18 results on '"Nechtman J"'
Search Results
2. Association of Hb santa ANA [α2β288(F4)LEU→PRO] And Hb porto alegre [α2β29(A6)SER→CYS] in a brazilian female
- Author
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Gonçalves, M. S., primary, Sonati, M. F., additional, Kimura, M., additional, Arruda, V. R., additional, Costa, F. F., additional, Nechtman, J. F., additional, and Stoming, T. A., additional
- Published
- 1994
- Full Text
- View/download PDF
3. A Novel β-Thalassemia Mutation [IVS-II-5 (G→C)] in a Chinese Family from Guangxi Province, P. R. China
- Author
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Jiang, N. H., primary, Liang, S., additional, Su, C., additional, Nechtman, J. F., additional, and Stoming, T. A., additional
- Published
- 1993
- Full Text
- View/download PDF
4. Types of Thalassemia Among Patients Attending a Large University Clinic in Kuala Lumpur, Malaysia
- Author
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George, E., primary, Li, H-J., additional, Fei, Y-J., additional, Reese, A. L., additional, Baysal, E., additional, Cepreganova, B., additional, Wilson, J. B., additional, Gu, L-H., additional, Nechtman, J. F., additional, Stoming, T. A., additional, Liu, J-C., additional, Codrington, J. F., additional, and Huisman, T. H. J., additional
- Published
- 1992
- Full Text
- View/download PDF
5. Association of Hb santa ANA [α2β288(F4)LEU→PRO] And Hb porto alegre [α2β29(A6)SER→CYS] in a brazilian female.
- Author
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Gonçalves, M. S., Sonati, M. F., Kimura, M., Arruda, V. R., Costa, F. F., Nechtman, J. F., and Stoming, T. A.
- Published
- 1994
- Full Text
- View/download PDF
6. Retrospective Validation of a 168-Gene Expression Signature for Glioma Classification on a Single Molecule Counting Platform.
- Author
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Tran PMH, Tran LKH, Satter KB, Purohit S, Nechtman J, Hopkins DI, Dos Santos B, Bollag R, Kolhe R, Sharma S, and She JX
- Abstract
Gene expression profiling has been shown to be comparable to other molecular methods for glioma classification. We sought to validate a gene-expression based glioma classification method. Formalin-fixed paraffin embedded tissue and flash frozen tissue collected at the Augusta University (AU) Pathology Department between 2000-2019 were identified and 2 mm cores were taken. The RNA was extracted from these cores after deparaffinization and bead homogenization. One hundred sixty-eight genes were evaluated in the RNA samples on the nCounter instrument. Forty-eight gliomas were classified using a supervised learning algorithm trained by using data from The Cancer Genome Atlas. An ensemble of 1000 linear support vector models classified 30 glioma samples into TP1 with classification confidence of 0.99. Glioma patients in TP1 group have a poorer survival (HR (95% CI) = 4.5 (1.3-15.4), p = 0.005) with median survival time of 12.1 months, compared to non-TP1 groups. Network analysis revealed that cell cycle genes play an important role in distinguishing TP1 from non-TP1 cases and that these genes may play an important role in glioma survival. This could be a good clinical pipeline for molecular classification of gliomas.
- Published
- 2021
- Full Text
- View/download PDF
7. Comparative analysis of transcriptomic profile, histology, and IDH mutation for classification of gliomas.
- Author
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Tran PMH, Tran LKH, Nechtman J, Dos Santos B, Purohit S, Satter KB, Dun B, Kolhe R, Sharma S, Bollag R, and She JX
- Subjects
- Astrocytoma genetics, Astrocytoma pathology, Biomarkers, Tumor genetics, Brain Neoplasms pathology, Cell Proliferation genetics, DNA Methylation genetics, Gene Expression genetics, Gene Expression Profiling methods, Glioma pathology, Humans, Neurons pathology, Prognosis, Brain Neoplasms genetics, Glioma genetics, Isocitrate Dehydrogenase genetics, Mutation genetics, Transcriptome genetics
- Abstract
Gliomas are currently classified through integration of histology and mutation information, with new developments in DNA methylation classification. However, discrepancies exist amongst the major classification methods. This study sought to compare transcriptome-based classification to the established methods. RNAseq and microarray data were obtained for 1032 gliomas from the TCGA and 395 gliomas from REMBRANDT. Data were analyzed using unsupervised and supervised learning and other statistical methods. Global transcriptomic profiles defined four transcriptomic glioma subgroups with 91.4% concordance with the WHO-defined mutation subtypes. Using these subgroups, 168 genes were selected for the development of 1000 linear support vector classifiers (LSVC). Based on plurality voting of 1000 LSVC, the final ensemble classifier confidently classified all but 17 TCGA gliomas to one of the four transcriptomic profile (TP) groups. The classifier was validated using a gene expression microarray dataset. TP1 cases include IDHwt, glioblastoma high immune infiltration and cellular proliferation and poor survival prognosis. TP2a is characterized as IDHmut-codel, oligodendrogliomas with high tumor purity. TP2b tissue is mostly composed of neurons and few infiltrating malignant cells. TP3 exhibit increased NOTCH signaling, are astrocytoma and IDHmut-non-codel. TP groups are highly concordant with both WHO integrated histology and mutation classification as well as methylation-based classification of gliomas. Transcriptomic profiling provides a robust and objective method to classify gliomas with high agreement to the current WHO guidelines and may provide additional survival prediction to the current methods.
