Search PubMed⌕ Search

Biomedical subjects

J C Shih

Publications and source records attributed to J C Shih.

At least 37 records · Page 2Linked to original sources
PubMed2001

First-trimester Down's syndrome screening by fetal nuchal translucency measurement in Taiwan.

BACKGROUND: Fetal nuchal translucency (NT) measurement is now widely used in many Western countries as a screening tool for Down's syndrome during the first trimester. However, at present there is no data on its use in Taiwan. The purpose of the present study was to evaluate the efficacy of NT measurement in first-trimester Down's syndrome screening in Taiwan. METHODS: We conducted a prospective study from October 1997 to May 1999. Sonographic measurement of fetal NT was performed in 1,249 fetuses at 9-14 weeks of gestation. Transabdominal ultrasound scanning was performed to obtain a sagittal section of the fetus for measuring the crown-rump length (CRL) and the maximum thickness of the subcutaneous translucency between the skin and the soft tissue overlying the cervical spine. Two different cut-off points were used for screening: a fixed cut-off point of at least 2.5 mm and a CRL-related cut-off point. In the latter method, fetuses with an NT measurement in the 95th percentile were considered at high risk for Down's syndrome. RESULTS: Three fetuses had Down's syndrome, with NT measurements of 2.1 mm, 2.7 mm, and 4.0 mm. The false positive rates for the fixed cut-off point and CRL-related cut-off point were 6.3% and 4.6%, respectively. Both methods had a sensitivity of 66.7%. However, the screening program using the CRL-related cut-off point had two advantages: a higher specificity (95.5% vs 93.8%) and a more reasonable distribution pattern for screening. CONCLUSION: This study showed that NT measurement is a potential screening tool for Down's syndrome during the first trimester in Taiwan. Using CRL-related cut-off points for screening is more reasonable than using a fixed cut-off point.

Adult↗
PubMed2001

In utero progressive pulmonary stenosis successfully treated with transcatheter intervention after delivery.

It is unclear whether pulmonary stenosis with intact ventricular septum is a secondary cardiac malformation. We report an infant with pulmonary stenosis (diagnosed by fetal echocardiography) with progressive obstruction in late gestation who presented with increasing transvalvular pressure gradients (15 mm Hg at 22 weeks' gestation to 47 mm Hg at 35 weeks). The tricuspid/mitral valve annulus ratio decreased from 1.25 at 24 weeks' gestation to 0.96 at 33 weeks. At 38 weeks' gestation, a male infant weighing 3,524 g, with Apgar scores of 9 and 9 at 1 and 5 minutes, respectively, was delivered by cesarean section. Critical pulmonary stenosis was confirmed by postnatal catheterization. These findings support the postulation that pulmonary stenosis is a progressive disorder. After percutaneous balloon dilatation, the transvalvular pressure gradient decreased and the right ventricular cavity increased gradually. The transvalvular pressure gradient had decreased to 15 mm Hg and the tricuspid/mitral valve annulus ratio was 0.93 at the age of 2 years.

Adult↗
PubMed2000

Substrate and inhibitor specificities for human monoamine oxidase A and B are influenced by a single amino acid.

Monoamine oxidase (MAO) is responsible for the oxidation of biogenic and dietary amines. It exists as two isoforms, A and B, which have a 70% amino acid identity and different substrate and inhibitor specificities. This study reports the identification of residues responsible for conferring this specificity in human MAO A and B. Using site-directed mutagenesis we reciprocally interchanged three pairs of corresponding nonconserved amino acids within the central portion of human MAO. Mutant MAO A-I335Y became like MAO B, which exhibits a higher preference for beta-phenylethylamine than for the MAO A preferred substrate serotonin (5-hydroxytryptamine), and became more sensitive to deprenyl (MAO B-specific inhibitor) than to clorgyline (MAO A-specific inhibitor). The reciprocal mutant MAO B-Y326I exhibited an increased preference for 5-hydroxytryptamine, a decreased preference for beta-phenylethylamine, and, similar to MAO A, was more sensitive to clorgyline than to deprenyl. These mutants also showed a distinct shift in sensitivity for the MAO A- and B-selective inhibitors Ro 41-1049 and Ro 16-6491. Mutant pair MAO A-T245I and MAO B-I236T and mutant pair MAO A-D328G and MAO B-G319D reduced catalytic activity but did not alter specificity. Our results indicate that Ile-335 in MAO A and Tyr-326 in MAO B play a critical role in determining substrate and inhibitor specificities in human MAO A and B.

