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Biomedical subjects

Y C Wang

Publications and source records attributed to Y C Wang.

At least 145 records · Page 8Linked to original sources
PubMed1995

Epidemiological study of head injuries in central Taiwan.

BACKGROUND: Head injury plays a major role in emergency neurosurgery and is the leading cause of neurosurgical mortality at Taichung Veterans General Hospital. Statistical data show that a similar condition exists in other teaching hospitals in the central Taiwan area, which includes more than one-quarter of the entire population and has more than one-third of the total land of Taiwan. A clinical statistical survey of head injuries in this area may provide a better understanding of the realistic situation in Taiwan. Reports on head injuries in Taipei City, Taipei area, and Hualian County are also cited for comparison. METHODS: The present study is based on a cooperative investigation of head injuries by 18 teaching hospitals in central Taiwan from July 1991 to June 1993. All patients received a neurological examination including the Glasgow coma scale (GCS), with recording by 20 Board-certified neurosurgeons. RESULTS: The 7050 cases collected included 5322 hospitalized cases, 1694 cases seen in the Emergency Room, and 34 deaths on arrival. The leading cause of head injuries was traffic accidents (5354 cases, 76.3%). Motorcycles contributed to the highest number of cases (3661, 68.4%); and trains contributed to the lowest number (8, 0.1%). Helmets were used in only 5.2% of 3503 motorcycle accidents. Based on the patients' or families' description in 4835 cases, the leading cause of the accident was careless driving (1180 cases, 24.4%). The 1088 cases of severe head injury were classified with a score less than 8 by the GCS; 498 of them died, or an 86.6% mortality (575 cases). CONCLUSIONS: Traffic accidents are the leading cause of head injuries, and motorcycles contribute to the major part of it in central Taiwan. Similar conclusions can be drawn for other areas including Taipei City, Taipei area, and Hualian County.

Accidents, Traffic↗
PubMed1995

[Inhibition of chemically induced microvascular leakage by ONO-1078, a leukotriene antagonist, in rat skin].

This study is to determine whether ONO-1078, a potent leukotriene antagonist, influences chemically induced rat skin microvascular leakage which is considered to be, at least in part, due to stimulation of sensory nerve ending and release of sensory neuropeptides. Evans blue dye was used as a tracer for plasma leakage. Intradermal injections of chemical stimuli, histamine (10 micrograms), capsaicin (10 micrograms) and formalin (0.5 mg), evoked Evans blue dye extravasation in rat skin. Intraperitoneal ONO-1078 dose-dependently inhibited the dye extravasation induced by these stimuli, with ID5v values of 1.98 mg.kg-1 for histamine, 1.78 mg.kg-1 for capsaicin, and 2.23 mg.kg-1 for formalin. In contrast to chlorpheniramine, a H1 receptor antagonist, the inhibitory effect of ONO-1078 was weaker on histamine, but more potent on capsaicin and formalin. The inhibitory effect of dexamethasone was more potent than that of ONO-1078 on these stimuli. On the other hand, ONO-1078 inhibited the dye extravasation induced by leukotriene D4 (0.05 micrograms), but showed no effect on those induced by substance P (0.5 micrograms, a sensory neuropeptide), a larger dose of histamine (100 micrograms), and bradykinin (1 microgram). These results suggest that inhibition of chemically induced skin microvascular leakage by ONO-1078 may be mediated by inhibiting the release of sensory neuropeptides from capsaicin-sensitive sensory fibers.

Animals↗
PubMed1995

[Relationship between CENP-B gene expression and the cell cycle].

The centromere/kinetochore is a specialized structure at the primary constriction of mammalian chromosomes. It participates in and is necessary for the mitotic chromosome movement. Centromere Protein B(CENP-B) is a highly conserved protein located at the centromere/kinetochore region. In this article, we explore the relationship between CENP-B expression and cell proliferation. HeLa cells were synchronized at different phases of the cell cycle and the synchronized cells were examined by flow cytometry and 3H-TdR labelling. ACA immunostaining showed the discrete single spots in nuclei of the cells at G1 and S phase, and spots in pairs mostly in those at G2 phase. Dot blot and Northern blot indicated that CENP-B gene was expressed at all phases of the cell cycle, but the expression level very much different with the highest at G2 phase and the lowest at S phase. Interestingly relatively high expression of CENP-B gene was also found in M phase, showing the continuity of the CENP-B gene expression during the cell cycle. This continuity implies a possibility that the assembly of the new centromere/kinetochore can not occur until centromere proteins reach a critical concentration when cells enter S phase and G 2 phase. Also, the continuous expression of centromere proteins may be necessary for the centromere/kinetochore function. In addition, the relationship between CENP-B gene expression and the nuclear skeleton was investigated. The nuclear skeleton-associated DNA extracted after Bam HI digestion were hybridized with 32P-labelled cDNA of CENP-B gene by means of Southern blot technique. The results that there stronger positive hybridization reaction in G 2 phase than in S phase indicated that CENP-B gene was more closely associated with the nuclear skeleton in G 2 phase cells than in S phase cells, which was in consistence with the level of the CENP-B gene expression at G 2 and S phase cells.

