Objective To observe the protective effect to Ulinastatin combined with Xingnaojing Injection (XI) for acute cerebral hemorrhage. Methods One hundred and eight cases of acute cerebral hemorrhage were randomly divided into treatment group ( N=56) and control group ( N=52) . All of the patients were given conventional western medical treatment including relieving cerebral edema, regulating blood pressure, maintaining electrolyte balance, anti-inflammation, preventing epilepsy. Additionally, the control group was given intravenous drip of Ulinstatin, and the treatment group was given intravenous drip of Ulinstatin and XI. The clearance of intracranial hematoma in the two groups was observed on treatment day 3, 7, 14, the absorption of cerebral edema was observed after treatment for one treatment course of 14 days, neurological deficit scores ( NDS) were compared on treatment day 14, 30, and the clinical efficacy was evaluated. Results ( 1) After treatment, hematoma area was reduced in the two groups ( P<0.05 compared with that before treatment); on treatment day 3, the difference of hematoma area was insignificant between the two groups (P>0.05); on treatment day 7 and 14, hematoma area in the treatment group was less than that of the control group, the difference being significant (P<0.05) . (2) On treatment day 14, the total effective rate for absorption of cerebral edema was 89.3% in the treatment group, and was 65.4% in the control group, the difference being significnat ( P<0.05) . ( 3) After treatment, NDS of the treatment group was less than that of the control group, and the total effective rate on NDS was 89.3% in the treatment, higher than 71.2% in the control group, the difference being significant ( P<0.05) . ( 4) In the treatment group, 3 cases had slight increase of aminotransferase. Eight cases of the control group had increased aminotransferase, and then the aminotransferase level recovered to normal after suspension. In the treatment group, 2 cases were dropped out for receiving emergency operation due to rehaemorrhagia during the treatment, and 3 cases were death for illness deterioration. In the control group, 7 cases gave up the treatment for illness deterioration and then were dead during the follow-up. Conclusion Ulinastatin combined with XI shows certain protective effect in treating acute cerebral hemorrhage.

Objective To establish an efficient, simple, low cytotoxicity and cheap transfaction system. Methods We have used the cationic polymer polyethylenimine(PEI) to study transient transfection in MCF-7 cells by testing different conditions, including cell concentrations, DNA concentrations, the ratio of PEI nitrogen to DNA phosphate(PEI-N∶DNA-P) and the time of cells grown in serum-free culture together with PEI-DNA complex. Results The optimized cell concentrations were 2?10 5 cells seeded per well in 24-well dishes 18-24?h before transfection. The DNA concentrations and ratio of PEI-N∶DNA-P are very important for optimal transfection and they affect each other. For 1??g DNA per well, the optimal PEI-N∶DNA-P is about 33∶1, however, as for 4??g DNA, it is 9∶1. The best time of cells grown in serum-free culture together with PEI-DNA complex is about 5-7?h.Conclusion With optimized conditions, we can establish an efficient, simple, low cytotoxicity and cheap transfection system by using PEI.

Abstract Ischemic stroke is characterized by high morbidity, disability and mortality. At present, there is a lack of effective treatment for ischemic stroke, so it is of great significance to reduce the incidence risk of ischemic stroke. Studies show that vitamin C can prevent atherosclerosis, thus reduce the incidence risk of ischemic stroke. However, this point is controversial due to the differences of study population, inconsistent evaluation methods of vitamin C content and the influence of various confounding factors. This paper reviews the related animal experiments, clinical trials and cohort studies, in order to provide reference for subsequent studies on reducing the incidence risk of ischemic stroke.

