Biomedical subjects

Chen-Jee Hong

Publications and source records attributed to Chen-Jee Hong.

At least 37 records · Page 2Linked to original sources

PubMed2005

Human kallikrein-2 gene polymorphism is associated with the occurrence of prostate cancer.

PURPOSE: Human glandular kallikrein, which is encoded by the human kallikrein-2 (KLK2) gene, is significantly associated with the occurrence of prostate cancer (PCa). We tested the association between a functional C748T polymorphism of the KLK2 gene and the occurrence of PCa. MATERIALS AND METHODS: Peripheral venous blood samples were obtained from 254 patients with PCa and 168 controls with benign prostatic hyperplasia. All control subjects had normal serum prostate specific antigen and proved to be free from malignancy on pathological examination of resected prostatic tissues. Serum prostate specific antigen, testosterone, Gleason score, clinical and pathological stage, tumor and prostate volume of the patients were investigated. The KLK2 gene polymorphism was determined by the polymerase chain reaction based restriction fragment length polymorphism method. RESULTS: The PCa group had a younger mean age +/- SEM (73.0 +/- 0.5 vs 74.7 +/- 0.5 years, p = 0.010) and higher C allele frequency (82.1% vs 74.7%, p = 0.010) than the control group. The frequency of the CC, CT and TT genotypes was 65.7%, 32.7% and 1.6% in patients with PCa, and 56.0%, 37.5% and 6.5%, respectively, in controls (p = 0.010). C allele carriers (CC and CT genotypes) were at significantly higher risk for PCa than TT homozygous subjects (p = 0.002). CC homozygous subjects were at significantly higher risk for PCa than T allele carriers (CT and TT genotypes) (p = 0.043). The PCa subgroup of patients with pathologically proved, localized PCa also had a higher frequency of the C allele (87.5% vs 74.7%, p = 0.026) and CC genotypes (78.7% vs 56.0%, p = 0.019) than controls. CONCLUSIONS: Our results suggest that the C allele of the functional C748T polymorphism of KLK2 may increase the risk of PCa.

Aged↗

PubMed2004

Association study of A2a adenosine receptor genetic polymorphism in panic disorder.

The adenosine A2a receptor (A2aAR) is thought to be implicated in the pathogenesis of panic disorder because caffeine, a potent antagonist for A2aAR, can precipitate panic attacks, and because disruption of the A2aAR gene increased anxiety-behaviors in mice. Recent studies demonstrated that the A2aAR 1976T > C genetic variant confers susceptibility to panic disorder though not by all studies. The present study tested the hypothesis that the A2aAR 1976T > C genetic variant confers susceptibility to panic disorder using a Chinese population of 104 panic disorder patients and 192 normal controls. We also tested whether the A2aAR 1976T > C polymorphism relates to the age of onset or subtype of panic disorders. Neither the distribution of the A2aAR 1976T > C genotypes (P = 0.296) or alleles (P = 0.864), nor the age of onset (P = 0.719) were significantly different among genotype groups. Furthermore, no association was demonstrated between this A2aAR polymorphism and either mitral-valve prolapse or agoraphobia in panic-disorder patients. These findings suggested that it is unlikely that the A2aAR 1976T > C polymorphism plays a major role in panic disorder pathogenesis in the Chinese population. The positive association between this polymorphism and panic disorder found in western population but not in Asian population suggests that this association could be ethnicity-dependent. The 1976C > T polymorphism may be in linkage disequilibrium with a functional variant that affects panic disorder, and the extent of this linkage disequilibrium is not similar for all ethnic populations.

Adult↗

PubMed2004

Association analysis for the muscarinic M1 receptor genetic polymorphisms and Alzheimer's disease.

In the ongoing search to reveal the pathophysiology of Alzheimer's disease (AD), the cholinergic system is important due to its role in cognitive function and its significance with respect to the results of postmortem pathology and animal model studies. For this investigation, we tested the hypothesis that the allelic variant (C267A) of the cholinergic receptor muscarinic 1 (CHRM1) confers susceptibility to AD or is related to its age of onset, in a sample population of 232 AD patients and 169 normal controls. The distribution of the CHRM1 genotypes (p = 0.919) and alleles (p = 0.327) did not differ significantly comparing AD patients and controls, even after stratification according to apolipoprotein E genotype. The onset age was not significantly different comparing the CHRM1 genotype groups. Our negative findings suggest that it is unlikely that the CHRM1 C267A polymorphism plays a substantial role in conferring susceptibility to AD. We propose that other genetic variations of CHRM1, relating either to AD or to the therapeutic response for AD, may need further investigation.