Amino Acid Sequence↗
PubMed2000

Current awareness in prenatal diagnosis.

In order to keep subscribers up-to-date with the latest developments in their field, John Wiley & Sons are providing a current awareness service in each issue of the journal. The bibliography contains newly published material in the field of prenatal diagnosis. Each bibliography is divided into 17 sections: 1 Books, Reviews & Symposia; 2 General Interest; 3 Normal Fetal Development; 4 Gametogenesis and Pre-implantation Diagnosis; 5 First Trimester Diagnosis; 6 Second Trimester Diagnosis; 7 Fetal Diagnosis by Ultrasound and Other Imaging; 8 Maternal Screening; 9 Screening for Carriers of Genetic Abnormality; 10 Technological Developments; 11 Confined Placental Mosaicism and Uniparental Disomy; 12 Molecular Cytogenetics; 13 Fetal Cells in Maternal Circulation; 14 Fetal Therapy; 15 Psychosocial Aspects; 16 Epidemiology and Environmental Factors; 17 Developmental Pathology. Within each section, articles are listed in alphabetical order with respect to author. If, in the preceding period, no publications are located relevant to any one of these headings, that section will be omitted.

Humans↗
PubMed2000

Regional cerebral cortical activation in monoamine oxidase A-deficient mice: differential effects of chronic versus acute elevations in serotonin and norepinephrine.

Mice deficient in monoamine oxidase A have previously been shown to demonstrate a chronic elevation of serotonin and norepinephrine in the brain. Using the autoradiographic [14C]iodo-antipyrine method, we examined cerebral cortical blood flow in conscious, restrained four- to five-month-old knock-out and wild-type animals following the intraperitoneal administration of either saline or D-fenfluramine. Knock-out animals administered saline, compared to their wild-type counterparts, demonstrated a significantly higher regional cortical blood flow in somatosensory and barrel field neocortex, an area which previous histological studies have shown to be characterized by abnormal serotonergic projection fibers and absent barrel formation. Regional cortical blood flow was significantly lower in knock-out than in wild-type mice in the entorhinal and midline motor cortex, with non-significant decreases noted in the olfactory, piriform and retrosplenial cortices and the amygdala. We compared the above findings to those obtained in response to D-fenfluramine which, in conjunction with its metabolite D-norfenfluramine, results in acute elevations of brain levels of serotonin and norepinephrine. Administration of D-fenfluramine (21. 2mg/kg) resulted in changes in regional cortical perfusion in most brain regions of both knock-out and wild-type mice that were opposite to the genotypic differences seen in perfusion in response to saline. Fenfluramine significantly increased regional cortical blood flow in the allocortex (olfactory, piriform, entorhinal) and the amygdala, and significantly decreased regional cortical blood flow in the somatosensory, barrel field, midline motor and retrosplenial cortices. Changes in regional perfusion in response to fenfluramine were topographically equivalent in knock-out and wild-type mice, although in knock-out mice such changes were of greater magnitude. Our study suggests that the effects on regional cortical blood flow of a lifelong absence of monoamine oxidase A, and the consequent chronic increase in serotonin and norepinephrine, differ from those attributable to acute increases in these neurotransmitters following fenfluramine administration. Such a differential response may reflect neurodevelopmental abnormalities and/or effects of a chronic physiological adaptation on the regulation of cortical activation.

Animals↗
PubMed2000

Prenatal depiction of angioarchitecture of an aneurysm of the vein of Galen with three-dimensional color power angiography.

A fetus with a large supratentorial cyst and cardiomegaly was encountered at 33 weeks of gestation. The cyst appeared as an aneurysmal, fluid-filled structure extending posteriorly with a finger-like appendage. Using color flow mapping, we disclosed rapid in-and-out blood flow with marked turbulence within the cyst. For evaluation of its blood supply and venous drainage of the vascular malformation, a three-dimensional reconstruction of the power Doppler image was conducted. The results revealed that the vascular malformation was supplied by a small contralateral aneurysm from the branches of Willis' circle, draining posteriorly into an abnormal falcine sinus and then into the superior sagittal sinus. No other fetal abnormality such as hydrocephalus or hydrops was discovered. The prenatal diagnosis of an aneurysm of the vein of Galen was made on the basis of the gray-scale, color Doppler findings, and also the angioarchitecture obtained by three-dimensional power Doppler imaging. The woman was admitted at 37 weeks of gestation due to labor onset and delivered the baby via the vaginal route without complication. Postnatal angiography and magnetic resonance imaging confirmed the diagnosis of an aneurysm of the vein of Galen, and the angioarchitecture depicted it before birth. We suggest that three-dimensional power Doppler ultrasonography may assist in the diagnosis of an aneurysm of the vein of Galen, and precisely delineate the complicated corresponding vasculature. This may guide postnatal management and predict the prognosis more accurately.

