AIM: By evaluating the effect of selective ni tric oxide synthase inhibitor, aminoguanidine (AG), on the contents of amino aci ds in the rat brain following cerebral ischemia, to investigate the effect of AG on cerebral ischemic injury and the possible mechanism. METHODS: Adult male SD rats, weighing 250-300 g, were matched ra ndomly. We made the focal cerebral ischemic model with thread embolism of left m iddle cerebral artery occlusion (MCAO). AG was administrated after MCAO. Rats we re killed at the scheduled time. The changes of infracted volume and the content s of aspartate, glutamate, glycine and ?-aminobutyric acid (GABA) from striatum , hippocampus and cortex were assayed, respectively. RESULTS: The cerebral infarct volume in AG group were significan tly lower than that in ischemic group. The contents of aspartate, glutamate, gly cine and GABA from striatum, hippocampus and cortex in ischemic group were marke dly higher than those in sham group. The contents of aspartate and glutamate in AG group were significantly lower than those in ischemic group, but the contents of glycine and GABA in AG group were higher than those in ischemic group. CONCLUSION: It may be concluded that AG has a beneficial effect on ischemic rat brain. The possible protective mechanism is that AG can reduce t he contents of aspartate and glutamate, increase the contents of glycine and GAB A.

Many studies have showed that nitric oxide(NO) might in duce dual effects during focal cerebral ischemic injury,namely neuroprotctive and neurotoxic effects.After cerebral ischemia, NO induced by endothelial NO synthase(eNOS) has neuroprotective effect. NO induced by neuronal NO synthase(nNOS) and inducible NO synthase(iNOS) has neurotoxic effect. Dual effects of nitric oxide have been becoming novel subjects for the protection of focal cerebral ischemic injury.

Objective To investigate the effects of nitric oxide(NO) and its donor(L-arginine) on focal cerebral ischemic injury in rats. Methods Forty-two healthy male SD rats weighing 250-300g were used. The animals were anesthetized with 20% urethane 1g? kg-1. Common carotid artery (CAA), external carotid artery(ECA) and internal carotid artery were(ICA) exposed through a median incision in the neck. Middle cerebral artery occlusion (MCAO) was produced by insertion of a 40 mm long nylon thread (0.3 mm in diameter) into ICA through ECA. The tip of the nylon thread was made into a ball of 0.5 mm in diameter with heat and the length of insertion was (18.5?0.5)mm on average. The animals were randomly divided into four groups: group 1: sham operation; group 2: ischemia group; group 3: low dose L-arginine(300mg?kg-1 intraperitoneal injection) and group 4: high dose L-arginine(500mg?kg-1 IP). Group 3 and 4 were further divided into 3 subgroups: subgroup A: L-arginine was given 1h after MCAO and the animals were killed 2h after medication (1h + 2h); subgroup B: L-arginine was given 3h after MCAO and the animals were killed 3h after medication(3h + 3h) and subgroup C: L-arginine was given 6h after MCAO and the animals were killed 3h after medication(6h + 3h) . The brain was removed immediately. The volume of cerebral infarct/volume of whole brain was calculated(%) . The NO, MDA content and NOS, SOD activity in the brain tissue of ischemic hemisphere were measured. Results L-arginine significantly decreased cerebral infarct volume and ameliorated focal cerebral ischemia. The effects in high dose group were better than in low dose group. L-arginine significantly increased NO content, decreased MDA content and enhanced the SOD activity in the focal ischemic cerebral tissue. Conclusions It may be concluded that L-arginine has beneficial effect on brain injury in acute ischemic stage and high dose provides better effects.

Objective To analyse the incidence, clinical features, histopathology and clinicopathological correlation in different age group of 524 cases with IgA nephropathy(IgAN) retrospectively. Methods 524 cases of IgA nephropathy were divided into three groups according to their age, and the clinical and renal pathological features were analyzed. Results In children group(≤15 years), the incidence of recurrent gross hematuria was 47. 2% and renal impairment 4. 6%. Malignant hypertension as first presentation associated with serious renal impairment occured in 3. 8% patients of youth and adult group (16 - 49 years). Higher incidence of nephrotic syndrome and acute renal failure was found in elder group (50 - 69 years). Conclusions The incidence Of IgAN in children and elder population is increased, especially in the children. They need a further follow-up. For elder patients considered as IgAN, a renal biopsy seems to be necessary. While youths and adults still account for the most part of IgAN patients.

Objective By exploring echocardiographic ch aracters and pathologic examination of noncompacted ventricular myocardium(NVM), to prevent life-threatening arrhythmias and embolism. Methods Echocardiographic examinations included four-chamber view, two-chamber view and short axis view of left ventricle, with an emphasis on observing left ventricular myocardium and endocardium approach to one-third of apex of heart. Results All 24 patients showed obvious echocardiographic findings characterized by prominent and excessive myocardial trabeculations and deep intratrabecular recesses in the affected ventricular cavity. Three cases complicated with other congenital heart malformations, 20 cases with congestive heart failure and only 2 cases were asymptomatic. Coronary arteriography was performed in 13 cases and revealed normal findings. Two cases eventually underwent heart transplantation because of severe congestive heart failure. Gross and histological findings demonstrated prominent muscular trabeculations, with deep intratrabecular recesses into lesion heart. Serial section from the base of the ventricle toward the apex revealed gradually weaker myocardium. Noncompaction of ventricular myocardium showed a thin, compacted epicardial and an extremely thickened endocardium by fibrous tissue. Conclusions Noncompaction of ventricular myocardium has characteristic echocardiographic manifestations and specific pathologic changes, which are different from those of primary enlarged type of cardiomyopathy.

