Objective To explore the distribution and characteristics on genotype of Mycobacterium tuberculosis and the relationship between Beijing genotype and drug-resistant phenotypes in Tianjin city. Methods 656 clinical strains were collected from Tianjin Center for Tuberculosis Control and ten other Tuberculosis Institute in Tianjin from January 2008 to June 2009.Information regarding administration, clinical as well as laboratory findings of patients were collected.Proportion method was adopted to detect the susceptibility on four anti-tuberculosis drugs, namely streptomycin (SM), isoniazid (INH), rifampicin (RFP) and ehambutol (EMB). Both Beijing and non-Beijing genotypes were differentiated by multiplex PCR. The relationship between Beijing genotype and drug-resistant phenotypes was analyzed. Results In this study, the overall resistance rate of MTB was 26.98%, with multidrug-resistant rate was 6.25%. Among 656 MTB strains, 600isolates (91.46% ) belonged to Beijing genotype. There was significant difference between Beijing and non-Beijing genotype (x2=4.26, P=0.039) among the Tianjin household registered population.Concerning the drug resistance, there was no significant difference between the two groups.Conclusion Beijing genotype strains were the predominant one in Tianjin. The proportion of people infected with the Beijing genotype strains in Tianjin household registration of patients was significantly higher than the proportion of patients in the floating population in the same region.Results from the statistical analysis did not reveal any statistically significant association between Beijing genotype and drug resistance.

OBJECTIVEPulmonary surfactant protein A (SP-A) plays an important role in the maintenance of pulmonary surfactant function and innative immune defence. This study aimed to explore the changes of SP-A concentration in the lungs of young rats with acute lung injury.

METHODSSprague-Dawley rats were randomly assigned to control and lung injury groups. Acute lung injury was induced by intraperitoneal injection of lipopolysaccharide (LPS) (4 mg/kg) in the lung injury group. The same amount of normal saline was given for the control group. The two groups were subdivided into 6 groups sacrificed at 6, 12, 24, 36, 48 and 72 hrs of injection (n=8 each). Western blot was employed to detect SP-A concentration in the lung tissues.

RESULTSSP-A concentration in the lung injury group was not different from the the control group within 12 hrs after LPS injection. SP-A concentration in the lung injury group was elevated significantly during 24-48 hrs after LPS injection, peaking at 36 hrs (6.94+/-0.80 vs 5.01+/-0.36; P< 0.01), compared with the controls. However, SP-A concentration in the lung injury group was significantly reduced 72 hrs after LPS injection compared with the controls (P< 0.01).

CONCLUSIONSThe changes of lung SP-A concentration in rats following acute lung injury were time-dependent. The transient elevation of SP-A concentration in the lungs indicated a strong compensation ability of SP-A in the host defence against acute lung injury.

Animals ; Female ; Lipopolysaccharides ; toxicity ; Lung ; chemistry ; Male ; Pulmonary Surfactant-Associated Protein A ; analysis ; Rats ; Rats, Sprague-Dawley ; Respiratory Distress Syndrome, Adult ; metabolism

OBJECTIVEAlveolar type II (AT II) cells play a crucial role in the maintenance of pulmonary surfactant homeostasis and pulmonary immunity. The effects of dexamethasone (Dex) on the ultrastructure of AT II cells after acute lung injury remain unknown. This study focused on the ultrastructural changes caused by acute lung injury and on the effects of Dex administration on these ultrastructural changes in young rats.

METHODSSeventy-two 21-day-old Sprague-Dawley rats were randomly divided into control, acute lung injury and Dex-treated groups. Rats in the lung injury group were intraperitoneally injected with 4 mg/kg lipopolysaccharide (LPS) in order to induce acute lung injury, while the control rats were injected with the same amount of normal saline (NS). The Dex-treated group was injected first with LPS followed 1 hr later by Dex (5 mg/kg) injection. Eight rats in each group were sacrificed 24, 48 and 72 hrs after LPS or NS injection. Lung samples were obtained from the lower parts of left lungs and fixed with 2.5% glutaraldehyde for transmission electron microscope examination.

RESULTSMicrovilli of AT II cells disappeared and the number of lamellar bodies (LBs) increased in the lung injury group 24 hrs after LPS injection. The ring-like arrangement of LBs around nuclei was present until 48 hrs after LPS injection. By 48 hrs after LPS injection, giant LBs with vacuole-like abnormalities appeared. The shape of nuclei became irregular and the border of the nuclei became blurred. By 72 hrs after LPS injection, the number of LBs was obviously reduced; nucleoli disappeared; and karyolysis occurred in some of the nuclei. In contrast, in the Dex-treated group, LBs crowded on one side of AT II cells and exocytosis appeared on the same side by 24 hrs after LPS injection. By 48 hrs, the number of LBs was reduced. The number of mitochondria increased, and some of them became swollen and enlarged. However, by 72 hrs, the number of LBs increased and the ring-like arrangement of LBs around the nucleus again appeared.

CONCLUSIONSUltrastructural changes of AT II cells following lung injury induced by LPS were time-dependent in young rats. Dex may ameliorate AT II cell injury and promote functional restoration of AT II cells in LPS-induced acute lung injury.