Autoantigens↗
PubMed1995

Effects of ONO-1078, a leukotriene antagonist, on cardiovascular responses induced by vagal stimulation, capsaicin, and substance P in guinea pigs.

AIM: To determine the role of ONO-1078, 4-oxo-8 -[p-(4-phenylbutyloxy) benzoylamino]- 2-(tetrazol-5-yl) -4H-1-benzopyran hemihydrate, in cardiovascular responses induced by vagal stimulation, capsaicin, and substance P. METHODS: Evans blue extravasation in the atrium and ventricle, and mean arterial pressure (MAP) were observed. RESULTS: Electric stimulation of vagus (ESV, 10 Hz, 5 ms, 2 or 10 V, for 90 s) increased Evans blue extravasation in the hearts of atropine (1 mg.kg-1, i.v.)-pretreated guinea pigs. Capsaicin (0.05 mg.kg-1, i.v.) and substance P (1 microgram.kg-1, i.v.) enhanced the dye extravasation and elicited a drop in MAP. ONO-1078 (0.03 and 0.1 mg.kg-1, i.v.) inhibited ESV-induced response, especially at stimulation of 2 V. ONO-1078 (0.03 mg.kg-1) attenuated capsaicin-induced cardiac microvascular leakage and hypotensive response, but failed to inhibit substance P-induced responses. CONCLUSION: ONO-1078 can modulate the cardiovascular responses in neurogenic inflammation, possibly mediated by inhibiting sensory neuropeptide release.

Animals↗
PubMed1994

Mammalian DNA ligase II is highly homologous with vaccinia DNA ligase. Identification of the DNA ligase II active site for enzyme-adenylate formation.

Mammalian cells contain three biochemically distinct DNA ligases. In this report we describe the purification of DNA ligase II to homogeneity from bovine liver nuclei. This enzyme interacts with ATP to form an enzyme-AMP complex, in which the AMP moiety is covalently linked to a lysine residue. An adenylylated peptide from DNA ligase II contains the sequence, Lys-Tyr-Asp-Gly-Glu-Arg, which is homologous to the active site motif conserved in ATP-dependent DNA ligases. The sequences adjacent to this motif in DNA ligase II are different from the comparable sequences in DNA ligase I, demonstrating that these enzymes are encoded by separate genes. The amino acid sequences of 15 DNA ligase II peptides exhibit striking homology (65% overall identity) with vaccinia DNA ligase. These peptides are also homologous (31% overall identity) with the catalytic domain of mammalian DNA ligase I, indicating that the genes encoding DNA ligases I and II probably evolved from a common ancestral gene. Since vaccinia DNA ligase is not required for DNA replication but influences the ability of the virus to survive DNA damage, the homology between this enzyme and DNA ligase II suggests that DNA ligase II may be involved in DNA repair.

Amino Acid Sequence↗
PubMed1994

Effects of ocular injury and administration of brain-derived neurotrophic factor on survival and regrowth of axotomized retinal ganglion cells.

Optic nerve transection in adult rats results in the death of approximately 50% of the axotomized retinal ganglion cells (RGCs) by 1 week and nearly 90% by 2 weeks after injury. The capacity of brain-derived neurotrophic factor (BDNF) to prevent this early, severe loss of RGCs was investigated in vivo by intravitreal injections of BDNF [5 micrograms in 5 microliters of bovine serum albumin/phosphate-buffered saline (BSA/PBS)] or vehicle (5 microliters of BSA/PBS). Using quantitative anatomical techniques, we show that (i) all RGCs survived 1 week after a single injection of BDNF at the time of axotomy. (ii) RGC densities decreased in the BDNF-treated retinas by 2 weeks but remained significantly greater than in the untreated controls. (iii) An enhanced RGC survival was obtained with single injections of BDNF from 6 days before to 5 days after axotomy. (iv) Repeated injections resulted in greater numbers of surviving RGCs, an effect that declined to undetectable levels by 6 weeks. (v) There were indications for an endogenous local source of trophic support whose expression was triggered by ocular injury, particularly to the anterior part of the eye. (vi) With multiple BDNF injections, there was profuse axonal sprouting around the optic disc. This remarkable intraretinal growth was not, however, reflected in increased RGC innervation of the peripheral nerve grafts, which are known to facilitate regeneration when used as optic nerve substitutes.