- Published
- 2020
- Full Text
- View/download PDF
8. A 73-gene proliferative transcriptomic signature predicts uterine serous carcinoma patient survival and response to primary therapy.
- Author
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Tran LKH, Tran PMH, Mysona DP, Purohit SB, Myers E, Lee WS, Dun B, Xu D, Liu H, Hopkins D, Nechtman J, Scelsi CL, Mittal PK, Kleven D, Wallbillich JJ, Rungruang B, Ghamande S, and She JX
- Subjects
- Aged, Aged, 80 and over, Cohort Studies, Cystadenocarcinoma, Serous mortality, Cystadenocarcinoma, Serous pathology, Cystadenocarcinoma, Serous therapy, Disease Progression, Female, Humans, Middle Aged, Prognosis, Reproducibility of Results, Retrospective Studies, Sequence Analysis, RNA, Tissue Array Analysis, Transcriptome, Tumor Cells, Cultured, Uterine Neoplasms mortality, Uterine Neoplasms pathology, Uterine Neoplasms therapy, Cystadenocarcinoma, Serous genetics, Uterine Neoplasms genetics
- Abstract
Objectives: To develop a transcriptomic signature capable of predicting overall survival (OS) for uterine serous carcinoma (USC)., Methods: RNAseq data for 58 USC patients were obtained from TCGA. Expression of 73 candidate genes was measured for 67 Augusta University (AU) samples using NanoString technology., Results: Analysis of the TCGA RNAseq data identified 73 genes that individually predict prognosis for USC patients and an elastic net model with all 73 genes (USC73) distinguishes a good OS group with low USC73 score from a poor OS group with high USC73 score (5-year OS = 83.3% and 13.3% respectively, HR = 40.1; p = 3 × 10
-8 ). This finding was validated in the independent AU cohort (HR = 4.3; p = 0.0004). The poor prognosis group with high USC73 score consists of 37.9% and 32.8% of patients in the TCGA and AU cohort respectively. USC73 score and pathologic stage independently contribute to OS and together provide the best prognostic value. Early stage, low USC73 patients have the best prognosis (5-year OS = 85.1% in the combined dataset), while advanced stage, high USC73 patients have the worst prognosis (5-year OS = 6.4%, HR = 30.5, p = 1.2 × 10-12 ). Consistent with the observed poor survival, primary cell cultures from high USC73 patients had higher proliferation rate and cell cycle progression; and high USC73 patients had lower rates of complete response to standard therapy., Conclusions: The USC73 transcriptomic signature and stage independently predict OS of USC patients and the best prediction is achieved using USC73 and stage. USC73 may also serve as a therapeutic biomarker to guide patient care., Competing Interests: Declaration of competing interest The authors declare no potential conflicts of interest., (Copyright © 2020 Elsevier Inc. All rights reserved.)- Published
- 2020
- Full Text
- View/download PDF
9. Delineating the angiogenic gene expression profile before pulmonary vascular remodeling in a lamb model of congenital heart disease.