Animals ; Dexamethasone ; pharmacology ; therapeutic use ; Lipopolysaccharides ; toxicity ; Pulmonary Alveoli ; drug effects ; ultrastructure ; Rats ; Rats, Sprague-Dawley ; Respiratory Distress Syndrome, Adult ; chemically induced ; drug therapy ; pathology

OBJECTIVETo evaluate the efficacy and safety of Capsule metadoxine in the treatment of alcoholic liver disease.

METHODSA randomized double blind multicenter placebo-controlled clinical study was performed to evaluate the therapeutic effectiveness and safety of capsule metadoxine. Patients in metadoxine group received capsule metadoxine 500mg tid po. Patients in placebo group received placebo 2 pillows tid po. The treatment duration was 6 weeks. Patients were followed up 2 weeks after the treatment. Patients were visited once every 3 weeks during the treatment period. Clinical symptoms and liver function were evaluated in all the patients before treatment, at week 3, week 6 and 2 weeks after therapy. CT scan was done in some patients before treatment and at the end point of therapy.

RESULTS254 patients were recruited in the study, 126 in metadoxine group and 128 in placebo group. Median ALT, AST, GGT level in metadoxine group were decreased from 80.0 U/L, 59.2 U/L, 123.0 U/L (before treatment) to 41.1 U/L, 36.0 U/L, 57.0 U/L (after 6 weeks therapy). The improvement in liver function was more significant in metadoxine group than in placebo group (P less than 0.05). For the patients who stopped drinking during the study, the total effective rate of improvement in liver function was 82.8% in metadoxine group, much higher than that in placebo group (55.7% , P=0.0000). For the patients who did not stop drinking during the study, the total effective rate of improvement in liver function was 65.4% in metadoxine group, which is not significantly higher than that in placebo group (44.8%, P=0.1767). The CT value ratio of liver to spleen was significantly improved in metadoxine group (P=0.0023), and there was no significant difference between the two groups (P=0.6293). The rate of adverse was 1.6% in both of groups.

CONCLUSIONCapsule metadoxine is an effective and safe treatment for alcoholic liver disease.

Administration, Oral ; Adult ; Aged ; Alanine Transaminase ; blood ; Alcohol Deterrents ; administration & dosage ; therapeutic use ; Analysis of Variance ; Aspartate Aminotransferases ; blood ; Capsules ; Double-Blind Method ; Drug Combinations ; Fatty Liver, Alcoholic ; blood ; drug therapy ; pathology ; Female ; Follow-Up Studies ; Humans ; Liver ; diagnostic imaging ; pathology ; Liver Diseases, Alcoholic ; blood ; drug therapy ; pathology ; Liver Function Tests ; Male ; Middle Aged ; Pyridoxine ; administration & dosage ; therapeutic use ; Pyrrolidonecarboxylic Acid ; administration & dosage ; therapeutic use ; Treatment Outcome ; Ultrasonography ; Young Adult ; gamma-Glutamyltransferase ; blood

OBJECTIVEThis study examined the relationship between the ultrastructural alterations of alveolar epithelial cells type II (AEC-II) and pulmonary surfactant protein A (SP-A) levels in the lung tissue of young rats with acute lung injury (ALI) in order to explore the possible mechanism of ALI.

METHODSForty-eight young Sprague-Dawley rats were randomly divided into control and ALI groups. The rats in the ALI group were intraperitoneally injected with 4 mg/kg of lipopolysaccharide (LPS) in order to induce ALI. The control subjects were injected with the same volume of normal saline. Rats were sacrificed at 24, 48 and 72 hrs after LPS or NS injection. Lung samples were obtained from the lower parts of the left lung and fixed with 2.5% glutaraldehyde for transmission electron microscope examination and for Western blot test of SP-A.

RESULTSThe microvilli of AEC-II disappeared 24 hrs after LPS injection. After 24 and 48 hrs of LPS injection, lamellar body (Lb) increased in number, enlarged in size and reduced in density, and the ring-like arrangement of Lb was present. By 48 hrs after LPS injection, giant Lb with vacuole-like deformity appeared. The contents of lung SP-A in the ALI group 24 hrs (6.52+/-0.62 vs 5.02+/-0.35; P<0.01) and 48 hrs (6.65+/-0.62 vs 5.01+/-0.36; P<0.01) after LPS injection were significantly higher than those in the control group. By 72 hrs after LPS injection, Lbs ruptured and were reduced in number. The shape of the nuclei was irregular and the border was blurred. The content of lung SP-A was greatly reduced in the ALI group 72 hrs after LPS injection compared with that in the control group (3.87+/-0.50 vs 5.22+/-0.36; P<0.01).

CONCLUSIONSThe alterations of AEC-II and lung SP-A were time-dependent in young rats with ALI induced by LPS. In the early stage of ALI, the lung SP-A content showed a compensatory increase. With the increasing injury of AEC-II cells, the secretion of SP-A presented with a decompensation and the lung SP-A content decreased. This may be one possible mechanism for the development of ARD.

Animals ; Female ; Lipopolysaccharides ; toxicity ; Male ; Microscopy, Electron ; Pulmonary Alveoli ; pathology ; ultrastructure ; Pulmonary Surfactant-Associated Protein A ; analysis ; Rats ; Rats, Sprague-Dawley ; Respiratory Distress Syndrome, Adult ; metabolism ; pathology