PubMed Health⌕ Search

Biomedical subjects

Y F Chen

Publications and source records attributed to Y F Chen.

At least 163 records · Page 9Linked to original sources

Effects of dietary salt on angiotensin peptides in kidney.

This study used a novel simple method for the extraction, separation, identification, and quantitation of angiotensin-like immunoactivity from tissue to examine the effects of altering dietary NaCl intake on intrarenal angiotensin I, II, and III levels in salt-sensitive, spontaneously hypertensive rats, salt-resistant Wistar-Kyoto rats, and Sprague-Dawley rats. Seven-week-old male spontaneously hypertensive rats, Wistar-Kyoto rats, and Sprague-Dawley rats were assigned randomly to a diet containing either 8% (high) or 1% (basal) salt and were maintained on these diets for 3 wk. Rats were then decapitated without prior anesthesia, and kidneys were rapidly (< 30 s) removed, snap frozen in liquid nitrogen, and stored at -80 degrees C. Frozen tissue was extracted in 2 M acetic acid and then subjected to solid-phase extraction with the cation exchange resin AG 50W X4. Angiotensin peptides were separated by reversed-phase high-performance liquid chromatography on a phenyl silica gel column with an eluent consisting of 20% acetonitrile in 0.1 M ammonium phosphate buffer, pH 4.9, and quantitated by radioimmunoassay. The elution of standard peptides under isocratic conditions revealed clear resolution of angiotensin I, II, and III and the (1-7) and (3-8) peptides. Recoveries of both labeled and unlabeled angiotensin peptide standards from the extraction step were > 90%. Renal angiotensin II stores were significantly higher in spontaneously hypertensive rats than in Wistar-Kyoto or Sprague-Dawley rats, independent of diet. Renal angiotensin II and III were further suppressed during dietary salt supplementation in both salt-resistant strains but not in the spontaneously hypertensive rat. These findings are consistent with an enhanced (compared with Wistar-Kyoto and Sprague-Dawley rats) role for angiotensin II in the kidney of the salt-sensitive, spontaneously hypertensive rat, particularly under conditions of dietary salt supplementation.

Angiotensin I↗

Postoperative diaphragmatic dysfunction in patients undergoing open-heart surgery.

Diaphragmatic elevation after cardiac surgery may result in compromized post operative respiratory function, prolonged ventilator use, longer intensive care unit (ICU) stays, poor quality of life and even mortality. 200 patients receiving open-heart surgery during the two years from October 1990 to October 1992 were studied retrospectively. 26 patients developed postoperative diaphragmatic elevation (Group 2). On the other hand, 174 patients did not (Group 1). The mean age of Group 1 (37.3 +/- 20.0 years) was younger than that of Group 2 (57.4 +/- 9.1 years), P < 0.0001. The mean aortic cross-clamp time was 70.1 +/- 38.1 minutes in Group 1. On the other hand, Group 2 had a longer crossclamp time (84.5 +/- 31.3 Minutes), p < 0.03. Our study revealed that the patients who suffered post operative diaphragmatic dysfunction were older and had a longer aortic crossclamp time than the patients who did not.

Adolescent↗

Surgical treatment of pericardial effusion in cancer patients.

31 cancer patients with symptomatic pericardial effusion were treated by subxiphoid pericardiotomy with simultaneous pleuropericardial window creation. There were no patients who died during surgery. In all patients, relief of cardiac compression by the effusion was immediate and complete. 10 patients died of advanced malignancy within 30 days after operation without evidence of recurrent pericardial effusion. During the period of follow-up, another seventeen patients died, and no death was related to pericardial effusion. It is concluded that pleuropericardial window through the subxiphoid approach is the treatment of choice for pericardial effusion in cancer patients. The procedure provides immediate and long-lasting relief of cardiac compression with acceptable mortality and morbidity.

Adult↗

The use of right gastroepiploic artery for the bypass of left anterior descending coronary artery--case reports.

