BACKGROUND: One of the main causes of the failure of central nerve regeneration is that the microenvironment (lack of nerve growth factor, inhibitory factor produced by excretion and formation of glial scar) in the injured central nerves is not favorable for the regeneration of axons. Therefore, it is important to improve the microenvironment of injured area for the regeneration of axons. Recently, olfactory ensheathing cells (OECs) have been attracting much attention as a key method to treat central nervous injury.OBJECTIVE: To investigate the effect of OECs on traumatic brain injury (TBI) in rats and whether they can reduce neurological impairment after TBI.DESIGN: A randomized controlled experimental trial based on experimental animals.SETTING: Department of neurosurgery in a hospital affiliated to a university.MATERIALS: The experiment was conducted in the Central Laboratory of Department of Neurosurgery, Kaifeng Railway Hospital from April 2003 to August 2003. Altogether 100 healthy adult SD rats of either gender,weighting 250- 350 g, were randomly divided into four groups: normal group, TBI group, normal saline group and OEC group with 25 rats in each. Each group was further divided into five subgroups with 5 rats in each.INTERVENTIONS: The models of TBI in rats were established, and OECs were transplanted into brain tissues immediately after injury. The scores of nerve injury were assessed in the rats at day 1, day 4, week 1, week 2 and week 4. The distribution of OECs in brain tissues was observed after the rats were sacrificed.MAIN OUTCOME MEASURES: Neurological function recovery of rats and distribution of OECs in brain tissues.RESULTS: At week 2 and week 4 after operation, neurological severity scores (NSS) in OEC group significantly differed from those of TBI group and normal saline group. HE staining or immunohistochemistry of GFAP and p75 revealed that OECs could survive in the transplanted site and migrate toward the surrounding tissues. The total number of p75 positive cells in five coronal tissue slices of 6 μm thick was added up at different intervals. The results showed that the number of OECs was decreased with the passing time.CONCLUSION: OECs can survive in the transplanted site and migrate to the surrounding tissues when they are transplanted into the iujured brain tissues immediately after TBI. Giving OECs can reduce neurological and motor dysfunction induced by TBI.

Aim To investigate the role of chemokine-like factor 1 ( CKLF1 ) in SH-SY5 Y cell migration and its molecular regulatory mechanism. Methods SH-SY5Y cells were stimulated with CKLF1 for 0. 5 h, 2 h, 8 h and 24 h, respectively. The migration distance and the percentage of migration cells were recorded by CELLocate analysis. The phosphorylation of focal ad-hesion kinase ( FAK) at Tyr-397 site was detected by Western blot analysis. By chemotaxis assays, we con-firmed the chemotaxis of CKLF1. Furthermore, FAK inhibitor PF-573228 and PLCγ inhibitor U73122 were used for the research of molecular regulatory mecha-nisms involved. Results CKLF1 promoted cell migra-tion and induced a strong increase in the phosphoryla-tion level of FAK-pY397 , which were significantly at-tenuated by the presence of U73122 ( a specific inhibi-tor for PLCγ) . In addition, the chemotaxis of CKLF1 was obviously blocked by the FAK inhibitor PF-573228 . Conclusion CKLF1 induces SH-SY5 Y cell migration via PLCγ/FAK signaling pathway.

Objective:To analyze the clinical features and genetic background of adrenoleukodystrophy(ALD).Methods:In this study, we reported a rare case of ALD who initially presented with progressive bilateral lower limb weakness. The clinical data of the patient and his family members were collected and the ABCD1 gene was sequenced for the patient and his three daughters by a high-throughput sequencing method.Results:The proband had a later onset of symptoms, a prolonged course of the disease, and initially exhibited bilateral lower limb weakness and nocturnal muscle spasms. The disease progressed to spastic quadriplegia, aphasia, dementia, swallowing difficulties, and urinary and fecal incontinence. Serum very-long-chain fatty acid concentrations were elevated. Subclinical cortisol secretion abnormalities were observed. Cranial imaging indicated symmetrical reduction in density around the lateral ventricles and white matter degeneration. The proband′s ABCD1 gene analysis revealed a novel heterozygous mutation c. 1367G>A, p. R456H. His three daughters carried the same nucleotide heterozygous mutation.Conclusion:This study investigates the clinical characteristics of ALD, providing additional clinical evidence for the diagnosis and treatment of this condition. Additionally, a novel mutation in the ABCD1 gene was identified, contributing to the genetic variation database.