Aged↗

PubMed2004

X-box binding protein 1 (XBP1) C--116G polymorphisms in bipolar disorders and age of onset.

X-box binding protein 1 (XBP1), a critical gene in the endoplasmic reticulum stress response, is located on chromosome 22q12, which has been linked with bipolar disorders in several studies. Recently, associations have been reported between a polymorphism (-116C --> G) in the promoter region of XBP1, and bipolar disorders in both case-control study and family-based association study, however, this finding is not yet confirmed by other research using independent sample populations. To replicate this finding and determine the association between onset age of bipolar disorders and the XBP1 C--116G polymorphism, we investigated the prevalence of this polymorphism in a Chinese population (153 bipolar disorder patients and 174 controls). We were unable, however, to demonstrate a significant association between the C--116G polymorphism and bipolar disorders (P = 0.674 for genotype and P = 0.436 for allele frequency) or age at onset (P = 0.563). Further, no association was demonstrated between this polymorphism and family history in bipolar disorder patients. These negative findings suggest that the XBP1 C--116G polymorphism does not play a major role in the pathogenesis of bipolar disorders in Chinese populations.

Adult↗

PubMed2004

Association study of PICK1 rs3952 polymorphism and schizophrenia.

Protein interacting with C-kinase-1 (PICKl) plays an important role in the targeting and clustering of neuronal receptors and amine transporters. The PICK1 gene may play a role in conferring susceptibility to schizophrenia as it has been mapped to chromosome 22q13.1, a region thought to contain a gene for schizophrenia. We tested the hypothesis that an allelic variant of the PICK1 gene was associated with a diagnosis of schizophrenia. The PICK1 rs3952 polymorphism was genotyped in 225 schizophrenia and 260 controls. Results demonstrated that the PICK1 rs3952 genotype and allele distribution was significantly different between the two groups. The positive association suggests that the PICK1 gene may play a role in the pathogenesis of schizophrenia.

Adult↗

PubMed2004

Case-control and family-based association studies between the neuregulin 1 (Arg38Gln) polymorphism and schizophrenia.

Genetic variations in the neuregulin 1 (NRG1), a critical gene in neuronal development, have been reported to be associated with schizophrenia in several reports. Association has been reported between a non-synonymous NRG1 polymorphism (Arg38Gln) and schizophrenia in a Chinese family-based association study; however, this finding is not yet confirmed by other research findings analyzed using independent sample. To replicate this finding and assess the association between age at onset of schizophrenia and the NRG1 Arg38Gln polymorphism, we investigated the prevalence of this polymorphism in a Chinese population (228 schizophrenic disorder patients and 269 controls). We were unable, however, to demonstrate a significant association between the NRG1 Arg38Gln polymorphism and schizophrenia (P = 0.869 for genotype and P = 0.597 for allelic frequencies) or age at onset (P = 0.940). Our family-based association study (15 schizophrenic bios and 221 schizophrenic trios) demonstrated 38Gln was transmitted in excess by the parent to the affected offspring (P = 0.052). However, this result contrasts with a previous finding in Chinese that 38Arg was transmitted in excess by the parent to the affected offspring. On the basis of the contrast between the findings of other study and our family-based study and the negative findings of our case-control association study, we conclude that NRG1 Arg38Gln polymorphism is not likely to play a major role in the pathogenesis of schizophrenia in Chinese populations.

Adult↗

PubMed2004

Expression of c-Fos-like immunoreactivity in the brain of mice with learned helplessness.

The learned helplessness (LH) developed after repeat inescapable stress is a well validated animal model of human major depression and is not species specific. c-Fos, the protein product of the protooncogene c-fos, is expressed in neurons under a variety of stressors and could reflect the regional neuronal activation. Using the LH paradigm in mice, we examined c-Fos expression in several brain regions related to stress response or major depression. The LH mice showed significantly lower c-Fos-like immunoreactivity (FLI) in the hippocampus dentate gyrus and the lateral septal nucleus, and higher FLI in the hypothalamic paraventricular nucleus compared with the naive mice. Our finding in the mice LH model supported previous studies in rats showing that the lateral septal nucleus and the hypothalamic paraventricular nucleus are important in LH behaviors. We further demonstrated that hippocampus dentate gyrus, a region important for learning and major depression, may also be involved in the LH behaviors. These related brain regions could provide a basis for further exploration of the molecular mechanisms underlying LH behaviors.

