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1.
Chinese Journal of Contemporary Pediatrics ; (12): 514-520, 2022.
Article in Chinese | WPRIM | ID: wpr-928637

ABSTRACT

OBJECTIVES@#To study the effect of sex on the clinical outcome of extremely preterm infants (EPIs)/extremely low birth weight infants (ELBWIs) by propensity score matching.@*METHODS@#A retrospective analysis was performed for the medical data of 731 EPIs or ELBWIs who were admitted from January 1, 2011 to December 31, 2020. These infants were divided into two groups: male and female. A propensity score matching analysis was performed at a ratio of 1:1. The matching variables included gestational age, birth weight, percentage of withdrawal from active treatment, percentage of small-for-gestational-age infant, percentage of use of pulmonary surfactant, percentage of 1-minute Apgar score ≤3, percentage of mechanical ventilation, duration of mechanical ventilation, percentage of antenatal use of inadequate glucocorticoids, and percentage of hypertensive disorders in pregnancy. The two groups were compared in the incidence rate of main complications during hospitalization and the rate of survival at discharge.@*RESULTS@#Before matching, compared with the female group, the male group had significantly higher incidence rates of neonatal respiratory distress syndrome, bronchopulmonary dysplasia (BPD), severe intraventricular hemorrhage, periventricular leukomalacia, necrotizing enterocolitis, and patent ductus arteriosus (P<0.05), while after matching, the male group only had a significantly higher incidence rate of BPD than the female group (P<0.05). There was no significant difference in the rate of survival at discharge between the two groups before and after matching (P>0.05).@*CONCLUSIONS@#Male EPIs/ELBWIs have a higher risk of BPD than female EPIs/ELBWIs, but male and female EPIs/ELBWIs tend to have similar outcomes.


Subject(s)
Female , Humans , Infant , Infant, Newborn , Male , Pregnancy , Bronchopulmonary Dysplasia/etiology , Infant, Extremely Low Birth Weight , Infant, Extremely Premature , Propensity Score , Retrospective Studies , Sex Characteristics
2.
Journal of Southern Medical University ; (12): 952-956, 2016.
Article in Chinese | WPRIM | ID: wpr-286867

ABSTRACT

<p><b>OBJECTIVE</b>To investigate the effect of docosahexaenoic acid (DHA) on invasiveness of aflatoxin B1 (AFB1)-induced hepatocellular carcinoma cells in vitro.</p><p><b>METHODS</b>HepG2.2.15 cells were exposed to different concentrations of AFB1 and DHA plus AFB1. The cell migration and invasion were assessed using wound-healing and Transwell assay, and flow cytometry was used to analyze the cell cycle changes. The ultrastructural changes of the cells were observed by transmission electron microscopy.</p><p><b>RESULTS</b>Compared with the control group, the cells exposed to2 µmol/L AFB1 showed obviously enhanced migration and invasion with decreased cell ratio in G1/G1 phase and increased cell ratio in G2/M phase but no changes in S phase cells; transmission electron microscopy revealed the presence of multiple nucleoli and significantly increased mitochondria and Golgi apparatus in the exposed cells. Compared with AFB1-exposed cells, the cells treated with DHA and AFB1 showed decreased migration and invasion abilities, and the G1/G1 phase cells increased and G2/M phase cells decreased significantly; ultrastructurally, the cells contained single nucleoli with decreased mitochondria and vacuolization occurred in the cytoplasm.</p><p><b>CONCLUSION</b>DHA can significantly inhibit AFB1-induced enhancement of cell migration and invasion in hepatocellular carcinoma cells in vitro.</p>


Subject(s)
Humans , Aflatoxin B1 , Pharmacology , Carcinoma, Hepatocellular , Pathology , Cell Cycle , Cell Movement , Docosahexaenoic Acids , Pharmacology , Golgi Apparatus , Hep G2 Cells , Liver Neoplasms , Pathology , Mitochondria , Neoplasm Invasiveness
3.
Journal of Southern Medical University ; (12): 1504-1508, 2011.
Article in Chinese | WPRIM | ID: wpr-333877

