Biomedical subjects

Y F Chen

Publications and source records attributed to Y F Chen.

At least 145 records · Page 8Linked to original sources

PubMed1997

Abdominal fluid collection secondary to acute pancreatitis: treated with percutaneous catheter drainage.

BACKGROUND: Complicated pancreatic inflammatory diseases are often life-threatening, multifocal, and multibacterial disorders. Untreated, these lesions often prove fatal. The purpose of the study is to describe interventional radiologic techniques for diagnosis and treatment of complicated peripancreatic fluid collections. METHODS: Between January 1994 and December 1995, 17 patients with abdominal fluid collection from complicated acute pancreatitis underwent percutaneous drainage following initial diagnosis with computed tomography (CT). These patients required multiple CT examinations, multiple catheter insertions, multiple catheter manipulations, and long-term catheter drainage. RESULTS: Twenty-five infected fluid collections among these 17 patients were percutaneously drained. Sixteen (94%) patients were successfully treated with catheter drainage alone. Surgical treatment was necessary in one patient because of segmental stricture of transverse colon caused by inflammation and adhesion of transverse mesocolon. Catheter drainage duration averaged 31 days. Patients required an average of three catheter manipulations and four abdominal CT scans. Mean hospital stay was 42 days (range, 11-95 days), and mean ICU stay was 25 days (range, 1-70 days). CONCLUSIONS: The study confirms that complicated peripancreatic fluid collections can be safely and effectively treated in most patients with percutaneous catheter technique.

Abscess↗

PubMed1996

Medroxyprogesterone attenuates estrogen-mediated inhibition of neointima formation after balloon injury of the rat carotid artery.

BACKGROUND: Estrogen blunts the neointimal proliferative response to balloon injury of the carotid artery in intact female rats and gonadectomized rats of both sexes. This study tested whether, in gonadectomized rats of both sexes. (1) progestin (medroxyprogesterone acetate, MPA) alters neointima formation in injured carotid arteries, (2) addition of MPA alters the antiproliferative effects of estrogen, and (3) an interaction between MPA and estrogen can be accounted for by MPA-induced alterations in serum 17 beta-estradiol levels. METHODS AND RESULTS: Male and female Sprague-Dawley rats were subjected to gonadectomy, then were randomly divided into four subgroups and treated with either (1) 17 beta-estradiol, (2) MPA, (3) 17 beta-estradiol + MPA, or (4) vehicle, and balloon injury of the right common carotid artery was carried out. Two weeks later, rats were killed by overdose of pentobarbital, and the carotid arteries were subjected to morphometric analysis for evaluation of myointimal thickening. Estradiol inhibited myointimal proliferation after vascular injury in gonadectomized rats of both sexes (P < .05). MPA alone did not alter neointima formation, but addition of MPA to estradiol completely blocked the antiproliferative effects of estrogen without altering serum 17 beta-estradiol levels. CONCLUSIONS: These data indicate that exogenous progestin given alone does not alter the vascular injury response in the rat carotid injury model but that addition of a progestin blocks the antiproliferative effects of estrogen in this model. These effects are seen in gonadectomized rats of both sexes. These findings have direct implications for postmenopausal hormone replacement therapy in humans.

Animals↗

PubMed1996

Estrogen reduces myointimal proliferation after balloon injury of rat carotid artery.