Animals↗

PubMed2004

Association study of the human partially duplicated alpha7 nicotinic acetylcholine receptor genetic variant with bipolar disorder.

The human alpha7 nicotinic acetylcholine receptor subunit (CHRNA7) gene cluster maps to the chromosome 15q13-q14 and is implicated as a candidate gene for bipolar disorder (BPD) by genetic linkage study. A -2 bp deletion polymorphism has been found in the duplicated CHRNA7 (CHRNA7-like) gene, which is located 1 Mb apart from CHRNA7. We tested the hypothesis that the allelic variant, 2 bp deletion (-2 bp), confers susceptibility to BPD or is related to the psychotic features of BPD. We genotyped the -2 bp polymorphism in 77 patients with BPD and 135 normal controls. The distribution of -2 bp genotypes showed a moderately significant difference between the BPD patients and controls (P=0.044). Three BPD patients carried more than two alleles of the -2 bp deletion genotype, while this genotype was not found in the control group. The -2 bp polymorphism was not associated with age of onset or psychotic features in BPD patients. The results of this study suggest that the -2 bp polymorphism or a nearby polymorphism may play a role in the pathogenesis of BPD. Determination of the functional impact of the -2 bp variant in the nervous system and, in particular, the effect of harboring more than two alleles of the -2 bp deletion needs further exploration.

Adult↗

PubMed2004

Personality traits in young female apolipoprotein E (apoE) epsilon4 and non-epsilon4 carriers.

Apolipoprotein E (apoE) is the major brain apolipoprotein, and is related to the functional integrity of the central nervous system. It has been reported that the apoE genetic polymorphism is associated with several components of childhood and adolescent temperament. To study the effect of the presence of the apoE epsilon4 allele on adult personality factors, tridimensional personality questionnaire (TPQ) scores were compared for epsilon4 and non-epsilon4 carriers in a sample population consisting of 135 young females. No significant differences were demonstrated comparing the scores for the two groups. Our findings suggest that the investigated apoE polymorphism does not play a major role in personality trait factors, as assessed by TPQ.

Adult↗

PubMed2004

The impact of polymorphism on prostate specific antigen gene on the risk, tumor volume and pathological stage of prostate cancer.

PURPOSE: A single nucleotide polymorphism with adenine (A) to guanine (G) substitution is identified at position -158 in the androgen response elements region of the prostate specific antigen (PSA) gene. We evaluated the relationship between the PSA -158A/G polymorphism and the risk, tumor volume and pathological stage of prostate cancer. MATERIALS AND METHODS: Peripheral venous blood samples were obtained from 122 patients with prostate cancer and 84 controls with benign prostatic hyperplasia. The diagnosis, tumor volume and pathological stage of prostate cancer were all determined according to the pathological reports of transrectal ultrasound guided prostate biopsy, transurethral prostate resection and radical prostatectomy. The PSA -158A/G polymorphism was determined by polymerase chain reaction based restriction fragment length polymorphism methods. RESULTS: Patients with prostate cancer had significantly greater frequencies of the G allele (87.3% vs 77.4%) and GG genotype (78.7% vs 61.9%) than the control group (p = 0.008 and 0.028, respectively). The OR of GG to AG and AA was 2.27 (p = 0.008). In the prostate cancer group the GG genotype was also associated with larger tumor volume (2.34 vs 0.82 ml) and higher pathological stage (organ confined cancer 68.2% vs 31.8% and extracapsular extension 100% vs 0%) than the GA and AA genotypes (p = 0.013 and 0.036, respectively). CONCLUSIONS: The PSA -158A/G polymorphism is associated with prostate cancer. The G allele increases the risk of prostate cancer and the GG genotype is associated with larger tumor volume and higher pathological stage.

Aged↗

PubMed2004

Association study of onset age, attempted suicide, aggressive behavior, and schizophrenia with a serotonin 1B receptor (A-161T) genetic polymorphism.