The right gastroepiploic artery (RGEA), a branch of the gastroduodenal artery, supplies the greater curvature of the stomach. It is capable of easily reaching the posterior and lateral surface of the heart as a reliable arterial conduit when appropriately harvested. In the previous reports, it has usually been anastomosed to the right coronary artery (RCA) or left circumflex coronary artery (LCX). Here, we present two cases of ischemic heart disease undergoing coronary revascularization. The RGEA was anastomosed to the left anterior decending coronary artery (LAD), which is the most important coronary artery in terms of patient outcome. Thallium-201 myocardial scintigraphy has proven that the RGEA can provide sufficient blood flow to the territory of the LAD. Thus, in coronary artery bypass grafting (CABG), the RGEA is a reliable arterial conduit for LAD revascularization.

Aged↗

The lectin Griffonia simplicifolia I-A4 (GS I-A4) specifically recognizes terminal alpha-linked N-acetylgalactosaminyl groups and is cytotoxic to the human colon cancer cell lines LS174t and SW1116.

The lectin GS I-A4 binds to terminal alpha-N-acetylgalactosaminyl (GalNAc) groups (which include the Tn antigen), but not to the closely related tumor-associated epitope, sialylated Tn antigen. The lectin also precipitates asialo OSM, but not its native sialylated form. Lectin histochemistry with human colonic tissues showed that GS I-A4 specifically stained specimens of colon cancer and colonic tissues from individuals with FAP; however, normal colonic tissues from patients without colonic disease were rarely stained with this lectin. Glycoconjugates bound by GS I-A4 were observed on the surface membranes of 2 human colon cancer cell lines, LS174t and SW1116, when fluorescein isothiocyanate (FITC)-conjugated GS I-A4 was used. GS I-A4 was toxic to these 2 human colon cancer cell lines in monolayer culture. A dose-response study conducted using 10-160 micrograms/ml, of GS I-A4 demonstrated significant dose-related toxicity against LS174t and SW1116 cells. At concentrations > 80 micrograms/ml, > 99% of LS174t and > 90% of SW1116 cells were killed. Four mM GalNAc specifically inhibited the cytotoxic effect of GS I-A4 (p < 0.001), whereas 4mM N-acetylglucosamine (GlcNAc) had no effect. Two other lectins that recognize terminal alpha-GalNAc residues, DBA and LBL, were significantly less cytotoxic to the colon cancer cells than GS I-A4. In the light of these findings, we speculate that GS I-A4 may have potential use as a diagnostic agent against colorectal cancer.

Acetylgalactosamine↗

Use of glutaraldehyde solution in the treatment of acute aortic dissections.

We report on a promising method for toughening and strengthening the fragile aortic wall that involves the direct application of a 25% glutaraldehyde solution and that has proved to be both technically simple and safe. The operation was successfully employed in 5 patients with acute aortic dissections, 3 with a Stanford type A and 2 with a type B dissection. Histologic examination of the glutaraldehyde-treated portions of the aortic wall showed no detectable difference between them and the sections of untreated aortic wall. All patients survived the operation. The duration of follow-up ranged from 9 to 31 months (mean, 14.0 months). All 5 patients were in good condition at the time of the last follow-up. The preliminary results indicate that the use of a 25% glutaraldehyde solution to strengthen the aortic wall during operations for the repair of acute aortic dissections, regardless of whether they are type A or type B, may reduce the incidence of catastrophic perioperative bleeding and promote favorable results.

Acute Disease↗

Clinical burn wound infection caused by L-forms of Staphylococcus aureus.

A patient with an infection with the L-form of Staphylococcus aureus occurring in burn wounds is reported. The authors conclude that the infection was attributable to a decrease in the host immunological functions and repeated administration of antibiotics resulting in the development of bacterial L-forms.

Adult↗

Sodium-proton (Na+/H+) exchange inhibition increases blood pressure in spontaneously hypertensive rat.