Adult↗
PubMed2000

Antenatal diagnosis of congenital hepatoblastoma in utero.

A fetus with a huge hepatic tumor was detected by sonography at 36 weeks of gestation. The mass appeared as a single, solid and polylobular tumor located in the right lobe of the liver. Foci of hemorrhage, necrosis and some tiny calcifications were seen. The adjacent right kidney appeared normal but was displaced. The right adrenal gland was not visualized. Three-dimensional power Doppler sonography further depicted the corresponding vascular anatomy of the tumor, including its vascularization pattern and blood supply. The tumor was situated to the right of the umbilical vein and portal sinus, possibly deriving its blood supply from the portal circulation. The fundamental findings suggested the diagnosis of hepatoblastoma by exclusion of other possibilities. The baby was delivered by Cesarean section at 36 weeks' gestation, due to signs of fetal distress. Unfortunately, hypotension, tachycardia, and tachypnea developed shortly after birth. Surgical intervention was performed, but intractable bleeding occurred intra-operatively. The infant died at 6 days of age. Autopsy confirmed the diagnosis of hepatoblastoma. We believe this is the first reported case of the antenatal diagnosis of congenital hepatoblastoma.

Adult↗
PubMed2000

Phe(208) and Ile(199) in human monoamine oxidase A and B do not determine substrate and inhibitor specificities as in rat.

It has been reported previously that reciprocally switching Phe(208) and Ile(199) in rat monoamine oxidase (MAO) A and B, respectively, was sufficient to switch their substrate and inhibitor preferences. In this study, the same mutants were made in the human forms of MAO. When compared with MAO A, MAO A-F208I showed a sixfold decrease in the specificity constant k(cat)/K(m) for both the MAO A- and the MAO B-preferring substrates 5-hydroxytryptamine and beta-phenylethylamine, respectively. The reciprocal point mutant MAO B-I199F had no effect on substrate affinity. To investigate if the region neighboring these two residues is responsible for conferring preferences, we have also made chimeric constructs by reciprocally switching the corresponding amino acid segments 159-214 in MAO A and 150-205 in MAO B. Chimerics MAO AB(159-214)A and MAO BA(150-205)B had small changes in K(m) and IC(50) values when compared with MAO A and B, respectively, but did not exhibit a preference switch. The results suggest that Phe(208) in MAO A and amino acid segments 159-214 and 150-205 in MAO A and B, respectively, influence the enzyme active site. However, substrate and inhibitor preferences of human MAO A and B are not determined by the respective residues Phe(108) and Ile(199) as in rat MAO nor by their neighboring regions.

Animals↗
PubMed2000

Ginkgo biloba abolishes aggression in mice lacking MAO A.

Mice deficient in monoamine oxidase A (MAO A) have increased brain levels of serotonin (5-HT) and norepinephrine and show enhanced aggression. We used MAO A knock-out (KO) mice as a model to study the effect of ginkgo biloba (EGb) on aggression. When EGb was administered to MAO A KO mice, their aggressive behavior in resident-intruder confrontations was reduced to levels seen in wild types. EGb did not affect the locomotive behavior of MAO A KO mice, which suggests that its effects on aggression were not due to sedation. EGb caused a significant 16.9% decrease in [3H]ketanserin binding to 5-HT2A receptors in the frontal cortex of MAO A KO mice but did not change the receptor affinity for [3H]ketanserin. This suggests that the antiaggressive effect of EGb may be mediated by 5-HT2A receptors and that EGb may be developed as a novel antiaggressive agent.

Aggression↗
PubMed2000

Analysis of the pharmacological and molecular heterogeneity of I(2)-imidazoline-binding proteins using monoamine oxidase-deficient mouse models.