BACKGROUND: Vascular disease progresses more slowly in females with functional ovaries than in males. The mechanisms of this vasoprotective effect of female sex are incompletely understood. This study tested (1) whether there is a sex difference in the development of myointimal proliferation after balloon injury of the rat carotid artery in vivo, (2) whether this response is estrogen or androgen dependent, and (3) whether there is a sexual dimorphism in expression of the c-myc proto-oncogene in intact and/or damaged rat carotid arteries. METHODS AND RESULTS: Ten-week-old male and female Sprague-Dawley rats were either gonadectomized or studied intact. Gonadectomized rats of both sexes were implanted with estradiol, testosterone, or nothing (control) 3 days before vascular injury. Two weeks later, the rats were killed by overdose of pentobarbital, and the injured right and uninjured control left carotid arteries were fixed and subjected to morphometric analysis for evaluation of the degree of myointimal thickening. Separate groups of intact male and female rats were killed at 1 and 2 hours after vascular injury, and total RNA from injured and uninjured vessels was subjected to Northern blot analysis for assessment of steady state c-myc mRNA levels. Neointimal area and the ratio of neointimal to medial area were significantly less in intact female rats than in intact male rats (P < .05). Gonadectomy of female rats was associated with a greater increase in neointima formation after balloon injury than that observed in intact females (P < .05), but testosterone replacement did not further enhance this response. Estradiol treatment significantly inhibited myointimal proliferation after vascular injury in gonadectomized rats of both sexes (P < .05). Neither gonadectomy nor gonadectomy plus testosterone replacement altered the myointimal proliferative response to balloon injury in male rats. Steady state c-myc mRNA levels were detectable in undamaged carotid arteries in intact rats of both sexes and were significantly greater in males than in females; c-myc mRNA levels were increased in both sexes after carotid injury, but the response was significantly larger in magnitude and more rapid in males than in females. CONCLUSIONS: These data indicate that the sex difference in myointimal proliferation after vascular injury is estrogen dependent. C-myc gene expression is greater in the undamaged carotid artery of the male than in that of the female, and the responsiveness of this gene to balloon injury of the artery is more rapid and more robust in the male than in the female rat. These findings have direct implications for the prevention and treatment of vascular disease in humans.

Animals↗

PubMed1996

Anterior hypothalamic norepinephrine, atrial natriuretic peptide, and hypertension.

Our laboratory has characterized a model of salt sensitive hypertension, the salt sensitive spontaneously hypertensive rat (SHR-S), in which dietary NaCl supplementation increases blood pressure by reducing norepinephrine release by nerve terminals in the anterior hypothalamic area (AHA), thus reducing activation of sympathoinhibitory neurons in the AHA. This, in turn, results in increased sympathetic outflow and higher blood pressure in the SHR. Two mechanisms have been shown to contribute to this effect: (i) reduced noradrenergic input into AHA via baroreflex pathways and (ii) local inhibition of NE release in AHA by the inhibitory neuromodulator atrial natriuretic peptide (ANP). Studies employing microinjection of a blocking monoclonal antibody to ANP directly into the AHA and the nucleus tractus solitarius (NTS) demonstrated for the first time that endogenous ANP in the brain is functionally active in the tonic control of blood pressure and baroreflex sensitivity in the SHR-S but plays a lesser role in the normotensive Wistar Kyoto (WKY) control. In the WKY, excitation of NTS neurons by baroreflex afferents leads to activation of sympathoinhibitory neurons in NTS and AHA, strong inhibition of sympathetic nervous system outflow, and a decrease in arterial pressure. In SHR-S, brain ANP acts at the levels of the NTS and the AHA to perturb this baroreflex regulatory pathway. ANP tonically activates sympathoinhibitory neurons in the caudal NTS of SHR-S, thereby restraining the rise in arterial pressure, and tonically inhibits baroreflex responsiveness to alterations in blood pressure. Thus ANP appears to act at a number of sites in brain to facilitate the development and maintenance of sympathetically mediated hypertension in the SHR-S model.

Animals↗

PubMed1996

Giant aneurysm of main pulmonary artery.

Aneurysm of the main pulmonary artery is an extremely rare entity. The first successful repair of an aneurysm of the main pulmonary artery was reported in 1971. Since then, surgical correction of the aneurysm of main pulmonary artery has been undertaken in only 6 cases. A thorough survey of the literature, including autopsy cases, medical cases, and surgical cases, shows the aneurysm in the present case to be one of the largest.

Aneurysm↗

PubMed1996

Sexual dimorphism of hypertension.

