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J J Lin

Publications and source records attributed to J J Lin.

At least 55 records · Page 3Linked to original sources
PubMed2000

Lack of association between angiotensin I-converting enzyme gene deletion polymorphism and cerebrovascular disease in Taiwanese.

BACKGROUND AND PURPOSE: Angiotensin I-converting enzyme (ACE) gene deletion polymorphism (D) has recently been suggested as a significant risk factor for cerebrovascular disease in studies involving Japanese and white populations. We investigated the role of ACE D polymorphism in the pathogenesis of cerebrovascular disease in Taiwanese. METHODS: To examine the association of ACE genotype and allele frequency with cerebrovascular disease, we conducted a study of 306 stroke patients and 300 control subjects matched by age and sex. RESULTS: Although the frequencies of both the homozygous deletion (DD) genotype and the D allele were greater in stroke patients than in control subjects, these differences were not significant. Further comparison of the frequencies of the DD genotype and the D allele in the three stroke subgroups (intracerebral hemorrhage, probable large-vessel disease, and probable small-vessel lacunar infarction) with the control group revealed no significant associations. Moreover, ACE gene polymorphism was not significantly associated with age of onset of stroke. Stepwise logistic regression analysis of the presence of the D allele and data on risk factors confirmed the lack of significant association between ACE deletion polymorphism and cerebrovascular disease. Moreover, no association was identified between ACE genotypes and any of the relative risk factors for cerebral infarction or severity of carotid atherosclerosis. CONCLUSIONS: Our results suggest that deletion polymorphism of the ACE gene is not associated with the pathogenesis of cerebrovascular disease in Taiwanese.

Alleles↗
PubMed1999

A comparative molecular field analysis study on several bioactive peptides using the alignment rules derived from identification of commonly exposed groups.

A 3D convex hull computation algorithm designed by us previously is used as a tool to align a series of structures randomly generated for eleven bioactive tachykinin peptides. There are 10 random structures generated for each peptide. A random structure is selected for each peptide to form a structural set of eleven structures. The total number of structural sets generated is 100. The convex hull computation algorithm is applied to each peptide structure generated. We count the frequency of atoms lying on the vertices of each hull computed. Vertices of the same atom type are gathered together as a set of commonly exposed atoms for a structural set generated. Structures are then aligned by treating the set of commonly exposed atoms as a set of correspondences using the FIT option of the SYBYL 6.4 program. All the structure sets are also aligned by using the coordinates of the backbone C alpha atoms as a set of correspondences through the same program. It is found that while a smaller degree of structural similarity for structures aligned by the convex hull alignment rule is detected, the overall SYBYL comparative molecular field analysis (CoMFA) statistics computed for the aligned structures using the alignment rule is better than that computed for the aligned structures using the C alpha atoms alignment rule. A similar conclusion is drawn for a subset of structures selected and probed by a different type of atoms using the SYBYL CoMFA program. These results indicate that computation of 3D convex hulls is a feasible way that one can use to align structures generated for highly flexible molecules of this kind.

Algorithms↗
PubMed1999

Expression of the Mf1 gene in developing mouse hearts: implication in the development of human congenital heart defects.

The transcription factor FKHL7 gene has recently been associated with the anterior segment dysgenesis disorder of the eye known as Axenfeld-Rieger anomaly (ARA). A growing body of evidence indicates that mutations in FKHL7 cause not only defects in the anterior segment of the eye but defects in the heart valves and septa as well. In order to evaluate its contribution to normal heart septation and valve formation, expression of the mouse homologue Mf1 in embryonic hearts was analyzed by in situ hybridization. A weak but significant level of Mf1 expression could be detected in the endocardium of mouse embryos as early as day 8.5 post-conception (p.c.). Mf1 expression was undetectable in the hearts of day 9.5 p.c. embryos, but by day 10.5-11 p.c., Mf1 transcripts could be found again in the endocardium of both the atrium and ventricle and a relatively strong signal was observed in the dorsal portion of the septum primum, in what appeared to be the spinal vestibule. At day 13 p.c. when aortic and pulmonary trunks are separated, relatively more Mf1 transcripts were detected in the leaflets of aortic, pulmonary, and venous valves, the ventral portion of the septum primum, as well as in the single layer of cells on the edges of the atrioventricular cushion tissues. Surprisingly, there was no signal detected in the developing interventricular septum. At day 15 p.c., overall Mf1 signals were greatly decreased. However, significant levels of expression could still be observed in the atrial septum, the tricuspid valve, the mitral valve, and in the venous valve but not in the interventricular septum. The temporal and spatial expression patterns of the Mf1 gene in developing mouse hearts suggest that Mf1 may play a critical role in the formation of valves and septa with the exception of the interventricular septum. This is further supported by our studies showing that mutations in the FKHL7 gene were associated with defects in the anterior segment of the eye as well as atrial septal defects or mitral valve defects. Dev Dyn 1999;216:16-27.

