OBJECTIVE: To investigate effects of polysulphone membrane filter continuous blood purification (CBP) on decreasing pancreatic amylase and various inflammatory mediators in the treatment of severe acute pancreatitis.METHODS: A total of 47 elderly patients with severe acute pancreatitis, who received CBP therapy was included in the experiment, and the blood routine test, blood biochemistry indexes and blood-gas analysis were performed prior to CBP therapy and continuous for 12 and 24 hours. Meanwhile, APACHE Ⅱ, SAPS Ⅱ and MODS scores were graded by recorded the heart rate, mean arterial pressure (MAP), central venous pressure (CVP), respiratory frequency and body temperature.RESULTS: Compared with pre-treatment, APACHE Ⅱ, SAPS Ⅱ and MODS scores, serum creatinine, hemodiastase, as well as C-reactive protein were decreased after treatment. After treatment, the oxygen index, such as heart rate, MAP, and CVP were declined, and the levels were increased progressively with time prolonged. During the course of CBP, the levels of HCO_3~-, Ga~(2+),and Mg~(2+) were increased than that of pre-treatment. The level of Ga~(2+), Mg~(2+) could maintain in a normal range during CBP therapy, however, it would be decreased when stop treatment.CONCLUSION: The improvement of cardio-pulmonary function relates to interstitial edema of tissue and organs. The effect on removing pancreatic amylase and various inflammatory mediators will be better with time prolonged. It is affirmative to treat elderly patients with severe acute pancreatitis by using CBP therapy.

Objective To construct sigF deletion mutant of Bacillus anthracis and the complementary strain of sigF deletion mutant in order to analyze the effect of losing sigF on formation of spores.Methods The spectinomycinadenyltransferase gene(spc) was inserted to replace sigF of B.anthracis by homologous recombination.A plasmid which contained sigF and sigF promotor was constructed and then transferred to the mutant to get a complementary strain of sigF deletion mutant.The characters of the mutant were analyzed by measuring growth curves, the ability of carbohydrate metabolism was compared, and spore formation was observed under a microscope.Results The sigF deletion strain A16D2△sigF was constructed from A16D2,which had a similar growth rate to the wild type A16D2 in logarithmic phase, but was not significantly different from the initial strain in the ability to use carbohydrates,although unable to form spores.The strain was found to maintain the state of asymmetric division by microfluidics experiment.Conclusion It is showed by this study that sigF is the essential gene of B.anthracis for spore formation, but not essential for vegetative growth.

OBJECTIVETo study the clinicopathologic features of primary cardiac valve tumors.

METHODSEleven cases of primary valve tumors collected from Fuwai Hospital during the period from 1983 to 2005 were enrolled into the study. The tumors were stained with hematoxylin and eosin and Weigert-Van Gieson stain. Immunohistochemistry was also carried out in selected examples.

RESULTSPrimary cardiac valve tumors were uncommon and accounted for only 3% (11/426) of all primary cardiac tumors. Most of them (10/11) were benign and malignancy was rarely encountered (1/11). The tumor subtypes included papillary fibroelastoma (4/11), cavernous hemangioma (4/11), glomus tumor (1/11), angiosarcoma (1/11) and hamartoma (1/11). Of the 11 tumors studied, 4 involved the tricuspid valve, 4 involved the mitral valve, 2 involved the pulmonary valve and 1 involved the aortic valve. The diagnosis was established by preoperative echocardiography in 7 patients. The remaining 4 cases were either misdiagnosed or undiagnosed.

CONCLUSIONSPreoperative diagnosis of primary cardiac valve tumors can be difficult due to lack of detailed information related to this group of lesions. Although benign cardiac valve tumors carry a good prognosis, the clinical outcome may be disastrous as a result of hemodynamic disturbances. Intraoperative frozen section examination is advisable for guiding proper surgical management.

Adolescent ; Adult ; Child ; Child, Preschool ; Diagnostic Errors ; Echocardiography ; methods ; Female ; Fibroma ; diagnosis ; diagnostic imaging ; pathology ; Heart Neoplasms ; diagnosis ; diagnostic imaging ; pathology ; Heart Valves ; diagnostic imaging ; pathology ; Hemangioma, Cavernous ; diagnosis ; diagnostic imaging ; pathology ; Humans ; Infant ; Male ; Middle Aged ; Reproducibility of Results ; Sensitivity and Specificity

OBJECTIVETo investigate the mechanisms of PTEN gene inactivation starting from DNA, mRNA and protein levels in ovarian cancers.

METHODSTumor tissue samples were obtained from 48 patients with epithelial ovarian cancers. Using four polymorphic markers (D10s541, D10s583, D10s1687 and D10s2491) within and flanking the PTEN gene located in chromosome 10q 23.3, polymerase chain reaction (PCR) and loss of heterozygosity (LOH) were introduced to examine LOH of PTEN gene; PCR-single strand conformation polymorphism (PCR-SSCP) was introduced to examine mutations of the fifth, sixth, seventh, and eighth exons of PTEN. Reverse transcriptase-polymerase chain reaction (RT-PCR) and immunohistochemistry (SP method) were applied to detect PTEN mRNA and PTEN protein expressions, respectively.

