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| 1 | Spinal cord injury in patients with systemic lupus Erythematosus Clinical manifestations, imaging characteristics and treatment显示文摘BACKGROUND: There are fewer reports on systemic lupus erythematosus (SLE) related myelitis, and definite and uniform therapeutic program is not available. OBJECTIVE: To observe the clinical manifestations, imaging characteristics, results of laboratory examination and treatment of SLE. DESIGN: A retrospective case analysis. SETTING: Department of Neurology, the Second Affiliated Hospital of Sun Yat-sen University. PARTICIPANTS: Totally 1 052 SLE inpatients were selected from the Second Affiliated Hospital of Sun Yat-sen University from January 1995 to May 2005, and they all accorded with the diagnostic standards for SLE set by American Rheumatism Association in 1982. 124 of them were diagnosed to have damage of central nervous system. Inclusive criteria: Patients with one of the focal physical signs, including mental and behavior disorders, headache, seizure and involvement of nervous system. Exclusive criteria: Patients with hypertensive encephalopathy, damage of nervous system due to uremia and infection of central nervous system. Spinal cord lesion occurred in 15 female cases of 23–51 years old. Informed consents were obtained from all the participants. METHODS: The physical signs, laboratory examinations, therapeutic program and prognosis were recorded in the 15 patients with symptoms of spinal cord lesions. All the patients underwent MRI scan of brain or lesioned segment of spinal cord, and 8 cases of them underwent lumbar puncture to determine intracranial pressure, routine and biochemical examinations were cerebrospinal fluid were performed. The disease activity of SLE in systems beyond central nervous system was evaluated with modified lupus activity criteria count (LACC). MAIN OUTCOME MEASURES: ① Incidence of SLE related myelitis, attack age distribution and its association with the activity of SLE; ② Comparisons of the clinical characteristics, cranial and spinal cord MRI manifestations, different therapeutic program and prognosis. RESULTS: All the 15 SLE patients were involved in the analysis of results. ① The incidence of SLE related myelitis was low (1%, 15/1 052). ② SLE related myelitis occurred mostly when the SLE symptoms were active, and only a few occurred at the stable period. ③ Among the SLE patients, MRI displayed abnormal changes in 71% (10/14), the typical changes appeared abnormal signals at corresponding spinal segments, manifested as prolonged T1 and T2 signals, thickened spinal segments. Lumbar segments were mostly involved. ④ Of the 9 patients treated with hormone impact, 7 cases (78%) had obvious improvements, and the effects were better in those treated with immunosuppressor combined with intravenous immunoglobulin of large dosage. CONCLUSION: ① Myelitis is a rare complication of SLE. ② MRI serves as a valuable supplementary approach in the diagnosis of SLE related myelitis without specificity. ③ Steroid pulse combined with immunosuppressor and intravenous immunoglobulin of large dosage is effective in the treatment. | Yamei Tang Fusheng Zhang Qingyu Shen Xiangpen Li Yigang Xing | 2007 | Neural Regeneration Research2007，2，3： | 1 |
| 2 | Valsartan Blocked Alcohol‐Induced, Toll‐Like Receptor 2 Signaling‐Mediated Inflammation in Human Vascular Endothelial Cells显示文摘 | Yushu Wang Yi Li Qingyu Shen Xiangpen Li Juan Lu Xiangping Li Deling Yin Ying Peng | 2014 | Alcohol Clin Exp Res2014，，10： | 1 |
| 3 | Renovascular hypertension causes cerebral vascular remodeling显示文摘Renovascular hypertensive rats (RHRs) were developed using the 2-kidney, 2-clip method. All RHRs at 10 weeks displayed high permeability of the cerebral surface blood vessels. Vascular casts of the RHRs showed that the vascular network was sparse. The arterioles of the RHRs at 10 weeks had smaller lumen diameters, but thicker vessel walls with hyalinosis formation compared with control animals. The endothelial cell membrane appeared damaged, and microthrombus formed. After ischemia, the infarction size was larger in RHRs than in control animals. These results suggest that cerebral arterioles in RHRs underwent structural remodeling. High blood pressure may aggravate the severity of brain injury in cerebral ischemia and affect the recovery of ischemia. | Yamei Tang Xiangpen Li Yi Li Qingyu Shen Xiaoming Rong Ruxun Huang Ying Peng | 2011 | Neural Regeneration Research2011，6，25： | 0 |
| 4 | Long-term existence of cerebral hypoxic tissue in a rat model of cerebral ischemia/reperfusion injury显示文摘BACKGROUND:Hypoxic tissue surrounding the ischemic core may represent the ischemic penumbra following cerebral infarction.However,some studies have shown that the duration of ischemic tissue is longer than previously believed. OBJECTIVE:To clarity whether cerebral hypoxic tissue could survive long-term and whether it is altered in rats following cerebral infarction;to establish an ischemia/reperfusion model in which hypoxic tissue exists for extended periods of time. DESIGN,TIME AND SETTING:A completely randomized grouping and controlled experiment was performed at the Experimental Animal Center of Sun Yat-sen University and Medical Research Center,the Second Affiliated Hospital of Sun Yat-sen University between June and December 2008. MATERIALS:4,9-diaza-3,3,10,10-tetramethyldodecan-2,11-dione dioxime(BnAO)(HL91),used as the hypoxic marker for autoradiography,was supplied by the Beijing Syncor