Animals↗
PubMed1999

Disinfection of denture base acrylic resin.

STATEMENT OF PROBLEM: During repair or adjustments of acrylic resin removable complete and partial dentures, particles of the acrylic resin from the interior of the prosthesis may expose dental personnel to microbial health hazards if the prosthesis has not been thoroughly disinfected. PURPOSE: This study investigates the efficacy of a commercially prepared microbial disinfectant (Alcide) on the external and internal surfaces of acrylic resins. MATERIAL AND METHODS: Four groups of acrylic resin were incubated in an experimental model to simulate the oral environment over time. Specimens were treated in 2 groups, disinfected and not disinfected, and then further grouped by breaking and not breaking. Analysis was performed with microbial colony counts, SEM, and statistical analyses. RESULTS: Viable microorganisms still remain on the internal and external surfaces of treated resins. CONCLUSION: Chlorine dioxide reduces, but does not eliminate, viable microorganisms on these dental prostheses.

Acrylic Resins↗
PubMed1999

Externalization of tropomyosin isoform 5 in colon epithelial cells.

Ulcerative colitis (UC) is associated with autoantibody response to a cytoskeletal protein, human tropomyosin (hTM) isoform-5 (hTM5). Because hTM5 is an intracellular protein, it may remain inaccessible to the autoantibodies. Therefore, we have investigated the possibility of externalization of hTM5 in colon epithelial cells. Freshly isolated colonic and small intestinal epithelial cells and LS-180 colon cancer cell line were examined for surface expression of hTM5 by flow cytometric analysis using hTM isoform-specific MoAbs. The extracellular release of hTM5 was determined by Western blot and radioimmunoprecipitation analyses. Physical association of hTM5 with a membrane-associated colon epithelial protein (CEP) was examined by co-immunoprecipitation of hTM5 with anti-CEP MoAb, and CEP with anti-hTM5 MoAb. Cell surface expression of hTM5 was observed in colonic epithelial and LS-180 cells but not in small intestinal epithelial cells. LS-180 cells spontaneously released hTM5 as well as CEP into the culture medium that was significantly stimulated by a calcium ionophore, A23187, but inhibited by phorbol-12-myristate-13-acetate, monensin and methylamine. Co-immunoprecipitation experiments revealed that hTM5 forms a complex with CEP. We conclude that hTM5 is externalized in colon but not in small intestinal epithelial cells. The physical association of hTM5 with CEP suggests a possible chaperone function of CEP in the transport of hTM5, a putative target autoantigen in UC.

Calcimycin↗
PubMed1999

Absence of G209A and G88C mutations in the alpha-synuclein gene of Parkinson's disease in a Chinese population.

A G209A mutation in the alpha-synuclein gene was recently discovered in a large Italian kindred and three unrelated Greek kindreds with autosomal dominant Parkinson's disease (PD). Subsequently, another mutation in the gene (G88C) was also identified in a German family with autosomal PD. These results indicate that the alpha-synuclein gene may have an important role in the pathogenesis of PD. This study was designed to screen the existence of both mutations of the alpha-synuclein gene among 100 Chinese patients with PD, including 80 with sporadic and 20 with familial PD. Results showed that none of our patients, both sporadic and familial PD, had either of the two mutations of this gene. We therefore conclude that although of great interest, these two mutations are not relevant for the pathogenesis of PD in a Han Chinese population.

Aged↗
PubMed1999

Requirement of a novel gene, Xin, in cardiac morphogenesis.

