Objective To investigate the causes and preventive measures of upper gastrointestinal bleeding in hyperbaric oxygen therapy for patients with severe closed head injury.MethodsThe clinical data of 24 cases of patients with upper gastrointestinal hemorrhage treated by hyperbaric oxygen therapy in the first people's Hospital of Fuyang District Hangzhou from May 2011 to May 2016 were analyzed, the occurrence time and clinical effect of upper gastrointestinal bleeding were analyzed.ResultsAmong the 24 cases of patients, 14 cases were treated for the first time that overt bleeding, including bleeding from the stomach liquid outflow of blood from 2 cases, gastric outflow 2 cases, hemorrhage after cure again received hyperbaric oxygen therapy 3 times again dominant bleeding 2 cases;6 cases hyperbaric oxygen treatment for third, 7, 10 times brown liquid or bloody fluid from the stomach outflow;4 cases hyperbaric oxygen treatment in patients with second and 3 courses of coffee liquid from the outflow tube, which accounted for 58.3%, 25.0%, 16.7% of the total, retrospectively;8 cases were with good recovery, 10 cases moderate disability, 4 cases severe disability, 2 cases vegetative state, 0 case died, the good recovery rate was 33.3%.ConclusionNot correctly grasp the time of hyperbaric oxygen therapy in the treatment of patients with severe closed craniocerebral injury will cause upper gastrointestinal hemorrhage, correct application of H2 receptor binding agent, developing targeted therapy programme can effectively prevent and treat upper gastrointestinal bleeding, so is worthy of the clinical's full attention.

Objective To study the changes of the bone density and metabolic makers in patients with lupus nephritis (LN) after long time prednisone treatment.Methods All patients were women.The healthy controls (group A, n =20),the patients with normal renal function (group B, n =25) were studied before and after 2 and 4 month prednisone treatment.Dual energy X ray absorptiometry was used to measure bone mineral density (BMD) in the lumbar spine at L2～L4,femoral neck,Ward′s triangle,great trochanter (GT) and ultradis (ULT).Simultaneously,the serum calcium,phosphate,alkaline phosphate enzyme,PTH M,BGP,24 hour urine calcium,creatinine and other biochemical indices were examined in all of them.Results ① There were no significant differences in BMD between both groups ( P

Objective To investigate the association between arsenic(+3 oxidation state) methyltransferase (AS3MT) genetic polymorphism and susceptibility to endemic arsenism.Methods Polymerase chain reactionrestriction fragment length polymorphism-single strand conformation polymorphism(PCR-RFLP-SSCP) technology was performed to detect mutations of AS3MT gene intron 8 and exon 9 in genome DNA of the 79 cases and 110 controls.PCR products with abnormal band forms were further sequenced to find the types and sites of mutation.Chi-square test and multivariate Logistic analyses were conducted.Results The incidence of the 9149 base mutation(A→C) in AS3MT gene intron 8(AS3MT-9149) in case group(19.0％,15/79) was lower than that in control group (23.6％,26/110).The incidence of the codon 287 mutation(ATG→AT/CG) in AS3MT gene exon 9(AS3MT-287)in case group(10.1％,8/79) was lower than that in control group (11.8％,13/110).However,statistical analysis indicated no significant difference in both mutations between two groups[AS3MT-9149:odds ratio(OR) =0.59,95％ confidence interval(CI):0.26-1.31,P =0.195; AS3MT-287:OR =0.85,95％ CI:0.32-230,P =0.751].Conclusions There are no significant association between the genetic polymorphisms of AS3MT-9149,AS3MT-287 and the susceptibility to endemic arsenism.Similarly,due to small sample amount,we can not exclude the possibility that these gene polymorphisms are related to susceptibility to endemic arsenism.

