Lin-Hua Yang

Renji Hospital

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Xiuyu Qin

Second Hospital of Shanxi Medical University

Lihong Hou

Xijing Hospital

Jianfang Chen

Shanxi Medical University

Xiu-E Liu

Xiue Liu

Second Hospital of Shanxi Medical University

Chunxia Dong

Peking University

Ruijuan Zhang

Zhengzhou University of Science and Technology

Lixian Chang

Institute of Hematology & Blood Diseases Hospital

Liuying Zhou

Chengdu Women's and Children's Central Hospital

Bao-Feng Chai

Shanxi University

Cooperative Institutions

Shanghai Jiao Tong University

Shanxi Medical University

Second Hospital of Shanxi Medical University

Renji Hospital

Sichuan University

Peking University

Chinese Academy of Sciences

Zhejiang University

Huazhong University of Science and Technology

Chinese Academy of Medical Sciences & Peking Union Medical College

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Clinical Observation on Treatment of Endometriosis with Neiyiqing

Lin-Hua Yang

Objective:To study response of Neiyiqing on the treatment of endometriosis.Methods:60 patients with endometriosis were divided into treatment group(30 cases,treated with Neiyiqing) and control group(30 cases,treated with gestrinone) randomly.After treatment,the clinical symptom,physical symptom and CA125 of serum were compared.Results:The improvements of dysmenorrhea symptoms of treatment group were better than that of control group obviously.There was no significant different between two groups in reducing CA125 of serum.Conclusion:Neiyiqing has similar curative effect and fewer side effects with gestrinone.

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[Construction and significance of recombinant hF9 minigene and its stable nonsense mutant cell lines].

PubMed (2013)

Gang Wang Bowen Jiang Lin-Hua Yang Xin Nie Chen-Liang Jia

This study was purposed to construct the recombinant hF9 minigene and its stable nonsense mutant cell lines, and to investigate its significance. Minigene hF9 was cloned into the mammalian expression vector pCMV-Tag3B; a nonsense mutant containing a premature termination codon (PTC) in the 121(st) amino acid residue was obtained by PCR site-directed mutagenesis; minigene hF9 and nonsense mutant were respectively transfected into HepG2 cells with G418 treatment to get stable HepG2-WT and HepG2-N cell lines. The results confirmed that the minigene hF9 and nonsense mutant were constructed successfully. The gene of interest was amplified by RT-PCR from the stable cell lines, and the minigene hF9 was expressed in the stable cell lines. It is concluded that the recombinant hF9 minigene and its stable nonsense mutant cell lines are constructed successfully. The cell lines can be used to screen the drugs treating the nonsense mutation-caused hemophilia according to PTC read-through approaches.

Minigene

Nonsense mutation

Nonsense

10.7534/j.issn.1009-2137.2013.02.034

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[Construction and identification of recombinant adenoviral vector for antisense klf4 gene].

Yaofang Zhang Ruijuan Zhang Lin-Hua Yang Yuan Zhang Jianfeng Zhou

This study was aimed to construct a recombinant adenovirus vector for antisense klf4 gene through AdEasy system. Human klf4 cDNA was reversely inserted into the multiple cloning sites (MCS)of the pShuttle-CMV by using the backbone plasmid AdEasy-l, the antisense klf4 gene was constructed through homologous recombination in E.coli BJ5183, then the adenoviruses were packaged and amplified in the HEK 293 ce1ls. The adenovirus vector for antisense klf4 gene confirmed by PCR, restriction analysis and DNA sequencing. After being transfected with the adenoviruses at 200 MOI for 48 hours, total RNA and protein were extracted from human umbilical vein endothelial cells (HUVEC). Klf4 mRNA and KLF4 protein expression levels were evaluated by Real-time PCR and Western-blot. The results showed that the recombinant adenovirus vector for antisense klf4 gene was successfully constructed, recombinant adenovirus could suppress the expression of klf4 mRNA and KLF4 protein in HUVECs. It is concluded that the adenovirus vector for antisense klf4 gene has been constructed successfully, which provides the material basis for further studying the biologic function and potential application of klf4.

HEK 293 cells

KLF4

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Relationships Study about Polymorphism of Matrix Metalloproteinase-9 with Coronary Heart Disease

Journal of Clinical Hematology (2007)

Lin-Hua Yang

Objective:To examine the matrix metalloproteinase-9 (MMP-9) C-1562T polymorphism in Shanxi province and study the relationships of this genetic variation with CHD.Method:Polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) was used for the detection of MMP-9 genotype on 64 CHD patients, including 37 myocardial infarction (MI) and 27 unstable angina (UA), and 84 healthy control subjects, and then the frequency of genotype was statistically computed.Result:Three genotypes of MMP-9, C/C、C/T、T/T had been detected in both groups. The frequencies of C/T genotype and T allele in CHD group were 26.6 % and 14.8 % respectively, while 21.4 %, 10.7 % in control group, there was no difference between them in statistics. When analyzed by subgroup, UA group (C/T 44.4 %, T 25.9 %) were significantly higher than those in the control group(C/T 21.4 %, T 10.7 %) ( P 0.05 ).Conclusion:The frequencies of C/T genotype and T allele of UA group in CHD were significantly higher than those in the control group, while in clinic, in the patients of C/T and T/T genotype which take one T allele at least, the proportion of below 65 years old was 61%, and among them, mostly were UA patients ( 72.7 %). This indicate that MMP-9 C-1562T may be an impressibility factor of UA below 65 years old in CHD.

Unstable angina

Matrix metalloproteinase 9

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[1059 g/c gene polymorphism of C-reactive protein in patients with deep vein thrombosis].