- Author
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Tian J, Fratz S, Hou Y, Lu Q, Görlach A, Hess J, Schreiber C, Datar SA, Oishi P, Nechtman J, Podolsky R, She JX, Fineman JR, and Black SM
- Subjects
- Angiopoietin-2 genetics, Angiopoietin-2 metabolism, Animals, Blotting, Western, Chemokine CCL2 genetics, Chemokine CCL2 metabolism, Disease Models, Animal, Down-Regulation genetics, Endothelial Cells metabolism, Fibroblast Growth Factor 2 genetics, Fibroblast Growth Factor 2 metabolism, Heart Diseases pathology, Heart Diseases physiopathology, Hemodynamics physiology, Microtubule-Associated Proteins genetics, Microtubule-Associated Proteins metabolism, Phenotype, Pulmonary Artery pathology, RNA, Messenger genetics, RNA, Messenger metabolism, Reproducibility of Results, Reverse Transcriptase Polymerase Chain Reaction, Sheep, Stress, Mechanical, Up-Regulation genetics, Gene Expression Profiling, Heart Diseases congenital, Heart Diseases genetics, Lung blood supply, Lung physiopathology, Neovascularization, Physiologic genetics, Pulmonary Circulation genetics
- Abstract
Disordered angiogenesis is implicated in pulmonary vascular remodeling secondary to congenital heart diseases (CHD). However, the underlying genes are not well delineated. We showed previously that an ovine model of CHD with increased pulmonary blood flow (PBF, Shunt) has an "angiogenesis burst" between 1 and 4 wk of age. Thus we hypothesized that the increased PBF elicited a proangiogenic gene expression profile before onset of vessel growth. To test this we utilized microarray analysis to identify genes that could be responsible for the angiogenic response. Total RNA was isolated from lungs of Shunt and control lambs at 3 days of age and hybridized to Affymetrix gene chips for microarray analyses (n = 8/group). Eighty-nine angiogenesis-related genes were found to be upregulated and 26 angiogenesis-related genes downregulated in Shunt compared with control lungs (cutting at 1.2-fold difference, P < 0.05). We then confirmed upregulation of proangiogenic genes FGF2, Angiopoietin2 (Angpt2), and Birc5 at mRNA and protein levels and upregulation of ccl2 at mRNA level in 3-day Shunt lungs. Furthermore, we found that pulmonary arterial endothelial cells (PAEC) isolated from fetal lambs exhibited increased expression of FGF2, Angpt2, Birc5, and ccl2 and enhanced angiogenesis when exposed to elevated shear stress (35 dyn/cm²) compared with cells exposed to more physiological shear stress (20 dyn/cm²). Finally, we demonstrated that blocking FGF2, Angpt2, Birc5, or ccl2 signaling with neutralizing antibodies or small interfering RNA (siRNA) significantly decreased the angiogenic response induced by shear stress. In conclusion, we have identified a "proangiogenic" gene expression profile in a lamb model of CHD with increased PBF that precedes onset of pulmonary vascular remodeling. Our data indicate that FGF2, Angpt2, Birc5, and ccl2 may play important roles in the angiogenic response.
- Published
- 2011
- Full Text
- View/download PDF
10. Effect of PPARgamma inhibition on pulmonary endothelial cell gene expression: gene profiling in pulmonary hypertension.
- Author
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Tian J, Smith A, Nechtman J, Podolsky R, Aggarwal S, Snead C, Kumar S, Elgaish M, Oishi P, Göerlach A, Fratz S, Hess J, Catravas JD, Verin AD, Fineman JR, She JX, and Black SM
- Subjects
- Animals, Arteries drug effects, Arteries pathology, Blood-Air Barrier drug effects, Blood-Air Barrier metabolism, Cattle, Cell Adhesion drug effects, Cell Adhesion genetics, Cell Cycle drug effects, Cell Cycle genetics, Cell Proliferation drug effects, Disease Models, Animal, Endothelial Cells drug effects, Endothelial Cells pathology, Humans, Hypertension, Pulmonary pathology, Neovascularization, Physiologic drug effects, Neovascularization, Physiologic genetics, Reproducibility of Results, Reverse Transcriptase Polymerase Chain Reaction, Sheep, Ubiquitin genetics, Vascular Endothelial Growth Factor A pharmacology, Zinc Fingers genetics, Anilides pharmacology, Endothelial Cells metabolism, Gene Expression Profiling, Gene Expression Regulation drug effects, Hypertension, Pulmonary genetics, Lung pathology, PPAR gamma antagonists & inhibitors
- Abstract
