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Biomedical subjects

H-C Liu

Publications and source records attributed to H-C Liu.

11 recordsLinked to original sources
PubMed2006

Debulking surgery for advanced thymoma.

AIMS: This study was conducted to evaluate the efficacy of debulking surgery in the treatment of locally advanced but operable malignant thymoma. METHODS: We reviewed 43 cases with incompletely resected stage III and IVa malignant thymoma managed between January 1987 and December 2002. RESULTS: Twenty-two had stage III and 21 had stage IVa disease. Maximal debulking was performed in 15 patients, nine with stage III and six with stage IVa disease. Nine patients also had myasthenia gravis (MG). Using univariate Kaplan-Meier analysis, we found that maximal debulking surgery, RT, and with the presence of MG were associated with better survival. Debulking resulted in a better outcome than non-debulking surgery (mean survival: 106 months vs 57.2 months). After adjustment with multivariate analysis, RT and MG were both associated with better survival. CT did not appear to be beneficial for advanced thymoma. CONCLUSIONS: RT is independently associated with a better outcome in locally advanced thymoma. Debulking surgery apparently allows for a better response to RT.

Adult↗
PubMed2006

Alloimmunization among patients with transfusion-dependent thalassemia in Taiwan.

The development of erythrocyte alloantibodies complicates transfusion therapy in patients with thalassemia. However, no data are available on the frequency of erythrocyte alloimmunization in patients with transfusion-dependent thalassemia in Taiwan. We analysed the clinical and transfusion records of 30 individuals (15 females and 15 males; mean age, 20 years; range, 4-31 years) with thalassemia who had regular transfusions for periods ranging from 0.5 to 20 years. Of the 30 patients, 28 who had beta-thalassemia major and two who had Hb H disease (alpha thalassemia), 11 (37%) were found to carry alloantibodies. All alloantibodies were clinically significant specificities, including four cases of anti-E, two of anti-E + c, two of anti-'Mi(a)', one of anti-'Mi(a)' + E, one of anti-D and one of anti-S. Alloimmunization to erythrocyte antigens is a frequent complication in transfusion-dependent thalassemia.

Adolescent↗
PubMed2005

Association studies of the adenosine A2a receptor (1976T > C) genetic polymorphism in Parkinson's disease and schizophrenia.

Given the implications with respect to the pathogenesis of dopaminergic dysfunction in schizophrenia and Parkinson's disease (PD), as well as the reciprocal antagonistic interactions between adenosine A2a receptor (A2aAR) and the dopamine D2 receptors, A2aAR may be a candidate gene conferring susceptibility to PD or schizophrenia. In this study, we tested the hypothesis that the A2aAR 1976T > C genetic variant confers susceptibility to or is related to the onset age of schizophrenia or PD using a sample population consisting of 94 PD and 227 schizophrenic patients. We also tested whether the A2aAR 1976T > C relates to antipsychotic-induced tardive dyskinesia in the schizophrenic population. The results demonstrated that in comparing PD patients and controls the distribution of the A2aAR 1976T > C genotypes (P=0.788) and alleles (P=0.702) did not vary significantly. Furthermore, the PD onset age was not significantly different amongst the three A2aAR 1976T > C genotypic groups. In comparing schizophrenic patients and controls, the distribution of the A2aAR genotypes (P=0.330) and alleles (P=0.632) also did not differ significantly. The onset age of schizophrenia and tardive dyskinesia (evaluated with Abnormal Involuntary Movements Scale) were similar within the three A2aAR genotypic groups. Our findings suggest that it is unlikely that the A2aAR 1976T > C polymorphism plays a major role in the pathogenesis of PD, schizophrenia, or antipsychotic-induced tardive dyskinesia in the Chinese population.

Age Distribution↗
PubMed2005

CEBPalpha mutations in childhood acute myeloid leukemia.

CEBPalpha: mutations have been described in adult acute myeloid leukemia (AML) and conferred a favorable prognosis. However, CEBPalpha mutation has not been reported in children. We investigated 117 children with de novo AML using DNA PCR assay followed by sequencing for each PCR product. CEBPalpha mutations were detected in seven patients, four had FAB M2, two M1 and one M4. CEBPalpha mutations only occurred in patients with intermediate cytogenetics and not in 56 children with AML1-ETO, CBFbeta-MYH11, PML-RARalpha or MLL rearrangements. Five patients had mutations occurred in both N-terminal part and basic-leucine zipper (bZIP) domain, one had an N-terminal frameshift mutation and the remaining one had an inframe insertion in the bZIP domain. Cloning analysis on five samples carrying more than one mutations demonstrated one homozygous combined mutations and four heterozygous biallelic mutations. Four of seven CEBPalpha mutation(+) patients had cooperating mutations with FLT3-ITD or N-ras mutations compared to 27 in 109 CEBPalpha mutation(-) patients. Our results showed that CEBPalpha mutations occurred in 6% of childhood AML and most exhibited combined mutations in both N-terminal part and bZIP domain.