A sexually dimorphic pattern of blood pressure, in which the male develops higher blood pressure than the age-matched female, has been observed both in human subjects and in laboratory animals. The mechanism(s) of this sexual dimorphism of blood pressure are not completely understood. This review summarizes sex differences in the epidemiology of hypertension in humans, the role of gonadal steroid hormones in the regulation of blood pressure of normotensive and hypertensive laboratory animals, and new insights into the molecular basis of the sexual dimorphism of hypertension and hypertensive vascular disease.

Animals↗

PubMed1996

Atrial natriuretic peptide blunts arterial baroreflex in spontaneously hypertensive rats.

We and other laboratories have reported that arterial baroreflex-mediated control of heart rate is blunted in spontaneously hypertensive rats (SHR) compared with normotensive controls. Recently, we reported that atrial natriuretic peptide (ANP) microinjected into the caudal nucleus tractus solitarii of SHR further blunts this defect. The present study tested the hypothesis that ANP modulates arterial baroreflex-mediated control of sympathetic nervous system activity. Nine-week-old, male SHR (n = 29) and normotensive Wistar-Kyoto control rats (n = 24) were instrumented for microinjection into the caudal nucleus tractus solitarii and for direct measurement of arterial blood pressure, heart rate, and lumbar sympathetic nervous system activity. After urethane- and alpha-chloralose-induced induced anesthesia, arterial baroreflex-mediated control of heart rate and lumbar sympathetic nerve activity was assessed during phenylephrine- (5 to 40 micrograms.kg-1.min-1) induced increases and sodium nitroprusside- (15 to 300 micrograms.kg-1.min-1) induced decreases in mean blood pressure before and after microinjection of ANP (50 ng) or monoclonal antibody to ANP (0.55 micrograms) into the caudal nucleus tractus solitarii. ANP reduced and the antibody enhanced the sensitivity of baroreflex-mediated control of both heart rate and lumbar sympathetic nerve activity in SHR but not in Wistar-Kyoto controls (P < .05). Arterial baroreflex sensitivity was unchanged with control microinjections of vehicle or mouse IgG in SHR. These data suggest that endogenous ANP in the caudal nucleus tractus solitarii may contribute to the development and/or maintenance of hypertension in SHR by blunting baroreflex-mediated control of sympathetic nervous system activity.

Animals↗

PubMed1996

Surgical correction of giant patent ductus arteriosus.

In reviewing the literature, there was only one report having the ductus over 30 mm in width. Recently, we utilized cardiopulmonary bypass, hypothermia, and low flow through a transpulmonary approach to close 2 cases of giant patent ductus arteriosus. Both cases complicated with systemic pulmonary hypertension. Its outside diameters were 31 mm and 36 mm respectively based on the measurement from magnetic resonance imaging. To our knowledge, its seem the biggest ductus in comparison to previous reports. Both cases survived the operation and doing well for a follow-up time of 5 years and 4 years 10 months respectively.

Adolescent↗

PubMed1996

Prevalence of dementia in an urban area in taiwan.

This two-stage epidemiologic study was to investigate the prevalence and types of dementia among elderly people in the Saa-Min district of Kaohsiung City in Taiwan. In stage one, the Chinese Mini-Mental Status Examination (CMMSE) and Blessed Dementia Rating Scale were employed. In stage two, a comprehensive neurobehavioral examination and neuropsychologic tests were administered by neurologists and neuropsychologists. Dementia was defined by DSM-III-R criteria. The National Institute of Neurological and Communication Disorders and Stroke-Alzheimer's Disease and Related Disorders Association guidelines for Alzheimer's disease (AD) and the National Institute of Neurological Disorder and Stroke-Association international pour la Recherche et l'Enseignement en Neurosciences criteria for vascular dementia (VaD) were applied. A total of 1,016 randomly selected elderly people participated in phase one: 131 people with CMMSE below cutoff values participated in phase two, of whom 45 were confirmed to have a form of dementia. The prevalence of dementia in this sample was 4.4% (3.2% in men and 5.8% in women): 2.0% for those 65 to 74 years old, 8.3% for those 75 to 84 and 24.4% for those > or = 85 years old; 6.0% for those who were illiterate, 3.3% for those who attended grade-school; and 2.8% for those who finished junior-high-school. AD (22 cases, 48.9%) was the most common cause of dementia, followed by VaD (11 cases, 24.4%) and mixed dementia (MIX: 5 cases, 11.1%). Old age and being female were significant high risk factors for AD. Medical history indicated that stroke and hypertension were significant risk factors for VaD. A relatively high prevalence of dementia was observed in this study, probably because we assessed neurobehavior in great detail. Although AD was the leading cause of dementia in the present population sample. VaD and MIX also comprised an important proportion, reflecting the high prevalence of stroke in Taiwan. Older women had high risk for AD, not for VaD; and those with a history of stroke and hypertension had high risk for VaD, not for AD.

