Objective To evaluate the expressive variety of NGF gene in injured sciatic nerves of rat. Methods For hemi-quanti- tative analysis, RT-PCR method was used in the detection of the levels of NGF mRNA in the distal stumps at 1 day and 1, 2, 4 weeks following transection of sciatic nerve. Results The 1evel of NGF mRNA was low in the normal sciatic nerve. But it was increased in the distal stump after sciatic nerve transection. The biphasic increase in NGF mRNA was characterized by a first very rapid and transient increase peaking at ist day after lesion, than a second prolonged and slow elevation starting around ist weed after lesion. Conclusion The process in NGF gene expression after sciatic nerve lesion was biphasicly increased.

Objective To observe CNTF gene expression and expressive variety during postnatal development in rat spinal cord. Methods The spatial expression of CNTF mRNA in spinal cord was examined by in situ hybridization with dig\|CNTF cDNA probe.Reverse transcription\|polymerse chain reaction(RT\|PCR),as hemi\|quantitative method was used to investigate the expressive variety of CNTF mRNA levels in spinal cord during postnatal development. Results Hybridized signals of CNTF mRNA was found only in part of glial cells on the peripheral region of the ventral and lateral white funiculi of spinal cord,but could not be detected in the gray matter of spinal cord.The expression of CNTF mRNA in spinal cord appeared with a lower level on the first postnatal day.It increased significantly at postnatal 15th days,the expression of CNTF mRNA reached the peak at 30th days,and it began to decrease on the 60th days. Conclusion This study indicated that CNTF mRNA might be expressed in part of glial cells in the white matter.There was expression in spinal cord on the 1st day after birth and the expression levels of CNTF mRNA possessed the changeable character during spinal cord development.

Objective: To investigate the dynamic expression of hepatic carnitine palmitoyltransferase-II (CPT-II) in the mitochondrial inner membrane during hepatocyte malignant transformation induced by lipid accumulation. Methods: Male Sprague-Dawley rats were divided randomly into control, fatty liver, and induced cancer groups, which were fed with normal, high-fat (HF), and HF containing 2-fluorenylacetamide (0.05%, 2-FAA) diets, respectively, for 14 weeks. One rat from each group was sacrificed every two weeks and the blood and liver samples were collected. Liver morphological changes were evaluated with hematoxylin and eosin staining, and the liver tissue samples were divided into control, fatty liver, degeneration, precancerous, and cancerous groups accordingly. Hepatic lipids were dyed by the oil red O method. The CPT-II expression was measured by immunohistochemistry and compared with the specific CPT-II concentration (ng/mg liver protein, ng/mg P) among different groups. Serum levels of circulating total cholesterol (Tch), triglyceride (TG), alanine aminotransferase (ALT), and aspartate aminotransferase (AST) were quantitatively analyzed. Results: Massive lipid accumulation hepatocytes was seen in rats on HF and HF containing 2-FAA diets. The lipid levels in the control group were significantly lower than those in the fatty liver (t = -11.556, P < 0.001), degeneration (t = -4.847, P = 0.04), precancerous (t = -13.652, P = 0.005), and cancerous groups (t = -10.896, P = 0.008). The serum TG and Tch levels in the degeneration, precancerous, and cancerous groups were 2-3 times higher than those in the control group (P < 0.05). After 2-FAA treatment, the morphological changes of rat hepatocytes showed the progression from degeneration and precancerosis to cancerosis, with hepatocyte injury. The serum AST and ALT levels in the degeneration, precancerous, and cancerous groups were significantly higher (4-8 times) than those in the control group (P < 0.05). The specific concentration of liver CPT-II expression was significantly reduced during hepatocyte malignant transformation, as confirmed by immunohistochemistry, with the CPT-II levels significantly lower in the cancerous group than in any of other groups (P < 0.05). Conclusion Low hepatic CPT-II expression might lead to abnormal lipid accumulation in hepatocytes, which should promote the malignant transformation of hepatocytes.