Adolescent↗
PubMed2004

Polymorphism of estrogen metabolism genes and cataract.

Cataract is the leading cause of visual impairment in older adults in the world. Age-related lens opacities are common and are frequent causes of loss of vision. The incidence of cataract increases significantly with increasing age in women only. The onset coincides with estrogen deficiency that occurs after menopause. Hormone replacement therapy has proven beneficial to selected postmenopausal women. Estrogen effects on biological system are modulated via the estrogen receptors (ER) and/or estrogen metabolites. Although ER have been detected in ocular tissue, whether ER polymorphism is related to cataract is not known at present. The polymorphisms of estrogen metabolizing enzymes are also related to the serum concentration and activity of estrogen. Polymorphism such as cytochrome P450c17 (A2/A2), cytochrome P450c1A (vt/vt) will result in increased formation of catechol estrogen, while people with catechol-O-methyltransferase (COMT) polymorphism COMT (L/L) will have decreased metabolism of catechol estrogen and decreased level of methoxyestradiol. COMT was also involved in tamoxifen metabolism which may further decrease the activity of COMT in breast cancer patients treated with tamoxifen. It is known that a 4-7% increase in cataract was found in tamoxifen-treated breast cancer patients than non-user. The 7.0% COMT (L/L) genotype in general population corresponded well with the 4-7% of cataract formation in tamoxifen-treated breast cancer patients. Our hypothesis is that breast cancer patients with COMT (L/L) genotype may be at increased risk of cataract formation after tamoxifen treatment.

Biomarkers, Tumor↗
PubMed2004

C-reactive protein and risk factors for peripheral vascular disease in subjects with Type 2 diabetes mellitus.

AIMS: To compare the importance of different inflammatory markers and traditional risk factors in predicting peripheral vascular disease (PVD) in patients with Type 2 diabetes mellitus. METHODS: A cross-sectional analysis of 30 Type 2 diabetic patients with PVD defined by ankle-brachial index (ABI) < 0.9, and 60 Type 2 diabetic patients without PVD (ABI > 1.0). Overnight blood was drawn and sent for study. RESULTS: Longer diabetic duration (15 +/- 8 vs. 10 +/- 7 years, P = 0.007), higher serum creatinine level (0.11 +/- 0.04 vs. 0.09 +/- 0.03 mmol/l, P = 0.001), higher total cholesterol/high-density lipoprotein-cholesterol (TC/HDL-C) ratio (5.2 +/- 1.6 vs. 4.3 +/- 1.1, P = 0.004) and increased hypertension status (70% vs. 52%, P = 0.014) and cerebral infarction (CI) history (23% vs. 3%, P = 0.009) were noted in Type 2 diabetes with PVD. Those with PVD also showed significantly higher serum levels of C-reactive protein (CRP) (median 0.282 vs. 0.102 mg/dl, P < 0.001) and interleukin (IL)-6 (10.6 +/- 1.81 vs 1.6 +/- 4.6 pg/ml, P = 0.001). Multivariate regression analysis showed that higher serum levels of C-reactive protein (CRP), longer diabetic duration, and use of angiotensin converting enzyme inhibitor (ACEI) were independently associated with PVD in Type 2 diabetes mellitus. CONCLUSIONS: Type 2 diabetic patients with PVD had longer diabetic duration, higher serum creatinine levels, higher TC/HDL-C ratio, higher hypertension and CI history and higher CRP and IL-6 levels. Only serum CRP level, diabetic duration, and use of ACEI were independently associated with PVD in Type 2 diabetes mellitus.

Aged↗
PubMed2003

FLT3-TKD mutation in childhood acute myeloid leukemia.

