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1.
Chinese Pharmacological Bulletin ; (12): 2397-2398, 2023.
Artigo em Chinês | WPRIM | ID: wpr-1013676

RESUMO

Methods The model of heart failure after myocardial infarction was established by left coronary artery liga-tion in rats. Two weeks after modeling, all rats were randomly divided into model group, LGZGD group, and captopril group. Meanwhile sham operation group was set up. The rats were given continuous intragastric administration with drug or distilled water for 28 days, once a day. The behavioral signs of rats in each group were observed. The cardiac function of rats in each group was examined by echocardiography. Serum BNP and NT-ProBNP content were detected by enzyme-linked immunoassay; The changes of myocardial his-topathological and collagen fibers in rats were detected using sirius staining. The contents of oxidative stress index including ROS, SOD in myocardial tissue of rats in each group were observed by DCFH-DA fluorescent probe and Enzyme-linked immunoassay. The ultra-structure of mitochondria was observed by transmission electron microscopy. Expressions of apoptotic proteins ( mitochondrial CytC, cytoplasmic CytC) were detec- ted by Western blot. Expression of proteins related to the Nrf2/BNIP3 pathway were examined by immunoflu-orescence and Western blot. Results LGZGD could significantly improve the cardiac function of rats, reduce the contents of BNP and NT-ProBNP, inhibit the excessive deposition of collagen in myocardial interstiti-um, reduce ROS, increase the content of SOD, improve mitochondrial structure damage, up-regulate the expression of Nrf2 and nuclear translocation, and reduce the expression of BNIP3. Conclusions LGZGD can inhibit the ventricular remodeling and prevent the occurrence of heart failure after myocardial infarction. Its pharmacological effects are mainly related to regulating the Nrf2/BNIP3 pathway, activating Nrf2, promoting its nuclear transfer, and further down-regulating BNIP3 , protecting mitochondrial function, and reducing cardiomyocyte apoptosis.

2.
Chinese Journal of Rehabilitation Theory and Practice ; (12): 892-896, 2020.
Artigo em Chinês | WPRIM | ID: wpr-905408

RESUMO

Autism spectrum disorder is a group of neurodevelopmental disorders that occur in early childhood. The specific pathogenesis is not clear. Abnormal development of neurons and glial cells is a significant feature of patients with autism spectrum disorder. This article reviewed the changes in neurons, astrocyte, microglial cell and oligodendroglia cell in autism spectrum disorder.

3.
Chinese Journal of Disease Control & Prevention ; (12): 1338-1341,1347, 2019.
Artigo em Chinês | WPRIM | ID: wpr-779517

RESUMO

Objective To explore the clinical effect of Bayesian discriminant analysis in predicting the risk of macrosomia. Methods 169 fetal macrosomia and 169 non-macrosomia were enrolled in a 1:1 matched case-control study. Conditional Logistic regression was used to select the discriminant indexes,and the discriminant indexes were put into the Bayesian discriminant model to obtain the Bayesian discriminant function. The discriminant function was the retrospectively examined and externally tested. Results The results of conditional Logistic regression model indicated that mother's height, early pregnancy body mass index (BMI), gestational diabetes, gestational weeks, the height of uterine and abdominal circumference were associated with the birth of fetal macrosomia. The Bayesian discriminant function were established: Fetal macrosomia:y1=-27.802+8.420×Mother's height+8.719×early pregnancy BMI+10.485×gestational weeks+3.375×gestational diabetes+2.862×height of uterine and abdominal circumference; Non-macrosomia y2=-17.477+7.161×Mother's height+7.217×early pregnancy BMI+7.862×gestational weeks+2.036×gestational diabetes-0.085×height of uterine and abdominal circumference. Wilks′ Lambda λ=0.489, P<0.001, the Bayesian discriminant function was statistically significant. The internal and external conformity rates of the Bayesian discriminant model were all more than 80%. Conclutions The birth of fetal macrosomia is related to many factors. The Bayesian discriminant model in the present study is valuable to discriminate macrosomia and provide an objective reference for more accurate identification of macrosomia in the future.

4.
Chinese Journal of Medical Genetics ; (6): 473-476, 2013.
Artigo em Chinês | WPRIM | ID: wpr-237224

RESUMO

<p><b>OBJECTIVE</b>To study a family with Bw subtype of ABO blood group system, and to review safety issues in relation with clinical transfusion.</p><p><b>METHODS</b>The molecular basis for the blood type was studied with serological assay, polymerase chain reaction-sequence specific primer (PCR-SSP) and DNA sequencing, TA clone and haplotype analysis in one blood donor whose ABO blood group were difficulty typed and her family. The bioinformatics analysis was carried out by biological analysis software to investigate the change of structure and function of enzymes influenced by the change amino acid. A retrospective survey was carried out to investigate what is the actual position that the donor blood was used in the clinical transfusion.</p><p><b>RESULTS</b>Three members from the family were found to have a Bw subtype. A substitution of nucleotide C by T at position 721 in exon 7 was discovered, which resulted in replacement of amino acid Arg to Trp. Review of clinical record suggested that there has been no significant abnormality association with past three blood transfusions.</p><p><b>CONCLUSION</b>A 721C>T mutation of the ABO gene probably underlies the Bw subtype. Further research is needed for understanding the clinical significance of this subtype in the blood transfusion.</p>


