China ; Critical Care ; history ; methods ; trends ; History, 20th Century ; History, 21st Century ; Humans

Humans ; Laryngeal Neoplasms ; Male ; Middle Aged ; Sarcoma

Adult ; Cranial Nerve Neoplasms ; diagnosis ; Diagnostic Errors ; Facial Nerve ; pathology ; Hemangioma ; diagnosis ; Humans ; Male

The framed storehouse and the open rolling shutter door equipment are designed and manufactured for the infrastructure construction.The multipurpose and moved frame operating platform is designed and manufactured according to the demands of loading and unloading as a whole for part medical equipments.In this way,the shortage of the storehouse space is solved and the usual training and moving become easier.

Background Oxidative stress is thought to be responsible to diabetes-complicated cataract.Our previous study demonstrated that as an iron chelator,deferiprone can protect lens from oxidative damage.Objective This further study aimed to investigate the role of deferiprone on the formation of diabetic-complicated cataract.Methods Forty 6-week-old Wistar rats were included in the study and randomized into 4 groups.Eight of them were used as the normal control group.Diabetes mellitus animal models were established in 22 rats by the carbonhydratediet and fat diet and the intraperitoneal injection of 40 mg/kg streptozocin (STZ).The deferiprone of 50 mg and 100 mg were intragastrically given in 8 model rats respectively after 3 days once a day for 8 weeks.The opacification of lenses was examined under the slit lamp weekly after treatment.The animals were sacrificed and the lenses were obtained at the eighth week of deferiprone injection.The concentrations of water-soluble protein ( WSP),urine-soluble protein (USP) and alkali-soluble protein (ASP) in rat lens suspension were detected by Bradford method.The super oxide dimutese (SOD),malondialdehyde (MDA) and glutathione (GSH) were determined spectrometically using xanthine oxidase,thiobarbituric acid,dithio bis-nitrobenzoic acid.Results No evidently differences were found in the content of the WSP,USP and ASP among the these groups( F=1.73,0.18,0.09,P＞0.05).The contents of MDA in 50 mg deferiprone group and 100 mg deferiprone group were ( 1.05 ± 0.10 ) mmol/g and ( 1.05 ± 0.22 ) mmol/g respectively,showing a significant decline in comparison with diabetic model group (P＜0.05).The SOD and GSH contents in lens were (321.29±16.57) U/mg,(322.07±22.16) U/mg and (7.83±0.65 ) mg/g,(7.70±0.77 ) mg/g respectively in 50 mg deferiprone group and 100 mg deferiprone group and were considerably elevated in comparison with ( 298.70± 14.69 ) U/mg and ( 5.47 ± 1.01 ) mg/g of diabetic model groups ( P＜0.05 ).No significant differences were found in the indexes mentioned above between 50 mg and 100 mg deferiprone groups(P＞0.05).Conclusions Deferiprone can reduce oxidative stress and improve the energy metabolism of the lens in diabetic rats.

OBJECTIVETo observe the effects of bitumen fume on neurotransmitter and ultrastructure of mice brain and to investigate the toxicity of bitumen fume on nerve system of mice brain.

METHODSThe experimental mice were forced to inhale the bitumen fume at different exposure level and in different time periods. The contents of the three transmitters dopamine (DA), norepinephrine (NE), 5-hydroxytryptamine (5-HT) in mice brain were measured by the fluorescence meanwhile ultrastructure of mice brain was observed by electronic microscope. The ultrastructure of mice brain was observed under transmission electron microscopy.

RESULTSThe contents of DA, NE and 5-HT in all groups decreased with the increasing of dose and prolonging of time (after 8 week, with the increasing of exposure lever, the content of DA, NE, 5-HT was respectively 2.194, 2.190, 2.181, 2.178 microg/g and 1.148, 1.138, 1.135 and 1.407, 1.403, 1.395 microg), but the results did not show significant differences. The structure of the mitochondria changes included the swollen mitochondria, chromatin margination, pyknosis and apoptosis in neuro cells and the processes of swollen astrocyte cells.

CONCLUSIONThe bitumen fume could induce changes of the ultrastructure of mice brain and affect the contents of neurotransmitter of mice brain.

