Objective To investigate the effect of mild hypothermia on brain edema after severe head injury (SHI) and its clinical significance. Methods Thirty-six patients with SHI were randomly divided into conventional therapy group (control group) and mild hypothermia therapeutic group (therapeutic group), with 18 patients in each group. The patients in the therapeutic group were treated with ice-cap, ice-blanket and ice-bag and lytic cocktail Ⅰas adjuvants, and a rectal temperature of 33 ℃ was maintained for 3~5 d. Intracranial pressure (ICP) of all the patients after operation were monitored postoperatively. The size of brain edema was measured with CT on day 0, 1, 3, 7, 14, 21 respectively after SHI. The size of brain edema at the trauma cite and ICP as well as the clinical outcome were compared and analysed. Results ICP of the control and therapeutic groups were（2.87±0.26）kPa and (1.67±0.23) kPa respectively on day 3 (P<0.01), and were (3.15±0.24)kPa and (1.78±0.24) kPa respectively on day 7 after brain injury (P<0.01). The area of brain edema was the largest on day 14 in the control group (140.90±22.95 cm3)and on day 3 in the therapeutic group (95.83±14.97 cm3). At day 14 posttrauma, the edema area in therapeutic group was 42% smaller than that in the control group (P<0.05). The rates of consciousness recovery within a week were 22.2% (4/18) in the control group and 55.6% (10/18) in the therapeutic group (P<0.05). The rates of unfavorable prognosis was 61.1% (11/18) in the control group and 33.3% (6/18) in the therapeutic group. Conclusion Mild hypothermia treatment can improve the prognosis through alleviating brain edema and stabilizing ICP after SHI.

Objective To investigate the effect of mild hypothermia on brain edema after severe head injury (SHI) and its clinical significance. Methods Thirty-six patients with SHI were randomly divided into conventional therapy group (control group) and mild hypothermia therapeutic group (therapeutic group), with 18 patients in each group. The patients in the therapeutic group were treated with ice-cap, ice-blanket and ice-bag and lytic cocktail Ⅰas adjuvants, and a rectal temperature of 33 ℃ was maintained for 3~5 d. Intracranial pressure (ICP) of all the patients after operation were monitored postoperatively. The size of brain edema was measured with CT on day 0, 1, 3, 7, 14, 21 respectively after SHI. The size of brain edema at the trauma cite and ICP as well as the clinical outcome were compared and analysed. Results ICP of the control and therapeutic groups were（2.87±0.26）kPa and (1.67±0.23) kPa respectively on day 3 (P<0.01), and were (3.15±0.24)kPa and (1.78±0.24) kPa respectively on day 7 after brain injury (P<0.01). The area of brain edema was the largest on day 14 in the control group (140.90±22.95 cm3)and on day 3 in the therapeutic group (95.83±14.97 cm3). At day 14 posttrauma, the edema area in therapeutic group was 42% smaller than that in the control group (P<0.05). The rates of consciousness recovery within a week were 22.2% (4/18) in the control group and 55.6% (10/18) in the therapeutic group (P<0.05). The rates of unfavorable prognosis was 61.1% (11/18) in the control group and 33.3% (6/18) in the therapeutic group. Conclusion Mild hypothermia treatment can improve the prognosis through alleviating brain edema and stabilizing ICP after SHI.

Breast Neoplasms ; diagnosis ; therapy ; Early Detection of Cancer ; Female ; Humans ; Practice Guidelines as Topic ; Receptor, ErbB-2 ; analysis

Objective To analyze retrospectively the clinical characteristics, pathogeny and therapy of traumatic interhemispheric subdural hematoma (ISH). Methods 31 ISH cases admitted since 1996 were reviewed and analyzed retrospectively concerning the clinical characteristics and therapies. Typically,ISH manifested itself with hemiplegia or monoplegia in the contralateral lower limb, called the falx syndrome, and unconsciousness was infrequent at the initial stage of the head injury. The pathogeny of ISH involved cracks of the bridging vein, hematomas in the interhemispheric small arteries and veins and probably coagulation dysfunction or anticoagulant therapy. Results In all 31 patients, 29 were cured and 2 died ofmultisystem organ failure (MSOF) and cerebral hernia respectively. The follow-up revealed that 6 cured patients developed interhemispheric subdural effusion. Conclusion CT scanning showing the interhemispheric hematoma exceeds 20 mL, or the interhemispheric hematoma is thicker than 1 cm can be referential to the diagnosis of ISH. For the ISH treatment, surgery and conservative management are suggested based on the functional disturbance or the stability of the disease. Patients with progressive neurologic deterioration should be operated without delay.

Objective To investigate the clinical efficacy of Gamma knife treatment on patients with functional pituitary prolactinoma(PRL)and its endocrine response.Method We retrospectively analyzed the clinical data of 135 cases of functional pituitary prolactinoma treated with Gamma knife in our hospital from Oct 1994 to Jan 2008.All patients were divided into 3 groups:group A(a central dose of 50 to 60 Gy,a marginal dose of 20 to 30 Gy);group B(a central dose of 40 to 50 Gy,a marginal dose of 15 to 25 Gy)and group C(a central dose of 30 to 40 Gy,amarginal dose of 12 to 20 Gy).The dose in the optic nerves of the 3 groups was under 9 Gy. Results After treated with Gamma knife,partial remission(PR)of the clinical symptoms appeared in 90 patients(66.7%);complete remission(CR)of those was showed in 35(25.9%)and no change of those appeared in 10(7.4%).No significant difference was found between age and both sex and tumor sizes in the 3 group(P<0.05).Different normal PRL rates was concluded by using different doses of Gamma knife(F=8.604,P=0.000).Pairwise comparison indicated that high dose of Gamma knife resulted in high PRL normal rates with statistical significance (P<0.05). Conclusion Gamma knife treatment used in patients with functional pituitary adenoma can not only control the growth of tumor,but also improve the dysfunction of endocrine,which should be adopted as the first choice for clinical treatment of functional pituitary prolactinoma.