Peroxisome proliferator-activated receptor type gamma (PPARgamma) is a subgroup of the PPAR transcription factor family. Recent studies indicate that loss of PPARgamma is associated with the development of pulmonary hypertension (PH). We hypothesized that the endothelial dysfunction associated with PPARgamma inhibition may play an important role in the disease process by altering cellular gene expression and signaling cascades. We utilized microarray analysis to determine if PPARgamma inhibition induced changes in gene expression in pulmonary arterial endothelial cells (PAEC). We identified 100 genes and expressed sequence tags (ESTs) that were upregulated by >1.5-fold and 21 genes and ESTs that were downregulated by >1.3-fold (P < 0.05) by PPARgamma inhibition. The upregulated genes can be broadly classified into four functional groups: cell cycle, angiogenesis, ubiquitin system, and zinc finger proteins. The genes with the highest fold change in expression: hyaluronan-mediated motility receptor (HMMR), VEGF receptor 2 (Flk-1), endothelial PAS domain protein 1 (EPAS1), basic fibroblast growth factor (FGF-2), and caveolin-1 in PAEC were validated by real time RT-PCR. We further validated the upregulation of HMMR, Flk-1, FGF2, and caveolin-1 by Western blot analysis. In keeping with the microarray results, PPARgamma inhibition led to re-entry of cell cycle at G(1)/S phase and cyclin C upregulation. PPARgamma inhibition also exacerbated VEGF-induced endothelial barrier disruption. Finally we confirmed the downregulation of PPARgamma and the upregulation of HMMR, Flk-1, FGF2, and Cav-1 proteins in the peripheral lung tissues of an ovine model of PH. In conclusion, we have identified an array of endothelial genes modulated by attenuated PPARgamma signaling that may play important roles in the development of PH.
- Published
- 2009
- Full Text
- View/download PDF
11. Role of acetylation and extracellular location of heat shock protein 90alpha in tumor cell invasion.
- Author
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Yang Y, Rao R, Shen J, Tang Y, Fiskus W, Nechtman J, Atadja P, and Bhalla K
- Subjects
- Acetylation, Adenosine Triphosphate metabolism, Benzoquinones metabolism, Cells, Cultured, Collagen metabolism, Drug Combinations, HSP90 Heat-Shock Proteins antagonists & inhibitors, Histone Deacetylase 6, Histone Deacetylase Inhibitors, Histone Deacetylases genetics, Humans, Hydroxamic Acids pharmacology, Immunoblotting, Immunoprecipitation, Indoles, Lactams, Macrocyclic metabolism, Laminin metabolism, Lysine chemistry, Lysine genetics, Matrix Metalloproteinase 2 metabolism, Mutagenesis, Site-Directed, Neoplasm Invasiveness, Panobinostat, Protein Processing, Post-Translational, Proteoglycans metabolism, Spectrometry, Mass, Matrix-Assisted Laser Desorption-Ionization, p300-CBP Transcription Factors metabolism, Breast Neoplasms metabolism, Breast Neoplasms pathology, HSP90 Heat-Shock Proteins metabolism, Histone Deacetylases metabolism
- Abstract
Heat shock protein (hsp) 90 is an ATP-dependent molecular chaperone that maintains the active conformation of client oncoproteins in cancer cells. An isoform, hsp90alpha, promotes extracellular maturation of matrix metalloproteinase (MMP)-2, involved in tumor invasion and metastasis. Knockdown of histone deacetylase (HDAC) 6, which deacetylates lysine residues in hsp90, induces reversible hyperacetylation and attenuates ATP binding and chaperone function of hsp90. Here, using mass spectrometry, we identified seven lysine residues in hsp90alpha that are hyperacetylated after treatment of eukaryotic cells with a pan-HDAC inhibitor that also inhibits HDAC6. Depending on the specific lysine residue in the middle domain involved, although acetylation affects ATP, cochaperone, and client protein binding to hsp90alpha, acetylation of all seven lysines increased the binding of hsp90alpha to 17-allyl-amino-demethoxy geldanamycin. Notably, after treatment with the pan-HDAC inhibitor panobinostat (LBH589), the extracellular hsp90alpha was hyperacetylated and it bound to MMP-2, which was associated with increased in vitro tumor cell invasiveness. Treatment with antiacetylated hsp90alpha antibody inhibited in vitro invasion by tumor cells. Thus, reversible hyperacetylation modulates the intracellular and extracellular chaperone function of hsp90, and targeting extracellular hyperacetylated hsp90alpha may undermine tumor invasion and metastasis.