A novel gene, Xin, from chick (cXin) and mouse (mXin) embryonic hearts, may be required for cardiac morphogenesis and looping. Both cloned cDNAs have a single open reading frame, encoding proteins with 2,562 and 1,677 amino acids for cXin and mXin, respectively. The derived amino acid sequences share 46% similarity. The overall domain structures of the predicted cXin and mXin proteins, including proline-rich regions, 16 amino acid repeats, DNA-binding domains, SH3-binding motifs and nuclear localization signals, are highly conserved. Northern blot analyses detect a single message of 8.9 and 5.8 kilo base (kb) from both cardiac and skeletal muscle of chick and mouse, respectively. In situ hybridization reveals that the cXin gene is specifically expressed in cardiac progenitor cells of chick embryos as early as stage 8, prior to heart tube formation. cXin continues to be expressed in the myocardium of developing hearts. By stage 15, cXin expression is also detected in the myotomes of developing somites. Immunofluorescence microscopy reveals that the mXin protein is colocalized with N-cadherin and connexin-43 in the intercalated discs of adult mouse hearts. Incubation of stage 6 chick embryos with cXin antisense oligonucleotides results in abnormal cardiac morphogenesis and an alteration of cardiac looping. The myocardium of the affected hearts becomes thickened and tends to form multiple invaginations into the heart cavity. This abnormal cellular process may account in part for the abnormal looping. cXin expression can be induced by bone morphogenetic protein (BMP) in explants of anterior medial mesoendoderm from stage 6 chick embryos, a tissue that is normally non-cardiogenic. This induction occurs following the BMP-mediated induction of two cardiac-restricted transcription factors, Nkx2.5 and MEF2C. Furthermore, either MEF2C or Nkx2.5 can transactivate a luciferase reporter driven by the mXin promoter in mouse fibroblasts. These results suggest that Xin may participate in a BMP-Nkx2.5-MEF2C pathway to control cardiac morphogenesis and looping.

Amino Acid Sequence↗
PubMed1999

Chemiluminescent detection of AFLP markers.

Nonradioactive amplified fragment-length polymorphism (AFLP) marker detection, a PCR-based, DNA-fingerprinting technique, was achieved by blotting AFLP products after electrophoresis onto a nylon membrane and subsequently hybridizing the blot with an alkaline phosphatase-labeled AFLP probe. Similar AFLP profiles were obtained by both a nonradioactive, chemiluminescent detection technique and by conventional AFLP marker detection using 32P-labeled AFLP primers. The suitability of the method using different gel systems combined with subsequent chemiluminescent detection of AFLP markers is validated by similar dendrograms that were generated using the unweighted pair group method with arithmetic averages (UPGMA). Moreover, chemiluminescent detection of AFLP markers using a universal AFLP nonradioactive probe has been successfully applied on prokaryotes such as Agrobacterium and eukaryotic genomes such as soybean and fungi.

Chromosome Mapping↗
PubMed1999

Immunodetection of Xenopus bone morphogenetic protein-1 in adult and embryonic cells.

In order to analyze biochemical properties of Xenopus bone morphogenetic protein-1 (XBMP-1), rabbit antiserum (alpha-B1) was raised against a synthetic peptide (P1) corresponding to a hydrophilic N-terminal region. XBMP-1B (Xtld) synthesized in the reticulocyte lysate was successfully immunoprecipitated by this antiserum. This precipitation was completely blocked when P1 was added to the reaction, indicating that alpha-B1 recognized XBMP-1B specifically. In Western blot analysis, two distinct sizes of protein (107 and 34 kD) were detected in hind limbs in metamorphosing animals. Both proteins were detected in various adult tissues such as lung, liver, kidney, heart, muscle, intestine, brain, and testis. The mixing of the liver and muscle extracts, and the following detection of immunoreactive proteins suggested that the 34 kD band was a proteolytic product of the 107 kD protein. In the embryonic extracts from the unfertilized egg (stage 0) to swimming tadpoles (stage 40), a 63 kD protein was detected in addition to the 107 kD protein. We also showed that the 107 kD protein was much more expressed in the animal half of the unfertilized eggs than in the vegetal half, but that it was ubiquitously expressed in the gastrula embryos. We suggest that the 63 and 107 kD proteins correspond to full-length proteins encoded by XBMP-1A and XBMP-1B genes, and these proteins are expressed in embryo and in various adult tissues.

Animals↗
PubMed1999

Benefit of bilateral pallidotomy in the treatment of generalized dystonia. Case report.

This 29-year-old man with cerebral palsy complicated by generalized dystonia was treated by simultaneous bilateral posteroventral pallidotomy. Postoperatively, there was slow, but steady, improvement in the patient's dystonia and disability. However, the improvement in abnormal movements was only prominent for cervical dystonia and oromandibular dyskinesia. The patient's Burke-Fahn-Marsden dystonia scores were 51 preoperatively and 37, 33.5 and 33.5, at 3, 6, and 12 months postoperatively, respectively, demonstrating a maximum improvement of 34%. These results suggest that pallidotomy can be an alternative therapy for those patients suffering from intractable generalized dystonia.

Adult↗
PubMed1999

Lack of association between deletion polymorphism of the ACE gene and ischemic vascular diseases in a Chinese population in Taiwan.