Aged↗

PubMed1995

The Bacillus subtilis flagellar regulatory protein sigma D: overproduction, domain analysis and DNA-binding properties.

Flagellar biosynthesis requires an alternative sigma (sigma) subunit of RNA polymerase to allow recognition of the promoters for flagellin and other late genes of the flagellar regulon. We have now overproduced and characterized Bacillus subtilis sigma D: the prototype of the sigma 28 family of flagellar sigma factors. Limited protease digestion studies indicate that sigma D contains an amino-terminal domain, comprising conserved regions 1.2 and 2, and a carboxyl-terminal domain containing conserved regions 3.2 and 4. The protease-sensitive region between these two domains correlates with a region of very low sequence conservation among bacterial sigma factors. Unlike the primary sigma factor, sigma D binds to DNA. In non-denaturing polyacrylamide gel electrophoresis the sigma D-DNA complex has an apparent equilibrium dissociation constant of 1 microM. Binding of sigma D to the promoter for flagellin, PD-6, appears to lead to an altered DNA structure near the -35 and -10 recognition elements as detected by DNase I footprinting and by the enhanced reactivity of several bases to dimethylsulfate.

Amino Acid Sequence↗

PubMed1995

Promoter architecture in the flagellar regulon of Bacillus subtilis: high-level expression of flagellin by the sigma D RNA polymerase requires an upstream promoter element.

Flagellin is one of the most abundant proteins in motile bacteria, yet its expression requires a low abundance sigma factor (sigma 28). We show that transcription from the Bacillus subtilis flagellin promoter is stimulated 20-fold by an upstream A+T-rich region [upstream promoter (UP) element] both in vivo and in vitro. This UP element is contacted by sigma 28 holoenzyme bound at the flagellin promoter and binds the isolated alpha 2 subassembly of RNA polymerase. The UP element increases the affinity of RNA polymerase for the flagellin promoter and stimulates transcription when initiation is limited by the rate of RNA polymerase binding. Comparison with other promoters in the flagellar regulon reveals a bipartite architecture: the -35 and -10 elements confer specificity for sigma 28, while promoter strength is determined largely by upstream DNA sequences.

Bacillus subtilis↗

PubMed1995

Effect of nickel addition on microstructure and properties of Ti-Co-Ni alloys.

The focus of this study was placed on the effect of nickel addition (5 wt%) on the microstructure, castability, biocorrosion resistance and some other properties of a series of cast high-cobalt (up to 25 wt%) Ti-Co-Ni alloys. Results indicated that melting temperatures of the present alloys were much lower than the melting temperature of pure titanium. Addition of 5 wt% Ni to replace an equivalent amount of Co slightly lowered the eutectoid and melting temperatures. Castability of the alloys was enhanced by the high alloy content and higher mould temperature. Substitution of 5 wt% Ni for Co increased the castability values. The phase transformation of beta-Ti to alpha-Ti was enhanced by nickel addition and higher mould temperature. Microhardness of the alloys increased with cobalt content and decreased with mould temperature. The addition of nickel lowered the hardness of the alloys. Breakdown potentials of the alloys were all higher than 900 mV and the critical anodic current densities were all lower than 8 microA cm-2.

Alloys↗

PubMed1995

Anti-inflammatory and analgesic activities from roots of Angelica pubescens.