BACKGROUND: The association of tumor necrosis factor alpha (TNF-α) gene polymorphisms with the onset and development of ankylosing spondylitis (AS) has been the focus of studies on AS in the field of genetics.OBJECTIVE: To explore the association of the polymophisms of TNF-α promoter gene at positions-308 and -238 with AS susceptibility and clinical pathological changes.DESIGN: A case-control study.SETTING:The Rheumatic Immunology Department of Changhai Hospital of the Second Military Medical University of Chinese PLA.PARTICIPANTS: Totally, 108 AS patients were recruited from Rheumatic Immunology Department of Changhai Hospital, Second Military Medical University of Chinese PLA from January 1999 to December 2003 ,they had no kinship. The ratio of men to women was 5.3: 1. They aged from 13 to 71 (30-± 12) years old, and AS was divided into Ⅰ- Ⅳ radiographic stages according to the sacro-iliac joint damage. A total of 100 healthy controls were randomly selected from the blood donators(Shanghai Hospital) who were aged from 19 -56 (33 ±9) years old, and the ratio of men to women was 4.9: 1. Informed consent was obtained from all the subjects.ti-coagulated with EDTA. Polymerase chain reaction amplification and purification of the TNF-α promoter region was made and the sequence of polymerase chain reaction products was examined and displayed by Chromas 1.62 softcorresponding radiographic stage of sacro-iliac joint damage was assessed to investigate the influence of gene polymorphisms on AS.MAIN OUTCOME MEASURES: DNA direct sequencing method was used to detect -238 and -308 allele phenotypes for investigating the association with clinical presentations.G and -238G/A allele was 98.1% (106 cases) and1. 9% (2 cases) respectively in AS group and 95.0% (95 cases) and 5.0% (5 cases) respecquency of TNF-α promoter gene at positions -308. 1.1(G/G) and - 308.1.2(G/A) alleles was 82.4% (89 cases) and 17.6% (192 cases) respectively in AS group, which was not significantly different compared respectively with 85.0% (85 cases) and 14.0% (14 cases) of the control of sacro-iliac joint damage and the frequency of TNF-α promoter gene at the position of - 308 (G/G) and (G/A): AS patients with(G/G) phenotype who were confirmed of radiographic stage Ⅰ, Ⅱ, Ⅲ, and Ⅳ were observed in 3/35/40/11cases,compared with (G/A) phenotype of 1/12/6/0 cases.The difference was statistically significant (χ2GMH = 4.77, P ＜ 0.05 ).CONCLUSION: Our data suggest that the polymorphisms of TNF-α promoter gene at positions of - 238 and - 308 allele has no association with AS susceptibility, but the polymorphisms of TNF - α promoter gene at the position of -308 might exert great influence on AS according to the radiographic stage of sacro-iliac joint damage.

OBJECTIVETo investigate the effect of silencing LSD1 gene by RNA interference on the proliferation, apoptosis on human lymphocytic leukemia Jurkat cell line and its mechanism.

METHODSThe hairpin- like oligonucleotide sequences targeting LSD1 gene was transfected into Jurkat cells by lipofectamine(TM) 2000. The LSD1 mRNA and protein were detected by RQ- PCR and Western blot. Cell growth was determined by MTT. Cell apoptosis was analyzed by flow cytometry. The expression of Bcl-2, Bax, procaspase- 3, and histone H3K4me, H3K4me2, H3K4me3, Act- H3, H3K9me were detected by Western blot.

RESULTSLSD1 mRNA was markedly suppressed by the shRNA targeting LSD1. LSD1 shRNA suppressed the proliferation and induced cells apoptosis of Jurkat cells. The cell apoptotic rate was (41.34±3.58)%, (3.45±1.54)%, (1.76±0.52)% in LSD1 shRNA, Neg-shRNA and Blank respectively, the difference among them was statistically significant (P<0.05). LSD1 shRNA down- regulated the expressions of Bcl- 2 and procaspase- 3, and up- regulated the expression of Bax. The methylation of H3K4me1, me2 and acetylation of Act- H3 improved without change of the methylation of H3K4me3.

CONCLUSIONSDeplete of LSD1 gene maybe through modifying the methylation of histone H3K4 to promote the cell apoptosis and inhibit cell growth in Jurkat cell line.

