Humans ; Ischemic Postconditioning ; Myocardial Reperfusion Injury

Brachytherapy ; adverse effects ; Female ; Humans ; Iodine Radioisotopes ; administration & dosage ; therapeutic use ; Male ; Medical Staff, Hospital ; Occupational Exposure ; analysis ; Radiation Dosage ; Radiation Monitoring

0.05). There was only 2/109 cases (5.8%) need a second course of antibiotics because of likely infection and 102/109 cases (93.5%)need not any moor antibiotics. The mean period of antibiotic treatment in group Ⅰ, group Ⅱa and group Ⅱb were (1.2?0.5) days,(4.8?0.8) days and (9.3?1.8) days,respectively.There were significant differences(all P

The sfa1 gene encoded a bifunctional enzyme with the activities of both alcohol dehydrogenase and glutathione-dependent formaldehyde dehydrogenase in Saccharomyces cerevisiae.The gene disruption cassette produced by PCR using the same long oligonucleotides which comprise 19 or 22 nucleotides complementary to sequences in the templates(pUG6 and pUG66 marker plasmid)at 3' end and 45 nucleotides at 5' end that annealed to sites upstream or downstream of the genomic target sequence to be deleted.After two linear disruption cassettes with a Cre/loxP mediated marker were transformed into the cells of Saccharomyces cerevisiae YS-1,the positive transformants were checked by PCR to correct the integration of the cassette and concurrent deletion of the chromosomal target sequence.Once correctly integrated into the genome,the select marker can be efficiently rescued by transformating the plasmid pSH47 into YS-1 and inducing the Cre expression with a Cre/loxP-mediated marker removal procedure.The expression of the Cre recombinase finally resulted in the removal of the marker gene,leaving behind a single loxP site at the chromosomal locus.The diploid mutant YS-1-sfa1 was generated,which could enhance the output of ethanol with 8.0% by shaking culture in flask compared with the original strain YS-1.

Objective To examine the expression of toll-like receptor 2(TLR2)in peripheral blood monocytes and explore its association with disease stages and clinical manifestations and to explore the patho- genesis of rheumatoid arthritis(RA).Methods The expression of toll-like receptor 2 in peripheral blood monocytes from 47 RA patientis(27 in active stage and 20 in stable stage)and 18 normal individuals were de- tected by flowcytometry and RT-PCR.Results The expression of toll-like receptor 2 in peripheral blood monocytes in patients with active disease was significantly increased compared to non-active patients and nor- mal individuals,The expression was found to correlate with the Disease Active Score(DAS),serum C-reactive protein(CRP)level and the erythrocyte sedimentation rate(ESR),but not correlate with rheumatoid factor (RF)and the anti-cyclic citrullinated peptide(CCP)antibody.Conclusion The expression of toll-like recep- tor 2 in peripheral blood monocytes of patients with active RA is significantly increased.And the expression is correlated with disease activity index.The innate immune system is activated in patients with active disease. And the increased expression may promote the activities of monocytes.

Objective To determine the effects of~(99)Tc-MDP on joint inflammation and bone destruc- tion in collagen-induced arthritis(CIA)rats model and its effect on tumor necrosis factor alpha(TNF-?). Methods CIA was induced by immunization of male SD rats with an emulsion of collagen.~(99)Tc-MDP or placebo was intravenous infused to rats for 20 days.Joint inflammation was assessed by arthritis index.Lesions of bone were assessed based on the histological changes in ankle joints,radiographic analysis in hind paw with Larsen score.Systemic TNF-?level was measured by radioimmune assay.Results~(99)Tc-MDP suppressed joint swelling(P

Air Pollutants, Occupational ; adverse effects ; analysis ; Dust ; analysis ; Environmental Monitoring ; instrumentation ; methods ; Humans ; Industry ; Inhalation Exposure ; statistics & numerical data ; Maximum Allowable Concentration ; Occupational Exposure ; statistics & numerical data ; Quartz

