Biomedical subjects

Jong-Min Woo

Publications and source records attributed to Jong-Min Woo.

10 recordsLinked to original sources

PubMed2006

Systematic identification and integrative analysis of novel genes expressed specifically or predominantly in mouse epididymis.

BACKGROUND: Maturation of spermatozoa, including development of motility and the ability to fertilize the oocyte, occurs during transit through the microenvironment of the epididymis. Comprehensive understanding of sperm maturation requires identification and characterization of unique genes expressed in the epididymis. RESULTS: We systematically identified 32 novel genes with epididymis-specific or -predominant expression in the mouse epididymis UniGene library, containing 1505 gene-oriented transcript clusters, by in silico and in vitro analyses. The Northern blot analysis revealed various characteristics of the genes at the transcript level, such as expression level, size and the presence of isoform. We found that expression of the half of the genes is regulated by androgens. Further expression analyses demonstrated that the novel genes are region-specific and developmentally regulated. Computational analysis showed that 15 of the genes lack human orthologues, suggesting their implication in male reproduction unique to the mouse. A number of the novel genes are putative epididymal protease inhibitors or beta-defensins. We also found that six of the genes have secretory activity, indicating that they may interact with sperm and have functional roles in sperm maturation. CONCLUSION: We identified and characterized 32 novel epididymis-specific or -predominant genes by an integrative approach. Our study is unique in the aspect of systematic identification of novel epididymal genes and should be a firm basis for future investigation into molecular mechanisms underlying sperm maturation in the epididymis.

Animals↗

PubMed2006

Tryptophan hydroxylase and serotonin transporter gene polymorphism does not affect the diagnosis, clinical features and treatment outcome of panic disorder in the Korean population.

Panic disorder may be associated with defective serotonin (5-HT) neurotransmission. This study was to investigate the association between the tryptophan hydroxylase (TPH) gene and a serotonin transporter gene promoter polymorphism (5-HTTLPR), with panic disorder in a Korean population. 244 Korean patients with panic disorder and the 227 controls were genotyped by a polymerase chain reaction-based method. The severity of panic disorders was assessed by number of panic attacks during the previous 1 month, as well as scores for anticipatory anxiety, panic distress, and agoraphobic distress, as determined by a visual analogue scale (VAS). All the subjects completed the assessment measures including Spielberger State-Trait Anxiety Inventory-State (STAI-S), Spielberger State-Trait Anxiety Inventory-Trait (STAI-T), Beck Depression Inventory (BDI), Symptom Checklist-90-Revised (SCL-90-R), Revised Anxiety Sensitivity Index (ASI-R), Clinical Global Impression Scale--Severity of Illness (CGI-S), Panic Disorder Severity Scale (PDSS), and the Hamilton Depression Rating Scale (HAMD). Responder analyses were conducted based on changes in CGI-I scores after 10 weeks of treatment. We found no significant differences in the genotype and allele frequencies in TPH A218C and 5-HTTLPR polymorphisms between the panic patients and the control group. Subgroup analyses in terms of comorbidities, response, and other primary clinical variables, indicated no differences in these polymorphisms. Our findings suggest that the TPH A218C polymorphism and 5-HTTLPR play no significant roles in the pathogenesis and clinical symptomatologies, at least in a Korean population.

Age of Onset↗

PubMed2006

Expression and relationship of male reproductive ADAMs in mouse.

A number of a disintegrin and metalloprotease (ADAM) family members are expressed in mammalian male reproductive organs such as testis and epididymis. These reproductive ADAMs are divided phylogenically into three major groups: ADAMs 1, 4, 6, 20, 21, 24, 25, 26, 29, 30, and 34 (the first group); ADAMs 2, 3, 5, 27, and 32 (the second group); and ADAMs 7 and 28 (the third group). Previous mouse knockout studies indicate that ADAM1, ADAM2, and ADAM3 have intricate expressional relationships, playing critical roles in fertilization. In the present study, we analyzed processing, biochemical characteristics, localization, and expressional relationship of the previously-unexplored, second-group ADAMs (ADAM5, ADAM27, and ADAM32). We found that all of the three ADAMs are made as precursors in the testis and processed during epididymal maturation, and that ADAM5 and ADAM32, but not ADAM27, are located on the sperm surface. Using sperm from Adam2(-/-) and Adam3(-/-) mice, we found that, among the three ADAMs, the level of ADAM5 is modestly and severely reduced in Adam3 and Adam2 knockout sperm, respectively. Further, we analyzed ADAM7, an epididymis-derived sperm surface ADAM from the separate phylogenetic group, in the knockout sperm. We found that the level of ADAM7 is also significantly reduced in both Adam2 and Adam3-null sperm. Taken together, our results suggest a novel expressional relationship of ADAM5 and ADAM7 with ADAM2 and ADAM3, which play critical roles in fertilization.