Acetylation ; Apoptosis ; Caspase 3 ; metabolism ; Cell Cycle ; Cell Line, Tumor ; Cell Proliferation ; Down-Regulation ; Histone Demethylases ; genetics ; Histones ; metabolism ; Humans ; Jurkat Cells ; Methylation ; Proto-Oncogene Proteins c-bcl-2 ; metabolism ; RNA Interference ; RNA, Messenger ; RNA, Small Interfering ; Transfection

Objective To assess perineural invasion in prostate needle biopsy ( PNIb) on patholog-ical staging , progression of prostate cancer . Methods This retrospective study recruited clinical data of 316 prostate cancer patients with mean age of 69 years from Jan.2006 to Mar.2013.The mean PSA before biopsy was 15.7μg/L.All patients underwent CT or MRI and radionuclide bone scan and had not been found local tumor invasion or distant metastasis .Transrectal ultrasound-guided prostate needle biopsy was performed to all candidates , and the preoperative diagnosis was localized prostate cancer .All patients were treated by laparoscopic radical prostatectomy (LRP).In this study, differences of Gleason score in prostatectomy speci-men, positive surgical margin (PSM), capsular invasion, seminal vesical invasion were analyzed between two groups:group A:patients with PNIb;group B:patients with no PNIb.We also studied the concordance of PNI distribution in PNIb and perineural invasion in prostatectomy specimen ( PNIp). Results The overall rate of PNIb was 32.5%.Difference of Gleason score ≤6 (16 in group A, 92 in group B), Gleason score=7 (46 in group A, 87 in group B), Gleason score ≥8 (41 in group A, 34 in group B) was statisti-cally significant (P<0.05).Of these two groups, differences in PSM (75 in group A, 43 in group B), cap-sular invasion (47 in group A, 36 in group B), and seminal vesical invasion (32 in group A, 23 in group B) were of statistical significant (P<0.05).At the multivariable logistic regression analysis , PNIb was inde-pendent predictor of PSM , capsular invasion, seminal vesicle invasion ( OR=11.358, OR=1.785, OR=2.364, P<0.05).All 22 patients with bilateral PNIb had bilateral PNIp .Of 81 patients with unilateral PNIb,55 had bilateral PNIp .The difference of distribution between PNIb and PNIp was of statistical signifi-cant (P<0.001). Conclusions PNIb is useful for evaluating the progression of prostate cancer .

Pediatric dilated cardiomyopathy( PDCM) is not only associated with infection,metabolism and other factors, but also a congenital cardiomyopathy. PDCM echocardiography ( ultrasonic cardiogram ) showed a severe enlargement of the left ventricle or double ventricle,with decreased left ventricle ejection con-traction. Clinical onset of disease concealment,often manifested as refractory heart failure,arrhythmia and sudden death( heart function often reached III～IV level) . The prognosis of the disease is poor,and mortality and mor-bidity are high,which may be the main cause of heart transplantation in children. Over the past three decades, treatment of left ventricular dysfunction has been the focus of research on adult cardiomyopathy,and treatment of PDCM has mostly extended from the treatment of dilated cardiomyopathy in adults. This article will provide the guidance of adult patients with cardiac dilation therapy,and is combined with recent research at home and abroad to illustrate the latest research and experience of PDCM treatment,and to explore the progress of PDCM treat-ment in recent years.

Objective:To explore the safety and clinical efficacy of orthotopic liver transplantation after treatment with gelatin sponge microparticles by transcatheter arterial chemoembolization (GSMs-TACE) for hepatocellular carcinoma with type II/III portal vein tumor thrombus.Methods:For this retrospective study, patients with hepatocellular carcinoma with portal vein tumor thrombosis undergoing GSMs-TACE before liver transplantation from January 2018 to June 2018. The clinical efficacy and safety were evaluated by alpha feto-protein (AFP), imaging changes, postoperative complications and survival time.Results:The median follow-up period was 24 months. The average number of GSMs-TACE was 1.5. No postoperative complications such as biliary fistula, abdominal hemorrhage, liver and kidney failure, arterial stenosis and biliary stricture occurred. After GSMs-TACE, there were varying degrees of tumor necrosis or thrombus, AFP decreased (n=5) and PIVKAII declined (n=7). The 1-year survival rate was 100% and the 1-year disease-free survival rate 71.4%. For two cases of lung metastasis, the recurrent time was 4 and 10 months respectively.Conclusions:GSMs-TACE plus liver transplantation offer good safety and clinical efficacy for hepatocellular carcinoma patients with portal vein cancer thrombus.