Assuntos
Adulto , Feminino , Humanos , Masculino , Sistema ABO de Grupos Sanguíneos , Classificação , Genética , Sequência de Aminoácidos , Sequência de Bases , Transfusão de Sangue , Éxons , Dados de Sequência Molecular , Linhagem , Reação em Cadeia da Polimerase , Estudos Retrospectivos
5.
Chinese Journal of Medical Genetics ; (6): 694-698, 2011.
Artigo em Chinês | WPRIM | ID: wpr-295551

RESUMO

<p><b>OBJECTIVE</b>To study two cases of rare para-Bombay blood types Bmh and Amh in order to determine clinical strategies of blood transfusion.</p><p><b>METHODS</b>ABO blood type was determined with serological assays. The samples were also genotyped with polymerase chain reaction-sequence specific primer (PCR-SSP) for potential mutations in α-1,2-fucosyltransferase gene (FUT1). The results were verified with direct sequencing.</p><p><b>RESULTS</b>Two rare para-Bombay blood types, namely Bmh and Amh, were identified by serological method, with one being BO1 which contained a FUT1 allele 547-548delAG deletion (h1h1), and another being A205O2 which contained FUT1 allele a 547-548delAG deletion and a FUT1 allele 658C/T missense mutation (h1h3).</p><p><b>CONCLUSION</b>FUT1 allele 547-548delAG deletion and 658C>T missense mutation in part form the molecular basis of para-Bombay blood types. As Bmh and Amh contain anti-HI in sera, great attention should be paid to avoid adverse reaction of blood transfusion in clinics.</p>


Assuntos
Humanos , Sistema ABO de Grupos Sanguíneos , Genética , Sequência de Bases , Tipagem e Reações Cruzadas Sanguíneas , Análise Mutacional de DNA , Éxons , Fucosiltransferases , Genética , Genótipo , Mutação , Análise de Sequência de DNA
6.
Chinese Journal of Hematology ; (12): 153-157, 2011.
Artigo em Chinês | WPRIM | ID: wpr-252006

RESUMO

<p><b>OBJECTIVE</b>To analyze the phenotype and genotype in three Chinese pedigrees with inherited dysfibrinogenemia.</p><p><b>METHODS</b>Laboratory tests including activated partial thromboplastin time (APTT), prothrombin time (PT), thrombin time (TT), reptilase time (RT), and the activities of antithrombin (AT:C), protein C (PC:C) and protein S(PS:C) were detected in three pedigrees. The activity and antigen of plasma fibrinogen (Fg) were analyzed by Clauss and immunoturbidimetry methods, respectively. The Fg of three probands was assessed by Western blot and sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE). The sequences of all the exons and exon-intron boundaries of the three Fg genes FGA, GFB and FGG were amplified by PCR and analyzed by direct sequencing.</p><p><b>RESULTS</b>Three probands had normal APTT, PT, PC:C, PS:C and AT:C, but prolonged TT and RT. The activity levels of the 3 probands's plasma Fg were reduced, but antigen levels were normal. Western blot and SDS-PAGE showed no abnormal molecular weight of Fg. The 3 heterozygous mutations of γ Arg275His, Aα Pro18Leu and Aα Arg16Cys were identified in the 3 probands, respectively.</p><p><b>CONCLUSION</b>The three probands with dysfibrinogenemia were caused by the mutations of γ Arg275His, Aα Pro18Leu and Aα Arg16Cys, respectively. Both Aα Pro18Leu and Aα Arg16Cys were first reported in Chinese population.</p>


Assuntos
Adulto , Feminino , Humanos , Pessoa de Meia-Idade , Afibrinogenemia , Genética , Povo Asiático , Genética , Sequência de Bases , Fibrinogênio , Genética , Genótipo , Mutação de Sentido Incorreto , Linhagem , Fenótipo
7.
Chinese Journal of Hematology ; (12): 149-153, 2010.
Artigo em Chinês | WPRIM | ID: wpr-283869

RESUMO

<p><b>OBJECTIVE</b>To identify the phenotype and genotype in four Chinese pedigrees with inherited coagulation factor V (FV) deficiency.</p><p><b>METHODS</b>The tests of activated partial thromboplastin time (APTT), prothrombin time (PT), FV activity (FV:C) and FV antigen (FV:Ag) were used for phenotype diagnosis. All the exons and exon-intron boundaries of F5 gene were amplified by PCR and analyzed by direct sequencing.</p><p><b>RESULTS</b>The APTT and PT in each of the four probands were obviously prolonged, and both activity and antigen of FV in the four probands were extremely lower compared with that of normal mixed plasma. Sequencing of F5 gene in proband 1 identified a heterozygous mutation, G16088C (Asp68His), and four polymorphisms, T35788C (Met385Thr), A47295G (His1299Arg), A58668G (Met1736Val) and A74083G (Asp2194Gly), which were located in the same chromosome; proband 2 was homozygous for two mutations, C46253T (Arg952Cys) and C46724T(Gln1109stop); the F5 gene of proband 3 showed a homozygous missense mutation, C67793G(Pro2006Ala); and proband 4 was homozygous for one missense mutation, C74022T (Arg2174Cys).</p><p><b>CONCLUSION</b>Five mutations (Asp68His, Arg952Cys, Gln1109stop, Pro2006Ala and Arg2174Cys) and four polymorphisms (Met385Thr, His1299Arg, Met1736Val and Asp2194Gly) may lead to type I inherited FV deficiency for these four probands, respectively. Gln1109stop, Pro2006Ala and Arg2174Cys haven't been identified before.</p>


Assuntos
Humanos , Fator V , Deficiência do Fator V , Genótipo , Linhagem , Fenótipo
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