In the present study, we extracted Angelica pubescens (AP) with various solvents in order to find the bioactive constituents that demonstrated analgesic and anti-inflammatory effects. The results were obtained as follows: (1) Methanol-, chloroform-, and ethyl acetate-extracts effectively reduced the pain that was induced by 1% acetic acid and a hot plate. (2) Methanol-, chloroform-, and ethyl acetate-extracts reduced the edema that was induced by 3% formalin or 1.5% carrageenan. (3) Sixteen compounds have been isolated and identified from the roots of AP. Among these compounds, columbianadin, columbianetin acetate, bergapten, umbelliferone, and caffeic acid significantly demonstrated anti-inflammatory and analgesic activities at 10 mg/kg. However, only osthole and xanthotoxin revealed anti-inflammatory activity. Isoimperatorin only demonstrated an analgesic effect. These results revealed that the anti-inflammatory and analgesic constituents from roots of AP were related to peripheral inhibition of inflammatory substances and to the influence on the central nervous system.

Analgesics↗

PubMed1995

Endothelin-A receptor antagonist prevents acute hypoxia-induced pulmonary hypertension in the rat.

Exposure to hypoxia is associated with increased pulmonary artery pressure and plasma endothelin-1 (ET-1) levels and with selective enhancement in ET-1 peptide and mRNA and endothelin-A (ETA) receptor mRNA levels in rat lung. The current study tested the hypothesis that endogenous ET-1 can account for hypoxia-induced pulmonary hypertension via a paracrine effect on ETA receptors in lung. Intravenous infusion of the ETA receptor antagonist BQ-123 (D-Trp-D-Asp-Pro-D-Val-Leu) (0.4 mg/microliters at 1 microliter/h) into Sprague-Dawley rats beginning 4 h before and for 90 min during normobaric hypoxia (10% O2) markedly attenuated the hypoxic response: mean pulmonary artery pressure increased from 17.2 +/- 0.7 to 29.0 +/- 1.2 mmHg in saline control rats but did not increase from baseline in BQ-123-treated rats. BQ-123 did not alter systemic arterial pressure, heart rate, or plasma endothelin-1 levels. These findings suggest that ET-1 synthesized in lung in response to hypoxia acts locally on ETA receptors to cause pulmonary hypertension.

Acute Disease↗

PubMed1995

Selective downregulation of ANP-clearance-receptor gene expression in lung of rats adapted to hypoxia.

To test the hypothesis that expression of atrial natriuretic peptide (ANP)-receptor genes is modified to provide a compensatory mechanism against hypoxic pulmonary hypertension, steady state mRNA levels for the ANP-A receptor (or guanylate cyclase-A; ANPAR), ANP-B receptor (or guanylate cyclase-B; ANPBR), and ANP-clearance receptor (ANPCR) were quantitated by Northern blot and slot-blot analysis in lung, kidney, spleen, and liver of hypoxia-adapted rats and air controls. Exposure of rats to short-term (48 h) and chronic (4 wk) hypoxia (10% O2, 1 atm) did not affect lung ANPAR-mRNA levels. Lung ANPBR-mRNA levels were unchanged by short-term hypoxia but selectively increased (approximately twofold) by chronic hypoxia. ANPCR-mRNA levels were selectively and significantly downregulated by 48-h and 4-wk hypoxia in lung but were unchanged or upregulated in other tissues. Lung ANPCR gene transcription, assessed by nuclear-runoff analysis, was decreased by hypoxia. These data support the conclusion that altered pulmonary ANP-receptor gene expression modulates the development of hypoxic pulmonary hypertension.

Adaptation, Physiological↗

PubMed1995

ETA-receptor antagonist prevents and reverses chronic hypoxia-induced pulmonary hypertension in rat.