- Published
- 2008
- Full Text
- View/download PDF
12. DNA microarray analysis of the uninoculated eye following anterior chamber inoculation of HSV-1.
- Author
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Zheng M, Qian H, Joshi RM, Nechtman J, and Atherton SS
- Subjects
- Animals, Antigens, CD19 metabolism, Antigens, Differentiation metabolism, B-Lymphocytes immunology, Eye Infections, Viral metabolism, Eye Infections, Viral virology, Female, Gene Expression Profiling, Herpes Simplex metabolism, Herpes Simplex virology, Immunoenzyme Techniques, Mice, Mice, Inbred BALB C, Oligonucleotide Array Sequence Analysis, RNA isolation & purification, Retinal Necrosis Syndrome, Acute metabolism, Retinal Necrosis Syndrome, Acute virology, T-Lymphocytes immunology, Up-Regulation, Anterior Chamber virology, Eye Infections, Viral genetics, Gene Expression Regulation physiology, Herpes Simplex genetics, Herpesvirus 1, Human physiology, Retinal Necrosis Syndrome, Acute genetics
- Abstract
Purpose: To use DNA microarray to analyze the expression patterns of genes in the uninoculated eye following uniocular anterior chamber inoculation of HSV-1., Methods: On Day 9 following inoculation of 2 x 10( 4) PFU of HSV-1 (KOS strain) or an equivalent volume of tissue culture medium into one anterior chamber of BALB/c mice, the uninoculated eyes were enucleated, pooled, and total RNA was isolated. cDNA was synthesized from the total RNA. The gene expression patterns were inferred based on the hybridization intensities of the probes on the cDNA array. The hybridization signals were globally normalized and filtered. The data were analyzed using hierarchical and gene tree clustering algorithms. Additional uninoculated eyes collected on Day 9 p.i. were stained for F4/80 and CD19., Results: Compared with the uninoculated eye of control mice, 3800 genes were upregulated at least twofold in the contralateral eye of HSV-1-infected mice. Among the 10 most upregulated genes, T cell-specific protein, MHC II antigen A, and MHC II k region locus 2 were upregulated 179-, 164-, and 162-fold, respectively. Ten T-cell receptor-related genes, 61 cytokine and chemokine genes, and 16 MHC genes were upregulated. Furthermore, 11 immunoglobulin and B cell genes and 11 macrophage-related genes were also upregulated. F4/80+ and CD19+ cells were observed on Day 9 p.i., Conclusions: The DNA microarray results support the idea that T cells and immunomodulatory factors (cytokines, chemokines) are likely to be involved in HSV-1 retinitis. These results also suggest that B cells and/or macrophages play a role in the pathogenesis of HSV-1 retinitis.
- Published
- 2003
- Full Text
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13. Inhibition of HIV-1 replication by an anti-tat hammerhead ribozyme.
- Author
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Jackson WH Jr, Moscoso H, Nechtman JF, Galileo DS, Garver FA, and Lanclos KD
- Subjects
- Animals, CD4-Positive T-Lymphocytes metabolism, COS Cells, Chloramphenicol O-Acetyltransferase genetics, Chloramphenicol O-Acetyltransferase metabolism, Genetic Vectors genetics, Moloney murine leukemia virus genetics, Plasmids genetics, RNA-Directed DNA Polymerase metabolism, Transduction, Genetic genetics, Transfection genetics, Viral Proteins antagonists & inhibitors, beta-Galactosidase genetics, tat Gene Products, Human Immunodeficiency Virus, Gene Products, tat antagonists & inhibitors, HIV-1 growth & development, RNA, Catalytic metabolism
- Abstract
Tat is a virally expressed regulatory protein involved in the replication of HIV-1, the etiological agent of AIDS. To investigate the effect of tat inhibition on HIV replication, we constructed a retroviral vector to express an anti-tat hammerhead ribozyme as part of the 3' untranslated region of beta-galactosidase transcripts. Initial testing of this vector in tat-expressing COS-7 cells reduced tat activity by 85-95% as measured by tat-dependent CAT assays. Amphotropic and HIV-pseudotyped retroviral particles generated with this vector were used in HIV challenge experiments to determine the ability of this reagent to control HIV replication. CD4(+) peripheral blood lymphocytes (PBLs) stably transduced with this vector were subsequently challenged with HIV. These cells were able to resist HIV infection for up to 20 days as measured by cell death and reverse transcriptase activity. These data yield proof of principle that a pseudotyped retroviral vector can target and deliver a protective ribozyme to CD4(+) cells., (Copyright 1998 Academic Press.)
