Adolescent ; Adult ; Child ; Female ; Fistula ; surgery ; Humans ; Male ; Recurrence ; Reoperation ; Retrospective Studies ; Thyroglossal Cyst ; surgery ; Young Adult

Objective To study the co-effects of methylene blue(MB) and exposure with the cold light source on cell DNA damage, and to explore the mechanism involved. Methods The alkaline single cell gel electrophoresis was used to determine cell DNA damage. Apoptosis of the cells was determined by flow cytometry analysis using Annexin V-FITC/PI staining. DCFH-DA probe was used to determine endocellular Reactive Oxygen Species (ROS). Results The levels of DNA damage in the SGC7901 adenocarcinoma cells treated with methylene blue in the light were significantly increased compared to that of control ( F = 8.39, P＜0.05 ). The DNA damage levels were related to the length of time of light exposure, and the damage was recovered to a certain level after light withdrew. Cell apoptosis ( x2=7.71,P ＜0.05)and endocellular ROS level (F = 34.11, P＜0.01＝ increased significantly in the exposure group. Conclusions Methylene blue chromoendoscopy can induce DNA damage and cell apoptosis, and the mechanism may be associated with ROS produced by the photochemical reaction.

Objective Pathogens from the nosocomial infection have been analyzed by MALDI‐TOF microbial identification system ,to evaluate mass spectrometry analysis advantage and explore the mass spectrometry method .Methods The pathogens have been analyzed by MALDI‐TOF microbial identification system ,by compared with the VITEK‐2 compact detection in the tes‐ting time ,detection rate and the amounts of identified strains .The homology differences have been analyzed by comparison calcula‐tion of common peaks from the fingerprint spectrums .Results Thirty‐one Escherichia coli strains ,28 Klebsiella pneumonia strains and 9 unusual pathogen strains have been identified by MALDI‐TOF MS for only 1 hours .It has more advantages than VITEK‐2 in the testing time and other aspects .Conclusion Nosocomial infection of pathogen shows a point source propagation mode centering on the department .MALDI‐TOF mass spectrometry is able to rapidly and correctly identify the pathogen .MALDI‐TOF microbial i‐dentification system is expected to be the major detecting technique in the field of the pathogen monitor and resistance monitoring a ‐nalysis .

Objective To find biological markers to predict the mathematical cognitive ability in order to set patients free from the pain and time-consuming behavioral tests. Methods 86 patients with stroke or brain traumatic injuries were recruited and acquired T1 and rest-ing-state functional MRI imaging data. And a mathematical task (7 calculation items, 2 counting items) and a word-reading task (140 items) was also finished. The partial correlative analysis was made between the score of mathematical task and the amplitude of low frequency fluc-tuation of each voxel of the whole brain with the word-reading performance as controlling task, and AlphaSim correction method was used with corrected P<0.05 (single voxel level:P<0.05;cluster size:>110 voxels). Results There were 5 cerebral regions whose amplitude of low frequency fluctuation significantly correlated with mathematical performance:left inferior parietal lobule (161 voxels, rpeak=0.34), left precu-neus/superior parietal lobule (141 voxels, rpeak=0.31), left middle temporal gyrus (359 voxels, rpeak=0.34), left middle frontal gyrus (491 vox-els, rpeak=0.36), and right middle frontal gyrus (156 voxels, rpeak=0.32). Conclusion The amplitude of low frequency fluctuation of left inferior parietal lobule, precuneus/superior parietal lobule, middle temporal gyrus, middle frontal gyrus, and right middle frontal gyrus could be used as predictors of mathematical cognitive ability for brain-damaged patients.