Animals↗
PubMed1994

Repeat operations in failed microvascular decompression for trigeminal neuralgia.

For the study of pathogenesis and treatment of recurrent trigeminal neuralgia, we performed 31 repeat operations from among 400 patients with trigeminal neuralgia in the past 10 years. Initially, of these 400 patients, 376 underwent microvascular decompression only, and 24 underwent partial sensory rhizotomy with or without microvascular decompression. Fifty-three patients (14%) had recurrences after microvascular decompression, of which 31 patients underwent repeat operations. Among the repeat operations, there was negative exploration in 16 patients (52%), arterial loop compression in 7 (22%), venous compression in 4 (13%), and Teflon compression or adhesion in 4 (13%). Twenty-one patients had early recurrences within 1 year, and 10 patients had late recurrences. Negative exploration and arterial compression were more likely in early recurrence (P = 0.01). Continuing demyelination might occur in patients with negative exploration, even when adequate decompression had been initially performed. Seventy percent of the patients had no recurring pain by way of partial sensory rhizotomy for negative explorations, redecompression of arterial loops, division of offending veins, or lysis and reposition of Teflon. About half of the patients had positive findings that were amenable without rhizotomy in the repeat operations. A repeat operation for failed microvascular decompression is a good choice if the condition of the patient is tolerant.

Arteries↗
PubMed1994

Subependymal giant cell astrocytoma with tuberous sclerosis--case report.

Tuberous sclerosis is a rare disease of autosomal dominant inheritance and may affect any organ, and less than 2% have a subependymal giant cell astrocytoma. In the present report, a 6-year-old girl with clinical features of tuberous sclerosis had an intraventricular tumor. CT scan and MRI of brain showed a tumor in the lateral ventricles extended into the Foramina of Monro and third ventricle causing severe hydrocephalus. She underwent left frontal craniotomy with partial removal of the tumor. The pathology was subependymal giant cell astrocytoma. Patient's neurological condition improved postoperatively and postoperative CT scan showed no hydrocephalus. Clinical and radiological follow-up of patients with tuberous sclerosis who had subependymal nodules in early childhood is important due to its possibility of subsequent transformation into intraventricular tumor.

Cerebral Ventricle Neoplasms↗
PubMed1994

[Effect of a leukotriene antagonist, ONO-1078, on electric stimulation of vagus (ESV)-induced bronchoconstriction and microvascular leakage in guinea pigs].

In atropine-pretreated guinea pigs, electric stimulation of vagus (ESV, 10 Hz, 5 ms, 2 V or 10 V, for 90 s) increased intrapulmonary pressure (IPP), and Evans blue extravasation in trachea, main bronchi, peripheral and distal intrapulmonary airways in a voltage-dependent manner. ONO-1078, a noval leukotriene antagonist, (0.03 and 0.1 mg.kg-1, iv) showed no remarkable inhibiting effect on ESV-induced increase of IPP. However, the agent significantly inhibited ESV-induced increase of Evans blue extravasation in the airways, especially in lower potency of stimulation (2 V). The results suggest that leukotrienes may be involved in airway microvascular leakage in response to neurogenic inflammation.

Airway Resistance↗
PubMed1994

Axotomy results in delayed death and apoptosis of retinal ganglion cells in adult rats.

Using quantitative anatomical techniques, we show that after intraorbital optic nerve transection in adult rats, virtually all retinal ganglion cells (RGCs) survive for 5 d and then die abruptly in large numbers, reducing the RGC population to approximately 50% of normal by day 7 and to less than 10% on day 14. During this period of rapid cell loss, some RGCs show cytochemical alterations indicative of apoptosis ("programmed cell death"), a change not previously categorized after axotomy in adult mammals. With intracranial lesions 8-9 mm from the eye, the onset of cell death is delayed until day 8 and is greater with cut than crush. The demonstration that axotomy results in apoptosis, the long interval between axonal injury and RGC death, and the different time of onset of the massive RGC loss with optic nerve lesions near or far from the eye suggest that axonal interruption triggers a cascade of molecular events whose outcome may be critically dependent on the availability of neuronal trophic support from endogenous or exogenous sources. The role of such molecules in RGC survival and the reversible nature of these injury-induced changes is underscored by the temporary rescue of most RGCs by a single intravitreal injection of brain-derived neurotrophic factor during the first 5 d after intraorbital optic nerve injury (Mansour-Robaey et al., 1994). The delayed pattern of RGC loss observed in the present experiments likely explains such a critical period for effective neurotrophin administration.