Background/Aims: To evaluate the causal correlation between complement components and non-viral liver diseases and their potential use as druggable targets. Methods: We conducted Mendelian randomization (MR) to assess the causal role of circulating complements in the risk of non-viral liver diseases. A complement-centric protein interaction network was constructed to explore biological functions and identify potential therapeutic options. Results: In the MR analysis, genetically predicted levels of complement C1q C chain (C1QC) were positively associated with the risk of autoimmune hepatitis (odds ratio 1.125, 95% confidence interval 1.018–1.244), while complement factor H-related protein 5 (CFHR5) was positively associated with the risk of primary sclerosing cholangitis (PSC;1.193, 1.048– 1.357). On the other hand, CFHR1 (0.621, 0.497–0.776) and CFHR2 (0.824, 0.703–0.965) were inversely associated with the risk of alcohol-related cirrhosis. There were also significant inverse associations between C8 gamma chain (C8G) and PSC (0.832, 0.707–0.979), as well as the risk of metabolic dysfunction-associated steatotic liver disease (1.167, 1.036–1.314). Additionally, C1S (0.111, 0.018–0.672), C7 (1.631, 1.190–2.236), and CFHR2 (1.279, 1.059–1.546) were significantly associated with the risk of hepatocellular carcinoma. Proteins from the complement regulatory networks and various liver diseaserelated proteins share common biological processes. Furthermore, potential therapeutic drugs for various liver diseases were identified through drug repurposing based on the complement regulatory network. Conclusions Our study suggests that certain complement components, including C1S, C1QC, CFHR1, CFHR2, CFHR5, C7, and C8G, might play a role in non-viral liver diseases and could be potential targets for drug development.

Objective:To analyze the clinical and pathological features and gene mutations of pancreatic acinar cell carcinoma (PACC).Methods:Clinical data of 34 patients with PACC admitted to the Department of Pancreatic Surgery of the First Affiliated Hospital of Naval Medical University from December 2009 to July 2018 were retrospectively analyzed to summarize its clinical characteristics, and the expressions of α1-ACT, CaM5.2, Syn and CgA in pancreatic tumor tissues were detected by immunohistochemistry. Next-generation gene sequencing technology was used to detect gene mutations in tumor specimens.Results:Among the 34 PACC patients, 23(68%) were males and 11(32%) were females; the age ranged from 25 to 75 years, with an average age of 54 years. The first symptom was abdominal pain or distension in 21 cases (62%), skin or scleral yellow staining in 4 cases(12%), and 9 cases(26%) were found in routine physical examination. BMI was 17.6-34.0 kg/m 2, of which 3 cases (9%) were <18.5 kg/m 2, 23 cases (68%) were 18.5-24.0 kg/m 2, and 8 cases (23%) were >24.0 kg/m 2. Preoperative examination showed elevated CA19-9 in 7 cases (20.6%), elevated CEA in 3 cases (8.8%), and elevated AFP in 7 cases (20.6%). Blood amylase was 16-247 U/L, with an average of 80 U/L. Enhanced CT showed that the lesion was irregular in shape, showing inhomogeneity and slightly low density, with areas of cystic degeneration and necrosis. The tumor was located in the head of the pancreas in 14 cases (41%), the body and tail of the pancreas in 19 cases (56%), and the neck of the pancreas in 1 case (3%). The largest tumor diameter was 1.5-15.5 cm, with an average of 5.4 cm. Postoperative pathologic stage I was confirmed in 4 cases (12%), stage Ⅱ in 14 cases (41%), stage Ⅲ in 14 cases (41%) and stage Ⅳ in 2 cases (6%). Immunohistochemical results showed that both α1-ACT and CaM5.2 were positively expressed (100%). Syn was positive in 8 cases (23.5%) and CgA was positive in 6 cases (17.6%). Ki-67 index was from 9% to 70%, with an average of 41%. Gene sequencing of pancreatic tumor tissue from 6 patients showed BRCA2 mutation in 2 patients (7155C>G), K-ras mutation in 1 patient (35G>T), RET mutation in 1 patient (200G>A), and LKB1 mutation (234G>T) in 1 patient, and one double mutation of K-ras and RET (35G>A, 1 798C>T). 30 patients were followed up, and the median survival was 38.3 months. Conclusions:PACC was a rare pancreatic tumor with no specific clinical manifestations. The positive expression rates of α1-ACT and CAM5.2 in tumor tissues were 100%. BRCA2, K-ras, RET and LKB1 were common gene mutations.