The current study was designed to determine the role of sodium-proton (Na+/H+) exchange in blood pressure regulation in sodium chloride (NaCl)-sensitive and NaCl-resistant spontaneously hypertensive rats and control Wistar-Kyoto rats (WKY) using 5-(N,N-hexamethylene)amiloride (HMA), a potent and selective inhibitor of Na+/H+ exchange. The response of mean arterial pressure to intravenous infusion of HMA was examined in conscious, unrestrained male rats maintained on normal (1%) or high (8%) NaCl diets for 3 weeks beginning at age 7 weeks. The HMA significantly increased mean arterial pressure in NaCl-sensitive spontaneously hypertensive rats and NaCl-resistant spontaneously hypertensive rats that were fed 1% NaCl, but not in WKY rats that were fed 1% NaCl; the 8% NaCl diet enhanced this pressor response in all 3 strains. The pressor response was accompanied by significant increases in plasma norepinephrine levels in NaCl-sensitive spontaneously hypertensive rats on both diets, but not in NaCl-resistant spontaneously hypertensive rats or WKY rats on either diet. There were no differences in steady-state levels (30-60 nM) of plasma HMA between diet groups in any strain. Therefore, administration of HMA in a dose at which it is highly selective for the Na+/H+ exchanger (Ki = 160 nM) caused a systemic pressor response in spontaneously hypertensive rats that was enhanced by dietary NaCl supplementation. With these data, it is suggested that inhibition of Na+/H+ exchange in vivo has a pressor effect greater in spontaneously hypertensive rats than in WKY rats and is further enhanced by NaCl supplementation.

Amiloride↗

Increased endothelin receptor gene expression in hypoxic rat lung.

Our previous studies demonstrated that exposure to hypoxia increases pulmonary artery pressure and plasma endothelin-1 (ET-1) levels and selectively enhances ET-1 gene expression in rat lung. The current study examined the effects of hypoxia (48 h, 10% O2, 1 atm) on ET-1 and endothelin A (ETA) and ETB receptor steady-state mRNA levels in lung, heart, pulmonary artery, thoracic aorta, superior vena cava, kidney, spleen, and liver of the rat. In lung, hypoxic exposure was associated with significant increases in ET-1 mRNA (4.1-fold), ET-1 peptide (1.5-fold) and ETA mRNA (2.3-fold) levels; ETB mRNA levels were unchanged. ET-1 mRNA was increased in response to hypoxia in pulmonary artery but not in aorta; both ETA and ETB receptor steady-state mRNA levels were increased in thoracic aorta, left atrium, and right ventricle, and tended to be increased in right atrium of hypoxia-exposed rats, compared with air controls. ETB but not ETA receptor steady-state mRNA levels were increased in pulmonary artery of hypoxia-exposed rats. No change in expression of either ET receptor steady-state mRNA levels was seen in organs perfused by the systemic vascular bed. In no case were ET receptor mRNA levels in hypoxic rats reduced below air control levels, despite elevations in local and/or circulating ET-1. These findings are consistent with a role for ET-1, acting through ETA receptors, in the pathogenesis of hypoxia-induced pulmonary hypertension.

Animals↗

Enhanced endothelin-1 and endothelin receptor gene expression in chronic hypoxia.

To test the hypothesis that endothelin (ET)-1 synthesis and ET receptor levels are increased selectively in the lung of rats with chronic hypoxic pulmonary hypertension, the current study examined the effects of exposure to chronic hypoxia (10% O2, 1 atm, 4 wk) on pulmonary arterial pressure, ET-1 levels in plasma and lung, and ET-1 and ETA and ETB receptor mRNA levels in lung, heart, pulmonary artery, aorta, kidney, spleen, and liver. Hypoxic exposure was associated with increases in pulmonary arterial pressure, plasma ET-1 levels, ET-1 mRNA in lung and pulmonary artery, and ET-1 stores and ETA and ETB receptor mRNA levels in lung. In thoracic aorta and the four heart chambers, ETA and ETB receptor mRNA levels were increased, but ET-1 mRNA levels were unchanged from air control levels. No change in ET-1 or ET receptor mRNA levels was seen in organs perfused by the systemic vascular bed, except in liver, where ETA receptor mRNA levels were decreased. The findings of concomitant increases in gene transcript levels for ET-1 and the ETA and ETB receptors in lung, but not in the great vessels or any other organ examined, are consistent with the hypothesis that increased ET-1 synthesis in the lung contributes to pulmonary vascular remodeling and the maintenance of chronic hypoxic pulmonary hypertension.

