Objective To investigate the application of 3.0 MR for Gamma knife radios surgery(GKS) for treatment trigeminal neuralgia(TN) and the effect of 3.0 MR on therapy.Methods Sixty-two patients with TN underwent GKS,between May 2005 to June 2011 at Wanjie Hospital were included as our subjects.3.0MR 3-D FIESTA sequence scan were performed before treatment,during treatment 3.0MR orientation guided to select the trigeminal neuralgia (TN) brain cistern segment target spot.The 4 mm collimator was used and the maximum dose was to 70-90 Gy.Results The followed up periods was 6-36 months,total effective rate was 92 ％,the total alleviate cases was 51 part for 8 cases,none for 3,ipsilateral facial numbness,tinnitus,masticatory muscle weakness was found.Conclusion 3.0MR can clearly display trigeminal neuralgia and duty blood vessel,nicety orientation TN root,and then enhance GKS treatment TN rate,as well as avoid complication.

OBJECTIVE To investigate the incidence rate of Pseudomonas aeruginosa whose ceftazidime resistance was induced by imipenem and the relationship of excretion pump with sensibility of imipenem and ceftazidime.METHODS The sensibility to 15 antibacterials and ceftazidime resistance induced by imipenem were detected by slip diffusion method,detect these bacteriumas′s MIC to Imipenem and Ceftazidime before and after excretion pump inhibitor hydroxide radical cyanogen chlorine phenylhydrazone(CCCP) were added by agar dilution,detect Ceftazidime′s MIC value which were added different concentration imipenem by agar dilution.RESULTS From 325 strains 116 strains(35.7%) were imipenem induced ceftazidime-resistant drug fast,from them 80.2% were imipenem-resistant and ceftazidime-sensitive,19.8% were imipenem and ceftazidime both sensitive.Sensibility to imipenem and ceftazidime was no marked change before and after CCCP added,MIC value of ceftazidime was step up 4-12 times by imipenem.CONCLUSIONS The incidence rate of ceftazidime-resistant P.aeruginosa induced by imipenem is high,clinical microbiological laboratory should evolve D-test to guide clinician use antibacterials more reasonable.

Objective To observe the effect of remifentanil combined with propofol to induce and sustain controlled hypotension in children during endoscopic sinus surgery(ESS). Methods Forty ASA Ⅰ children undergoing adenoidectomy in ESS were divided into control group and controlled hypotension group by random digits table with 20 cases in each group. No controlled hypotension in control group. Anesthesia was induced with propofol,remifentanil and atracurium, and maintained with continuous infusion of propofol 2 min until the target mean arterial pressure (MAP)(55 - 60 mm Hg, 1 mm Hg = 0.133 kPa) was reached,and MAP was maintained at this level during operation in controlled hypotension group. During 15 min before surgical procedure pharynx nasalis blood flow was measured and recorded with laser Dopper flowmetry continuously. The quality of the surgical field in term of blood loss and dryness was established at 15 min after operation starting. Results Controlled hypotension was induced within (2.5 ± 0.3 ) min, the infusion rate ofMAP and heart rate at 15 min after controlled hypotension and 15 min after operation starting were significantly lower than those at controlled hypotension instantly in controlled hypotension group and control group (P ＜ 0.05 ). The pharynx nasalis blood flow decreased at 15 min after controlled hypotension from baseline [(68.3 ± 8.3 )% vs. (99.8 ± 7.9 )%] (P ＜ 0.05 ). The operation time and the quality of the surgical field in term of blood loss and dryness in controlled hypotension group were better than those in control group [(21 ± 4) min vs. (32 ± 6) min and ( 1.8 ± 0.1 ) scores vs. (3.5 ± 0.5) scores] (P ＜ 0.05 ). The awakeextubate time was within 10 min in two groups, and there were no anesthesia related complications.Conclusion Remifentanil combined with propefol can induce and sustain controlled hypotension,reduce pharynx nasal is blood flow and provide good surgical conditions in children for ESS.

