Objective To investigate the value of methylprednisolone pulse therapy on the acute treatment of multiple sclerosis.Methods 46 cases of the acute phase of patients with multiple sclerosis treatment in the hospital's department of neurology were chosen,who were divided in accordance with the principle of randomized controlled study group and the control group,each group of 23 patients.The study group was given methylprednisolone in the treatment and control group were given dexamethasone treatment.The clinical efficacy and complications of the treatment of patients were compared.Results The study group markedly in 14 cases,effective 54 cases,the total effective rate was 82.6％ ;the control group,10 casesmarkedly effective in 4 cases,9 cases ineffective,the total effective rate was 60.9％ ; compared the two sets of data decline before treatment,there was a statistically significant difference (x2 =5.236,P ＜ 0.05).After the treatment,the two groups of patients with EDSS scores compared with EDSS scores of the study group was significantly lower than that of the control group,the difference was statistically significant(t =3.135,P ＜ 0.05).Conclusion In acute phase of patients with multiple sclerosis,methytprednisolone pulse therapy can reduce the incidence of complications,and reduce the patient's nervous system damage,which can improve the quality of life in patients.

Objective To study the expressions and prognostic significance of high mobility group protein A1 (HMGA1) and high mobility group protein A.2 (HMGA2) in pancreatic carcinoma.Methods The expressions of HMGA1 and HMGA2 were examined by immunohistochemical SP method in 60 cases of pancreatic carcinoma and 30 cases of normal pancreatic tissues.The relationship between the expression and prognosis was also analyzed.Results The expressions of HMGA1 and HMGA2 in pancreatic carcinoma were significantly higher than those in normal tissues,and the positive expression rates were 70.0％ vs.6.7％ (x2 =32.105,P =0.000) and 73.3％ vs.3.3％ (x2 =39.200,P =0.000).The expression of HMGA1 in pancreatic carcinoma was correlated with histological grade (x2 =6.774,P =0.034),TNM stage (x2 =4.776,P =0.029) and lymphatic metastasis (x2 =12.614,P =0.000).The expression of HMGA2 in pancreatic carcinoma was correlated with histological grade (x2 =8.200,P =0.017) and TNM stage (x2 =7.253,P =0.007).The expression of HMGA1 was positively associated with HMGA2 expression (r =0.393,P =0.001).Kaplan-Meier analysis showed that the median survival time of HMGA1 and HMGA2 positive patients were shorter than those patients with HMGA1 negative and HMGA2 negative (14.0 months vs.24.0 months,x2 =14.568,P =0.000;15.0 months vs.21.0 months,x2 =7.270,P =0.007).Conclusion HMGA1 and HMGA2 are highly expressed in pancreatic carcinoma,and play synergistic roles in the generation and progress of pancreatic carcinoma.There is certain value of combined detection of HMGA1 and HMGA2 to predict the prognosis of pancreatic carcinoma.

Alzheimer's disease (AD) is a neurodegenerative disorder characteristic of neurons reducing, senile plaques, neurofibrillary tangles and so on, and the most common cause of dementia among the elderly. Many efforts have been made to understand the epigenetic mechanisms involved in the development of AD, such as gene methylation and histone acetylation, although the exact mechanisms are not yet entirely clear. Here, we provide a review of the epigenetic mechanisms and related research in AD, which may provide a new direction for the research as well as the development of the epigenetic drugs.

With the progress and development of the DNA test and imaging technique, and the evolu-tion of evidence rule which bring the discussions about whether the individual identification using imag-ing data is outdated, and other disputes such as whether radiologic evidence could be suitable for con-temporary evidence and be used to solve the posture difference of imaging test. This article summaries the domestic and foreign researches of individual identification using imaging data in the past 20 years and reviews the problems above.