ABSTRACT

<p><b>OBJECTIVE</b>To evaluate the effect of metformin on the apoptosis of renal cell carcinoma (RCC) cells in vitro and its mechanisms.</p><p><b>METHODS</b>Fluorescent microscopy and flow cytometry were used to examine the changes in the apoptosis of 786-O cells after metformin treatment. The possible signaling molecules involved in this process were analyzed by immunoblot analysis of AMP-activated protein kinase (AMPK) signaling and caspase 9.</p><p><b>RESULTS</b>Metformin induced apoptosis and caspase 9 activation in 786-O cells in low-serum medium but not in normal-serum medium. Metformin also induced AMPK activation in 786-O cells, but this activation was not associated with the cell proliferation inhibition or apoptosis-inducing effect of metformin.</p><p><b>CONCLUSION</b>Metformin can induce apoptosis of RCC cells in vitro, suggesting its potential as a therapeutic agent for RCC.</p>


Subject(s)
Humans , Apoptosis , Carcinoma, Renal Cell , Pathology , Caspase 9 , Metabolism , Cell Line, Tumor , Cell Proliferation , Kidney Neoplasms , Pathology , Metformin , Pharmacology
4.
Journal of Southern Medical University ; (12): 1226-1229, 2010.
Article in Chinese | WPRIM | ID: wpr-289958

ABSTRACT

<p><b>OBJECTIVE</b>To obtain recombinant N-and C-terminal of FKBP38 and prepare anti-FKBP38 polyclonal antibody for Western blotting (WB), immunohistochemical (IHC) and immunofluorescence (IF) analyses.</p><p><b>METHODS</b>The N-terminal (1-207 aa) and C-terminal (209-387 aa) cDNA of FKBP38 were sub-cloned from the full-length cDNA of FKBP38 and ligated to prokaryotic expression plasmid pGEX-6P-1 for construction of the recombinant vectors pGEX-6P-1-FKBP38-N and pGEX-6P-1-FKBP38-C. After sequencing, the recombinant vectors were transformed into E.coli BL21 and GST-tagged FKBP38-NT and FKBP38-CT were induced by IPTG. The proteins were purified by Glutathione affinity chromatography column and characterized by SDS-PAGE. Rabbits were immunized with the purified recombinant protein to prepare the antiserum, which were analyzed by WB, IHC and IF.</p><p><b>RESULTS</b>The recombinant vectors pGEX-6P-1-FKBP38-N and pGEX-6P-1-FKBP38-C were successfully constructed. After IPTG induction, the E.coli transformed with these plasmids expressed GST-tagged protein, which was successfully purified. Western blotting demonstrated that the purified antibody could specifically bind to FKBP38 in various cell lines. Immunofluorescence assay showed that FKBP38 was located mainly on the mitochondria. Immunohistochemical analysis revealed cytoplasmic location of FKBP38 in breast cells.</p><p><b>CONCLUSION</b>We successfully expressed and purified N- and C-terminal of FKBP38, and FKBP38 polyclonal antibody we prepared can specifically recognize FKBP38 in SB, IF and IHC assays, which facilitates further functional investigation of FKBP38.</p>


Subject(s)
Humans , Antibodies, Monoclonal , Fluorescent Antibody Technique , Genetic Vectors , Genetics , Immunohistochemistry , Recombinant Proteins , Genetics , Allergy and Immunology , Tacrolimus Binding Proteins , Genetics , Allergy and Immunology
5.
Chinese Pharmacological Bulletin ; (12)2003.
Article in Chinese | WPRIM | ID: wpr-680453

ABSTRACT

Aim To study the expression of caspase-12 mRNA and protein following focal cerebral ischemia-reperfusion in rats,and explore the effect of endoplasmic reticulum pathway on neuronal apoptosis.Methods 60 male Wistar rats were randomly divided into sham-operated group and ischemic group.The middle cerebral artery occlusion(MCAO)models were established by using the intraluminal suture occlusion method,neuronal apoptosis was detected by TUNEL staining,the expression of caspase-12 protein was detected by immunohistochemical staining,the expression of caspase-12 mRNA was detected by RT-PCR method.Results In ischemic group,the number of apoptotic cells and the expression of caspase-12 mRNA and protein were gradually increased following prolonged cerebral reperfusion,reached the peak at 24 h.The number of apoptotic cells and the expression of caspase-12 mRNA and protein in ischemic group were significantly less than those of sham-operated group at all times(P

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