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Background Toll-like receptor 4 (TLR4) is an immune related receptor.It plays an important role in inducing inflammation response.The inflammatory response secondary to optic nerve crush will results in serious retinal damage.It is worthy of studying the expression and effect of TLR4 in retina after optic nerve crush.Objective This experimental study was to explore the role of TLR4 in the loss of retinal ganglion cells(RGCs) after optic nerve crush.Methods Twenty-four SPF adult health Sprague-Dawley (SD) rats were used in the study and radomized into two groups based to the experimental time.The optical nerve crush models were established by crushing the optical nerve in the right eyes of the rats,and the left normal eyes served as controls.The rats were sacrificed by over anesthesia and retinas were isolated 3 days and 7 days after operation.Expression of TLR4 in the retinas was detected using immunofluorescence method.Reverse trancription PCR (RT-PCR) and Western blot were applied respectively for the detection of TLR4 mRNA and protein in the retinas.The apoptosis of RGCs was evaluated using TUNEL staining.The use and care of experimental animals followed theGuide for the Care and Use of Laboratory Animals of NIH.This study was approved by the Institutional Animal Care and Use Committee at the Zhongshan Ophthalmic Center.Results The expression of TLR4 in rat retinas presented with green fluorescence mainly in the inner layer of retinas.The fluorescence was enhanced in the model 3 days group and the model 7 days group compared with the corresponding control groups.The relative expressing values of TLR4 mRNA in the retinas were 2.92±0.06and 3.92±0.12 in the model 3 days and 7 days groups,respectively,which were significantly higher than 2.87±0.12and 3.44±0.17 in the control 3 days and 7 days group (t3d =-12.888,P＜0.001 ;t7d =-4.669,P=0.010).In the model 3 days group and model 7 days group,the grey values of TLR4 protein were 1.14±0.05 and 1.49±0.03,and those in the control 3 days and 7 days groups were 0.99 ± 0.09 and 1.38 ± 0.07,showing significant differences between them(t3d =-11.324,P＜0.001 ;t7d =-5.638,P=0.005).Apoptotic RGCs were obviously increased in the optic nerve damage group in comparison with the control group.Conclusions The TLR4 is over-expressed in the inner layer of retina after optic nerve crush,which suggestes that TLR4 is probably involved in the loss of RGCs after optic nerve crush.
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Objective To explore the pathophysiological mechanisim underlying the development and progression of chronic subdural hematoma (CSDH) through an ultrastructural observation of the outer membrane of CSDH. Methods A total of 8 samples of CSDH outer membrane were obtained from the 8 patients who had uncergone surgery of hematoma removal in our department from January 2008 to January 2009.CT scanning revealed 2 cases of low hematoma density,2 cases of hematoma isodensity, 2 cases of high hematoma density and 2 cases of mixed hematoma desity.Conventional light microscopy and electron microscopy were used to observe the ultrastructure of the outer membrane. Results Light microscopy showed numerous dilatated and congested macrocapillaries with a wide vascular lumen in the outer membrane of the hematoma capsule.Electron microscopy showed weak, discontinous or partially dissolved endothelial cells in the macrocapillaries.Scattered red blood cells in the extracellular space were found, indicating bleeding within the outer membrane.Eosinophils increased with enlarged granules within the cellular cytoplasm.Neutrophils and macrophages were also present in some specimens.Fibroblasts showed a state of significant proliferation and activation. Conclusions There are abundant newly formed vascular networks in the outer membrane of CSDH. Neomembrane formation, neovascularization and repeated micro-haemorrhages from these fragile new vessels may play a key role in the development and progression of CSDH.
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Objective To discuss the etiological relationship between brain trauma and glioma.Methods A case of post-traumatic glioblastoma was reported with regard to his clinical manifestations,imaging features and pathological characteristics, and the related literatures were present. Results This case is consistent with the criteria on the glioblastoma mutiforme following cerebral trauma in literatures.Conclusion The development of a brain tumour following a cortical injury is possible, although rare. The presupposition for the development of a glioma following brain trauma is a predisposing genetic alteration of brain cells.
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<p><b>OBJECTIVE</b>To find out the optimal approach to decompress externally the severe injured brain and to avoid possible complications caused by external decompression.</p><p><b>METHODS</b>68 patients who underwent external decompression after traumatic brain injury were admitted into Tianjin Medical University General Hospital for cranioplasty from 1995 to 2001. Complications were retrospectively investigated and analyzed in all patients. The findings were compared between the patients who accepted the decompressive craniectomy in our hospital and in local hospitals. chi(2)-test was employed for statistical analysis and complication evaluation.</p><p><b>RESULTS</b>Large craniectomy definitely caused some side effects to patients. Among various complications, several of them showed significantly high incidence (P<0.05) in patients who underwent the decompressive operation in local hospitals such as shunt-dependent hydrocephalous, subdural fluid collection, and CSF leakage from scalp incision. The rest of the complications had no remarkable difference (P<0.05) between the two groups including dilation or/and migration of lateral ventricle underlying the cranial defect, skin flap concavity, encephalomalacia of the decompressive area, seizure and infection.</p><p><b>CONCLUSIONS</b>To reduce the incidence of iatrogenic side effects, surgical craniectomy should be performed according to the strict indication and standard and any abuse should be avoided.</p>