ObjectiveToevaluatethelevelofsemanticmemoryofpatientswithbraininjuryusinglocalizationofsemanticmemorytest,andtocomparethedifferenceofsemanticmemorybetweenpatientgroupandnormalcontrolgroup,andtoanalyzetherelationshipbetweensemanticmemoryimpairmentandthepositionofbraininjury.Methods25patientswithbraininjury(16withleft braininjury,9withrightbraininjury)and24normalpersonsweretestedwithassociationjudgmenttestofpictureandwordversion.ResultsThescoresofassociationjudgmenttestofbothpictureandwordversionwerelowerinleftbraininjuredpatientsthan normalcontrols(P<001)orrightbraininjured(P<005).Thescoresofpicturecorrelatedwithwordversion(r=0542,P<001).Theincidenceofsemanticmemoryimpairmentwasmoreinleftbraininjurythanright(P<001),aswellasintheleftbasal gangliainjurythanright(P<005).ConclusionAssociationjudgmenttestofpictureandwordversioncanbeusedtoevaluatethe levelofsemanticmemoryofpatients.Semanticmemoryimpairmentisoftenseeninpatientswithbraininjury.Semanticmemoryis lefthemispherelateralized.

OBJECTIVETo observe the dynamic time-phase expressions of key genes of brain-gut CaM signal pathway of spleen Qi deficiency rats and the intervention effect of Sijunzi decoction.

METHODMale Wistar rats were randomly divided into the normal control group, model 14 d, 21 d, 28 d groups, and Sijunzi decoction 14 d, 21 d, 28 d groups. Except for the normal control group, the remaining groups were included into the spleen Qi deficiency model with the bitter cold breaking Qi method (ig 7.5 g · kg⁻¹ · d⁻¹ of Rheum officinale, Fructus aurantii immaturus, Magnolia officinalis preparation) and the exhaustive swimming method. On the 7th day after the modeling, the Sijunzi decoction groups were orally administered with Sijunzi decoction 20 g · kg⁻¹ · d⁻¹. The expressions of key genes CaM/CaMK II of CaM signaling pathway in hippocampus and intestine at different time points by immunohistochemical method and Western blot. At the same time, the intervention effect of Sijunzi decoction on spleen Qi deficiency rats and its mechanism were analyzed.

RESULTSpleen Qi deficiency rats showed higher intestinal CaM/CaMK II expression and lower hippocampus CaM/CaMK II expression than normal rats (P < 0.05, P < 0.01). After the treatment of Sijunzi decoction, spleen Qi deficiency rats showed reduction in intestinal CaM/CaMK II expression and increase in hippocampus CaM/CaMK II expression (P < 0.05, P < 0.01).

CONCLUSIONThe formation of spleen Qi deficiency syndrome may be related to the high expression of CaM/CaMK II in small intestine tissues and its low expression in hippocampus tissues. Sijunzi decoction may achieve the therapeutic effect in spleen Qi deficiency syndrome by reducing the CaM/CaMK II expression in intestinal tissues and increasing it in hippocampus tissues.

Animals ; Brain ; drug effects ; enzymology ; metabolism ; Calcium-Calmodulin-Dependent Protein Kinase Type 2 ; genetics ; metabolism ; Calmodulin ; metabolism ; Drugs, Chinese Herbal ; administration & dosage ; Humans ; Intestines ; drug effects ; enzymology ; metabolism ; Male ; Qi ; Rats ; Rats, Wistar ; Spleen ; drug effects ; Splenic Diseases ; drug therapy ; enzymology ; genetics ; metabolism

OBJECTIVETo study the mutagenicity and teratogenicity induced by ammonium dinitramide(ADN).

METHODSAccording to technical specifications for toxicity determination of chemicals, Salmonella typhimurium reverse mutation assay (Ames assay), in vivo mammalian erythrocyte micronucleus test, sperm malformation test and teratogenesis test were used to detect the mutagenicity and teratogenicity induced by AND.