The selective endothelin-A (ETA)-receptor antagonist BQ-123 has been shown to prevent chronic hypoxia-induced pulmonary hypertension in the rat. Therefore in the current study we utilized BQ-123 to test the hypothesis that blockade of the ETA receptor can reverse as well as prevent the increase in mean pulmonary artery pressure, right ventricle-to-left ventricle plus septum ratio, and percent wall thickness in small (50-100 microns) pulmonary arteries observed in male Sprague-Dawley rats exposed to normobaric hypoxia (10% O2, 2 wk). Infusion of BQ-123 (0.4 mg.0.5 microliter-1.h-1 for 2 wk in 10% O2) begun after 2 wk of hypoxia significantly reversed the established pulmonary hypertension and prevented further progression of right ventricular hypertrophy during the third and fourth week of hypoxia. BQ-123 infusion instituted before exposure to hypoxia completely prevented the hypoxia-induced pulmonary hypertension, right ventricular hypertrophy, and pulmonary vascular remodeling. These findings suggest that, in the lung, hypoxia induced an increase synthesis of endothelin-1, which acts locally on ETA receptors to cause pulmonary hypertension, right heart hypertrophy, and pulmonary vascular remodeling, while ETA-receptor blockade can both prevent and reverse these processes.

Animals↗

PubMed1995

Endothelin-receptor antagonist bosentan prevents and reverses hypoxic pulmonary hypertension in rats.

The current study examined the effects of bosentan, an orally active antagonist of endothelin-A and -B receptors, on the development and maintenance of hypoxia (10% O2)-induced pulmonary hypertension and vascular remodeling in the rat. Pretreatment with bosentan (100 mg.kg-1.day-1, 1 gavage/day for 2 days) completely blocked the pulmonary vasoconstrictor response to acute hypoxia. Chronic bosentan treatment (100 mg.kg-1.day-1 po in the food) instituted 48 h before hypoxic exposure prevented the subsequent development of pulmonary hypertension, attenuated the associated right heart hypertrophy, and prevented the remodeling of small (50-100 microns) pulmonary arteries without altering systemic arterial pressure. Institution of bosentan treatment (for 4 wk) after 2 wk of hypoxia produced a significant reversal of established hypoxia-induced pulmonary hypertension (from 36 +/- 1 to 25 +/- 1 mmHg), right heart hypertrophy, and pulmonary vascular remodeling despite continuing hypoxic exposure. These findings support the hypothesis that endogenous endothelin-1 plays a major role in hypoxic pulmonary vasoconstriction and/or hypertension, right heart hypertrophy, and pulmonary vascular remodeling and suggest that endothelin-receptor blockade may be useful in the treatment of hypoxic pulmonary hypertension humans.

Animals↗

PubMed1995

Gender and dietary NaCl in spontaneously hypertensive and Wistar-Kyoto rats.

We recently reported that high dietary NaCl exposure significantly increases both daytime and nighttime mean arterial pressure in male spontaneously hypertensive rats (SHR) but only nighttime values in male normotensive Wistar-Kyoto rats (WKY). In the present study we used a telemetry monitoring system to evaluate the effects of high dietary NaCl exposure on diurnal variation of mean arterial pressure and heart rate in male and female SHR and WKY. After implantation of a radio-frequency transducer, rats were fed either high (8%) or basal (1%) NaCl diets for 2 weeks. High dietary NaCl ingestion significantly increased both daytime and nighttime mean arterial pressure in male SHR compared with males receiving a basal NaCl diet, resulting in greater 24-hour values (163 +/- versus 154 +/- 1 mm Hg, high versus basal NaCl diet; P < .05). High dietary NaCl ingestion significantly increased only nighttime blood pressure in male WKY, with no significant effect on 24-hour mean arterial pressure (102 +/- 2 versus 101 +/- 3 mm Hg, high versus basal). High dietary NaCl exposure did not affect daytime or nighttime mean arterial pressure in female SHR (24-hour mean arterial pressure, 144 +/- 2 versus 141 +/- 2 mm Hg, high versus basal NaCl diet). Twenty-four-hour mean arterial pressure tended to be lower in female WKY receiving a high NaCl diet than females ingesting a basal diet (101 +/- 3 versus 106 +/- 1 mm Hg), but the difference was not significant.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