OBJECTIVETo study the clinical effect and safety of early postnatal application of glucocorticoids in the prevention of bronchopulmonary dysplasia (BPD) in preterm infants.

METHODSThe databases including PubMed, Cochrane Library, Embase, CNKI, Wanfang Data, and VIP were comprehensively searched for articles on early postnatal application of glucocorticoids in the prevention of BPD in preterm infants published up to June 2016. Review Manager 5.3 was used for the Meta analysis of 16 randomized controlled trials (RCTs) that met the inclusion criteria.

RESULTSA total of 2 962 participants were enrolled in the 16 RCTs, with 1 486 patients in the trial group and 1 476 in the control group. The Meta analysis showed that early postnatal application of glucocorticoids reduced the incidence rate of BPD at a corrected gestational age of 36 weeks (OR=0.73, 95%CI: 0.61-0.87, P=0.0004), but there was an increase in the risk of hyperglycemia (OR=1.61, 95%CI: 1.24-2.09, P=0.0003), hypertension (OR=1.63, 95%CI: 1.11-2.38, P=0.01), and intestinal perforation (OR=1.51, 95%CI: 1.12-2.04, P=0.007).

CONCLUSIONSAt present, it is not recommended to use glucocorticoids to prevent BPD in preterm infants. Its advantages and disadvantages need further studies, with special focuses on the adverse effects of hyperglycemia, hypertension, and intestinal perforation.

Bronchopulmonary Dysplasia ; prevention & control ; Glucocorticoids ; adverse effects ; therapeutic use ; Humans ; Hyperglycemia ; chemically induced ; Hypertension ; chemically induced ; Infant, Newborn ; Infant, Premature ; Intestinal Perforation ; chemically induced

Angiogenesis Inhibitors ; adverse effects ; Antibodies, Monoclonal ; adverse effects ; Antibodies, Monoclonal, Humanized ; Bevacizumab ; Carcinoma, Non-Small-Cell Lung ; drug therapy ; Hemorrhage ; chemically induced ; Humans ; Hypertension ; chemically induced ; Lung Neoplasms ; drug therapy ; Proteinuria ; chemically induced ; Thromboembolism ; chemically induced

Adult ; Arsenic Poisoning ; pathology ; Chronic Disease ; Hemosiderin ; metabolism ; Hemosiderosis ; metabolism ; pathology ; Humans ; Hypertension, Portal ; chemically induced ; metabolism ; pathology ; Liver Cirrhosis ; chemically induced ; metabolism ; pathology ; Male ; Pancytopenia ; chemically induced ; metabolism ; pathology ; Splenomegaly ; chemically induced ; metabolism ; pathology

OBJECTIVETo analyze and evaluate the reproductive effects of occupational exposure to mercury among female workers and to identify relative sensitive indicators.

METHODSDocuments on the relations of occupational exposure to mercury and reproductive effects on female workers were collected through computer and manually that were published in Chinese language during 1989-2006. After strict selection, homogeneity test and integrated analysis for the abstracted data of the eligible studies were conducted using Review Manager Statistic Software. Combined RR value was used as the index for total effect on each project for Meta-analysis.

RESULTSIn total, 14 original research papers were included (totally 2148 subjects and 2044 controls). When comparing to the controls, the occupational exposure to mercury was significantly associated with longer menstrual period (RR = 1.82, 95% CI: 1.45-2.30), menstrual cycle delay (RR = 2.03, 95% CI: 1.74-2.37) and the changes of menstrual blood volume (RR = 2.06, 95% CI: 1.47-2.09), dysmenorrhea (RR = 2.14, 95% CI: 1.54-2.99), pregnancy-induced hypertension (RR = 2.17, 95% CI: 1.32-3.57), stillbirths (RR = 2.54, 95% CI: 1.41-4.56) and low birth weight (RR = 3.39, 95% CI: 1.38-8.33)/birth defect (RR = 2.67, 95% CI: 1.55-4.60) of their offspring (P < 0.05).

CONCLUSIONOccupational exposure to mercury could cause dysfunction of the menstrual period, menstrual cycle, menstrual blood volume, as well as dysmenorrhea for female workers being exposed to mercury and inducing adverse reproductive outcomes, including pregnancy-induced hypertension, stillbirth, low birth weight and birth defects of their offspring.

Adolescent ; Adult ; Dysmenorrhea ; chemically induced ; Female ; Humans ; Hypertension, Pregnancy-Induced ; chemically induced ; Infant, Low Birth Weight ; Infant, Newborn ; Menstrual Cycle ; drug effects ; Mercury ; adverse effects ; Middle Aged ; Occupational Exposure ; adverse effects ; Pregnancy ; Pregnancy Complications ; chemically induced ; Stillbirth ; Young Adult

Acute Disease ; Female ; Humans ; Hypertension ; chemically induced ; Middle Aged ; Organophosphate Poisoning ; Pesticides ; poisoning ; Skin Absorption

Animals ; Hypertension, Pulmonary ; chemically induced ; physiopathology ; Monocrotaline ; adverse effects ; Rats ; Rats, Sprague-Dawley ; Thrombomodulin ; metabolism