BACKGROUND: The association between deletion/insertion polymorphism of the angiotensin I-converting enzyme (ACE) gene and ischemic vascular diseases (IVDs) is still unclear. This study was designed to evaluate the role of ACE gene polymorphism in the pathogenesis of IVDs in a Chinese population living in Taiwan. METHODS: A case-control study was carried out to examine the association of the ACE gene genotype and the allele frequency in 400 IVD patients, including 214 patients with ischemic cerebrovascular disease (ICVD) and 186 patients with ischemic heart disease (IHD), compared with 200 control individuals. RESULTS: Although the patients with ICVD and IHD were found to have higher frequencies of the D/D genotype (22% and 43%) and the D allele (20% and 42%) than the controls (16% and 39%), the statistical differences were not significant, as shown by chi 2 analysis (p > 0.05). Upon further comparison of the frequencies of the D allele among the two sexes and different age subgroups, there was still no significant association. CONCLUSIONS: Deletion polymorphism of the ACE gene was not associated with IVD in a Chinese population in Taiwan. The unique or synergistic effect of other genes that might contribute to the pathogenesis of IVDs needs further investigation.

Aged↗
PubMed1998

The cancer growth suppressor gene mda-7 selectively induces apoptosis in human breast cancer cells and inhibits tumor growth in nude mice.

A differentiation induction subtraction hybridization strategy is being used to identify and clone genes involved in growth control and terminal differentiation in human cancer cells. This scheme identified melanoma differentiation associated gene-7 (mda-7), whose expression is up-regulated as a consequence of terminal differentiation in human melanoma cells. Forced expression of mda-7 is growth inhibitory toward diverse human tumor cells. The present studies elucidate the mechanism by which mda-7 selectively suppresses the growth of human breast cancer cells and the consequence of ectopic expression of mda-7 on human breast tumor formation in vivo in nude mice. Infection of wild-type, mutant, and null p53 human breast cancer cells with a recombinant type 5 adenovirus expressing mda-7, Ad.mda-7 S, inhibited growth and induced programmed cell death (apoptosis). Induction of apoptosis correlated with an increase in BAX protein, an established inducer of programmed cell death, and an increase in the ratio of BAX to BCL-2, an established inhibitor of apoptosis. Infection of breast carcinoma cells with Ad.mda-7 S before injection into nude mice inhibited tumor development. In contrast, ectopic expression of mda-7 did not significantly alter cell cycle kinetics, growth rate, or survival in normal human mammary epithelial cells. These data suggest that mda-7 induces its selective anticancer properties in human breast carcinoma cells by promoting apoptosis that occurs independent of p53 status. On the basis of its selective anticancer inhibitory activity and its direct antitumor effects, mda-7 may represent a new class of cancer suppressor genes that could prove useful for the targeted therapy of human cancer.

Adenoviridae↗
PubMed1998

Melanoma differentiation associated gene-9, mda-9, is a human gamma interferon responsive gene.

Subtraction hybridization using a cDNA library prepared from temporally spaced mRNAs from human melanoma cells treated with recombinant human fibroblast interferon (IFN-beta) plus mezerein (MEZ) that induces terminal differentiation (tester cDNA library) and a temporally spaced cDNA library prepared from actively proliferating melanoma cells (driver cDNA library) produced a Temporally Spaced Subtracted (TSS) cDNA library. This approach resulted in the identification of melanoma differentiation associated (mda) genes displaying both enhanced and suppressed expression during growth inhibition and differentiation. In the present report, we describe a novel cDNA mda-9 that consists of 2084 nucleotides, and encodes a protein of 298 amino acids with a predicted M(r) of approx. 33 kDa. Treatment of human SV40-immortalized normal melanoma cells with immune interferon, INF-gamma, induces growth suppression and enhances mda-9 expression without inducing terminal differentiation. These results establish that induction of terminal differentiation in human melanoma cells, using the combination of a type I interferon (IFN-beta) + MEZ, can elicit signaling pathways and gene expression changes also regulated by type II immune interferon.

Amino Acid Sequence↗
PubMed1998

Mesoderm induction by heterodimeric AP-1 (c-Jun and c-Fos) and its involvement in mesoderm formation through the embryonic fibroblast growth factor/Xbra autocatalytic loop during the early development of Xenopus embryos.