Objective To study effects of 1 800 MHz electromagnetic field exposure in pregnancy on the ultrastructure of the hippocampus of offspring rats. Methods Ninety Wistar rats(female and male was 2:1) were mated,and the pregnant rats were exposed to 1 800 MHz microwave field with power density of 0.5 mW/cm2 or 1.0 mW /cm2,12 h/d,for 21 consecutive days,the rats in the control group received dummy exposure. Three rats aged 3 days and 72 days were selected from groups for ultrastructure observation of hippocampus. Results No significant pathological changes were observed in nerve cells and capillary vessels in the hippocampus. Conclusion The results of the present paper indicate that pregnancy exposure to 1 800 MHz electromagnetic field,may not lead to abnormal ultrastructure changes in hippocampus of offspring rats

Objective To investigate and to analyze the extend,structure,regional distribution,and causes of the hearing disability in Guangxi,from the information gathered from the second national sample survey among the disabled;to evaluate the present situation of hearing disability among Guangxi residents;and to provide basis for setting up effective preventing and intervening program for the hearing disabled.Methods The sampling methods was used to carry out a selective examination among 200 sample areas,including 25 counties and 100 villages.There were about 400 residents in each area,22 569 families,80 712 people involved in the survey with the sampling rate of 1.730%.The standard time began at 0 o'clock,April 1st,2006.Results Among the 5 837 disabled,1 467 were hearing disabled,accouting for 25.13% of the total.70 were grade 1 hearing diability(4.770% of the total number of the disabled);127 were of grade 2 hearing diability (8.660% of the total number of the disabled);689 grade 3 hearing diability (46.98% of the total number of the disabled);581 grade 4 hearing diability(39.600% of the total number of the disabled).The distribution of primary causes indecated that 911 were age related hearing loss,accounting for 62.10%;155 had unknown cause,accounting for 10.570%;158 ontological disease,accounting for 10.770%;111 systemic disease,accounting for 7.57%;132 had other reasons,accounting for 8.99%.Among all,821 were male (560%),646 were female (440%).The gender ratio was 1.27:1.910 were rural residents (620%),557 urban residents (38%).The age distribution was:3 under six (0.20%),10 from 7 to 17 (0.68%),215 from 18 to 59 (14.66%),1 239 over 60 (84.46 %).Conclusion Hearing disability is of the highest incidence among all kinds of disability in Guangxi.Most of the hearing impaired are associated with age and ear disease.Therefore prevention,education and treatment can help reduce the incidence of hearing disability.

Objective: To investigate the beneficial effect of NG-nitro-L-arginine(L-NA) on cerebral ischemic injury and the possible mechanism by evaluating the effect of nitric oxide synthase(NOS) inhibitor,L-NA,on the contents of aspartate,glutamate,glycine and?-aminobutyric acid(GABA),respectively,in striatum,hippocampus and cortex of rat brain following cerebral ischemia. Methods:The model of focal cerebral ischemia in rat was prepared.Rats were divided into sham-operated group,ischemic group and L-NA group.Each group was further divided into 3 subgroup(n=6 for each): the middle cerebral artery occlusion(MCAO) was maintained for 2,6 and 12h,respectively.L-NA(20 mg/kg,ip) was administrated after MCAO,two times a day,for 3 consecutive days.The changes of infarcted volume and the contents of amino acids were assayed. Results:The infarcted volume(IV%) was not significantly different among the ischemic groups with or without L-NA administrated 2 or 6 h after MCAO;and was markedly decreased in the ischemic group with L-NA administrated 12 h after MCAO(P

AIM: To evaluate the effect of aminoguanidine (AG) on inflammatory factors and neuronal apoptosis after focal cerebral ischemic injury in rats and the possible mechanism of protective effect of AG against cerebral ischemic injury. METHODS: Thirty male SD rats (weighing 250 g-280 g) were randomly divided into three groups: (1) sham operated group (SH group, n=10), (2) ischemic groups (IS group, n=10), (3) AG group (n=10). In AG group, AG at dose of 100 mg?kg-1 was given intraperitoneally twice a day for 3 consecutive days. In IS group, normal saline was given instead of AG. Focal cerebral ischemia was produced by middle cerebral artery occlusion (MCAO) for 12 h. A nylon thread with rounded tip was inserted into left internal carotid artery cranially until resistance was felt. The distance from bifurcation of common carotid artery to the tip of the thread was about 18-19 mm. Focal cerebral ischemia was confirmed by left Horner's syndrome and right side hemiplegia. In SH group, the carotid artery was exposed but no thread was inserted. The expression of tumor necrosis factor-?(TNF-?) was determined by immunochemistry and the content of interleulin-1?(IL-1?) was measured by radioimmunoassay. The expressions of Bcl-2 and Bax protein were detected by flow cytometry. RESULTS: The expression of TNF-? and the content of IL-1? were markedly increased after MCAO. Significantly increased DNA fragmentation, the indication of apoptosis, was detected after MCAO. The expression of TNF-? and the content of IL-1? were significantly lower in AG group than those in IS group. The percentage of apoptosis cells and expression of Bax protein were markedly lower in AG group than those in IS group but still significantly higher than those in SH group. The expression of Bcl-2 protein was markedly higher in AG group than that in IS group. No significant difference in the expression of Bcl-2 protein between IS and SH group was observed. CONCLUSION: AG inhibits the increase in the expression of TNF-? and the content of IL-1?, and protects neurons from apoptosis induced by focal cerebral ischemia through increasing the Bcl-2 protein expression and inhibiting the Bax protein expression.