Animals ; Brain ; metabolism ; ultrastructure ; Female ; Hydrocarbons ; toxicity ; Male ; Mice ; Mice, Inbred Strains ; Neurotransmitter Agents ; analysis

Carcinoma, Squamous Cell ; genetics ; pathology ; virology ; Cervical Intraepithelial Neoplasia ; genetics ; pathology ; virology ; DNA, Viral ; metabolism ; Female ; Gene Amplification ; Humans ; In Situ Hybridization, Fluorescence ; Lymphatic Metastasis ; Neoplasm Grading ; Neoplasm Staging ; Papillomaviridae ; genetics ; Papillomavirus Infections ; metabolism ; RNA ; genetics ; Telomerase ; genetics ; Uterine Cervical Neoplasms ; genetics ; pathology ; virology

OBJECTIVEThe study aimed to test if Paridis Rhizoma total saponins (PRTS) could induce apoptosis of human gastric cancer cell MKN-45.

METHODBased on the previous researches, PRTS was set by different concentrations to treat human gastric cancer cell for 12 h (5, 10, 20 mg x L(-1)). Fluorescent staining methods were adopted to observe apoptotic morphological changes of MKN-45. The apoptosis rates were analyzed by flow cytometry with Annexin V-FITC/PI staining. The enzymatic activities of caspase-3 and caspase-8 were measured by ELISA. The protein levels of Fas and FasL were detected by Western blotting.

RESULTUnder a fluorescence microscope, MKN-45 treated by PRTS was seen typical apoptotic morphological features. PRTS significantly increased the rate of apoptosis. Compared with the control group, there exsited significant differences in apoptosis rate of PRTS concentration of 20 mg x L(-1) (P < 0.01); besides, the enzymatic activities of caspase-3 and caspase-8 were promoted obviously after the effect of PRTS on MKN-45 cells for 12 h (P < 0.01). The protein levels of Fas and FasL in the MKN-45 were upgraded significantly.

CONCLUSIONPRTS can induce apoptosis of human gastric cancer cell MKN-45 , which is concerned with caspase-3 and caspase-8 and upgraded Fas and FasL.

Apoptosis ; drug effects ; Caspase 3 ; genetics ; metabolism ; Caspase 8 ; genetics ; metabolism ; Cell Line, Tumor ; Drugs, Chinese Herbal ; pharmacology ; Fas Ligand Protein ; metabolism ; Humans ; Magnoliopsida ; chemistry ; Rhizome ; chemistry ; Saponins ; pharmacology ; Signal Transduction ; drug effects ; Stomach Neoplasms ; drug therapy ; genetics ; metabolism ; physiopathology ; fas Receptor ; metabolism

Air ; analysis ; Chromatography, Gas ; methods ; Ethylene Oxide ; analysis ; Furans ; analysis ; Methylene Chloride ; analysis ; Workplace

Objective To investigate the potential role of angiotensinⅡ(AngⅡ)-angiotensinⅡreceptor 1 (ATRI) pathway on inflammatory activation in the lung of rats. Method Twenty four Sprague-Dawley rats were randomly divided into four groups: control group, Ang II group, AngⅡ+losartan group and losartan group. Lung wet/dry weight (W/D) was recorded to assess lung injury. The total lung homogenates were prepared to detect nuclear factor-kappa B (NF-?B) activation by electrophoretic mobility gel shift assary (EMSA), tumor necrosis factor (TNF)-?mRNA expression by reverse transcription polymerase chain reaction (RT-PCR), myeloperoxidase (MPO) and malondialdehyde (MDA) by colorimetry. Plasma yon Willebrand Factor (vWF) were assessed by enzyme-linked immunosorbent assay (ELISA). Meanwhile, pathological changes were examined under optical microscope. Results Histologically, alveolar edema, hemorrhage, and massive inflammatory cell infiltration were observed in AngⅡgroup, but not in control group and losartan group. Compared with AngⅡgroup, histological injury was lesser in AngⅡ+ losartan group. In AngⅡgroup, lung W/D, NF-?B activation, TNF-?mRNA expression, MPO, MDA and vWF were markedly higher than those in the other three groups. There were not significant differences of lung W/D, NF-?B activation, TNF-?mRNA expression, MPO, MDA and vWF in control group, AngⅡ+ losartan group and losartan group. Conclusions Systemic infusion of AngⅡcould up- regulate inflammatory mediator expression and induce lung injury in rats. AngⅡ, acting mainly through ATRI, induced inflammatory activation in the lung of rats.