Objective To investigate the causes, diagnosis and treatment of gastrolienal portal hypertension. Methods During recent 10 years, 32 cases of gastrolienal portal hypertension were admitted. Clinicopathological features were analyzed. Results The main causes of this entity was chronic pancreatitis or pseudocyst of the pancreas (14 cases), tuberculosis of lymph nodes in retroperitoneum (7 cases) , retroperitoneal malignant lymphoma (3 cases) and pancreatic tumors (8 cases). Definite diagnosis was made in all 32 cases during the hospitalization. Twenty cases underwent surgery including splenectomy (11 cases) , splenectomy plus portal-azygous disconnection (5 cases) , splenectomy plus distal pancreatectomy (4 cases) , endoscopic varicose vein ligation combined with partial splenic embolization (2 cases), and endoscopic varicose vein ligation ( 5 cases). Conclusion A definite diagnosis of gastrolienal portal hypertension lies in the surgeon's recognition of this entity. Splenectomy is the most effective symptomatic treatment.

Objective To study the characteristics of clustering of cardiovascular risk factors in patients less than 50 years-old of premature stable coronary heart disease(PSCHD)complicated with nonalcoholic fatty liver(NAFL).Methods One hundred and six patients with documented PSCHD were recruited into this study and their clinical data,including biochemical parameters,high-sensitivity C-reactive protein(hsCRP),white blood cell(WBC)count,ete.,were analyzed based on whether they had NAFL by B-type ultrasound scanning and their homeostasis model assessment ratio(Homa-IR)by the criteria for metabolic syndrome formulated by the International Diabetes Federation.Results Thirty-two (30.1percent)of 106 patients of PSCHD complicated with NAFL,and 74(69.9 percent)without NAFL. As compared to patients without NAFL,patients with NAFL had higher fasting blood glucose(FBS),serum level of insulin(INS),total cholesterol(TC),triglyceride(TG),serum activity of alanine aminotransferase(ALT),hsCRP,WBC count,body mass index(BMI),Homa-IR,and higher proportion of those with abnormal blood glucose,hypertension.metabolic syndrome(MS)and carotid atherosclerosis (CA)(P＜0.05),respectively.Bi-variate correlation analysis revealed that hsCRP positively correlated to BMI,TG,ALT and Homa IR(r=0.420,P=0.000;r=0.200,P=0.040;r=0.218,P=0.048:and r=0.546,P=0.000,respectively)and inversely correlated with serum level of high-density lipoprotein cholesterol(HDL-C)(r=-0.220,P=0.023).WBC count positively correlated with FBS(r=0.211,P=0.030).BMI,hsCRP,ALT,and proportions of hypertension,diabetes,MS,NAFL and CA in patients with Homa-IR above median were significantly higher than those in patients with that below median ( P＜0.05,respectively).Conclusions More risk faetors for chronic inflammatory reaction,cardiovascular disease and insulin resistance were clustered more obviously in patients of PSCHD complicated with NAFL.

ObjectiveTo study the potential of using temporal clustering analysis(TCA)technique in localizing an epileptogenic zone.MethodsTwelve patients with epilepsy were examined using resting functional MRI(fMRI). The patients had detectable focal lesions on cranial MRI.TCA was performed to analyze resting fMRI data in order to identify the timing of interictal epileptiform discharges (IEDs).Standard event-related fMRI analysis in SPM99 was used to generate maps of the activation induced by epileptic brain activities.Comparisons were made between TCA Resultsand SPM motion trochoid.ResultsEight of the twelve subiects showed activations in the brain regions that were consistent with those lesions determined on anatomic MRI.The remaining four subiects showed no clear activation in the areas of detectable lesions. In addition, correlation was found between TCA Resultsand motion trochoids.ConclusionsTemporal cluster analysis,an exploratory data-driven technique,may provide the timing information about interictal epileptiforill discharges.However,the Resultsfrom this novel fMRI analytical technique need to be interpreted with caution as it is vulnerable to motion artifact.