Animals↗

Mithramycin inhibits myointimal proliferation after balloon injury of the rat carotid artery in vivo.

BACKGROUND: Smooth muscle proliferation and extracellular matrix formation in the subintimal region of blood vessels that have been subjected to intimal injury are responsible for restenosis following balloon angioplasty of the coronary arteries and for accelerated atherosclerosis in a variety of other pathophysiological states. The immediate early-response gene c-myc is overexpressed in proliferating vascular smooth muscle cells in vitro, and c-myc antisense oligomers have been shown to reduce c-myc expression and to inhibit proliferation of vascular smooth muscle cells in culture. Mithramycin is a commercially available G-C-specific DNA binding drug that selectively inhibits transcription of genes, such as c-myc, that have G-C-rich promoter sequences. This study tested the hypothesis that mithramycin inhibits transcription of the c-myc proto-oncogene and prevents myointimal proliferation after balloon injury of the rat carotid artery in vivo. METHODS AND RESULTS: Ten-week-old male Sprague-Dawley rats received mithramycin (150 micrograms/kg IP) or distilled H2O 1 hour before and 1 hour after balloon injury of the right common carotid artery. After 2 weeks, the rats were killed by overdose of pentobarbital, and the injured right and uninjured control left arteries were pressure-fixed and subjected to morphological analysis for evaluation of the degree of myointimal thickening. Separate groups of rats were killed at 2 and 6 hours after vascular injury, and total RNA from injured and control vessels of mithramycin- and vehicle-treated rats was subjected to Northern analysis for assessment of steady-state c-myc mRNA levels. The areas of neointima and the ratios of neointimal to medial area were significantly less in mithramycin-treated than in control rats (0.6 +/- 0.1 versus 1.2 +/- 0.1 mm2, P < .01 and 95 +/- 16% versus 190 +/- 14%, P < .01). Lumen size was significantly greater in mithramycin-treated than in control rats (1.5 +/- 0.1 versus 0.8 +/- 0.1 mm2, P < .01). Steady-state c-myc mRNA levels were increased 10-fold and 2-fold (compared with undamaged carotid arteries) at 2 and 6 hours after balloon injury, respectively; mithramycin treatment reduced c-myc mRNA levels at 2 and 6 hours by 66% and 53%, respectively. CONCLUSIONS: These results support the hypothesis that systemic administration of mithramycin immediately (1 hour before and after intervention effectively inhibits transcription of the c-myc proto-oncogene and prevents myointimal proliferation after balloon injury of the rat carotid artery in vivo. Because mithramycin has been shown to be well tolerated by humans and to effectively inhibit transcription of c-myc in proliferating human cells, this agent may be useful in the prevention of coronary restenosis.

Angioplasty, Balloon↗

The role of atrial natriuretic peptide and endothelin in hypoxia induced pulmonary hypertension.