Animals↗
PubMed1994

Bromocriptine treatment of postoperative prolactinoma patients.

BACKGROUND: Prolactinoma is the leading cause of pituitary adenoma. It causes amenorrhea in women and impotence in men. Surgical and bromocriptine treatment are the mainstays of therapy in most of the patients with this disease. Determining the outcome for postoperative hyperprolactinemia patients who received bromocriptine treatment was the main purpose of this study. METHODS: Thirty-two patients who received operation for prolactinoma have been investigated. Twenty of them had received bromocriptine treatment before conception, 14 were diagnosed as having macroadenoma and all of them had post-operative hyperprolactinemia. RESULTS: Five patients needed bromocriptine treatment of more than 12.5mg/day to decrease the serum prolactin level. Three patients received radiotherapy postoperatively. Other patients were bromocriptine sensitive. Eight of them had menses restored, and of these, five became pregnant. CONCLUSIONS: Operation can successfully treat most of the patients with microadenoma. If there has postoperative hyperprolactinemia, bromocriptine treatment should be the first choice before radiotherapy.

Adolescent↗
PubMed1994

[The performances of attention deficit/hyperactivity disorder on neuropsychological tests of children].

The purpose of this study was to investigate the Attention Deficit/Hyperactivity Disorder (ADHD) by neuropsychological tests of children. There were two groups of subjects; one group was 23 ADHD children, the other group was 33 normal children. All of the subjects were 5 to 8 years old (mean = 7.05). The social economic status differences were nonsignificant between the two groups (chi-square = 0.52, p > 0.05). The instruments were WISC-R, Tests of Psycholinguistic Abilities, Diagnostic Arithmetic Test, and Reitan-Indiana Neuropsychological test for yound children. The findings were: (1) For all IQs (verbal, performance, full), the ADHD group was significantly lower than the normal group, and there were 8 (34.8%) ADHD children who were mental retards, 3 (13.0%) ADHD children were borderline mental retards, and there was just one (3.0%) normal child who was a borderline mental retard. (2) For academic abilities (Tests of Psycholinguistic Abilities, and Diagnostic Arithmetic Tests), the ADHD group was significantly (p < 0.05) lower than the normal group, and the higher the grade, the larger the difference. (3) For neuropsychological tests, if cut-off points of performance level (0, 1, 2, 3) were percentile 5, 10, and 25 for all of the subjects, then there 12 variable criteria were lower than the Reitan's, 3 variable criteria were higher than the Reitan's, 29 variable criteria were similar with Reitan's, and 8 variables were indiscriminate between individuals. (4) The motor functions and higher cognitive abilities of the ADHD group were worse than those of the normal group.

Attention Deficit Disorder with Hyperactivity↗
PubMed1993

A retinoblastoma-binding protein related to a negative regulator of Ras in yeast.

The growth suppression function of the retinoblastoma protein (Rb) is though to be mediated by Rb binding to cellular proteins. p48 is one of the major proteins that binds to a putative functional domain at the carboxy terminus of the Rb protein. Here we report the isolation of a full-length complementary DNA (RbAp48) encoding p48. Complex formation between p48 and Rb occurs in vitro and in vivo, and apparently involves direct interaction between the proteins. Like Rb, p48 is a ubiquitously expressed nuclear protein. RbAp48 share sequence homology with MSI1, a negative regulator of the Ras-cyclic AMP pathway in the yeast Saccharomyces cerevisiae. Furthermore, like MSI1, human RbAp48 suppresses the heat-shock sensitivity of the yeast ira1 strains and RAS2Val19 strains. Interaction with p48 may be one of the mechanisms for suppression of growth mediated by Rb.

Amino Acid Sequence↗
PubMed1993

Molecular and cytogenetic analyses of autism in Taiwan.

Karyotypic and DNA analyses were both performed on 104 autistic children referred from Taichung Autism Education Academy and Tainan Autism Association in Taiwan. The frequency of fragile sites of the autistic patients did not differ significantly from that of the normal individuals. Of the 12 autistic children with chromosomal abnormalities, 8 had the fragile X, 2 had Down syndrome, and the remaining had other aneuploid constitutions. The results of this study illustrate the contribution of chromosomal abnormalities or variants to the pathogenesis of infantile autism.

Adolescent↗
PubMed1993

Host T-cell primary allosensitization to MHC class-I- and class-II-expressing human cardiac myocytes requires the presence of a second signal.