Meifang Wang Lin-Hua Yang Xiaoling Yang Ruijuan Zhang Chunxia Dong

This study was aimed to investigate the distribution of 1059 G/C gene polymorphism of C-reactive protein(CRP) in deep vein thrombus (DVT) and its clinical significance. Polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) was used to screen 1059 G/C polymorphism in exon 2 of C-reactive protein gene in 61 cases of DVT and 60 healthy controls. The frequency of mutation was calculated. The results showed that there was no statistical difference of 1059 G/C genotype and mutation frequency of allele between deep vein thrombosis group and control group (p > 0.05). It is concluded that the 1059 G/C gene polymorphism of CRP displays certain difference in races and areas, and whether 1059 G/C gene polymorphism of CRP is a dangerous factor for deep vein thrombosis, which needs to be deeply explored.

Gene polymorphism

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Polymorphism of Platelet Glycoprotein IIIa PIA2 with Coronary Heart Disease

Chinese Journal of Thrombosis and Hemostasis (2007)

Lin-Hua Yang

Objective To examine the polymorphism of platelet glycoprotein Ⅲa (GPⅢa) T1565C in Shanxi province and study its association with coronary heart disease (CHD).Methods Polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) was used for the detection of GPⅢa genotype on 64 CHD patients, including 37 myocardial infarction (MI) and 27 unstable angina (UA), and 84 healthy control subjects, and then the frequency of mutation was statistically computed.Results Two genotypes of GPⅢa, T/T,T/C had been detected in both groups. The frequencies of GPⅢa C/T were very low both in CHD(1/64) and control group(0).Conclusion Whether GPⅢaT1565C is a heredity factor of CHD in Shanxi which require more resuarch.

Unstable angina

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[Screening and analysis of coagulation factor VIII inhibitor in patients with hemophilia A].

Ao‐Li Zhang Lin-Hua Yang Xiu-Er Liu Hua Zhao Jianhua Zhang

In order to detect coagulation factor VIII (FVIII) inhibitor in patients with severe hemophilia A (HA) and preliminarily study the genetic mutation in patients with inhibitor positive. Totally 58 patients with HA (FVIII: C < 1%) were enrolled. FVIII: C activity was measured by one-stage coagulation assay. FVIII inhibitor was screened by using APTT method and FVIII inhibitor in screened positive patients with HA was quantitatively analyzed by using Bethesda method. Using genomic DNA as template, 12, 14, 16 exons of FVIII in screened positive patients were amplified, and the mutations of amplified products were detected by direct sequencing. The results indicated that the FVIII inhibitor could be detected in 4 patients (6.9%) from 58 HA patients, no gene mutations in 12, 14, 16 exons of FVIII were found. It is concluded that the positive rate of FVIII inhibitor in HA patients is lower than that reported in literature. The causes of inhibitor production needs to further investigate.

genomic DNA

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A comprehensive immune repertoire signature distinguishes pulmonary infiltration in SARS-CoV-2 Omicron variant infection

Frontiers in Immunology (2024)

Xuechuan Li Hongyi Zhu Peipei Xu Jie Zhang Zhe Wang

The coronavirus disease 2019 (COVID-19) global pandemic has been the most severe public health emergency since 2019. Currently, the Omicron variant of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has been the most dominant. The most prominent symptom of SARS-CoV-2 infection is respiratory. Meanwhile, the fatality of COVID-19 was mainly from pneumonia. However ,in patients with SARS-CoV-2 infection who have pneumonia and those who do not, the differences in the immune repertoire still require further investigation.

Infiltration (HVAC)

2019-20 coronavirus outbreak

10.3389/fimmu.2024.1486352

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[A novel mutation causes congenital factor V deficiency].

PubMed (2003)

Lihong Hou Fei Xie Xiue Liu Li Zhang Yanli Guo

To investigate the gene defect in a hereditary coagulation factor V (FV) deficiency family.The plasma FV actigen was measured by one-stage clotting assay. The FV antigen was assayed by Biotin-Avidin enzyme linked immunosorbent assay (BA-ELISA). The full length of exon 1 to exon 25 and the 5' untranslated sequence of FV genomic DNA were analyzed by polymerase chain reaction (PCR) and direct sequencing of the amplified fragments, meanwhile the defect was identified by T/A cloning sequencing.The plasma coagulant activity and amount of FV of the proband were marked deficient (1% and 1.54%, respectively). DNA sequence analysis for the proband revealed a causative mutation in a heterozygous status. It was one base pair deletion in exon 4 at nucleotide 675 inherited from her mother.A novel mutation in the FV gene was identified in the proband with congenital FV deficiency. The mutation was 675delA in exon 4 resulting in a frameshift and a premature termination codon.

Proband

genomic DNA

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[FVIII intron 22 homologous region mediated recombinations and genotyping methods of hemophilia A].

PubMed (2014)

Zhiping Guo Lin-Hua Yang

The intron 22 inversion is caused by intrachromosomal homologous recombination of the Int22h (intron 22 homologous region) repeats in opposite orientation, accounting for almost 45%-50% of all cases of severe hemophilia A. By contrast, recombinations between similarly oriented int22h repeats in the same chromosome, homologous chromosomes or chromatids may cause deletion or duplication of the intermediate region between the two int22h copies, resulting in false-positive or false-negative possibility that obscure the characterization of intron 22 inversion. The modified long distance PCR(LD-PCR) and inverse shifting PCR(IS-PCR) would distinguish all the possible int22h-mediated rearrangements.

Non-allelic homologous recombination

Chromosomal inversion

Gene conversion

10.7534/j.issn.1009-2137.2014.03.055

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