Located on the presynaptic and postsynaptic terminals of serotonergic neurons, serotonin 1B receptors (5-HT1B) are involved in the modulation of serotonergic activity. The implications of 5-HT1B study of animal models of schizophrenia and antipsychotic activity involving defective sensory processes suggest that this receptor may be involved in the pathogenesis of schizophrenic disorders. In a population-based association study, we tested the hypothesis that the allelic variant, A-161T, of the 5-HT1B gene confers susceptibility to schizophrenic disorders and is associated with age of onset, aggressive behavior and attempted suicide. We genotyped the A-161T polymorphism in 110 patients with schizophrenic disorders and in 215 normal controls. No association was demonstrated between 5-HT1B genotype or allele frequencies and schizophrenic disorders, except for a trend for later age at disease onset in A/A homozygote schizophrenics in comparison with A/T heterozygote patients (p = 0.071). No significant difference in genotype distribution was determined comparing patients with and without aggressive behavior, and those with and without a history of suicide attempt. These findings suggest that the investigated 5-HT1B genetic polymorphism does not play a major role in the pathogenesis of schizophrenic disorders.

Adult↗

PubMed2004

Association analysis of brain-derived neurotrophic factor Val66Met polymorphisms with Alzheimer's disease and age of onset.

Because of a decrease in central brain-derived neurotrophic factor (BDNF) levels in Alzheimer's disease (AD) and the important role of BDNF in neuronal survival, BDNF may represent a candidate gene conferring susceptibility to AD. Recently, a functional BDNF Val66Met polymorphism has been associated with AD in an Italian population. In the present study, we investigated a possible role of this BDNF polymorphism in the susceptibility of AD or AD onset in a Chinese population. Comparing AD patients and controls, the distribution of the BDNF genotypes and alleles did not differ significantly. The onset age was not significantly different comparing the three BDNF genotype groups. Our negative findings suggest that it is unlikely that the BDNF Val66Met polymorphism plays a major role in the pathogenesis of AD in the Chinese population and do not support previous findings that homozygosity for the 66Val allele confers an increased risk for AD. Further studies with genetic variations in BDNF relating either to AD-associated depression or to the AD treatment response are suggested.

Age of Onset↗

PubMed2004

Association study of a brain-derived neurotrophic factor (BDNF) Val66Met polymorphism and personality trait and intelligence in healthy young females.

Brain-derived neurotrophic factor (BDNF), a member of the nerve-growth-factor family, plays an important role in neuronal survival and development, and it can modulate serotonergic activity. Further, BDNF has been implicated in the expression of personality traits and in cognitive function. We tested the associations between functional BDNF Val66Met genetic variants, and personality trait and intelligence in a cohort of 114 healthy young Chinese females. Subjects with the Val/Val genotype had a significantly higher mean performance IQ than Val/Met carriers, especially for the Object Assembly subtest. No significant association was demonstrated for the BDNF polymorphism and any of the Tridimensional Personality Questionnaire personality-factor scores, including harm avoidance. These results suggest that genetic variants of the BDNF gene may play a role in specific cognitive functions, but not in overall intelligence. In contrast to a recent report, however, this polymorphism does not appear to be associated with the neuroticism-related personality trait.

Adult↗

PubMed2004

Association study of a brain-derived neurotrophic factor (Val66Met) genetic polymorphism and panic disorder.

Brain-derived neurotrophic factor (BDNF), a member of the neurotrophic factor family, plays an important role in the development, maintenance and function of several neuronal systems. Recent studies have demonstrated that antidepressants, commonly used for panic disorder treatment, can increase central BDNF. In addition, animals with BDNF deficits have higher levels of anxiety when exposed to stressors in comparison to normal controls. The present study tested the hypothesis that the BDNF gene Val66Met polymorphism is associated with panic disorder. In this study, therefore, the incidence of this polymorphism was compared in 103 panic disorder patients and 180 normal controls. The genotype and allele frequencies for the BDNF gene Val66Met polymorphism did not differ comparing the two groups. Furthermore, no association was demonstrated between this BDNF polymorphism and either mitral valve prolapse or agoraphobia in panic disorder patients. These findings suggest that the investigated BDNF polymorphism does not play a major role in the pathogenesis of panic disorder in this Chinese population. Further studies exploring the relationship between genetic variations of BDNF and the cerebral atrophy associated with, and antidepressant treatment response in, panic disorder may be appropriate.

Adult↗

PubMed2004

Association study of a functional catechol-O-methyltransferase genetic polymorphism with age of onset, cognitive function, symptomatology and prognosis in chronic schizophrenia.