RESULTSWhen the exposure doses of AND were 8-5000 pg/plate, the result of Ames assay was negative. As compared with control group, the micronucleus rate of mice exposed to 113.8 mg/kg AND significantly increased(P<0.05), the sperm malformation rates of mice exposed to 54.4-272.0 mg/kg AND did not increased significantly. The survival rate of fetuses decreased, the rate of assimilated fetuses increased, the rate of fetus sternum agenesis enhanced in mice exposed to 319 mg/kg AND, as compared with controls. The rates of in the 4th-6th fetus sternum agenesis in groups exposed to 21.3, 79.7 and 319 mg/kg AND were higher than that in control group. The malformation rate of fetus bowels in groups exposed to 319 mg/kg AND was higher than that in control group. The teratogenic index of ADN was 30.

CONCLUSIONAND may be a mutagen and induce the teratogenic effect.

Animals ; Embryo, Mammalian ; drug effects ; pathology ; Female ; Male ; Mice ; Mice, Inbred Strains ; Micronucleus Tests ; Mutagenicity Tests ; Nitrites ; toxicity ; Pregnancy ; Quaternary Ammonium Compounds ; toxicity ; Spermatozoa ; drug effects ; pathology ; Sternum ; drug effects ; pathology

OBJECTIVETo study the acute, subacute and subchronic toxicity induced by ammonium dinitramide (ADN), and to ascertain the gradation and target organs of acute toxicity induced by AND.

METHODSAccording to technical specifications for toxicity determination of chemicals, the oral tests for acute, subacute and subchronic toxicity induced by AND were performed for 90 days.

RESULTSThe oral LDx for mouse and rat was 568.9 mg/kg and 616.6 mg/kg ADN respectively. The gradation of acute toxicity induced by AND was low level. The results of oral subacute and subchronic toxicity tests (for 28 and 90 days) showed that a gain in weight in group exposed to 123 mg/kg AND was significantly lower than that in control group (P<0.05), the TBIL and ALT in group exposed to 61.6 and 123 mg/kg AND significantly increased and the ratio of liver weight to body weight obviously decreased, as compared with control group, the number of animals with hepatic pathological changes in group exposed to 61.6 and 123 mg/kg AND was significantly higher than that in control group (P<0.05).

CONCLUSIONThe gradation of acute toxicity induced by ADN was low level. When the exposure dose of AND was 30.8 mg/kg, the adverse effect was not observed, and the target organ was liver.

Animals ; Body Weight ; Female ; Liver ; drug effects ; pathology ; Male ; Mice ; Mice, Inbred Strains ; Nitrites ; toxicity ; Quaternary Ammonium Compounds ; toxicity ; Rats ; Rats, Sprague-Dawley ; Toxicity Tests, Acute ; Toxicity Tests, Subchronic

Humans ; Arthritis, Psoriatic/drug therapy* ; Interleukin-17 ; Interleukin Inhibitors ; Antirheumatic Agents/therapeutic use* ; Tumor Necrosis Factor-alpha/therapeutic use* ; Interleukin-23/therapeutic use*

Objective To investigate the expression and the role of DCL1 gene in human glioma. Methods Thirty-nine glioma samples and 10 control tissues resected from healthy brain tissue with traumatic brain injury were collected for analysis. Real-time quantitative PCR was employed to detect the DCL1 gene expression at the mRNA level. Plasmid pCS2-DLC1was transfected into the glioma cell line U251 and pCS2-MT was transfected as control group; Western blotting was employed to detect the DCL1 gene expression at the protein level: the expression of Myc; MTT assays were performed to assess the proliferation of glioma cell line U251. Results Glioma tissues showed a significant increased DCL1 gene expression at mRNA level as compared with the control brain tissues (P=0.000). The DLC1 gene expression at mRNA level in the Grade Ⅰ gliomas was obviously higher than that in Grade Ⅱ,Ⅲ or Ⅳ ones (P=0.001). Over-expression of Myc in pCS2-DLC1 transfected group was found, while no obvious Myc expression was noted in the control group. The pCS2-DLC1 transfected group showed higher proliferation level of U251 cell lines than the pCS2-MT control group (P=0.002). Conclusion High expression level of DLC1 might contribute to the formation and development of glioma.