Objective To demonstrate high mobility group box chromosomal protein 1(HMGBI) expression in synovium and joint,and to identify the role of HMGB1 in the pathogenesis of synovitis and joint destruction in adjuvant-induced arthritis(AA).Methods AA of 15 male rats were induced in SD rats by intradermal injection of 100?l Freud's complete adjuvant in the foot pad of the left hind paw.All rats were killed at the 18th day.Synovium and joints were collected for histopathology studies and determining the expression of HMGB1 by immunohistochemistry,and serum was collected for determining the expression of HMGB1 by western blotting analysis.Results Immunostaining of specimens from normal rats showed that HMGB1 was primarily confined to the nucleus of synoviocytes with occasional cytoplasmic staining.In contrast, inflammatory synovial tissues from AA rats showed a distinctly different HMGB1 staining pattern.Nuclear HMGBI expression was accompanied by a cytoplasmic staining in many mononuclear cells.The cytoplasmic HMGB1 expression in synovium of AA rats is significantly higher than that of normal rats.Additionally,HMGBI was highly expressed in the nuclei and cytoplasm of the subchondral chondrocytes and inflammatory cells in bone erosion in AA rats(P＜0.01),while fewer positive cytoplasmic staining of HMGB1 was found in chondrocytes and fewer positive nuclear staining was found in bone cells in normal rats.HMGB1 concentration was significantly higher in serum of AA rats than that in normal rats(P＜0.001).Conclusion The cytoplasmic HMGBI expression in synovium and joints is greatly upregulated;the level of HMGB1 in serum is increased in AA rats which suggests a patbogenetic role of HMGB1 in synovitis and bone destruction of adjuvant-induced arthritis.

The expressions of StAR (steroidogenic acute regulatory protein) mRNA in testes from 7,14,23 and 37 day-old piglets were studied by tissue in situ hybridization. The results indicated that in the testes of piglets, StARmRNA was expressed in Leydig cells of pig testes. The expression level of StARmRNA was lower in 7 days piglets but higher in 14,23,37 days. The results indicated that StAR gene played an important role in steroid biosynthesis.

OBJECTIVETo investigate the effects of angiotensin converting enzyme inhibitor (ACEI) captopril on Calpain-mediated cardiomyocytes apoptosis and cardiac function in diabetic rats.

METHODSThirty adult male SD rats were randomly divided into 3 groups (n = 10), normal control group (NC group), diabetes mellitus group (DM group)and captopril treated group (Cap group). Streptozocin (STZ) were used to make the model of diabetes mellitus, captopril was administrated by gavage at the dose of 50 mg/kg every day, while in NC group and DM group the same volume of normal saline was administrated. Twelve weeks later, left ventricular systolic pressure (LVSP), left ventricular end-diastolic pressure (LVDEP), maximal rise rate of left ventricular pressure (+ dp/dtmax) and maximal fall rate of left ventricular pressure (- dp/dtmax) were detected; Western blot was used to detect the expression of Calpain-1 Calpain-2, Bcl-2, Bax and total Caspase3 protein; apoptosis index (AI) were assessed by terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling (TUNEL).

RESULTSCompared with NC group, LVDEP was significantly higher; LVSP, + dp/dtmax and - dp/dtmax were significantly decreased (P < 0.05); Bcl-2 protein expression was decreased; the expression of Calpain-1, Calpain-2, Bax and total Caspase3 protein were increased; the value of AI was significantly increased. Compared with DM group, LVDEP was significantly lower; LVSP, + dp/dtmax and - dp/dtmax were significantly increased (P < 0.05); Bcl-2 protein expression was increased, the expression of Calpain-1, Calpain-2, Bax and total Caspase3 protein were decreased; the value of AI was significantly decreased (P < 0.05).

CONCLUSIONCaptopril can protect diabetic myocardial structure through inhibiting activation of Calpain-1 and Calpain-2, up-regulating the expression of Bcl-2, down-regulating the expression of Bax to inhibit Caspase3 dependent apoptosis, thereby improving the ventricular function and myocardial structure.

Angiotensin-Converting Enzyme Inhibitors ; pharmacology ; Animals ; Apoptosis ; drug effects ; Calpain ; metabolism ; Cardiomyopathies ; pathology ; Caspase 3 ; metabolism ; Diabetes Mellitus, Experimental ; metabolism ; pathology ; physiopathology ; Male ; Myocytes, Cardiac ; cytology ; drug effects ; Proto-Oncogene Proteins c-bcl-2 ; metabolism ; Rats ; Rats, Sprague-Dawley ; bcl-2-Associated X Protein ; metabolism