[Brain impairment induced by oral intake of lead and its effects on expression of Hoxa9 Gen in Rats].

OBJECTIVE: To observe effects of oral intake of lead on the expression of Hoxa9 gen and the ability of learning and memory and explore the the toxic molecular mechanisms of lead. METHODS: Thirty male Wistar rats were chosen and randomly divided into the low lead dosage group, the high lead dosage group and the control group, 10 rats in each group. The low lead dosage group and the high lead dosage group were given respectively 0.06%, 0.2% lead acetate orally while the control group was given distilled water orally. The Y-maze test was used to measure the ability of learning and memory, the graphite heat atomic absorption spectrum method to determine the lead concentration in blood and brain, and the in situ hybridization (ISH) method to determine the expression of Hoxa9 mRNA in brain. RESULTS: (1) The number of electric shocks of the lead poisoned rats were significantly increased over time. The number of electric shocks of the lead poisoning rats was much higher than that of the control group (P < 0.01) (at the end of the experiment, the low lead dosage group: 31.8 +/- 2.26; the high lead dosage group: 37.3 +/- 1.70; the control group: 18.4 +/- 1.51). (2) The brain of the lead poisoned rats including the hippocampus, the cerebellum and the cerebral cortex were significantly atrophic and the apoptosis and necrosis occurred in the cells of the brain. Purkinje's cells in the cerebellum showed significant necrosis and disappearance. The structure of brain in rats of the control group demonstrated no atrophy. (3) The expression of Hoxa9 mRNA in the lead poisoned rats was significantly decreased compared with the control group. There were few Hoxa9 positive cells in the brain of the lead poisoned rats, but many of them were observed in the control group. CONCLUSION: Lead may inhibit the expression of Hoxa9 and induce atrophy and necrosis of brain, which gives rise to a damage of learning and memory.

Surgical treatment of giant esophageal leiomyoma.

AIM: To summarize the operative experiences for giant leiomyoma of esophagus. METHODS: Eight cases of giant esophageal leiomyoma (GEL) whose tumors were bigger than 10 cm were treated surgically in our department from June 1980 to March 2004. All of these cases received barium swallow roentgenography and esophagoscopy. Leiomyoma located in upper thirds of the esophagus in one case, middle thirds of the esophagus in five cases, lower thirds of the esophagus in two cases. Resection of tumors was performed successfully in all of these cases. Operative methods included transthoracic extramucosal enucleation and buttressing the muscular defect with pedicled great omental flap (one case), esophagectomy and esophago-gastrostomy above the arch of aorta (three cases), total esophagectomy and esophageal replacement with colon (four cases). Histological examination confirmed that all of these cases were leiomyoma. RESULTS: All of the eight patients recovered approvingly with no mortality and resumed normal diet after operation. Vomiting during meals occurred in one patient with esophagogastrostomy, and remained 1 mo. Reflux esophagitis occurred in one patient with esophago-gastrostomy and was alleviated with medication. Thoracic colon syndrome (TCS) occurred in one patient with colon replacement at 15 mo postoperatively. No recurrence occurred in follow-up from 6 mo to 8 years. CONCLUSION: Surgical treatment for GEL is both safe and effective. The choices of operative methods mainly depend on the location and range of lesions. We prefer to treat GEL via esophagectomy combined with esophago-gastrostomy or esophagus replacement with colon. The long-time quality of life is better in the latter.

[Protective effect of Gastrodia elata and E-gelatin on lead-induced damage to the structure and function of rat hippocampus].

OBJECTIVE: To observe the counteraction of Gastrodia elata and E-gelatin on the effect of subchronic lead poisoning on the ability of learning and memory and the ultrastructure in hippocampus. METHODS: Subchronic lead acetate exposure was given to rats (0.2 g x kg(-1) x d(-1)). Single and combined administration of Gastrodia elata (4 g x kg(-1) x d(-1)) and E-gelatin (1 g x kg(-1) x d(-1)) were conducted at the same time. Pb concentration in blood, and the ability of learning and memory (Y-maze test) of rats were measured. Ultrastructure of CA3 pyramidal cells in hippocampus under transmission electron microscope was observed. RESULTS: Blood Pb concentrations in each group (Pb group: 690.6 micro g/L, Pb + Gastodiae eleta group: 688.8 micro g/L, Pb + E-gelatin group: 663.8 micro g/L, Pb + combined group: 667.2 micro g/L) were higher than that in the control (28.24 micro g/L, P < 0.01). But there was no significant difference (P > 0.05) among these groups. In Y-maze test, the number of electric stroke in Pb group is higher than that in control (P < 0.01). Gastrodia elata or E-gelatin used singly could significantly reduce the number of electric stroke of lead-exposed groups (P < 0.05 in the first month and P < 0.01 in the second and third month). And the effect of combined use of them was more efficient than single use (P < 0.01). Under electron microscope, no anomaly was seen in the pyramidal cells of CA3 area in hippocampus of control group. But there was significant anomaly such as neucleus separation in the cells of Pb exposed group. In Pb-Gastrodia elata group, there were some stress response phenomena such as the occurrence of huge mitochondria while in Pb-E-gelatin group, the anomaly was mild. The cells in the CA3 area in hippocampus of the pb-Gastrodia-E-gelatin group were almost normal, and also showed some stress response phenomena. CONCLUSION: Gastrodia elata and E-gelatin may protect the neurons in CA3 area of hippocampus against damage induced by lead to improve the ability of learning and memory, and they have synergistic effect.

[The antagonistic action of Gastrodia elata combined with E-gelatin on lead-induced down regulation of c-fos expression in rat brain].

OBJECTIVE: To observe the effect of lead on the expression of c-fos mRNA in hippocampus and cerebellum and the ability of learning and memory in rat, and to observe the antagonistic action of Gastrodia elata and E-gelatin on the effect mentioned above. METHODS: Rats were exposed to lead acetate (0.2 g x kg(-1) x d(-1) and 0.1 g x kg(-1) x d(-1)). The single and combined administration of Gastrodia elata (4 g x kg(-1) x d(-1)) and E-gelatin (1 g x kg(-1) x d(-1)) were conducted at the same time. Blood lead concentration in rats were measured. The ability of learning and memory by Y-maze test were examined. The expression of c-fos mRNA in hippocampus and cerebellum during Y-maze test were observed by in situ hybridization (ISH). RESULTS: (1) Blood lead concentrations were significantly increased in both high and low doses of lead-exposed rats (P < 0.01). But there were no differences among high dose groups or low dose groups (P > 0.05). (2) In Y-maze test, the number of electric stroke during learning in lead-exposed group was significantly increased (P < 0.01) while that in Gastrodia elata and E-gelatin groups was significantly decreased (P < 0.05), and that in combined use group was more significantly decreased (P < 0.01). (3) There were much more deep-colored c-fos positive cells in CA3 area of hippocampus in low dose of Pb-exposed with Gastrodia elata + E-gelatin group. These cells were also found in high Pb with combined use or single use group, but which were not so densely distributed as the former. And they were hardly found in high and low doses of Pb alone groups. The changes of expression of c-fos cells in cerebellam were similar to those in hippocampus. CONCLUSION: The down regulation of c-fos expression may be one of the molecular mechanism of lead-induced impairment of learning and memory. Gastrodia elata and E-gelatin may antagonize the effect of lead on c-fos expression, and combined use of both drugs may potentiate the antagonism.