Star Medicinal,China, and the flesh eluent Na^(99)Tc^mO_4 to mark HL91 was supplied by Guangzhou Medical Isotope Center of the China Institute of Atomic Energy.2-(2-nitro-1H-imidazole-1-yl)-N-(2,2,3,3,3-pentafluoropropyl) acetamide(EF5) and its antibody ELK3-51,used as a hypoxic marker for immunofluorescence,were supplied by the University of Pennsylvania,USA. METHODS:Male Sprague Dawley rats were randomly divided into four groups:1.5-hour ischemia/reperfusion group(1.5 h IR),2-hour ischemia/reperfusion group(2 h IR),3-hour ischemia/reperfusion group(3 h IR),and permanent ischemia(PI) group,with 21 rats in each group. The middle cerebral artery occlusion model was established using the intraluminal suture method, while reperfusion was performed by removing the suture at each observation time point.However,in the PI group,the suture was left in the artery. MAIN OUTCOME MEASURES:Area and average absorbance of fluorescence,representing hypoxic tissue,were measured by image-analysis. RESULTS:Autoradiography revealed positive hypoxia at days 1 and 14 postoperatively in the 1.5 h IR group.Immunohistochemistry results demonstrated that hypoxic tissue existed in the 1.5 h IR group on days 1,3,7,and 14,with decay of the area,but no significant weakening of fluorescent intensity.Hypoxic tissues were not observed at day 7 postoperatively in the 2 h and 3 h IR groups, as well as PI group. CONCLUSION:Similar to human cerebral infarction,hypoxic tissues in rats exist for an extended period of time following cerebral infarction,and diminish over even longer periods.Moreover,the 1.5 h IR rat model was the suitable model for studying long-term hypoxic tissue after cerebral infarction. | Yidong Wang Jingrui Pan Yu Qiu Xiangpen Li Mei Li Ying Peng | 2009 | Neural Regeneration Research2009，4，5： | 0 |
| 5 | Stereotaxic microinjection of adenovirus-mediated human tissue Kallikrein gene reduces apoptosis in a rat model of middle cerebral artery occlusion显示文摘BACKGROUND:Several studies have demonstrated that Kallikrein gene transfer provides neuroprotection. Whether the neuroprotective effects of human tissue Kallikrein (HTK) are associated with apoptosis remains unclear. OBJECTIVE: To investigate the effects of HTK on apoptosis in the peripheral cerebral infarct region. DESIGN, TIME AND SETTING: The completely randomized grouping, gene engineered, controlled experiment was performed at the Lin Baixin Laboratory Center, the Second Affiliated Hospital of Sun Yat-sun University between September 2007 and April 2008. MATERIALS: Ninety clean, healthy, male, Sprague Dawley rats were included. pUC19-HTK plasmid was constructed in the Laboratory for Neurology, the Second Affiliated Hospital of Sun Yat-sen University, China. bcl-2, bax, caspase-3, and β-actin were designed and purified by Shanghai Shuiyuan Company, China. METHODS: Middle cerebral artery occlusion (MCAO) model was established in all rats. At 72 hours after MCAO model establishment, rats were randomly divided into 3 groups, with 30 rats per group: blank control, saline, and pAdCMV-HTK. The saline and pAdCMV-HTK groups were respectively stereotactically micro-injected with 5 μL physiological saline or pAdCMV-HTK at the area surrounding the cerebral infarction region. Only puncture was performed, without any injection, in the blank control group. MAIN OUTCOME MEASURES: At 72 hours after MCAO establishment, as well as at 24 hours, 72 hours, and 7 days subsequent to treatment, exogenous HTK expression was detected by immunohistochemistry. Apoptosis was examined by terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling (TUNEL), while mRNA levels of bcl-2, bax, and caspase-3 were detected by reverse transcription-polymerase chain reaction. In addition, neurological severity scores were evaluated prior to and after treatments. RESULTS: Ninety rats were included in the final analysis. HTK was primarily detected in the cytoplasm at 24 hours after pAdCMV-HTK injection. Thereafter, HTK expression gradually increased and reached a peak level at 72 hours after injection, which was significantly different from the blank control and saline groups (P < 0.05). At 7 days, HTK expression began to decrease, but remained higher than the saline and blank control groups (P < 0.05). Apoptotic cells aggregated around the cerebral infarction region. Compared with the saline and blank control groups, the mean number of TUNEL-positive cells was notably decreased in the pAdCMV-HTK group at each time point after treatment (P < 0.05). mRNA levels of bcl-2, bax, and caspase-3 were elevated in all groups at 24 hours after treatment, peaked at 72 hours, and then gradually decreased again at 7 days. Compared with the saline and blank control groups, bcl-2 slightly increased, but was not significantly different from the pAdCMV-HTK group (P > 0.05). bax and caspase-3 mRNA levels were significantly reduced at 24 and 72 hours after treatment (P < 0.05). At 72 hours and, in particular, at 7 days after treatment, neurological severity scores were significantly less in the pAdCMV-HTK group compared with the saline and blank control groups (P < 0.05–0.01). CONCLUSION: HTK could protect neural cells in the peripheral cerebral infarction region from apoptosis, which resulted in a better outcome. This may be related to modulated bcl-2 expression and reduced bax and caspase-3 expression. | Ruiyan Lu Lianhong Yang Qingyu Shen Mei Li Xiangpen Li Ying Peng | 2008 | Neural Regeneration Research2008，3，8： | 0 |
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