Objective To investigate influence of Ang-(1-7) on the inducible nitric oxide synthase (iNOS) activity and gene expression following focal cerebral ischemia/reperfusion in rats. Methods Cerebral ischemia/reperfusion injury was induced by intraluminal thread occlusion of middle cerebral artery in the adult male Sprague-Dawley (SD) rats. Ang-(1-7) or artificial cerebrospinal fluid (aCSF) was continuous administrated by implanted Alzet osmotic minipumps into lateral cerebral ventricle after reperfusion. Experimental animals were divided into sham-operated group ( sham operation + aCSF), aCSF treatment group(MCAO+aCSF)and ang-(1-7)treatment groups(MCAO+Ang-(1-7))at low(1 pmol·0.5 μl-1·h-1),medium (100 pmol·0.5 μl-1·h-1)or hith(10 nmol·0.5 μl-1·h-1)dose levels.The activity of iNOS in ischemic tissues were measured by iNOS detection kits. Reverse transcription( RT)-PCR was used to determine messenger RNA (mRNA) of the iNOS in ischemic tissues. Results The cerebral ischemic lesion resulted in a significant increase of iNOS expression compared with sham operation group. The high-dose Ang-(1-7) markedly enhanced (iNOS) activity ( 160. 83 vs 116. 75 U/mg, F = 19. 22,P＜0.01; 151.87 vs 113.07 U/mg, F=63.52,P＜0. 01) and gene expression(0.43 vs 0.38, F=21.83,P ＜ 0. 01; 0. 40 vs 0. 35, F = 19.49, P ＜ 0. 01 ) compared with aCSF treatment group at 24 hours and 48hours after reperfusion, whereas medium and low-dose Ang-( 1-7 ) didn't stimulate iNOS activation.Conclusions The obtained results suggest that high-dose Ang-(1-7) upregulate iNOS expression following ischemic stroke.Moreover,overdose Ang-(1-7)(10 nmol·0.5 μl-1·h-1)may have Ang Ⅱ-like effects in iNOS expression increase.

Objective To investigate the clinical and imageological features of pituitrin-induced delayed encephalopathy. Methods Clinical data of 8 patients with delayed encephalopathy caused by pituitrin were analyzed retrospectively. Results All of the 8 patients presented diffent degree neuropsychic symptoms at 4～12 d after stop using the pituitrin. The extrapyramidal and psychiatric symptoms of the cases were found,such as hypermyotonia(8 cases),hypokinesia(6 cases),extremity buffeting(3 cases),emotional and behavior disorder(6 cases). The 8 cases with EEG examination showed:there were gently to midrange widespread dysfunction in 4 cases,severe widespread dysfunction in 1 case. The levels of serum Na+ in 5 cases were decrease slightly. The 8 cases with brain MRI examination showed that the abnormal signals were mainly located in lentiform nucleus and head of caudate nucleus with long T1 and T2-weighted images,and including thalamus or midbrain abnormalities signal in 1 case,respectively. Conclusions The manifestations of pituitrin-induced delayed encephalopathy are extrapyramidal symptoms and cerebral disorders. The characteristics of brain MRI are abnormal signals in lentiform nucleus and head of caudate nucleus with long T1 and T2-weighted images. The supposed pathogenesis may be nerve necrosis induced by Charcot's artery spasm and hyponatremia.

Objective To improve the recognition of rapid eye movement(REM) sleep behavior disorder(RBD) as an early marker for ?-synucleinopathies.Methods By studying a typical case of RBD followed with multiple system atrophy-P,the clinical features,pathogenesis and its correlation with ?-synucleinopathies of RBD were elucidated.Results This case manifested a serial of paroxysmal increased activities of the limbs and behavioral disturbances during his REM sleep,and parkinsonism features appeared 9 years later.His cranial MRI showed the abnormal long T1 and T2 signals at bilateral centrum ovale,corona radiate and basal ganglia area of the cerebral hemisphere.Conclusions RBD is clinically characterized with paroxysmal behavioral disorder in the REM sleep,the changes of the brain stem,striatum and cortical perfusion are attributed to the RBD pathogenesis.Closely linked to a-synucleinopathies,RBD may be clinical harbinger of those disorders.

In order to definitude the influence caused by the different sampling in voice assessment.Method:We comparing the results acquired by total section and subsection sampling.Result:The results acquired by subsection tended to normal more than those acquired by total section. Conclusion:Subsection sampling voice assessment might conceal the drgree of the disease state of patients

In order to study the effect of chronic noise exposure on auditory center, seven guinea pigs were .exposured to 105 dB A noise 8h daily for 45 d. Then the animals were killed by decapitation. The superior olive and inferior colliculus were taken immediately to make the samples of electron microscope. The mitochondria swelling, membrane rupture, cristae breaking, ballooning degeneration were found. The rough surfaced endoplasmic reticulum was swollen and expanded. The lysosome and secondary lysosome were increased. The cell interstitial edema and synaptic besicle decrease were observed. The nuclear chromatid was decreased and nucleolus was kept to the side. The laminae of neurilemma of nerve fibers were dissociated, swollen and broken. The results indicate that the ultrastructure, neural cells and fibers in the auditory center are damaged by chronic noise exposure and most of these damages are irreversible.