The goal of our studies is to elucidate the role of atrial natrluretic peptide (ANP) and endothelin-1 (ET-1) and their receptor mechanisms in hypoxia-induced pulmonary hypertension and the control of pulmonary artery pressure in patients with pulmonary hypertension. Our experimental model is the male Sprague-Dawley rat subjected to normobaric hypoxia (10% O2, 1 atm) x 4 weeks or less. Our hypothesis is that ET-1 and ANP gene expression are enhanced by exposure to hypoxia and that the ET-1 and ANP so generated have causal and protective, respectively, effects on the development of hypoxia-induced pulmonary hypertension. Results from our studies demonstrated that ANP gene expression and ANP secretion in the heart, and the sensitivity to both endogenous and exogenous ANP in the pulmonary vasculature of hypoxia adapted rats are enhanced during hypoxic exposure. These data defined a role for ANP as a modulator hormone that protects against the development of acute hypoxic pulmonary vasoconstriction and chronic hypoxic pulmonary hypertension. Our studies also demonstrated that ET-1 and endothelin-A receptor (ET-AR) gene expression were selectively enhanced in the pulmonary vasculature by exposure to hypoxia, and that the ET-1 so generated is an important mediator in acute and chronic hypoxia-induced pulmonary hypertension. These results suggest that the intrapulmonary ET-1, acting on ET-AR receptors in the pulmonary vasculature mediates the hypoxia-induced pulmonary vasoconstriction and hypertension. In addition, our recent experiments have demonstrated that administration of BQ-123, a selective ET-AR antagonist, abolished the pulmonary vasoconstrictor response to acute (0-90 min) and chronic (2 weeks) hypoxia, further suggesting that ET-1 plays an important role in the pathogenesis of hypoxia-induced pulmonary hypertension in the rat. Results from our studies also indicate that selective ANP analogs and ET-AR antagonists may be clinically useful for the treatment of pulmonary hypertension.

Animals↗

Surgical correction of sinus venosus atrial septal defect associated with partial anomalous pulmonary venous connection to high superior vena cava--case report.

A 63-year-old woman complained of general malaise and insomnia initially. Atrial septal defect was diagnosed by transthoracic echocardiography thereafter. She had not received complete cardiac studies until progressive dyspnea was noted half a year later. After a series of examinations, sinus venosus type atrial septal defect (ASD) associated with partial anomalous pulmonary venous connection to high superior vena cava (SVC) and persistent left SVC was documented. Surgical correction was performed later. The postoperative course was smooth and her condition improved gradually at 10-month follow-up.

Female↗

Surgical management of the hypopharyngeal and cervical esophageal cancer.

Between December 1979 and December 1992, 15 patients with hypopharyngeal and cervical esophageal cancer were treated surgically. Total pharyngolaryngectomy and partial cervical esophagectomy were performed and the defects were reconstructed with cervical skin flaps in 2 cases. The free jejunal segments were used in 6 cases following total pharyngolaryngectomy and cervical esophagectomy, cervical esophagectomy (larynx preserved) was repaired with free jejunal graft in 1 case. The pharyngogastric anastomosis following total pharyngolaryngoesophagectomy were performed in 4 cases, one of them, used pectoralis major myocutaneous flap for resection of soft tissue and skin of the neck. The pectoralis major myocutaneous flap and forearm free flap in 1 case respectively were used to reconstruct the deficits of total laryngectomy and partial pharyngectomy, and partial pharyngolaryngectomy. In our series, 1, 3, 5 years survival rates were 73.3% (11/15), 50% (6/12) and 55.6% (5/9), respectively. The advantages and disadvantages of a variety of operative procedures and the cervical lymph nodes management will be discussed.

Adult↗

Correction of aortico-left ventricular tunnel in a small Oriental infant: a brief clinical review.

In reviewing 56 cases of aortico-left ventricular tunnel from 39 reported articles, none of the patients operated on were Oriental. In this report, a 4 month-old male infant was successfully operated on. The tunnel was closed with a Dacron patch on the aortic orifice. The child is now free from symptoms, except for mild residual aortic regurgitation, and is developing normally 5 year-11 month after repair. A brief clinical review has been attempted in these reported cases.

Aorta↗

Effectiveness of coenzyme Q10 on myocardial preservation during hypothermic cardioplegic arrest.

A prospective, randomized, double-blind trial assigned 11 patients to receive coenzyme Q10 and 11 to receive none. Patients pretreated with coenzyme Q10 had a lower left atrial pressure and a lesser incidence of low cardiac output. They also had a wider pulse pressure. The right and left ventricular myocardial ultrastructure was better preserved in patients receiving preoperative treatment with coenzyme Q10. There was no demonstrable benefit to the atrial myocardium.

Adult↗