ADAM Proteins↗

PubMed2005

Molecular, biochemical, and cellular characterization of epididymal ADAMs, ADAM7 and ADAM28.

The mammalian epididymis is critical for sperm to acquire motility and fertilizing capacity. This maturation process involves the interaction of epididymal secretory proteins with sperm. We analyzed mouse a disintegrin and metalloprotease (ADAMs) 7 and 28 expressed specifically or predominantly in the epididymis. We found that these ADAM genes are expressed in an epididymal region-specific manner and their gene expression is regulated by both androgen and testicular factors (ADAM7) or only testicular factors (ADAM28). We identified an ADAM28 transcript isoform that lacks the transmembrane domain. Protein analysis revealed that ADAM7, but not ADAM28, is transferred from the epididymis to the sperm surface and redistributed in the sperm head during acrosome reaction. These processes were shown to occur without processing of the protein. Taken together, our results indicate that the two epididymal ADAMs closely related in phylogeny are differential in various characteristics and ADAM7 has unique secretory feature and interactive relationship with sperm.

ADAM Proteins↗

PubMed2005

Complementary DNA cloning, genomic characterization and expression analysis of a mammalian gene encoding histidine-rich calcium binding protein.

A protein complex present at the junctional sarcoplasmic reticulum (SR) membrane is implicated in the Ca(2+) release process during muscle contraction. The histidine-rich Ca(2+)-binding protein (HRC) is an emerging component associated into the SR protein complex. We cloned cDNAs for rat and monkey HRCs, showing a conserved sequence organization in common with other mammalian HRCs. Genomic analysis revealed that each mammalian HRC gene is present as a single copy in the genome, consisting of 6 exons and 5 introns. Developmental expression analysis using mouse embryos and postnatal hearts demonstrated that Hrc transcription begins at 12.5 days postcoitum and its level increases gradually, reaching an adult level in the range 5-20 days after birth. Comparing the Hrc gene and other SR genes, we found that the timing and pattern of gene expression vary among the SR genes and the full-level expression of these genes is achieved in the heart after postnatal day 20. Collectively, our study provides comprehensive information about the structure and expression of the mammalian HRC gene, together with the comparative expression data of the related SR genes.

Amino Acid Sequence↗

PubMed2004

Identification and integrative analysis of 28 novel genes specifically expressed and developmentally regulated in murine spermatogenic cells.

Mammalian spermatogenesis is a highly ordered process that occurs in mitotic, meiotic, and postmeiotic phases. The unique mechanisms responsible for this tightly regulated developmental process suggest the presence of an intrinsic genetic program composed of spermatogenic cell-specific genes. In this study, we analyzed the mouse round spermatid UniGene library currently containing 2124 gene-oriented transcript clusters, predicting that 467 of them are testis-specific genes, and systematically identified 28 novel genes with evident testis-specific expression by in silico and in vitro approaches. We analyzed these genes by Northern blot hybridization and cDNA cloning, demonstrating the presence of additional transcript sequences in five genes and multiple transcript isoforms in six genes. Genomic analysis revealed lack of human orthologues for 10 genes, implying a relationship between these genes and male reproduction unique to mouse. We found that all of the novel genes are expressed in developmentally regulated and stage-specific patterns, suggesting that they are primary regulators of male germ cell development. Using computational bioinformatics tools, we found that 20 gene products are potentially involved in various processes during spermatogenesis or fertilization. Taken together, we predict that over 20% of the genes from the round spermatid library are testis-specific, have discovered the 28 authentic, novel genes with probable spermatogenic cell-specific expression by the integrative approach, and provide new and thorough information about the novel genes by various in vitro and in silico analyses. Thus, the study establishes on a comprehensive scale a new basis for studies to uncover molecular mechanisms underlying the reproductive process.

Animals↗

PubMed2004

Topiramate and divalproex in combination with risperidone for acute mania: a randomized open-label study.