OBJECTIVE We have previously shown that inhibition of phosphodiesterase-4(PDE4)protects against neuronal damage in models of Parkinson's dis-ease(PD).However,the mechanisms have not yet been completely revealed.Here we aimed to elucidate the pharmacological effects and mechanisms of action of rof-lupram(ROF),an novel PDE4 inhibitor,in experimen-tal models of PD.METHODS The survival rate,apopto-sis rate and toxicity level of SH-SY5Y cells were deter-mined by MTT,flow cytometry and lactate dehydroge-nase detection kit.At the same time,LYT staining was used to detect the changes of lysosome fluorescence intensity:Western blotting was used to detect the changes of lysosome associated proteins,Sirtuin1 and α-Syn;NAD/NADH assay kit was used to determine the change of NAD content.To explore whether SIRT1 inhibitor(EX527)and lysosomal inhibitor could block the effect of ROF.In addition,ROT was used to stimulate C57BL/6J mice to construct a mouse model of PD to verify the effect and mechanism of ROF.The changes of motor function were evaluated by behavioral experiments(pole climb-ing,bar rotating and balance beam experiments).Super-oxide dismutase kit and Western blotting were used to detect the changes of SOD activity and expression of related proteins in substantia nigra.RESULTS We showed that pretreatment with ROF significantly attenu-ated cell apoptosis in ROT-treated SH-SY5Y cells.Fur-thermore,ROF significantly enhanced the lysosomal function,as evidenced by the increased levels of mature cathepsin D(CTSD)and lysosomal-associated mem-brane protein 1(LAMP1)through increasing NAD+/NADH and the expression of sirtuin 1(SIRT1).Pretreatment with an SIRT1 inhibitor selisistat(SELI,10 μ mol·L-1)attenuated the neuroprotection of ROF,and ROF-increased expression levels of LAMP1 and mature CTSD.Moreover,inhibition of CTSD by pepstatin A(20 μmol·L-1)attenuated the protective effects of ROF.In vivo study was conducted in mice exposed to ROT(10 mg·kg-1·d-1,ig)for six weeks;then,ROT-treated mice received ROF(0.5,1 and 2 mg·kg-1·d-1,ig)for four weeks.ROF significantly ameliorated motor deficits,which was accompanied by increased expression levels of tyro-sine hydroxylase,SIRT1,mature CTSD,and LAMP1 in the substantia nigra pars compacta.CONCLUSION Taken together,these results demonstrate that ROF exerts a neuroprotective action in PD models.The mech-anisms underlying ROF neuroprotective effects appear to be associated with NAD+/SIRT1-dependent activation of lysosomal function.

Objective To investigate the risk factors associated with post traumatic cerebral infarction (PTCI) after craniotomy hematoma evacuation for severe traumatic brain injury (sTBI) so as to provide clinical reference for the early prevention of postoperative PTCI.Methods A retrospective case control study was conducted to analyze the clinical data of 558 sTBI patients who received craniotomy hematoma evacuation admitted to Changsha Hospital of Traditional Chinese Medicine from October 2006 to June 2016.There were 340 males and 218 females,aged 15-71 years,with an average of 47.8 years.Among them,75 patients were at the age of less than 30 years,315 were at 30-50 years,and 168 were above 50 years.According to the Glasgow coma score (GCS),there were 127 patients with 3-4 points,124 with 5-6 points,and 307 with 7-8 points.The patients were divided into PTCI group (51 patients)and non-PTCI group (507 patients).The related indicators of the two groups of patients after admission were collected,including gender,age,injury cause,GCS,skull base fracture,traumatic subarachnoid hemorrhage (tSAH),cerebral hernia,hypotension,the time from injury to craniotomy,and whether decompressive craniectomy was performed.Univariate analysis was first performed for these factors,followed by multivariate logistic regression analysis.Results There were no significant differences in gender,age,injury cause,skull base fracture,and decompressive craniectomy between PTCI group and control group (P ＞ 0.05).In the PTCI group,there were 29 patients with GCS of 3-4 points,17 with 5-6 points,and five with 7-8 points;there were 48 patients with tSAH,37 patients with cerebral hernia,and 18 patients with hypotension.In terms of the time from injury to craniotomy,it took ＜ 3 hours in 30 patients,3-6 hours in 12,6-12 hours in five,and ＞ 12 hours in four.In the non-PTCI group,there were 98 patients with GCS of 3-4 points,107 with 5-6 points,and 302 with 7-8 points.There were 34 patients with tSAH,117 with cerebral hernia,and 35 with hypotension.In terms of the time from injury to craniotomy,it took ＜3 hours in 294 patients,3-6 hours in 130,6-12 hours in 68,and ＞ 12 hours in 15.The differences between the two groups were statistically significant (P ＜ 0.05).Multivariate logistic regression analysis indicated that GCS of 3-6 points,tSAH,cerebral hernia,time from injury to craniotomy,and hypotension were significantly associated with PTCI after operation for sTBI (P ＜ 0.01).Conclusions GCS of 3-6 points,tSAH,cerebral hernia,duration from injury to craniotomy,and hypotension time ＞ 3 hours are the high risk factors of PTCI in sTBI patients after craniotomy.For patients with these high risk factors,craniotomy should be performed in time,and the perioperative blood pressure and intracranial pressure stability should be maintained so as to relieve vasospasm.