- Published
- 1998
- Full Text
- View/download PDF
14. Sickle cell disease in a Brazilian population from Sao Paulo: a study of the beta s haplotypes.
- Author
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Goncalves MS, Nechtman JF, Figueiredo MS, Kerbauy J, Arruda VR, Sonati MF, Saad SO, Costa FF, and Stoming TA
- Subjects
- Base Sequence, Blotting, Southern, Brazil, Gene Frequency, Haplotypes, Humans, Molecular Sequence Data, Polymerase Chain Reaction, Globins genetics, Sickle Cell Trait blood
- Abstract
In this study we have determined the frequency of beta S haplotypes in a Brazilian sickle cell disease population from Sao Paulo, Brazil, by analyzing sequence variations in the immediate 5' flanking and second intervening sequence (IVSII) regions of the gamma globin genes. This association between sequence differences and beta s haplotype backgrounds was determined by screening genomic DNA samples using dot blot analysis of polymerase chain reaction products. We studied 148 beta s chromosomes, and found that haplotype 20 (CAR or Bantu) significantly predominated in this population. This is in agreement with the findings of the historical Portuguese Atlantic slave trade from Africa to South America.
- Published
- 1994
- Full Text
- View/download PDF
15. Association of Hb Santa Ana [alpha 2 beta (2)88(F4)Leu- > Pro] and Hb Porto Alegre [alpha 2 beta (2)9(A6)Ser- > Cys] in a Brazilian female.
- Author
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Gonçalves MS, Sonati MF, Kimura M, Arruda VR, Costa FF, Nechtman JF, and Stoming TA
- Subjects
- Anemia blood, Base Sequence, Brazil, Child, Chronic Disease, Female, Hematologic Tests, Humans, Molecular Sequence Data, Mutation, Splenomegaly blood, Anemia genetics, Hemoglobins, Abnormal genetics, Splenomegaly genetics
- Published
- 1994
- Full Text
- View/download PDF
16. Alpha and beta thalassaemia among Chinese children in Guangxi Province, P.R. China: molecular and haematological characterization.
- Author
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Liang R, Liang S, Jiang NH, Wen XJ, Zhao JB, Nechtman JF, Stoming TA, and Huisman TH
- Subjects
- Alleles, Child, Child, Preschool, China, Chromosome Deletion, Female, Fetal Hemoglobin analysis, Hemoglobin H analysis, Hemoglobins analysis, Hemoglobins, Abnormal analysis, Humans, Male, Mutation, alpha-Thalassemia blood, beta-Thalassemia blood, alpha-Thalassemia genetics, beta-Thalassemia genetics
- Abstract
We have studied nearly 100 patients with beta-thalassaemia major and 60 patients with Hb H disease who were attending the Haematology Clinic of Guangxi Medical College. Treatment of the patients was limited and only a few patients with beta-thalassaemia major received blood transfusion(s). As a result, the severe anaemia has led to early death at 3-4 years for beta zero-thalassaemia homozygotes, and 8-12 years for beta(+)-thalassaemia homozygotes. Four beta-thalassaemia alleles are responsible for nearly 90% of all beta-thalassaemia chromosomes. This information has resulted in the initiation of a prenatal testing programme at the local level. The patients with Hb H disease maintained a haemoglobin level of 6-10 g/dl and early death was infrequently observed. The --SEA deletion was the major type of alpha-thalassemia-1, while three smaller deletions (-2.7, -3.7 and -4.2 kb) and two nondeletional alpha-thalassaemia determinants (Hbs Constant Spring and Quong Sze) were the alpha-thalassaemia-2 types.
- Published
- 1994
- Full Text
- View/download PDF
17. A novel beta-thalassemia mutation [IVS-II-5 (G-->C)] in a Chinese family from Guangxi Province, P.R. China.
- Author
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Jiang NH, Liang S, Su C, Nechtman JF, and Stoming TA
- Subjects
- Base Sequence, Child, China, Female, Humans, Molecular Sequence Data, Mutation, beta-Thalassemia genetics
- Published
- 1993
- Full Text
- View/download PDF
18. The Brazilian type of nondeletional A gamma-fetal hemoglobin has a C----G substitution at nucleotide -195 of the A gamma-globin gene.
- Author
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Costa FF, Zago MA, Cheng G, Nechtman JF, Stoming TA, and Huisman TH
- Subjects
- Base Sequence, Brazil, Chromosome Deletion, DNA genetics, Humans, Molecular Sequence Data, Mutation, Globins genetics
- Published
- 1990
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