The gene coding for catechol-O-methyltransferase (COMT), which is involved in the metabolism of catecholamines, has long been implicated as a candidate gene for schizophrenia. This study aimed to assess the relationship between a functional polymorphism (Val158Met) of the COMT gene and age of onset (AOO), symptomatology, global cognitive function and prognosis in patients with schizophrenia. The study enrolled 154 patients with schizophrenia from chronic wards. Results failed to show a significant association between the Val158Met polymorphism and the Brief Psychiatric Rating Scale scores, Mini-Mental State Examination scores, and Social and Occupational Functioning Assessment Scale scores, but COMT Val158Met heterozygotes had a later AOO than homozygous patients. However, by further expanding the number of patients to 228 patients, the differences in AOO among the three COMT genotypic groups was not significant. The COMT Val158Met polymorphism did not appear to significantly affect susceptibility, symptomatology, global cognitive function and prognosis in Chinese patients with schizophrenia, but the possible association with AOO merits further investigation.

Adolescent↗

PubMed2004

Association study of adrenergic beta3 receptor (Trp64Arg) and G-protein beta3 subunit gene (C825T) polymorphisms and weight change during clozapine treatment.

Weight gain, a common adverse effect of clozapine, may impair health and affect patient compliance during treatment with this agent. The aim of this study was to investigate the relationship between genetic variants of the adrenergic beta3 receptor (ADRB3) and the G-protein beta3 subunit (GNB3) and clozapine-induced body weight change (BWC). Eighty-seven treatment-resistant schizophrenic patients were weighed before and after 4 months of clozapine treatment, with the subjects gaining an average of 2.6 kg in body weight. No statistically significant relationship was demonstrated for the investigated ADRB3 Trp64Arg and the GNB3 C825T polymorphisms in terms of BWC post-treatment, suggesting these two polymorphisms do not play a significant role in clozapine-induced BWC. Further exploration of other genetic variants implicated in clozapine-induced BWC is important, however, in order to predict and reduce clozapine-associated weight gain.

Adolescent↗

PubMed2004

Association study of catechol-O-methyltransferase gene and dopamine D4 receptor gene polymorphisms and personality traits in healthy young chinese females.

Human personality traits, which are substantially heritable, may be modulated by monoamine neurotransmitters. It has been demonstrated that the catechol-O-methyltransferase (COMT) Val158Met genetic polymorphism, a functional polymorphism that may affect monoamine metabolism, is possibly associated with specific personality traits. In addition, a polymorphism in the dopamine D4 receptor (DRD4) gene exon 3 has been associated in some, but not all, studies with the novelty seeking personality trait, as evaluated by the Tridimensional Personality Questionnaire (TPQ). In this study, associations between these two polymorphisms and TPQ personality traits were investigated in a sample population of 120 healthy young Chinese females. The results of this analysis reveal that the COMT Val158Met polymorphism was significantly associated with novelty seeking (p = 0.017) and reward dependence scores (p = 0.015) in our sample. However, no significant differences were demonstrated comparing TPQ-specific scores for subjects bearing different DRD4 genotypes. The present study suggests that the functional COMT Val158Met genetic polymorphism contributes to individual differences in the personality traits novelty seeking and reward dependence. Similar to the results of a recent meta-analytic review, however, no association was demonstrated between this DRD4 polymorphism and novelty seeking in our young Chinese female sample population.

Adult↗

PubMed2004

Association study of serotonin 1B receptor (A-161T) genetic polymorphism and suicidal behaviors and response to fluoxetine in major depressive disorder.

Serotonin 1B receptors (5-HT1B) are autoreceptors involved in the local inhibitory control of serotonin release, and have been suggested to play a role in the pathogenesis of major depressive disorder (MDD) and the antidepressant effects of the selective serotonin reuptake inhibitors in patients. We genotyped the 5-HT1B A-161T polymorphism in 160 patients with MDD and 160 normal controls. We then tested the hypothesis that the allelic variant, A-161T, of the 5-HT1B gene confers susceptibility to MDD or is associated with suicide attempt. We also examined the association of this polymorphism with therapeutic response in 116 of the MDD patients who received fluoxetine treatment for 4 weeks. No significant difference was found in the A-161T genetic polymorphism between MDD patients and controls. The genotype distribution between patients with and without suicide attempt, or between fluoxetine treatment responders and nonresponders were also similar. Our findings suggest that 5-HT1B A-161T genetic polymorphism does not play a major role in the susceptibility to MDD, nor is it related to suicidal attempt or the therapeutic response to fluoxetine in MDD.

Adult↗