The changes of hair cells after acute radiation injury to cochlea were studied with scanning electron microscope in guinea pigs. Outer hair cell cilia were disordered, fused, and lost in the early stage after 40Gy ?-ray irradiation of the bullae of guinea pigs. From 15 to 30d after radiation, reconstruction of cilia besides early changes, and ball shape materials on the side of inner hair cells were found. The possible mechanism of these changes is also discussed

The effects of different doses of r-ray on cochlea are reported in this paper. Significant hearing loss and severe cochlea hair cells injury were found while radiation dose was more than 80 Gy. With 40 Gy to 60 Gy, slight hearing loss, but cochlea hair cells and support cells impairment were observed. With 20 Gy, no hearing loss and no hair cell damage were found. The results indicated that the damage increases with a dose of radiation and there is a delay effect of radiation on cochles.

Objective To explore the effect of caspase-9 inhibitor on low fetal bovine serum ( FBS)-induced apop-tosis in cartilage endplate chondrocytes in SD rat vertebrae.Methods Disc cartilage endplates were obtained from 3-month old SD rats and subjected to sequential digestion to harvest chondrocytes for primary culture, and apoptosis was in-duced by 1%FBS for 48 hours.Three groups of chondrocytes were treated by 1% FBS, caspase-9 inhibitor ( Z-LEHD-FMK) and DMSO, respectively.After 48 hours, apoptosis was detected by DAPI staining and flow cytometry.The expres-sion of procaspase-9, active caspase-9 and active caspase-3 was monitored by Western blot.Results Compared with the 1%FBS group (40.8 ±0.84)%and DMSO group (40.2 ±1.56)%, the apoptosis rate of the caspase-9 inhibitor group (26.3 ±2.56)% was significantly lower (P<0.05).The expressions of active caspase-9 and active caspase-3 in the caspase-9 inhibitor group were significantly lower than those in the other two groups (P<0.05).Conclusions Caspase-9 inhibitor can inhibit low FBS-induced apoptosis in cartilage endplate chondrocytes of rat vertebrae, and might become a new drug for the treatment of disc degeneration.

Objective To develop an apoptosis model of nucleus pulposus cells in cell culture.Methods To mimic the nutrient-deficient microenvironment of degenerative intervertebral disc,nucleus pulposus cells derived from infant SD rat disc were cultured under serum limiting conditions.Nucleus pulposus cells were cultured in culture medium contai-ning 1%, 3%, 5%, 8%and 10%fetal bovine serum( FBS) respectively to select the optimum FBA concentration.Apoptosis was assessed by flow cytometry, Western blot,cell counting kit, and immunofluorescence technique.Results The flow cy-tometry revealed that apoptosis rate of the nucleus pulposus cells increased with decreasing concentration of FBS, and 3%FBS used in the experimental group was the most effective concentration to induce apoptosis(P<0.05).Western blot dem-onstrated significantly higher expression of Bax and caspase-3 enzyme in the 3%FBS group than in the 10%FBS group, while bcl-2 activity decreased.The results of CCK-8 test indicated that the nucleus pulposus cells got slower proliferation in the medium containing 3%FBS.Immunofluoresence analysis showed that FAS expression was significantly higher in the 3%FBS group than in the 10%FBS group.Conclusions 3%FBS condition may induce apoptosis in the nucleus pulposus cells and compromise the cell function to induce intervertebral disc degeneration.The caspase family should be involved in the process.

BACKGROUND:Previous studies have shown that chitosan can promote the repair of peripheral nerve injury and methylprednisolone can improve the microenvironment around nerve injuries, which are commonly used in clinical treatment of acute central nervous system injury.
OBJECTIVE:To observe the effects of modified chitosan and methylprednisolone combination on repair of sciatic nerve injury in rats.
METHODS:The rat sciatic nerve was transected and microscopical y anastomosed immediately. Then, modified chitosan, methylprednisolone, methylprednisolone+modified chitosan, and saline were injected respectively around the anastomosis site, compared with the sham surgery group.
RESULTS AND CONCLUSION:Compared with other groups, the combination group showed shorter claw extending reflex recovery time (P<0.05). Significant differences were found between the combination group and other groups in nerve conduction velocity, the remnant rate of gastrocnemius wet weight, the diameter and section area of gastrocnemius cells (P<0.05). The nerve fibers through the anastomotic site were significantly increased, with consistent thickness and arrangement and less neurodegeneration when observed 12 weeks after operation. In conclusion, the modified chitosan combined with methylprednisolone could significantly promote the sciatic nerve repair.