Mood stabilizers and atypical antipsychotics are commonly combined for the treatment of bipolar mania. The aim of this study was to compare the effectiveness and tolerability of topiramate and divalproex in combination with risperidone for treating acute mania patients in a naturalistic treatment setting. Seventy-four patients who met the DSM-IV criteria for bipolar mania were enrolled in this study. In order to assess the efficacy and the extrapyramidal symptoms (EPS), the Young Mania Rating Scale (YMRS), Clinical Global Impression (CGI) and Simpson-Angus Rating Scale (SARS) were measured at the baseline and at weeks 1, 3 and 6. From the baseline to the endpoint, the YMRS and CGI scores were reduced by 67.9% and 56.6% in the topiramate plus risperidone group (TPMG). The YMRS and CGI scores were also reduced by 63.7% and 58.2% in the divalproex plus risperidone group (DVPG). The weight and body mass index (BMI) increased significantly by 3.6% and 3.3% from the baseline to the endpoint in the DVPG, while they decreased by 0.5% and 0.4%, respectively, with no significant difference in the TPMG. There were no serious adverse events in either group. Despite the methodological limitations, topiramate was effective and tolerable for treating acute mania and may also be a promising alternative to a weight-gain liable mood stabilizer (MS) such as divalproex.

Acute Disease↗

PubMed2003

Identification and characterization of ADAM32 with testis-predominant gene expression.

Members of the ADAM (A Disintegrin And Metalloprotease) family of cell surface proteins have been discovered in a variety of tissues and species. We have cloned and sequenced a mouse cDNA encoding a novel member of the ADAM family. This mouse ADAM gene was named ADAM32 after an human homologue previously sequenced but not characterized. The cDNA sequence of ADAM32 has an open reading frame which encodes 750 (mouse ADAM32) and 787 (human ADAM32) amino acids, sharing 69% homology between the two species. The deduced amino acid sequences of mouse and human ADAM32 cDNAs contain all of the domains common to ADAM family members. Comparison of amino acid sequences showed that ADAM32 is highly homologous to ADAM2 and ADAM3, sperm surface proteins required for fertilization. We found that the ADAM32 gene is expressed predominantly in the testis. Examination of transcription in pre-pubertal and adult mouse testes revealed that expression of ADAM32 begins during meiotic prophase, in pachytene spermatocytes. These results suggest a potential role for ADAM32 in sperm development or fertilization. Genome database searches revealed that the mouse and human ADAM32 genes are located on chromosomes 8 and 8q11, respectively. The ADAM32 gene covers a relatively large region of the genome (120 kb for mouse ADAM32 and 180 kb for human ADAM32) and consists of multiple small exons (at least 22 exons in mouse ADAM32 and 25 exons in human ADAM32).

ADAM Proteins↗

PubMed2002

Catechol O-methyltransferase genetic polymorphism in panic disorder.

OBJECTIVE: The authors examined the distribution of catechol O-methyltransferase (COMT) genotypes in patients with panic disorder as well as the relationship between a COMT polymorphism and the clinical characteristics of these patients. METHOD: Fifty-one patients with panic disorder and 45 healthy comparison subjects were tested for a genetic polymorphism of COMT. Clinical variables were assessed for the patients with panic disorder. RESULTS: The frequency of the L/L genotype was significantly higher in the patients with panic disorder than in the healthy subjects (19.6% versus 2.2%). Panic disorder was significantly associated with the L allele and L/L genotype. Patients with panic disorder who had the L/L genotype showed poorer treatment response than those with other genotypes. CONCLUSIONS: These results suggest that the L/L genotype of the COMT gene may be related to the development and treatment outcome of panic disorder in some patients.

Adult↗

PubMedDate not supplied

The association between panic disorder and the L/L genotype of catechol-O-methyltransferase.

To clarify the role of catechol-O-methyltransferase (COMT) polymorphism in panic disorder (PD), we investigated a large group of Korean PD patients (N = 178) and controls (N = 182) using a case-control study. We also assessed the response to paroxetine treatment and other clinical variables in the PD patients. The increase in the COMT(L) allele was not statistically significant in PD (p = 0.104). However, compared with the sum of the other genotypes, the frequency of the L/L genotype was significantly higher in PD (p = 0.042). The odd ratios (ORs) also indicated a significant effect of the homozygosity for the COMT(L) allele on an increased risk for PD (OR=2.38; 95% CI 1.03-5.51). In addition, patients with L/L genotype had higher trait-anxiety levels (p = 0.030) and poorer treatment response to paroxetine than those with other genotypes (p = 0.002). Our results suggest that the COMT L/L genotype is associated with PD and the genetic variant of the COMT enzyme may be related to the clinical severity and treatment response to paroxetine in PD.

Adult↗