Mutations of receptor tyrosine kinases are implicated in the constitutive activation and development of human hematologic malignancies. An internal tandem duplication (ITD) of the juxtamembrane domain-coding sequence of the FLT3 gene (FLT3-ITD) is found in 20-25% of adult acute myeloid leukemia (AML) and at a lower frequency in childhood AML. FLT3-ITD is associated with leukocytosis and a poor prognosis, especially in patients with normal karyotype. Recently, there have been three reports on point mutations at codon 835 of the FLT3 gene (D835 mutations) in adult AML. These mutations are located in the activation loop of the second tyrosine kinase domain (TKD) of FLT3 (FLT3-TKD). The clinical and prognostic relevance of the TKD mutations is less clear. To the best of our knowledge, there has been no report to describe FLT3-TKD mutations in childhood AML. In this pediatric series, FLT3-TKD mutations occurred in three of 91 patients (3.3%), an incidence significantly lower than that of FLT3-ITD (14 of 91 patients, 15.4%) in the same cohort of patients. None of them had both FLT3-TKD and FLT3-ITD mutations. Sequence analysis showed one each of D835 Y, D835 V, and D835 H. Of the three patients carrying FLT3-TKD, two had AML-M3 with one each of L- and V-type PML-RARalpha, and another one had AML-M2 with AML1-ETO. None of our patients with FLT3-TKD had leukocytosis at diagnosis. At bone marrow relapse, one of the four patients examined acquired FLT3-ITD mutation and none gained FLT3-TKD mutation.

Adolescent↗
PubMed2003

Gender-specific contribution of the GABA(A) subunit genes on 5q33 in methamphetamine use disorder.

Family and twins studies have suggested that genetic factors are involved in the development of substance use disorders. Several unrelated case/control association studies have reported associations of the GABA(A) subunit genes on 5q33 with the development of alcohol dependence. We hypothesized that these particular GABA(A) subunit genes also contribute to the development of methamphetamine use disorder. To test our hypothesis, we recruited cases using a series of questionnaires. Among the polymorphic SNPs, significant differences between cases and controls were identified in the female sample in the rs2279020 of the GABA(A)alpha1 subunit gene, and the novel SNP rs4480617 in the GABA(A)gamma2 subunit gene. No associations were found in the male sample. Further haplotype analysis identified several marker blocks significantly associated with methamphetamine use disorder in females; each block consists of the rs4480617. Our study provides preliminary evidence that the GABA(A) subunit genes on 5q33 may preferentially contribute to methamphetamine use disorder in females.

Adolescent↗
PubMed2003

Identification of chicken lymphocyte antigen 6 complex, locus E (LY6E, alias SCA2) as a putative Marek's disease resistance gene via a virus-host protein interaction screen.

Marek's disease virus (MDV) is a naturally occurring oncogenic avian herpesvirus that causes neurological disorders and T cell lymphoma disease in domestic chickens. Identification and functional characterization of the individual factors involved in Marek's disease (MD) resistance or pathogenesis will enhance our understanding of MDV pathogenesis and further genetic improvement of chickens. To study the genetic basis for resistance to MD, a strategy that combined protein-protein interaction screens followed by linkage analysis was performed. The MDV protein US10 was used as the bait in an E. COLI two-hybrid screening of a cDNA library derived from activated splenic T cells. The chicken LY6E, also known as SCA2 and TSA1, was found to specifically interact with US10. This interaction was confirmed by an in vitro protein-binding assay. Furthermore, LY6E was found to be significantly associated with MD traits in an MD resource population comprised of commercial chickens. Previously, LY6E was implicated in two independent DNA microarray experiments evaluating differential gene expression following MDV infection. Given that LY6E is involved in T cell differentiation and activation, we suggest that LY6E is a candidate gene for MD resistance and deserves further investigation on its role in MDV pathogenesis, especially with respect to the binding of US10.

Animals↗
PubMed2002

Association analysis for genetic variants of the NMDA receptor 2b subunit (GRIN2B) and Parkinson's disease.

Recent studies have implicated N-methyl-D-aspartate (NMDA) receptor dysfunction in the pathogenesis and treatment of Parkinson's disease (PD). The NMDA receptor is composed of several subunits, of which, the receptor 2b subunit (GRIN2B) is of particular significance for PD. This subunit is found enriched in the basal ganglia, and PD-monotherapy potential has been determined for GRIN2B antagonists. For this study of a sample population consisting of 101 PD patients and 108 controls, we tested the hypothesis that an ACC --> ACT transversion (2664(th) nucleotide of the coding sequence) affecting codon 888 (tyrosine) of GRIN2B confers susceptibility to PD, or relates to the age of onset. Comparing PD patients and controls, the distribution of the GRIN2B genotypes (p = 0.754) and alleles (p = 0.269) did not differ significantly. The onset age was not significantly different comparing the three genotypic groups (p = 0.189). Our negative findings suggest that it is unlikely that the GRIN2B C2664T polymorphism plays a substantial role in conferring susceptibility to PD in the Chinese population. Further studies with other genetic variations of NMDA subunits, relating either to PD or to the therapeutic response for PD, are suggested.

Age of Onset↗