Objective To investigate the voice recovery by means of observing the changes of the acoustic parameters in the patients after vocal cord polyp operation by microlaryngoscope.Methods Follow up on the voice changes by means of morphology evaluations and voice analysis applied to 30 cases of patient with vocal cord polyp before the operation and in each week for 4 weeks after the operation.Results 86.67% patients were observed to have improved external appearance of their vocal cords 2 weeks after surgery.There is statistically significant difference in 2-,3-,4-week respectively after the operation compared with the preoperative group(P0.05).Conclusion 2 weeks is needed for the patients with vocal cord polyp to have improved vocal cords and one month needed at least to have the voicing functions recovered.Therefore the resting time should be proposed to patients with vocal cord polyp as a resting guideline.

Objective To evaluate the effects of smecta in prolonged hemorrhagic shock.Methods The modified Wigger's method was used to induce hemorrhagic shock in anesthetized rabbits.Twenty-nine rabbits were randomly divided into hemorrhagic shock group(n=14),smecta group(n=15),with smecta solution being administered via a gavage tube before shock.The plasma levels of endotoxin,tumor necrosis factor ?(TNF?),interleukin-6(IL-6) and nitric oxide(NO) were detected at pre-shock and post-shock,immediately after resuscitation and 2h after resuscitation.Blood culture was done at pre-shock,immediately after resuscitation,2h after resuscitation.The survival rates of 24h and 48h were observed.Results The plasma levels of endotoxin,TNF?,IL-6 and NO markedly increased after shock,and were maintained at high level in shock group (P

Objective To evaluate the effects of aminoguandine(AG) used as a selective inhibitor of the inducible isoform of nitric oxide synthase(iNOS) and L NAME used as a non selective inhibitor of nitric oxide synthase(NOS) on severe hemorrhagic shock Methods Forty rabbits were bled to mean arterial pressure of 4 4 66 kPa via femoral artery Hypotention was maintained for 120 min, the shed blood was then returned, followed by an infusion with Ringer′s solutions Animals were randomly divided into three groups: hemorrhagic shock group (n=14), AG group (AG 20mg/kg was infused intravenously ,n=14), L NAME group (L NAME 30mg/kg was infused intravenously with ,n=12) Plasma levels of endotoxin, tumor necrosis factor(TNF?) and nitric oxide (NO) were determined before and after shock, immediately after resuscitation and 0 5h, 2h, 4h after resuscitation The 24h and 48h survival rates were recorded Lung, intestine, liver and kidney tissues were obtained 48 h after shock for microscopic examination Results The plasma endotoxin, TNF? and NO levels markedly increased and were kept at high levels after shock Lower plasma levels of endotoxin TNF? and NO, less tissue damages and high survival rates were observed in AG group as compared with those in L NAME group and shock group Conclusions The endotoxin,TNF? and NO play an important role in the development of irreversible shock AG is beneficial in the treatment of hemorrhagic shock, while L NAME does not improve the outcome of shock

BACKGROUND: The number of dementia patients ceaselessly increases with the extension of the life expectancy and the ageing of the population; hence the survival rate of patients with post-stroke dementia(PSD) has become an important issue of public health. Although it is generally believed that dementia could shorten human life expectancy, there is rare report regarding the impact of PSD on the survival rate of the patients in developing countries.OBJECTIVE: To investigate the impacts of ischemic dementia on the survival rate of the patients to explore the risk factors that would affect the survival rate of patients after cerebral infarction(CI).DESIGN: A prospective randomized controlled study based on patients.SETTING: The second department of neurology of a field surgery institute in a military university hospital of Chinese PLA.PARTICIPANTS: Totally 619 cases of acute CI including 313 males and 306 females aged between 55 and 85 years old[mean of (70. 3 ±9.5) years old] were selected form the Department of Neurology of the Daping Hospital of the Third Military Medical University of Chinese PLA between 1st May 1998 and 28th December 1999.INTERVENTIONS: Data including human factor, vascular factor and CI characters of 619 cases of ischemic cerebral stroke were collected and they also received neuropsychological test. Dementia was diagnosed in CI patients at admission and 3 months after CI according to DSM-Ⅳ criteria. Two-year follow up was conducted for the analysis of survival rate in PSD patients and survival-correlated predicting factors.and survival rate in CI patientsRESULTS: Totally 146 total patients(23.6% ) were diagnosed as PSD at 3 month after CI, of which 39 cases were pre-stroke dementia and 107 cases were CI-correlated dementia. The survival rate of PSD patients was 49.3%after(19.4 ±8.3) months of follow-up. The survival rate of patients with CI-correlated dementia was 53.7% while the non-dementia patients was 92.0% after(21.3 ± 9.1 ) months of follow-up. There was significant correlation between PSD and survival rate as indicated by multifactor analysis ( RR = 4. 91, 95% CI = 3.85 - 13.49) . The rest predicting factors included age(RR=1. 12, 95% CI=1.06-1.18), BarthelIndex(BI, RR=1.63,95% CI=1.15-2.31), auricular fibrillation(AF, RR=1.47, 95%CI = 1.17 - 1.85) and CI history( RR = 2. 81, 95% CI = 1.53 - 5.16).CONCLUSION: Dementia could reduce the survival rate of CI patients and it could be set as a predicting factor for post-infarction survival rate.