Objective To study the neuroprotective effects of neuregulin-1?(NRG-1?) on the nervous behavioral function,cerebral infarction volume,brain water content(BWC),neuronal apoptosis and aquaporin-4(AQP-4) expression in astrocytes after cerebral ischemic reperfusion and the related mechanism in mice.Methods Intraluminal thread methods were applied to establish the middle cerebral artery occlusion reperfusion models in the mice.Neuregulin-1?(2?g / kg) was injected into the internal carotid artery for treatment.The nervous behavioral function was evaluated with Bederson's test.The cerebral infarction volume was observed with tetrazolium chloride staining.The BWC was measured by dry-wet weight comparing.The apoptosis positive cells were counted by immunofluorescence assay.The expression of AQP-4 was determined by immunohistochemical assay.Results Nervous behavioral malfunction appeared in all the mice with left middle cerebral artery occlusion and/or reperfusion.The infarction focus showed in the ischemic hemisphere after the injury.The BWC,the number of neuronal apoptosis cells and AQP-4 expression in astrocytes were higher than those in the sham group. In the NRG-1? treatment group,the nervous behavioral function was improved 24 hours after ischemia,the number of apoptosis positive cells reduced and the infarction volume decreased significantly compared with the control group(P0.05).In the groups of reperfusion for 22,46 and 70 hours,the five indexes mentioned above were significantly different from those in the corresponding control groups(P

Objective To explore the neuroprotective effect and mechanism of picroside II on ERK1/2 signal transduction pathway after cerebral ischemia injury in rats.Methods The focal cerebral is-chemic models were established by inserting a monofilament threads into middle cerebral artery occlusion (MCAO) in 100 Wistar rats and treated by injecting picroside II (20 mg/kg) intraperitoneally.The neu-robehavioral function was evaluated by modified neurological severity score points ( mNSS) test.The cerebral infarct volume was measured by tetrazolium chloride ( TTC) staining.The apoptotic cells were counted by terminal deoxynucleotidyl transferase dUTP nick end labeling ( TUNEL) assay.The expression of pERK1/2 in cortex was determined by the immunohistochemistry ( IHC) and Western Blot ( WB) .Results mNSS test showed that severe neurological dysfunction was found in model and LPS groups,and the scores of mNSS were significantly increased;meanwhile the scores of mNSS in treatment group and U0126 group were signifi-cantly lower than that in model and LPS groups (P<0.05).TUNEL assay showed that the apoptotic cell inde-xes (ACI) in different groups were (0.06±0.02),(0.27±0.03),(0.07±0.02),(0.26±0.03)and(0.09± 0.05) ,and the ACI in treatment and U0126 groups was obviously lower than that in model and LPS groups (P<0.05) .With IHC and WB,pERK1/2 level in model group was the highest,which was slightly higher than that of LPS group,and pERK1/2 expression in treatment and U0126 groups was significantly decreased com-pared with that in model and LPS groups (P<0.05) .Conclusion The activation of ERK1/2 by cerebral is-chemia could induce the cell apoptosis.Picroside II might reduce cell apoptosis by inhibiting the activation of ERK1/2 in ischemic brain injury.

Objeetive To investigate the optimized concentration,effectiveness and histological change of Pingyangmycin by local injection of keloids for two weeks.Methods The appropriate concentration was analyzed,based on the Vancouver scar scale.48 eases of keloids were randomly divided into 4 groups with different concentrations of Pingyangmycin (1,0.5,0.25,and 0.125 mg/ml).Each case was iniected for five times at two weeks intervals,and then the statistical results (pair t test) and the histological changes were evaluated.Results Statistically,0.5 mg/ml group was more effective (P=0.0026),and this group had significant differences from the others (SNK test).The rate of the recurrence for one year was 12.00% in the whole effective cases.The keloid tissue after treatments,histologically,showed the thicker epidermis and larger papillary layer of the dermis,more inflammatory cells.Conclusions 0.5 mg/ml Pingyangmycin is the most appropriate concentration in this study and 0.25 mg/ml is the effective one.This treatment for keloid is convenient,safe,effective,low recrudescence and few side effects.