Objective To investigated the biological procedure of allograft decalcified bone matrix(DBM)and bone cement(BC)combined with bovine bone morphogenetic protein (bBMP)used for the repair of femoral defect caused by microwave－ induced hyperthermia in dogsby 99mTc－ MDP bone scintigraphy.Method The canine femoral defect(length 25mm,width 10mm)was caused by microwave－ induced hyperthermia(50℃ ,20minutes)and the composite material was implanted .Then the canine femurs were examined by 99mTc－ MDP bone scintigraphy respectively at different postoperative time and the results were compared with that of X－ ray photography and histological observation.Bone cement was implanted in the other femur as a contrast.Results It could be observed at the first and the second month that the radioisotope was gathered in the place where the composite material was implanted and the amount of radioisotope gathered in was the most abundant at the third month and it was lasted to the fourth month. That of the sixth month was decreased to that of the second month.The radiation count of the first, the second, the third the fourth and the sixth month were 93.9± 12.7, 110.7± 16.4,222.1± 24.0,201.3± 26.9 and 111.6± 20.7 respectively,and the count of the third month and the fourth month were more than that of the first, the second and the sixth month(P<0.01).Conclusion The composite material could be remodeled easily and the new bone could be formed by the induction of bBMP. So it could be merged with the normal bone.While the 99mTc－ MDP bone scintigraphy is the object and reliable index to determine the biological procedure of the composite material in dogs.

Adenoma ; metabolism ; pathology ; surgery ; Aged ; Diagnosis, Differential ; Endodermal Sinus Tumor ; pathology ; Female ; Humans ; Immunohistochemistry ; Neprilysin ; metabolism ; Ovarian Neoplasms ; metabolism ; pathology ; surgery ; Sex Cord-Gonadal Stromal Tumors ; pathology ; Stromal Cells ; metabolism ; pathology ; Vimentin ; metabolism

Induced pluripotent stem cells (iPSCs) can be propagated indefinitely, while maintaining the capacity to differentiate into all cell types in the body except for the extra-embryonic tissues. This iPSC technology not only represents a new way to use individual-specific stem cells for regenerative medicine but also constitutes a novel method to obtain large numbers of disease-specific cells for biomedical research. However, the low efficiency of reprogramming and genomic integration of oncogenes and viral vectors limit the potential application of iPSCs. Chemical-induced reprogramming offers a novel approach to generating iPSCs. In this study, a new combination of small-molecule compounds (SMs) (sodium butyrate, A-83-01, CHIR99021, Y-27632) under conditions of transient folate deprivation was used to generate iPSC. It was found that transient folate deprivation combined with SMs was sufficient to permit reprogramming from mouse embryonic fibroblasts (MEFs) in the presence of transcription factors, Oct4 and Klf4, within 25 days, replacing Sox2 and c-Myc, and accelerated the generation of mouse iPSCs. The resulting cell lines resembled mouse embryonic stem (ES) cells with respect to proliferation rate, morphology, pluripotency-associated markers and gene expressions. Deprivation of folic acid, combined with treating MEFs with SMs, can improve the inducing efficiency of iPSCs and reduce their carcinogenicity and the use of exogenous reprogramming factors.

Background Granulocyte colony-stimulating factor(G-CSF)has been reported to have beneficial effect on cardiac dysfunction in post infarction and doxorubicin-induced cardiomyopathy.Objective To investigate the effects of G-CSF on cardiac remodeling in cardiac hypertrophy induced by angiotensin Ⅱ(Ang Ⅱ).Methods Thirty-six male wild type mice(WT)were allocated randomly to receive subcutaneously G-CSF(10 ?g/kg per day, n=9),or Ang Ⅱ(2.88 mg/kg per day,n=9),or Ang Ⅱ plus G-CSF(Ang Ⅱ 2.88 mg/kg+G-CSF 10 ?g/kg,n =9)for 4 weeks with untreated WT(n=9)as controls.Blood pressure and cardiac function were measured. Heart weight/body weight ratio,myocyte cross-sectional area and fibrosis area were determined.The mRNA ex- pression of osteopontin(OPN)in myocardium was detected by RT-PCR.The expressions of angiotensin converting enzyme(ACE),ACE2 and phosph-p70S6 kinase protein in myocardium were assessed by Western-Blot.Results Ang Ⅱ significantly elevated blood pressure(SBP,Ang Ⅱ:139.7?1.6 vs WT:108.7?2.3 mmHg,P0.05),but significantly attenuated the myocyte cross-sectional area(Ang Ⅱ+G-CSF:181.06?0.11 vs Ang Ⅱ:202.02?0.16 ?m~2,P