We have previously demonstrated the involvement of AP-1/Jun in fibroblast growth factor (FGF) signaling by loss-of-function assay (Dong, Z., Xu, R.-H., Kim, J., Zhan, S.-N., Ma, W.-Y., Colburn, N. H., and Kung, H. (1996) J. Biol. Chem. 271, 9942-9946). Further investigations by gain-of-function are reported in this study. AP-1 transactivation activity was increased by the treatment of animal cap explants with FGF. Ectopic overexpression of two components of AP-1 (c-jun and c-fos together, but not alone) produced posteriorized embryos and induced mesoderm formation in animal cap explants, indicating that both AP-1 heterodimers are required for mesoderm induction. Since Ras/AP-1 functions downstream of FGF signaling, we then tested the involvement of Ras/AP-1 in mesoderm maintenance mediated by embryonic FGF/Xbra using dominant-negative mutants. Mesoderm maintenance mediated by embryonic FGF/Xbra was blocked by dominant-negative mutants of Ras/AP-1, and AP-1 enhanced the expression of Xbra. Further studies demonstrated the inhibition of Ras/AP-1-mediated mesoderm formation by dominant-negative mutants of the FGF receptor and Xbra. These results indicate that Ras/AP-1 and FGF/Xbra signals are involved in the mesoderm maintenance machinery and mesoderm formation through the synergistic action of the diversified signal pathways derived from the FGF/Xbra autocatalytic loop.

Animals↗
PubMed1998

Peritoneal loss of insulin-like growth factor-I and binding proteins in end-stage renal disease.

The kinetics of peritoneal transport of insulin-like growth factor (IGF) system-related proteins during dialysis is not well characterized. We studied temporal changes in dialysate and serum concentrations of IGF-I and IGF-II as well as IGF binding protein (BP)-1, -2, and -3 in ten children with end-stage renal disease (ESRD) undergoing continuous cycling peritoneal dialysis (CCPD) during a 4-h peritoneal equilibration test (PET). Dialysate concentrations of IGF-I, IGF-II, and all three IGFBPs demonstrated a time-dependent increase during PET. Despite their transport, the serum concentrations of these proteins did not change significantly during the PET. Dialysate/serum ratios for IGF-I, IGF-II, and IGFBP-1, -2, and -3 were significantly increased at 2 h and increased further at 4 h, at which time values averaged 1.3+/-0.2%, 3.1+/-0.5%, 6.2+/-1.0%, 2.4+/-0.2%, and 1.3+/-0.2% of serum levels, respectively. The transperitoneal clearance (microl/min per 1.73 m2) of the three IGFBPs was inversely related to both their molecular weight and plasma concentration. However, peritoneal clearance of IGF-I and -II was similar to that of the larger and more-abundant IGFBP-3. Mass transfer rates (microg/h per 1.73 m2) for the IGFs and their binding proteins were directly proportional to their prevailing plasma concentration. Based on estimates of mass transfer, only a small molar excess of IGFBPs was removed from the circulation relative to the combined molar concentration of IGF-I and IGF-II. Hence, it seems unlikely that any beneficial effect of CCPD on growth in children with ESRD is mediated via a preferential loss of IGFBPs into the dialysate fluid.

Blotting, Western↗
PubMed1998

Tropomyosin isoforms in intestinal mucosa: production of autoantibodies to tropomyosin isoforms in ulcerative colitis.

BACKGROUND & AIMS: Autoantibodies against tropomyosins (TMs) have been reported in ulcerative colitis (UC). In this study the hTM isoforms (hTM1-5) present in intestinal epithelial cells and in smooth muscle were investigated, and the immunoreactivity against hTMs by immunoglobulin G (IgG) produced in vitro by colonic mucosal lymphocytes (LPMCs) from patients with UC, Crohn's disease (CD), and controls was examined. METHODS: TMs were extracted from colonic and jejunal epithelial cells and smooth muscle, and hTM isoforms were identified using isoform-specific monoclonal antibodies by enzyme-linked immunosorbent assay and transblot analysis. The immunoreactivity of IgG produced by colonic LPMCs was analyzed against the recombinant hTM isoforms. RESULTS: The major hTM isoforms present in colonic and jejunal epithelial cells are hTM5 and hTM4, whereas intestinal smooth muscle contains the hTM1-3 isoforms. The IgG synthesized in vitro by LPMCs from UC (n = 19) recognized hTM5 and hTM1, more significantly (P < 0.04 to <0.001) when compared with CD (n = 12) and controls (n = 17). However, IgG produced by LPMCs from CD did not show such anti-hTM reactivity. Mucosal anti-hTM IgG mainly belonged to the IgG1 subclass. CONCLUSIONS: Intestinal epithelial cells and smooth muscle have distinct hTM isoforms. Patients with UC, and not CD, show mucosal autoantibody response against hTM isoforms, particularly hTM5 and hTM1.

Adult↗