,分别予以常温治疗和亚低温治疗,于伤后第1、3、5、7、14天采血.用酶联免疫吸附(ELISA)法测定血清ABAb浓度,观察各时间点血清ABAb浓度的变化,分析各时间点两组血清ABAb浓度与格拉斯哥预后评分(GOS)的相关性.另取20例健康体检者作为对照组.结果 (1)所有sTBI患者在伤后各时间点血清ABAb浓度高于正常对照组(P＜0.01).(2)HT组于伤后各时间点血清ABAb浓度低于NT组,且差异有统计学意义(P＜0.01).(3)NT组于伤后各时间点血清ABAb浓度与GOS评分呈负相关,出院时HT组预后也较NT组为佳.结论 HT能够降低sTBI患者血清ABAb含量,具有脑保护作用,其脑保护机制可能与HT能减轻血清ABAb介导的损伤性脑细胞炎性反应有关.

Abstract：

Objective To disclose the Probably protective mechanism of mild hypothermia protecting brain through investigating the contents charges of Antibrain-Antibody(ABAb)in serum in patients with severe traumatic brain injury(sTBI) and the influence of mild hypothermia on serum levels of ABAb.Methods A total of 80 cases with sTBI were treated with normothennia - treated (NT) (NT group, re =40)and mild hypothermia( HT) (HT group, n =40) respectively. ELISA was used to measure serum levels of ABAb. Groups at 1、3、5、7 and 14 days after injury to observe the contents changes of ABAb in serum and the influence of mild hypothermia. Simultaneous analysis two groups at each time point of serum ABAb concentration and Glasgow outcome scale (GOS) of relevance was performed Contrast analysis of clinical prognosis for patients in the two groups was carried out to reveal the protective mechanism of mild hypothermia protecting on patients with sTBL 20 serum specimens of normal persons were used as control group. Results (1) All sTBI patients at each time point after injury, serum ABAb levels were higher than the normal control group ( P ＜0.01). (2) Concentration of antibodies in the serum ABAb levels in HT group at each time point was lower than in NT group( P＜0.01). (3) Concentration of serum ABAb levels in NT group at each time point of injury was negatively correlated with the GOS score; prognosis at discharge in HT group was better than in NT group. Conclusions HT can reduce the serum ABAb levels in sTBI patients, improve the prognosis, have brain protective effect The brain protective mechanisms may be related to the mild hypothermia which reduce the serum ABAb - mediated inflammatory damage on brain cells.     

Evaluating the prognosis and degree of brain injury by combined S-100 protein and neuron specific enolase determination

BACKGROUND: S-100 and neuron specific enolase (NSE) possess the characteristics of specific distribution in brain and relative stable content. Some studies suggest that combined detection of the both is of very importance for evaluating the degree of brain injury. OBJECTIVE: To observe the changes of S-100 protein and NSE levels at different time points after acute brain injury, and evaluate the values of combined detection of the both for different injury degrees, pathological changes and prognosis. DESIGN: Case-control observation. SETTING: Department of Neurosurgery, Second Affiliated Hospital, Lanzhou University. PARTICIPANTS: Thirty-four inpatients with brain injury, 19 males and 15 females, aged 15 to 73 years, who received treatment between September 2005 and May 2006 in the Department of Neurosurgery, Second Affiliated Hospital, Lanzhou University, were recruited. The patients were admitted to hospital at 24 hours after brain injury. After admission, skull CT confirmed that they suffered from brain injury. Following Glasgow coma score (GCS) on admission, the patients were assigned into 3 groups: severe group (GCS 3 to 8 points, n =15), moderate group (GCS 9 to 12 points, n =8) and mild group (GCS 13 to 15 points, n =11). Following Glasgow outcome scale (GOS) at 3 months after brain injury, the patients were assigned into good outcome group (GOS 4 to 5 points, good recovery and moderate disability included, n =19) and poor outcome group (GOS 1 to 3 points, severe disability, vegetative state and death, n =15). Ten subjects who received health examination concurrently were chosen as normal control group , including 6 males and 4 females , aged （45.4±14.3）years. In our laboratory, the normal level of NSE was ≤15.2 ng/L, and that of S100 was ≤ 0.105 μg/L. METHODS: ①Blood samples of control group were collected when the subjects received health examination. Blood samples of patients with brain injury were collected at 24 hours, 3, 7 and 14 days after injury. According to the instructions of NSE and S-100 kits purchased from Roche Company, serum NSE and S-100 levels were determined by electrochemiluminescence immunoassay (ECLIA). ②Analysis of variance was used for intergroup comparison, Spearman correlative analysis for comparison of different GCS and GOS, and linear regression analysis for comparison of correlation of two factors. MAIN OUTCOME MEASURES: ①The dynamic changes of NSE and S-100 of patients with different brain injuries and their correlations with GCS. ② The dynamic changes of NSE and S-100 of patients with different outcomes and their correlations with GOS. RESULTS: Thirty-four patients with brain injury and ten healthy persons were involved in the result analysis. ①Overall change rule of NSE and S100 after brain injury: NSE of patients with brain injury reached its peak at 24 hours after injury, then was gradually decreased with time and was below normal level in the 2nd week. The overall tendency of S-100 was the same as that of NSE in patients with brain injury. ② The dynamic changes of NSE and S100 of patients with different brain injuries and their correlations with GCS: NSE and S-100 levels at 24 hours after injury were significantly negatively correlated with those on admission （r = －0.537,－0.731, P < 0.05）. At 24 hours after injury, serum NSE and S-100 levels of patients with mild, moderate and severe brain injuries were significantly higher than those of control group (P < 0.05); At 14 days after brain injury, serum NSE and S-100 levels of patients with mild and severe brain injury were close to those of control group (P > 0.05); While at 24 hours, 3, 7 and 14 days after brain injury, the serum NSE and S-100 levels of patients with severe brain injury were significantly higher than those of control group (all P < 0.05). NSE level of patients with mild brain injury was decreased to normal level at 7 days after injury and that of patients with moderate brain injury at 14 days after injury. S-100 level of patients with mild and moderate brain injury was decreased to normal level at 14 days after injury. Serum NSE and S-100 levels of patients with severe brain injury always kept over normal level and those of patients with mild brain injury reached peak value at 3 days after injury. ③ The dynamic changes of NSE and S-100 levels of patients with different outcomes and their correlations with GOS: serum NSE and S-100 levels at 24 hours after injury were significantly negatively correlated with GOS （r =－0.573,－0.756, P < 0.05）. It suggested that the severer the injury was, the lower the GOS was. At 24 hours, 3, 7 and 14 days after injury, serum NSE and S-100 levels of patients in good outcome group were significantly lower than those of poor outcome group (P < 0.05). CONCLUSION: The injury degree and prognosis of patients with brain injury are correlated with serum NSE and S-100 levels. The detection of serum S-100 and NSE levels after injury can be used for evaluating injury and prognosis of brain injury     