OBJECTIVESince glucose-6-phosphate dehydrogenase (G6PD) deficiency is the most common hereditary hemolytic erythrocyte enzyme deficiency, most cases have single nucleotide mutations in the coding region, and current test methods for gene mutation have some missed detections, this study aimed to investigate the feasibility of RT-PCR sequencing in the detection of gene mutation in G6PD deficiency.

METHODSAccording to the G6PD/6GPD ratio, 195 children with anemia of unknown cause or who underwent physical examination between August 2013 and July 2014 were classified into G6PD-deficiency group with 130 children (G6PD/6GPD ratio <1.00) and control group with 65 children (G6PD/6GPD ratio≥1.00). The primer design and PCR amplification conditions were optimized, and RT-PCR sequencing was used to analyze the complete coding sequence and verify the genomic DNA sequence in the two groups.

RESULTSIn the G6PD-deficiency group, the detection rate of gene mutation was 100% and 13 missense mutations were detected, including one new mutation. In the control group, no missense mutation was detected in 28 boys; 13 heterozygous missense mutations, 1 homozygous same-sense mutation (C1191T) which had not been reported in China and abroad, and 14 single nucleotide polymorphisms of C1311T were detected in 37 girls. The control group showed a high rate of missed detection of G6PD deficiency (carriers) in the specimens from girls (35%, 13/37).

CONCLUSIONSRT-PCR sequencing has a high detection rate of G6PD gene mutation and a certain value in clinical diagnosis of G6PD deficiency.

Adolescent ; Child ; Child, Preschool ; Female ; Glucosephosphate Dehydrogenase ; genetics ; Glucosephosphate Dehydrogenase Deficiency ; diagnosis ; genetics ; Humans ; Infant ; Male ; Mutation ; Reverse Transcriptase Polymerase Chain Reaction ; methods ; Sequence Analysis, DNA

The global incidence rate of nonalcoholic steatohepatitis (NASH) continues to rise. The pathogenesis of NASH is complex, and there is no effective clinical treatment. Previous study has shown that DEAD box protein 5 (DDX5) can significantly alleviate the NASH process in mice. This study screened the natural product library of the research group and found that the active compound hypercalin B (HB) in Hypericum beanii N. Robson, a traditional Chinese medicine, can upregulate the expression of DDX5 protein in a dose-dependent manner. In this study, an in vitro model of NASH stimulated by palmitic acid (PA) and an animal model of NASH induced by the methionine- and choline-deficient diet (MCD) were constructed. Different concentrations of HB were used to investigate the effect and mechanism of HB in alleviating NASH progression. All animal experiments in this paper were approved by the Ethics Committee of China Pharmaceutical University (NO: 2021-02-003). In vitro model results showed that HB significantly reduced the intracellular lipid deposition induced by free fatty acid (FFA). Animal experiments showed that HB improved liver injury by significantly reducing lipid accumulation in the liver of NASH mice, and reducing serum aspartate transaminase (AST) and alanine transaminase (ALT) levels. Moreover, HB could inhibit liver inflammation by reducing the mRNA levels of liver pro-inflammatory cytokines including interleukin 6 (IL-6), interleukin 1β (IL-1β), and tumor necrosis factor α (TNFα). Further research showed that HB could reduce the phosphorylation level of the mechanical target of rapamycin (mTOR) and reduce the expression of sterol regulatory element binding protein 1 (SREBP1) and fatty acid synthase (FASN), thereby improving lipid metabolism and alleviating NASH progression, and the effects of HB against NASH were dependent on DDX5. In conclusion, HB can improve lipid metabolism and inhibit inflammatory activation by suppressing mTORC1 pathway via upregulating DDX5 protein, and showed promising anti-NASH activity in vitro and in vivo.