Objective To investigate the effects of inosine on the neuronal apoptosis and the expression of cytochrome C mRNA after focal cerebral ischemia and reperfusion in rats,and to explore the neuroprotective mechanisms of inosine. Methods SD rats model of focal ischemic reperfusion was induced by intraluminal middle cerebral artery occlusion (MCAO) with a nylon monofilament suture. Inosine (100 mg/kg) was injected intraperitoneally twice following MCAO. Apoptosis was determined by terminal deoxynucleotidy1 transferase-mediated uridine 5'-triphosphate-biotin nick end -labeling (TUNEL) staining. In situ hybridization was performed to examine the expression of cytochrome C mRNA. Results TUNEL-positive cells were observed 2 h after reperfusion and peaked at 1 d and 2 d after reperfusion in cortex and striatum respectively. Inosine reduced the number of TUNEL-positive cells at and after reperfusion 12 h. Cytochrome C mRNA expressed in cortex and striatum of ischemic hemisphere as early as at 2 h after reperfusion and reached a peak at 12 h and 1 d in cortex and striatum respectively. Inosine could diminish the expression of cytochrome C mRNA at and after reperfusion 12 h. Conclusions Inosine might play a neuroprotective role by inhibiting the neuronal apoptosis and the expression of cytochrome C mRNA which were induced by cerebral ischemia reperfusion injury.

Objective To investigate the effects of aquaporin4 (AQP4) on the brain injury after cerebral ischemic reperfusion and to search the new method that can prevent and cure the injury. Methods Locally injection of naked DNA ( pcNDA3.1/Zeo), which carries AQP4 gene and reporter gene green fluorescent protein(GFP), in the brain was performed 12 h before ischemic challenge to up-regulate the AQP4 expression. The expressed level of AQP4, the infarction size and neurological deficit scores were estimated in three groups. Results (1) Exogenous AQP4 expression in the brain did not affect the healthy rat neurological deficit score; (2) Rat neurological deficit scores were 7.9?0.7, and 7.1?0.9 respectively in 12 h and 24 h after reperfusion in AQP4 injected group, which were lower than that in plasmid control group when both groups were challenged with reperfusion after ischemia; (3) Expression of AQP4 in the brain was higher in AQP4 injected group than plasmid control group and control group in early stage after reperfusion; (4) Expression of exogenous AQP4 in the brain increased the cortex and striatum infarction size 24 h after reperfusion, which were (261.0?18.2) mm 3 and (21.9?1.9) mm 3, respectively, in AQP4 injected group more than plasmid control group. Conclusions (1) Increased local AQP4 expression in brain does not affect neurological function in the healthy rat; (2) Pre-expression of AQP4 increase infarction size and neuro-functional injury; (3) Modification of AQP4 activity and regulation of AQP4 expression level would be the new strategy for the prevention of cerebral edema and the reduction of cerebral injury after stroke.