BACKGROUND: In subjects with different inflammatory and autoimmune diseases, soluble vascular cell adhesion molecule-1 (sVCAM-1) in sera increases, and its change may become an important monitoring index of immunological function, but its change rule has been unclear in acute cerebral infarction.OBJECTIVE: To observe the change of sVCAM-1 in sera of subjects with cerebral infarction and its clinical significance, and compare between the subjects with cerebral hemorrhage and normal population.DESIGN: A case controlled analysis.SETTING: Second Department of Brain, Research Institute of Surgery,Daping Hospital, Third Military Medical University of Chinese PLA.PARTICIPANTS: A total of 132 inpatients were selected from Second Department of Brain, Research Institute of Surgery, Daping Hospital, Third Military Medical University of Chinese PLA between May 2002 and April 2004. Among them, 89 subjects with cerebral infarction were classified into large infarction group (n=25,＞ 10 cm3), medium infarction group (n=31,4-10 cm3) and small infarction group (n=33, ＜ 4 cm3) respectively according to the size of infarct focus. There were 43 subjects in cerebral hemorrhage group, and 30 healthy persons were as normal control group.METHODS: Blood samples were isolated from subjects with cerebral infarction at hour 24, days 3, 7 and 14 after onset of the disease, while the blood samples were extracted from subjects with cerebral hemorrhage at hour24 and day 14 after the onset of the disease. 4 mL venous blood was obtained from the three groups. The serum concentration of sVCAM-1 was determined with double antibody sandwich method (DASM) in all the examinees.MAIN OUTCOME MEASURES: ①Dynamic change of the serum concentration of sVCAM-1 in the course of acute cerebral infarction, and compared with the other two groups. ②Comparison of the serum concentration of sVCAM-1 in different size of infarct focus. ③Change of the serum concentration of sVCAM-1 in acute cerebral infarction subjects complicated with infection.RESULTS: A total of 162 subjects were involved in the result analysis. ①The serum concentration of sVCAM-1 at the 24th hour after cerebral infarction was significantly higher in subjects with cerebral infarction than in subjects with cerebral hemorrhage group and normal control group [(1 184.5±68.3) ,(693.9±41.7), (576.1±39.8) μg/L,P＜0.01].Serum sVCAM-1 in the cerebral infarction subjects increased from the 24th hour to the 7th day after infarction gradually, while from the 7th day to the 14th day decreased gradually. However, the serum sVCAM-1 in the cerebral infarction subjects at day 14 was still markedly higher than that in the cerebral hemorrhage group and the normal control group (P ＜ 0.01 ). ②The serum concentration of sVCAM-1 was significantly higher in the large cerebral infarction group as compared with medium and small cerebral infarction groups [(1 217.4±59.3) ,(1 132.6±51.9) ,(983.7±54.2) μg/L,P ＜ 0.01]. ③The serum concentration of sVCAM-1 was significantly higher at days 3, 7and 14 in cerebral infarction subjects complicated with infection than in subjects without infection (P ＜ 0.01 ).CONCLUSION: The sVCAM-1 participates pathological change process of cerebral infarction, which can be regarded as monitoring index of cerebral infarction change. To block its production and expression can provide a new approach for improving the prognosis of cerebral infarction.

AIM: To observe the effect of glycine on the myocardial ischemic injury in mice METHODS: Mice were supplied with 20% glycine twice daily (0 025 mL/g, ig), or 40% Injection salviae miltiorrhizae composita (ISMC, 0 025 mL/g, ig) One week later, 0 02 U/g pituitrin was injected intraperitoneally The electrocardiogram was recorded, and activities of nitric oxide synthase (NOS), superoxide dismutase (SOD) and the content of malondiadehyde (MDA) in the myocardium were examined RESULTS: Glycine reduced changes in J spot in electrocardiogram Both glycine and ISMC increased activities of SOD and NOS, inhibited increase in MDA content in the myocardium induced by pituitrin There was no difference in above parameters between glycine-treated and ISMC-treated mice. CONCLUSION: These results demonstrated that glycine can protect myocardium from ischemic injury, the mechanism may be related to increase in activities of NOS, SOD and supressing the lipid peroxidation.