Denervation study of synapses of organ of corti of old world monkeys

Fine structural characteristics of synapses in the spiral organ of Corti were examined, with reference to differences between inner and outer haircell systems, and to location of neurons of origin of efferent axons. Surgical interruption of crossed olivocochlear bundle, of vestibular nerve, of facial nerve, and excision of superior cervical ganglia were used to determine the pathways of efferent axons. Interruption of the vestibular nerve near the brainstem results in degeneration of all efferent terminals on outer hair cells. Mid-line lesions at, and caudal to, the facial colliculus result in degeneration of about half of these efferent terminals. Efferent synaptic bulbs to the inner hair-cell system are small, of the order of one micron, and form type 2 junctions with afferent dendrites. They tend to have more large dense-core vesicles (about 80 nm) than the large efferent terminals of the outer hair-cell system, and appear to be the terminals of axons in the habenula perforata, which exhibit varicosities laden with large dense core vesicles. The varicosities are unaffected by excision of the superior cervical ganglia. So far as our material can reveal, it appears that the varicosities in the habenula perforata do not survive vestibular root interruption, nor do the efferent processes in the internal spiral bundle or at the base of inner hair cells. Most interestingly, the afferent processes of the inner hair-cell system, as identified for example by their relation to pre-synaptic bodies in the inner hair cells, are subject to a trans-synaptic reaction after severance of the vestibular root. They undergo a dramatic cytological transformation, characterized by increase of volume, engorgement with microtubules, microfilaments, microvesicles of various sizes, and clusters of lysosomes. Thus, both the efferent and afferent terminals of the inner hair-cell system show marked cytological differences from the corresponding terminals of the outer hair cell system.     

Summary of legislation of 1935 of interest to the department of Mental Hygiene

Psychiatric Quarterly -     

Summary of legislation of 1941 of interest to the Department of Mental Hygiene

Psychiatric Quarterly -     

Asymmetry of on- and off-pathways of blue-sensitive cones of the retina of macaques

Macaque retinal ganglion cells whose receptive-field center recieves input from blue-sensitive cones show an overt asymmetry of the frequency of ON-center and OFF-center varieties, an asymmetry not present in ganglion cells whose center receives input from the other two cone types. A similar asymmetry of ON/OFF responses is found in the local electrotetinogram (d-wave) mediated by signals from blue-sensitive cones. ‘Blue-ON-center’ ganglion cells have larger receptive-field centers and shorter conduction latencies than other opponent-color varieties, suggesting an appreciable degree of receptor convergence and presumably large cell bodies. Intracellular stainings of these neurons with Procion Yellow show that they correspond to diffuse stratified (Parasol) ganglion cells whose flat-topped dendritic arborization stratifies in the sclerad half of the inner plexiform layer. In view of the known characteristics of macaque bipolar cells and of the ON/OFF asymmetry, it is proposed that these ganglion cells are postsynaptic to cone-specific flat bipolars possibly mediating sign-inverting synaptic contacts. The results also indicate a reversal, for the blue-cone pathway, of the ON/OFF lamination of the inner plexiform layer that has recently been described in other species.     

Mechanism of action of tubocurarine on nicotinic cholinoreceptors of neurons of the sympathetic ganglia of rats

Tubocurarine (Tc) effect on membrane currents elicited by acetylcholine (ACh) was studied in isolated superior cervical ganglion neurons of rat using patch-clamp method in the whole-cell recording mode. The "use-dependent" block of ACh current by Tc was revealed in the experiments with ACh applications, indicating that Tc blocked the channels opened by ACh. Mean lifetime of Tc-open channel complex, tau, was found to be 9.8 +/- 0.5 s (n = 7) at -50 mV and 20-24 degrees C. tau exponentially increased with membrane hyperpolarization (e-fold change in tau corresponded to the membrane potential shift by 61 mV). Inhibition of the ACh-induced current by Tc (3-30 microM/1) was completely abolished by membrane depolarization to the level of 80-100 mV. Inhibition of ACh-induced current was augmented at increased ACh doses. It is concluded that the open channel block produced by Tc is likely to be the only mechanism for Tc action on nicotinic acetylcholine receptors in superior cervical ganglion neurons of rat.