RESULTSLOH of PTEN gene was observed in 19 of 48 (39.6%) ovarian cancers. PTEN mutations were found only in 2 (4.2%) of the cases. Absence of PTEN mRNA expression was 18.8% (9 of 48). Immunostaining of 48 cancer samples revealed that 13 (27.1%) were PTEN immunostain negative. Of these 13 samples, only 2 (15.4%) had structural, biallelic inactivation by intragenic PTEN mutations and loss of the remaining wild-type allele; 7 (53.8%) showed evidence of LOH, 5 of these 7 samples showed deletion of PTEN mRNA expression, another 2 samples showed positive expression of PTEN mRNA; 4 (30.8%) tumors had neither PTEN gene mutation nor LOH but exhibited no PTEN protein expression, 2 of these 4 cases showed deletion of PTEN mRNA expression, another 2 showed positive expression of PTEN mRNA. For the cases of PTEN protein absent staining, the rate of LOH was 69.2% (9 of 13), higher than 28.6% (10 of 35) for the positive staining (P < 0.05).

CONCLUSIONSPTEN gene inactivation may contribute to epithelial ovarian carcinogenesis. There may be several mechanisms of PTEN gene inactivation in ovarian cancers. Protein expression deletions may be a significant mechanism.

Adult ; Aged ; Chromosomes, Human, Pair 10 ; Exons ; Female ; Gene Deletion ; Gene Expression Regulation, Neoplastic ; Genes, Tumor Suppressor ; Humans ; Loss of Heterozygosity ; Middle Aged ; Mutation ; Ovarian Neoplasms ; genetics ; metabolism ; PTEN Phosphohydrolase ; biosynthesis ; genetics ; Polymerase Chain Reaction ; Polymorphism, Single-Stranded Conformational ; RNA, Messenger ; biosynthesis ; genetics

Objective:To analyze the effect of different glucocorticoid administration routes in the treatment of children's secretory otitis media and impacts on immunologic function.Methods:Clinical data of children with secretory otitis media received treatment at our hospital from January 2016 to June 2016 were analyzed.Patients were divided into two groups by different glucocorticoid administration routes,Group A:intratympanic injection;Group B:oral administration.After one week,clinical effects and immunologic functions were tested and compared between the two groups.Results:A total of 87 patients were analyzed,Group A 45 cases,Group B 42 cases.After one week treatment,both of the two groups got significantly improved in audiology indexe (P<0.05),however,these index were more better in Group A when compared with those of Group B(P<0.05).Meanwhile,Group A patients got higher cure rate than that of Group B (91.1%,41/45 vs 73.8%,31/42;X2=4.558,P=0.033).Both of the two groups got significantly improved in CD3+T,CD4+T and CD4/CD8 (P<0.05) and decreased in CD8,IL-4,IFN-γ and IL-4/IFN-γ(P<0.05),but these markers changed more significant in Group A (P<0.05).Group A patients had a lower recurrence rate than Group B patients one year after treatment, the difference was statistically significant (9.76%,4/41 vs 29.03%,9/31;Log-rank X2=4.698,P=0.030).Conclusion:The treatment of children's secretory otitis media,the intratympanic injection of glucocorticoid shows a better effect than that of oral cortico-steroids.

Background: Several studies have shown that proton pump inhibitors (PPIs) can enhance the sensitivity of gastric cancer (GC) cells to chemotherapy and inhibit tumor proliferation and invasion. Aims: To investigate whether PPI could enhance chemosensitivity by inhibition of cell cycle-related genes in GC cells. Methods: Two human GC cell lines, AGS and HGC27 were treated with pantoprazole in different concentrations, and the cell viability was detected by CCK-8 assay. Transcriptome sequencing combined with KEGG enrichment analysis were used to determine the effect of PPI on cell cycle of GC cells, and the changes of cell cycle and its related genes were validated by flow cytometry, real-time PCR and Western blotting, respectively. Bioinformatics websites were employed to analyze the major differentially expressed cell cycle-related genes in GCs and their relationship with patients' prognosis. After transfection with FOXM1 plasmid or control plasmid, the inhibitory effect of PPI combined with cisplatin on GC cells was determined by CCK-8 assay. Results: PPI inhibited the proliferation of GC cells effectively in vitro. Transcriptome sequencing showed that the expression levels of G2/M phase-related genes, including FOXM1, PLK1, and AURKB were down-regulated in PPI-treated GC cells, and G2/M arrest was suggested by KEGG enrichment analysis. All these changes were proved by flow cytometry, real-time PCR and Western blotting. Bioinformatics analysis revealed that FOXM1, PLK1, and AURKB genes were highly expressed in GCs and correlated with a poor prognosis. The inhibitory effect of PPI combined with cisplatin on GC cells was superior to that of cisplatin alone, but could be partially reversed by overexpression of FOXM1. Conclusions: PPI treatment can induce G2/M arrest in GC cells by inhibiting cell cycle-related genes, and subsequently enhance the sensitivity of GC cells to chemotherapy.