Objective The aim of this study was to investigate the effects of hesperidin ( HDN) on antioxidant ac-tivity in mice.Methods HDN scavenging free radicals was detected by spectrophotometry, inhibition of mitochondrial swelling was detected by pyrogallol autoxidation, and erythrocyte hemolysis was detected by Fe2+phenanthroline.The mice were fed with HDN at different concentrations (0, 80, 160, 320 mg/kg) by gastric gavage for 12 days.ELISA and spec-trophotometric methods were used to assay the amount of MDA in mouse liver and kidney tissues and the activity of antioxi-dant enzymes ( SOD, CAT, GSH-PX) , and the antioxidant enzyme gene mRNA expression was analyzed by RT-PCR.Re-sults Compared with the control group, the radical (· OH, O2 -· , DPPH· ) clearance rate was significantly increased in the HDN groups.There was a significant decrease of oxidative hemolysis of erythrocytes and mitochondrial swelling in vitro. MDA content in the mouse liver and kidney tissues and serum showed a decrease, and the activity of antioxidant enzymes ( SOD, CAT, GSH-PX) in the HDN group was significantly higher than that in the control group.There was an up-regula-tion of mRNA expression of antioxidant enzyme in mouse liver and kidney tissues.Conclusions The results showed that HDN can eliminate free radicals, reduce cell oxidative damage caused by free radicals, inhibit superoxide production, up-regulate antioxidant enzyme gene expression and enhance their enzyme activity, thus showing a good antioxidant effect.

Objective To investigate the effects of ginsenoside Rg3 on growth and apoptosis of gastric cancer cell line MKN-45 and SGC-7901 in vitro. Methods MKN-45 and SGC-7901 cells at logarithmic growth phase were obtained, and were cultured with ginsenoside Rg3 of different concentrations (20, 30, 40, 50 μg/mL) for 24, 48 h or 24, 48 and 72 h. Cells cultured without ginsenoside Rg3 were served as controls. The inhibition rates of ginsenoside Rg3 on MKN-45 and SGC-7901 cells were detected by MTT assay, apoptosis rate of SGC-7901 cells was determined by Annexin V/PI double staining flow cytometry, cell cycles of SGC-7901 cells were analysed by flow cytometry, and morphological changes of SGC-7901 cells in 50 μg/mL ginsenoside Rg3 treatment group were observed by transmission electron microscopy. Results The inhibition rates on MKN-45 and SGC-7901 cells in each ginsenoside Rg3 treatment group were significantly higher than those in control group (P < 0.05), and the inhibition rates increased with the concentrations of ginsenoside Rg3 and time of culture ( P < 0.05). Compared with control group, the apoptosis rates of SGC-7901 cells and percentages of cells in G_1/G_1 cell cycle in each ginsenoside Rg3 treatment group were significantly increased in a concentration and time dependent manner. Typical morphology of SGC-7901 cell apoptosis was observed by transmission electron microscopy in 50 μg/mL ginsenoside Rg3 treatment group. Conclusion Ginsenoside Rg3 has significant inhibition effect on gastric cancer cell lines in vitro with a concentration and time dependent manner, the mechanism of which may involve the induction of gastric cell line apoptosis.

Objective To explore the peripheral blood microRNA (miRNA) expression of patients with gastric cancer,and to establish specific peripheral blood miRNA expression profile of gastric cancer,which would provide the evidencc for investigating the role of miRNA in the genesis and development of gastric cancer and looking for new molecular markers of gastric cancer.MethodsA total of 6 gastric cancer patients and 6 healthy volunteers were selected.The totat RNA of peripheral blood was extracted for miRNA expression profile examination and hioinformation analysis. The results of microarray were verified by real-time PCR. The online miRNA target gene pr(e)diction software was used to predict and screen miRNA differentially expressed target genes. Results Compared with control group,there were 54 differentially expressed miRNA in gastric cancer group,of which the expression of 35 miRNA (miRNA-504,mi RNA-183,miRNA- 938,miRNA-1285,miRNA- 576-3p,miRNA-663,etc) were up-regulated and 19 miRNA (miRNA-433,miRNA-193b,miRNA-329,miRNA 409-3p,miRNA 154,el(e)) were down-regulated.The results of real-time PCR indicated that there was a good consistency between PCR verificd results and microarray results in 2 up-regulated miRNA (miRNA 504 and miRNA-183) and 2 down-regulated miRNA (miRNA-443 and miRNA- 193b).ConclusionThere is specific peripheral blood miRNA expression profile of patients with gastric cancer,and these differentially cxpressed miRNA will likely become new diagnostic biomarkers of gastric cancer.