The I(2) subgroup of imidazoline-binding sites was identified as monoamine oxidases (MAOs), but it is unclear whether there are I(2)-binding sites located on proteins distinct from MAOs. To address this issue, we characterized I(2)-binding proteins in liver and brain of wild-type and MAO A- and MAO B-deficient mice. I(2)-binding sites were identified using [(3)H]idazoxan and the photoaffinity adduct 2-[3-azido-4-[(125)I]iodophenoxyl]methylimidazoline ([(125)I]AZIPI). [(3)H]Idazoxan labeled binding sites with ligand recognition properties typical of I(2) sites in both brain and liver of wild-type mice. High-affinity, specific [(3)H]idazoxan binding were not altered in MAO A knockout (KO) mice. In contrast, [(3)H]idazoxan binding was completely abolished in both liver and brain of MAO B KO mice. In wild-type mice, [(125)I]AZIPI photolabeled three proteins with apparent molecular masses of approximately 28 (liver), approximately 61 (brain), and approximately 55 kDa (liver and brain). The photolabeling of each protein was blocked by the imidazoline cirazoline (10 microM). Photolabeling of the approximately 61- and approximately 55-kDa proteins was not observed in MAO A and B KO mice, respectively. In contrast, photolabeling of the liver approximately 28-kDa protein was still observed in MAO-deficient mice, indicating that this protein is unrelated to MAOs. These data indicate that I(2) imidazoline-binding sites identified by [(3)H]idazoxan reside solely on MAO B. The binding sites on MAO A and the liver approximately 28-kDa protein may represent additional subtypes of the family of the imidazoline-binding sites.

Adrenergic alpha-Antagonists↗
PubMed2000

Yang-Gan-Wan protects mice against experimental liver damage.

The hepatoprotective effect of Yang-Gan-Wan (YGW, Pro-Liver pill), a Chinese herbal remedy, was investigated in mice that were treated with allyl alcohol (AlOH), acetaminophen (AA) or carbon tetrachloride (CCl4). Mice were pretreated daily with 200 mg/kg YGW for 10, 14 and 18 days before treatment with 85 mg/kg AlOH, 475 mg/kg AA or 20 microl/kg CCl4, respectively. YGW dramatically abolished the elevated activities of alanine aminotransferase (ALT) and sorbitol dehydrogenase (SDH) and reduced the necrosis induced by AlOH. YGW also decreased the elevated activities of ALT and SDH and reduced the necrosis induced by AA and CCl4. This study demonstrates that YGW has protective effects against liver damage induced by AlOH, AA, and CCl4.

Acetaminophen↗
PubMed2000

Yang-gan-wan protects mice against apoptosis induced by anti-Fas antibody (Jo2).

We investigated the protective effect of yang-gan-wan (YGW, Pro-Liver pill), a Chinese herbal remedy, against liver apoptosis (programmed cell death) induced by anti-Fas antibody (Jo2). Mice were pretreated daily with 200 mg/kg YGW for 14 days before treatment with 10 microg/20 kg body weight Jo2. YGW significantly reduced the elevated activity of alanine aminotransferase (ALT) and also reduced the elevated activity of sorbitol dehydrogenase (SDH) produced 4 hrs after treatment with Jo2. YGW also increased the survival of mice treated with Jo2 by about 1 hr in 11 out of 16 mice (69%). Most of the mice died 9 hrs after Jo2 injection. This study demonstrates that YGW has protective effects against liver apoptosis induced by Jo2.

Alanine Transaminase↗
PubMed1999

Ketanserin and tetrabenazine abolish aggression in mice lacking monoamine oxidase A.

Mice deficient in monoamine oxidase A (MAO A) have elevated brain levels of 5-HT and manifest enhanced aggression. We used these mice as a model to study the role of 5-HT in aggression. Our results show that ketanserin and tetrabenazine (TBZ) strikingly abolished the aggressive behavior of MAO A-deficient mice. The anti-aggressive effect of ketanserin may be primarily mediated by 5-HT(2A) receptors. Another specific 5-HT(2A) antagonist, [R-(+)-a-(2, 3-dimethoxyphenyl)-1-[2-(4-fluorophenylethyl)]-4-piperidine-methan ol (MDL 100907), also blocks the aggression of mutant mice but was less dramatic. Ketanserin and TBZ are both antagonists of the vesicular monoamine transporter (VMAT2). The anti-aggressive effect of TBZ and part of the effect of ketanserin may be mediated by the VMAT2. Using radioligand binding and autoradiography, we also showed that the numbers of VMAT2, 5-HT(1A), 5-HT(2A) and 5-HT(2C) sites are decreased in brains of mutant mice, which may reflect down-regulation by excess 5-HT. This study suggests that ketanserin and TBZ may be developed as novel anti-aggressive agents.

Adrenergic Uptake Inhibitors↗