Normal FHCMs, or transformed cell lines derived from FHCMs, such as W1, even after induction of MHC antigens by pretreatment with IFN-gamma, failed to induce proliferation of allogeneic human PBMCs in vitro. To test the hypothesis that antigen-specific T-cell activation and proliferation require not only the binding of the TCR with its ligand, the MHC molecule, but also a second signal that involves the interaction of T-cell surface molecules with their natural ligands on the stimulating cells, a mAb against CD28 was used. Cocultures of allogeneic PBMCs with IFN-gamma-pretreated irradiated FHCMs or the W1 cell line in microtiter plates containing immobilized anti-CD28 mAb induced marked stimulator cells MHC class-II-specific proliferative responses. The W1 cell line and FHCMs failed to express detectable levels of the BB1/B7 molecule (the natural ligand for CD28) as determined by flow microfluorometry or mRNA levels coding for BB1/B7 as determined by RT-PCR. These data suggest that one of the probably reasons for the failure of MHC-expressing cardiac myocytes to induce allogeneic activation is the absence of costimulatory signals.

Base Sequence↗
PubMed1993

Evidence from mutation spectra that the UV hypermutability of xeroderma pigmentosum variant cells reflects abnormal, error-prone replication on a template containing photoproducts.

Xeroderma pigmentosum (XP) variant patients are genetically predisposed to sunlight-induced skin cancer. Fibroblasts derived from these patients are extremely sensitive to the mutagenic effect of UV radiation and are abnormally slow in replicating DNA containing UV-induced photoproducts. However, unlike cells from the majority of XP patients, XP variant cells have a normal or nearly normal rate of nucleotide excision repair of such damage. To determine whether their UV hypermutability reflected a slower rate of excision of photoproducts specifically during early S phase when the target gene for mutations, i.e., the hypoxanthine (guanine) phosphoribosyltransferase gene (HPRT), is replicated, we synchronized diploid populations of normal and XP variant fibroblasts, irradiated them in early S phase, and compared the rate of loss of cyclobutane pyrimidine dimers and 6-4 pyrimidine-pyrimidones from DNA during S phase. There was no difference. Both removed 94% of the 6-4 pyrimidine-pyrimidones within 8 h and 40% of the dimers within 11 h. There was also no difference between the two cell lines in the rate of repair during G1 phase. To determine whether the hypermutability resulted from abnormal error-prone replication of DNA containing photoproducts, we determined the spectra of mutations induced in the coding region of the HPRT gene of XP variant cells irradiated in early S and G1 phases and compared with those found in normal cells. The majority of the mutations in both types of cells were base substitutions, but the two types of cells differed significantly from each other in the kinds of substitutions, but the two types differed significantly from each other in the kinds of substitutions observed either in mutants from S phase (P < 0.01) or from G1 phase (P = 0.03). In the variant cells, the substitutions were mainly transversions (58% in S, 73% in G1). In the normal cells irradiated in S, the majority of the substitutions were G.C --> A.T, and most involved CC photoproducts in the transcribed strand. In the variant cells irradiated in S, substitutions involving cytosine in the transcribed strand were G.C --> T.A transversions exclusively. G.C --> A.T transitions made up a much smaller fraction of the substitutions than in normal cells (P < 0.02), and all of them involved photoproducts located in the nontranscribed strand. The data strongly suggest that XP variant cells are much less likely than normal cells to incorporate either dAMP or dGMP opposite the pyrimidines involved in photoproducts. This would account for their significantly higher frequency of mutants and might explain their abnormal delay in replicating a UV-damaged template.

Base Sequence↗
PubMed1993

Prevalence of attention deficit hyperactivity disorder in primary school children in Taiwan.

Chinese versions of Conners' Teacher's Rating Scale (CTRS) and the Werry-Weiss-Peters Activity Scale (WWPAS) were applied to 4,290 randomly selected primary school children in Kaohsiung. Using relative operational characteristic analysis to determine the best cut-off points, the validity of the WWPAS and CTRS for estimating the prevalence of attention deficit hyperactivity disorder (ADHD) was established. It was found that CTRS had satisfactory results, but the WWPAS did not have an optimal cut-off score. Using CTRS as a screening tool, the estimated overall prevalence rate of ADHD among Kaohsiung primary school children was found to be 9.9%, while the rate in boys (14.9%) was 3.3 times higher than in girls (4.5%). The assumption that hyperactivity is uncommon among Chinese children was proven to be unreliable.

Attention Deficit Disorder with Hyperactivity↗