Background: The incidence rate and mortality of colorectal cancer (CRC) in China are increasing, and the age of onset is tending to be younger. Aims: To analyze the results of colonoscopy in patients positive for CRC screening, and to explore the significance of a CRC screening protocol that combines risk assessment questionnaire with fecal occult blood test (FOBT) in early diagnosis of colorectal neoplasms. Methods: Individuals who were positive for the first stage of screening (questionnaire + FOBT) in a community CRC screening program in Shanghai Huangpu District from May 2013 to October 2019 and then received the second stage of screening (colonoscopy) in Ruijin Hospital Luwan Branch were enrolled consecutively. Biopsy or polypectomy specimens were taken for pathological examination if any lesions were found endoscopically. Patients who underwent colonoscopy due to changes in bowel habits in the same period were served as controls. The detection rates of colorectal neoplasms in these two groups and the disease characteristics in the screening positive group were analyzed. Results: The screening positive group included 1 329 residents positive for the first stage of screening. The overall detection rate of colorectal lesions was 63.3%, and the detection rates of CRC, colorectal polyps and adenomatous polyps were 2.6% (34 cases), 60.7% (807 cases) and 35.2% (468 cases), respectively. While in control group (n=22 438), the rates were 43.6%, 1.8%, 41.5%, and 21.6%, respectively, all were significantly lower than those in screening positive group (all P<0.05). In screening positive group, the overall detection rate of colorectal lesions was higher in male than in female (73.7% vs. 54.2%, P<0.05) and increased with aging (P<0.05). Most of the CRC cases were in 60-79 years old age group with no gender difference. All CRC and most of the adenomas with dysplasia were greater than or equal to 1 cm in diameter, while most of the adenomas without dysplasia, hyperplastic polyps and inflammatory polyps were less than 1 cm in diameter. Conclusions: The community CRC screening program practiced in China can increase the detection rates of CRC and precancerous lesions effectively.

METTL3 and METTL14 are two components that form the core heterodimer of the main RNA m6A methyltransferase complex (MTC) that installs m6A. Surprisingly, depletion of METTL3 or METTL14 displayed distinct effects on stemness maintenance of mouse embryonic stem cell (mESC). While comparable global hypo-methylation in RNA m6A was observed in Mettl3 or Mettl14 knockout mESCs, respectively. Mettl14 knockout led to a globally decreased nascent RNA synthesis, whereas Mettl3 depletion resulted in transcription upregulation, suggesting that METTL14 might possess an m6A-independent role in gene regulation. We found that METTL14 colocalizes with the repressive H3K27me3 modification. Mechanistically, METTL14, but not METTL3, binds H3K27me3 and recruits KDM6B to induce H3K27me3 demethylation independent of METTL3. Depletion of METTL14 thus led to a global increase in H3K27me3 level along with a global gene suppression. The effects of METTL14 on regulation of H3K27me3 is essential for the transition from self-renewal to differentiation of mESCs. This work reveals a regulatory mechanism on heterochromatin by METTL14 in a manner distinct from METTL3 and independently of m6A, and critically impacts transcriptional regulation, stemness maintenance, and differentiation of mESCs.
Animals ; Mice ; Methylation ; Chromatin ; Histones/metabolism* ; RNA, Messenger/genetics* ; Methyltransferases/metabolism* ; RNA/metabolism*