Apnea ; epidemiology ; pathology ; therapy ; Birth Weight ; China ; epidemiology ; Female ; Gestational Age ; Humans ; Infant, Newborn ; Infant, Very Low Birth Weight ; Male ; Risk Factors ; Time Factors

Objective To explore the mechanism of effects of cardiac sympathetic anesthesia on left ventricular ejection fraction(LVEF) and left cardiac cavity size of patients with dilated cardiomyopathy.Method 121 consecutive patients with dilated cardiomyopathy were divided into cardiac sympathetic nerve blockade group(TEA group) and control group(c group).In TEA group,5％ lidocaine was injected into thoracic epidural cavity for about 4 to 8 weeks in addition with routine therapy.In c group,only routine therapy was used.We observe the changes of LVEF and left cardiac cavity size before and after treatment in both groups. Result In TEA group,after anesthesia,LVEF was increased from(31.3± 12.8) to(47.3± 21.3),P<0.001;left ventricular end－ diastolic diameter was reduced from(69.1± 7.1)to (65.1± 8.0),P<0.001;left atrial diameter was decreased from(44.0± 6.2)to(39.4± 7.2),P< 0.001. Conclusion Cardiac sympathetic anesthesia can effectively improve the ejection performance of dilated cardiomyopathy and make the dilated cardiac cavity turn to normal level.

Chondrodysplasia Punctata ; congenital ; Humans ; Infant, Newborn ; Male

Administration, Oral ; Anti-Bacterial Agents ; administration & dosage ; Cytomegalovirus Infections ; drug therapy ; immunology ; virology ; Erythromycin ; administration & dosage ; Female ; Humans ; Infant ; Male ; T-Lymphocyte Subsets ; immunology ; Virus Replication

Humans ; Infant, Newborn ; Male ; Protein C ; metabolism ; Protein C Deficiency

Acquired Immunodeficiency Syndrome ; immunology ; HIV Infections ; immunology ; Humans ; Medicine, Chinese Traditional ; T-Lymphocytes ; physiology

Objective To explore the influence of melatonin receptor agonist Neu-P11 on the expression of IRS-1 and GLUT-4 in insulin-resistant 3T3-L1 adipocytes. Methods Insulin resistant 3T3-L1 adipocytes were induced with high glucose/ high insulin for 24 hours, and then they were divided into 4 treatment groups; melatonin, Neu-P11, melatonin+luzindole and Neu-P11 + luzindole. And non-treated insulin-resistant 3T3-L1 adipocytes were taken as control. Glucose consumption was detected by enzymatic method. IRS-1 and GLUT-4 protein expressions were detected by Western blotting analysis. Results After the insulin-resistant adipocytes were treated with melatonin and Neu-P11, the glucose consumption andthe expressions of IRS-1, GLUT-4 proteinswere significantly increased compared with the non-treated control group (P<0. 05). The expressions of IRS-1, GLUT-4 proteins in melatonin + luzindole (melatonin receptor antagonist) and Neu-P11 + luzindole groups were significantly decreased compared with melatonin alone or Neu-P11 alone groups (P<0. 05), and were similar to those in thenon-treated control group. Conclusion Melatonin receptor agonist Neu-P11 can increase glucose consumption, insulin sensitivity in insulin resistant-adipocytes, which might be associated with the up-regulation of IRS-1 and GLUT-4 protein expression.

Objective: The objective of present study was to examine the changes of melatonin receptor agonist Neu-P11 on expression of PKB and P-PKB in 3T3-L1 adipocytes and to research the variation mechanisms.Methods: 3T3-L1 pre-adipocytes were cultivated and differentiated in adipogenic cocktail by IBMX, DEX and insulin; Confirm the establishment of insulin resistance model. The changes of PKB and P-PKB protein expressions before and after drug action were detected by Western blot; Results: Expression of PKB and P-PKB reduced significantly by comparison with IS (P < 0.05). Melatonin and Neu-P11 can increase obviously the expression of PKB and P-PKB (P < 0.05). But Luzindole can block the effect of melatoninl, Neu-P11 increasing PKB (P < 0.05), will also be able to block that the melatonin increase P- PKB (P < 0.05), but it can"t block that Neu-P11 increases P - PKB .

Aim To evaluate the effect and safety of azithromycin injection produced in China and cefazolin in the treatment of respiratory tract infections.Methods 50 patients with respiratory tract infections were divided randomly into two groups. Patients in the test group recieved azithromycin in the dosage of 250 mg?d-1,qd for 5 d iv with double dosages at the first time and patients in the control group recieved cefazolin in the dosage of 2.0 g,bid,iv for 5～10 d. Results No statistical significant differences of overall clinical effect were observed between two groups .The fully recovery,effective and side reaction rates for the test group were 46.67%,90% and 3.3%,respectively,and for control group the data were 60%,95%,and 0%, respectively.Conclusion Azithromycin injection produced in China is effective and safe in the treatment of respiratory infections.

This study is to investigate the effect of artesunate on transforming growth factor-beta1 (TGF-beta1) induced epithelial-mesenchymal transition (EMT) and its possible mechanism. After the in vitro cultured RLE-6TN cells were treated with TGF-beta1 then artesunate intervened on it, after 24 h, expression of the markers of mesenchymal cell was assayed using Western blotting and real-time PCR analysis. Western blotting was also used to detect the effect of TGF-beta1 on the Smad3 and Smad7 expressions of RLE-6TN cells. Morphological alterations were examined by phase-contrast microscope, and ultrastructure changes by electron microscope. Incubation of RLE-6TN cells with TGF-beta1 resulted in the up-regulation of the expression of the mesenchymal cell markers, after artesunate intervened on it, resulted in the down-regulation of the expression. Meanwhile, incubation with artesunate intervened on RLE-6TN cells could lead to the apparent down-regulation of the expression of Smad3 and up-regulation of Samd7 and the transition of RLE-6TN cells to mesenchymal-like by TGF-beta1 induction, after artesunate intervened on it, RLE-6TN cells to epithelial-like. TGF-beta1 induced epithelial-mesenchymal transition process; artesunate can inhibit TGF-beta1-induced epithelial-mesenchymal transition process, the possible mechanism is up-regulation of the expression of Smad7 and down-regulation of the expression of Smad3, meanwhile inhibits phosphorylation of Smad3.
Actins ; genetics ; metabolism ; Animals ; Artemisia ; chemistry ; Artemisinins ; isolation & purification ; pharmacology ; Cell Line ; Cell Proliferation ; drug effects ; Epithelial Cells ; cytology ; metabolism ; Epithelial-Mesenchymal Transition ; drug effects ; Idiopathic Pulmonary Fibrosis ; pathology ; Plants, Medicinal ; chemistry ; Pulmonary Alveoli ; cytology ; RNA, Messenger ; metabolism ; Rats ; Smad3 Protein ; genetics ; metabolism ; Smad7 Protein ; genetics ; metabolism ; Transforming Growth Factor beta1 ; pharmacology ; Vimentin ; genetics ; metabolism