BACKGROUND: Activation of leucocyte and endothelial cell in ischemic area of brain and the expression of adhesive molecule on the surface can cause aggregation and infiltration of leucocyte which deteriorated cerebral injury due to cytotoxicity. Ligustrazine can inhibit thrombosis and improve microcirculation.OBJECTIVE: To observe the effect of ligustrazine on adhesion of leucocyte and endothelial cell in focal area after cerebral ischemia-reperfusion injury.DESIGN: Randomized controlled animal study.SETTING: Second Division of Brain, Department of Neurology, Daping Hospital of the Third Military Medical University of Chinese PLA; Department of Psychiatry, the Second People's Hospital of Yuxi, Yunnan Province.MATERIALS: The experiment was carried out at the Second Cerebral Laboratory of Neurological Department of Daping Hospital Affiliated to the Third Military Medical University of Chinese PLA. A total of 32 male Wistar rats weighing 250-300 g were randomly divided into normal control group (n=8), cerebral ischemia-reperfusion group (n=12) and cerebral ischemia-reperfusion + ligustrazine group (n=12).METHODS: Rats in ligustrazine group were venously injected with 15 g/kg ligustrazine phosphoric acid, and rats in normal control group and cerebral ischemia-reperfusion group were venously injected with the same volume of saline. Cerebral ischemia-reperfusion injury and adhesive changes of leucocyte in focal area after administration of ligustrazine were observed with immunofluorescent labeling technique and micro-ultra-speed imaging system.MAIN OUTCOME MEASURES: ① Adhesive density index of leucocyte of arteriole in focal area after cerebral ischemia-reperfusion injury; ② Adhesive changes of leucocyte in focal area after administration of ligustrazine.RESULTS: All experimental animals were involved in the finalanalysis.① As compared with those in control group, adhesive density index of leucocyte of arteriole in focal area in cerebral ischemia-reperfusion group was increased, broken stress between leucocyte and endothelial cell was decreased remarkably, adhesion was increased obviously, and there was significant difference (P ＜ 0.01). ② As compared with those in cerebral ischemia-reperfusion group, adhesive density index and adhesion of leucocyte in ligustrazine group were decreased and reached the lowest values after 24 hours. Broken stress was increased and maintained at a higher level. There was no significant difference from that in normal control group till 24 hours.CONCLUSION: Ligustrazine can relieve adhesion between endothelial cell and leucocyte after cerebral ischemia-reperfusion injury.

Objective To evaluate the effect of vertebral artery kinking on cerebral hemodynamics. Methods The patients with vertebral artery kinking on digital subtraction angiograph (DSA) were selected from 223 patients with vertebral-basilar artery transient ischemic attack, then the changes of vertebral artery hemodynamics were evaluated using transcranial color Doppler (TCD). Results There were 84 patients with vertebral artery kinking among 223 patients with vertebral-basilar artery transient ischemic attack. Patients with vertebral artery kinking were older and had more vascular risk factors than patients without vertebral artery kinking. Compared with the control group, patients showed decreased blood flow rate such as peak velocity (Vp) and mean velocity (Vm), increased pulsatility index (PI) and resistant index (RI) in vertebral artery kinking group. Conclusions Vertebral artery kinking is common abnormal artery among patients with vertebral-basilar artery transient ischemic attack, it leads to hemodynamic changes. Age and vascular risk factors are potential causes of vertebral artery kinking.

Objective To observe the effects of sleep deprivation(SD)on learning and memory and phos-phorylated cyclic AMP responsive element binding protein(pCREB) expression in hippocampus of mice,and to explore the mechanism of cognitive change after SD. Methods Twenty female C57BL/6J mice were randomly divided into sleep deprivation group(SD, n = 10) and normal cage control group (CC,n = 10). Touch method was used to establish the sleep deprivation model. 30 days after SD,all the animals were subjected for Morris Water Maze (MWM) to test mean escape latency and percentage of time spent in the target quadrant. pCREB level in hippocampus was tested with Western blot. Results The mean escape latency in SD group in the second and third day of MWM was (29.31 ±4.93) s and (25.33 ±5.06)s, respectively, and was longer than that in CC group ((26.05 ±5.96)s and (19.35 ±7. 85)s,respectively). Mice in SD group spent less time in the target quadrant than that in CC group((23.61 ±9.86)% and (37.46 ±7. 51)%,.respectively, P<0.05). Results of Western blot for pCREB revealed that the pCREB level in hippocampus in sleep deprivation group was significantly lower than that in control group(0.71 ±0.03 and 0.82 ±0.06, respectively, P<0.01) . Conclusion The impairment of spatial learning and memory ability in sleep deprivation animals may be associated with the reduction of pCREB in hippocampus.

Objective To detect the expression of TNF α and ICAM 1 in cerebral ischemia reperfusion injury. To explore their probable modulation mechanism.Methods Immunohistochemistry was used to examine the expression of TNF α and ICAM 1.The MPO activity was determined by spectrophotometry.Result The expression of TNF α and ICAM 1 were obviously rised after cerebral ischemia reperfusion (P< 0.05).Conclusion The up regulation of TNF α and ICAM 1 after cerebral ischemia reperfusion induced the accumulation of leukocytes, which involved in ischemia reperfusion injury mechanism. TNF α play an important role in expression of ICAM 1.