Objective To investigate the role of a subunit of N-methyl-D-aspartate (NMDAR), a receptor-channel complex, in the neurotoxicity secondary to brain injury and explore its mechanism of action. Methods The animal model of brain injury was established in rats by free-fall metal and the treatment model was induced by injecting AP5 into the lateral ventricle. NMDAR1 mRNA expression levels after brain injury were determined by in situ hybridization. Result NMDAR1 mRNA expression increased significantly at 15 min, utmostly lowered at 72 h and returned to the normal level at 168 h after brain injury. In response to AP5 treatment, NMDAR1 mRNA expression in the treatment group was lower than that in the injured group at 15 min and recovered the normal level at 72 h after brain injury. Conclusion Excessive expression of NMDAR1 mRNA might be involved in the secondary cerebral impairerment after brain injury and the treatment with AP5, a competitive antagonist of NMDAR1, functions to offer neuroprotection.

Objective To investigate the role of a subunit of N-methyl-D-aspartate (NMDAR), a receptor-channel complex, in the neurotoxicity secondary to brain injury and explore its mechanism of action. Methods The animal model of brain injury was established in rats by free-fall metal and the treatment model was induced by injecting AP5 into the lateral ventricle. NMDAR1 mRNA expression levels after brain injury were determined by in situ hybridization. Result NMDAR1 mRNA expression increased significantly at 15 min, utmostly lowered at 72 h and returned to the normal level at 168 h after brain injury. In response to AP5 treatment, NMDAR1 mRNA expression in the treatment group was lower than that in the injured group at 15 min and recovered the normal level at 72 h after brain injury. Conclusion Excessive expression of NMDAR1 mRNA might be involved in the secondary cerebral impairerment after brain injury and the treatment with AP5, a competitive antagonist of NMDAR1, functions to offer neuroprotection.

Objective To evaluate the treatment of aneurysms rupture during endovascular embolization.Methods Nine aneurysms ruptured during the embolization and were treated with endovascular embolization.The reasons of aneurysms rupture during embolization,the prevention and the first aid after aneurysms rupture were analysed.Results Seven patients recovered and 2 died.Conclusions The optimal treatment of aneurysms rupture during endovascular embolization is effective,(J Intervent Radiol,2007,16: 132-134)

Objective To analyze the gene expression profiles in relation to the migration ability of adult human bone marrow-derived neural stem cells (Md-NSCs), and identify the genetic basis of the high migration potential of Md-NSCs in the central nervous system (CNS). Methods Adult human bone marrow stromal celIs(BMSCs) obtained from adult healthy volunteers were induced to differentiate into Md-NSCs in vitro, and the expressions of the genes related to cell invasiveness and metastasis were investigated by microarray analysis. Quantitative real-time PCR (RT-PCR) was used to verify the microarray results. Results The results of microarray analysis revealed significant overexpressions of the genes MMP1, MMP2, MMP17, ITGA3, RhoB, RhoC and RhoD in the Md-NSCs as compared with the expressions in fresh normal human adult bone marrow cells depleted of red blood cells. Quantitative RT-PCR verified the overexpression ofMMP2 gene by 2.84×100 folds, ITGA3 gene by 2.22×102folds, and RhoC gene by 4.92×100 folds. Conclusion The high migration potential of the Md-NSCs in the CNS is probably associated with the overexpression of the genes that promote cell invasiveness and metastasis. These overexpressed genes are also important oncogenes, and therefore the tumorigenicity of the Md-NSCs warrants further investigation.

Objective To explore the role of forskolin, a reagent elevating the cellular content of cAMP, in blood-brain barrier (BBB) damage in rats after cerebral injury damage. Methods Sixty male SD rats were equally randomized into normal control group, sham-operated group, injured group and forskolin treatment group. Rat models of cerebral injury in the later 2 groups were induced by the improved device of Feeney weight-dropping. Foskolin treatment group was peritoneally administered forskolin 5 mg/kg 0.5 h after the brain injury. Twenty g/L Evens blue was given through intravenous injection 23 h after the injury; all the rats were sacrificed 24 h after the injury. The permeation of Evens blue was observed qualitatively with a fluorescence microscope and measured quantitatively with a spectrophotometer. Results No obvious permeation of Evens blue was noted in the surrounding areas of the damaged tissue of normal controls and sham-operated group; Evans blue significantly permeated in the injured group; as compared with that in the injured group, the permeation of Evens blue was significantly decreased in the forskolin treatment group (P＜0.05). The level of Evens blue in the cortex and hippocampus of both side of the brain in the injured group was significantly higher that that in the normal controls and sham-operated group (P＜0.05); the level of Evens blue in the cortex of the left side of the brain in the forskolin treatment group was significantly lower that that in the injured group, but obviously higher than that in the normal controls and sham-operated group (P＜0.05).Conclusion Forskolin, the reagent elevating the cellular content of cAMP, can significantly prevent BBB opening.