BACKGROUND: It has been demonstrated that insulin-like growth factor-1 (IGF-1) is a kind of neurotrophic factor and protects from cerebral ischemia/reperfusion injury, the expression of IGF-1 is associated with the attack of ischemic stroke. The effects of IGF-1 and its receptor (IGF-1R) on neurobehavioral function are to be further studied.OBJECTIVE: To observe the effects of IGF-1 and IGF-1R on neurobehavioral function in rat models of cerebral ischemia/reperfusion injury.DESIGN: A randomized controlled observation.SETTING: Institute of Cerebrovascular Diseases, Affiliated Hospital of Qingdao University Medical College.MATERIALS: The experiments were carried out in Shandong Key Laboratory for Prevention and Treatment of Brain diseases. Twenty-eight healthy adult Wistar rats of clean degree, weighing 220-260 g, were provided by the experimental animal center of Shandong University.METHODS: The rats were randomly divided into experimental group (n =24) and sham-operated group (n =4). The middle cerebral artery occlusion/reperfusion (MCAO/R) models were established by inserting a thread through left external-internal carotid arteries. The sham-operated rats were given the same treatments except inserting thread. ①Neurologic deficit test: The rats in the experimental group were assessed according to Bederson standard after 1-hour ischemia and 6, 12-hour, 1, 3, 7 and 14-day reperfusion respectively. The sham-operated rats were assessed at corresponding time points; Without neurologic deficit was marked as 0 point; flexion of anterior claws as 1 point; unable to act against the pushing from the contralateral side as 2 points; circling while walking as 3 points; shaking as 4 points;unconscious mind as 5 points. ② Sample collection and treatment: The samples in the experimental group were collected after 1-hour ischemia and 6, 12-hour, 1, 3, 7 and 14-day reperfusion, and those in the sham-operated group ere collected at 24 hours postoperatively. The rats were anesthetized, brain samples were got at about 5 mm posterior to optic chiasma after brains were removed completely, then serial coronal sections (5 μm) were prepared, and 1 from 10 sections was stuck to the cover glasses treated with poly-L-lysine. ③ Morphological observation of neurons: The neurons in brain were observed by toluidine blue staining. ④ Detection of IGF-1 and IGF-1R: The expressions of IGF-1 and IGF-1R in cortex and striatum were detected with immunohistochemical technique, 4 fields were randomly selected to count the positive cells under high-power microscope (×400).MAIN OUTCOME MEASURES: ① The neurologic deficit; ② Morphological changes of neurons in brain; ③ Expressions of IGF-1 and IGF-1R in cortex and striatum.RESULTS: All the 28 rats were involved in the analysis of results. ① The neurologic deficit: The scores of neurologic deficit were (1.50±058) and (1.50±0.78) in rats after 7 and 14-day reperfusion, which were lower than that in rats after 6-hour reperfusion [(3.00±0.00), P ＜ 0.05]. ② Morphological changes of neurons in brain: The neurons in ischemic area appeared as paryopyknosis and became irregular in shape, there were obvious gaps around the cells, also deeply stained as purplish blue, nucleolus disappeared, and there were many scattered cellular fragments. ③ Expressions of IGF-1 and IGF-1R in cortex and striatum: The numbers of IGF-1 positive cells in cortex were (8.75±2.06), (11.13±1.14),(19.75±3.18), (17.38±3.11 ) and (11.23±2.28) respectively in rats after 6, 12-hours and 1, 3, 7-day reperfusion, which all were higher than that in sham-operated rats [(3.88±1.46), P ＜ 0.05], the numbers of IGF-1 positive cells in striatum were(8.25±2.21), (11.34±2.21), (18.23±2.64), (18.56±2.34) and (11.31±2.14) respectively in rats after 6, 12 hours and 1, 3, 7days reperfusion , which were also higher than that in sham-operated rats [(4.12±2.24), P ＜ 0.05]. The numbers of IGF-1R positive cells in cortex were (7.63±1.50), (10.50±2.34), (15.55±3.12), (15.37±3.01), (8.86±2.75) respectively in rats after 6, 12-hours and 1,3,7-day reperfusion, which all were higher than that in sham-operated rats [(4.13±1.81), P ＜0.05]. Those in striatum were (8.33±2.31), (10.24±2.09), (14.72±2.17), (14.24±2.77), (8.38±2.05), which were also higher than that in sham-operated rats [(3.76±2.35), P ＜ 0.05].CONCLUSION: The neurological function is damaged after cerebral ischemia/reperfusion, but it has a trend of self-recovery. The expressions of IGF-1 and IGF-1R are mainly distributed in cortex and striatum. Higher expressions of IGF-1 and IGF-1R maintain during 12 hours to 7 days after reperfusion and have a peak value at 1-3 days, which suggests that early expression of IGF-1 and IGF-1R are certain related to the recovery of neurological function.