OBJECTIVE: To investigate the effect of Yiqi Wenyang Huoxue Huatan Fang (YWHHF) on alleviating hypoxia-hypercarbia pulmonary hypertension by inhibiting endothelial-mesenchymal transition (EndoMT) BMP-7/Smads pathway. METHODS: Fifty male healthy SD rats of clean grede, weighting (180~220) g, were randomly divided into 5 groups (=10):normoxia group (N), hypoxia-hypercarbia group (HH); YWHHF high dose group (YH), middle dose group (YM) and low dose group (YL). The rats in N group were kept in normal oxygen environment, the remaining four groups were intermittently exposed to hypoxia-hypercarbia environment (9%~11% O, 5%~6% CO) for 4 weeks, 6 days a week, 8 hours per day. The rats in YH, YM, YL groups were received YWHHF gavage in a dosageof 0.6, 0.3, 0.15g/kg respectively (3 ml/kg),the rats in N and HH groups were received equal volume of normal saline. After 4 weeks, the mean pulmonary arterial pressure(mPAP) was detected,the right ventricular free wall and left ventricle plus ventricular septum were isolated to determine the right ventricular hypertrophy index. Lung ultrastructural changes were surveyed under an electronic microscopy, the changes of pulmonary artery structure surveyed by immunofluorescence, the mRNA levels of alpha-smooth muscle actin (α-SMA)、platelet endothelial cell adhesion molecule-1 (CD31)、bone morphogenetic protein-7 (BMP-7)、drosophila mothers against decapentaplegic protein1/5/8 (Smad1/5/8) were detected by RT-PCR, and the protein levels of α-SMA、CD31、BMP-7、p-Smad1/5/8 and Smad1/5/8 were detected by Western blot. RESULTS: Compared with N group, mPAP and the right ventricular hypertrophy index were increased,some significant injuries also were discovered under microscopic observation,the mRNA and protein expression of α-SMA was increased, and the mRNA expressions of CD31、BMP-7、Smad1/5/8 were decreased in the other four groups, the protein expressions of CD31、BMP-7、p-Smad1/5/8 were decreased(<0.05). Compared with HH group, the above changes in YH、YM、YL groups were all improved (<0.05). CONCLUSIONS YWHHF can inhibit EndoMT to alleviate pulmonary hypertension, and the mechanism may be related to the promotion of the expression of BMP-7/Smads pathway.
Animals ; Hypercapnia ; Hypertension, Pulmonary ; chemically induced ; Hypoxia ; Male ; Pulmonary Artery ; Rats ; Rats, Sprague-Dawley

Enbucrilate ; adverse effects ; therapeutic use ; Female ; Humans ; Hypertension, Portal ; diagnosis ; etiology ; Liver Cirrhosis, Biliary ; drug therapy ; Middle Aged ; Pulmonary Embolism ; chemically induced ; diagnosis ; Sepsis ; chemically induced ; etiology

OBJECTIVETo observe the changes in pulmonary artery protein kinase C (PKC) activity in rats with chronic inflammatory pulmonary hypertension (PHT).

METHODSChronic inflammatory PHT was induced in rats with monocrotaline. The PKC activities in the rat pulmonary arteries were measured by radioactive assay during the development of PHT.

RESULTSWith the development of chronic inflammatory PHT, the total and cytosolic fractions of PKC activity in PHT rat pulmonary arteries increased initially with subsequent decrease (Plt;0.05), but the membranous fraction of PKC activity and the membrane-to-cytosol PKC activity ratio increased continuously (P<0.05).

CONCLUSIONThe up-regulation of PKC activity and the translocation of PKC might be associated with the development of chronic inflammatory PHT in rats.

Animals ; Chronic Disease ; Hypertension, Pulmonary ; chemically induced ; enzymology ; Inflammation ; chemically induced ; enzymology ; Male ; Monocrotaline ; Protein Kinase C ; metabolism ; Pulmonary Artery ; enzymology ; Rats ; Rats, Wistar

OBJECTIVESTo study the role of hepatic sinusoid capillarization during the formation of portal hypertension in fibrotic rats induced by dimethylnitrosamine (DMN).

METHODSHepatic fibrotic rats were induced by administration of DMN intraperitoneally three times a week for 4 weeks. The rats were harvested on day 2 and weeks 1, 2, 3, 4, 5, 6, 8, 12 and 24. The formation of liver fibrosis and hepatic sinusoid capillarization were observed by morphologic methods. Pressure of portal vein (Ppv) was directed measured with intubation tube method by mesentry anterior vein.

RESULTSThe Ppv was getting higher and higher with the administration of DMN. After four weeks, the Ppv was higher than that of control [(1.10+/-0.18)kPa vs (0.52+/-0.04)kPa, t=6.41, P<0.01]. The dynamic change of hepatic sinusoid capillarization was in accordance with that of Ppv, which normalized gradually after the DMN was stopped. Significant positive correlation existed between the dynamic change of Ppv and the expression of vWF, laminin and alpha-SMA in sinus (r=0.833, P<0.01; r=0.953, P<0.01; r=0.919, P<0.01).

CONCLUSIONHepatic sinusoid capillarization is the vital cause for portal hypertension in fibrotic rats induced by DMN.

Animals ; Capillaries ; pathology ; Dimethylnitrosamine ; Hypertension, Portal ; chemically induced ; etiology ; pathology ; Liver ; blood supply ; pathology ; Liver Cirrhosis, Experimental ; chemically induced ; complications ; pathology ; Male ; Rats ; Rats, Wistar