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Biomedical subjects

Y T Chen

Publications and source records attributed to Y T Chen.

At least 145 records · Page 8Linked to original sources

Differences in cervical cancer mortality among black and white women.

OBJECTIVE: To determine whether stage of disease and treatment patterns account for mortality differences between black and white women with cervical cancer. METHODS: Using data obtained from the Surveillance, Epidemiology, and End Results (SEER) Program for 1988-1994, we determined the associations between race and stage, and race and treatment. Racial differences in survival for up to 7 years of follow-up were adjusted for age, marital status, SEER location, International Federation of Gynecology and Obstetrics (FIGO) stage of disease, lymph node status, grade, histology, and treatment. RESULTS: Cumulative mortality was 36% (366 deaths in 1029 women) for black women and 24% (1215 deaths in 5021 women) for white women; unadjusted hazard ratio was 1.60 (95% confidence interval [CI] 1.43, 1.80). Black women were more likely to present with advanced disease than white women (43.8% compared with 34.8%). In a model adjusting for demographics and FIGO stage, the hazard ratio for black women compared with white women decreased to 1.35 (95% CI 1.19, 1.54). Treatment varied by race, with black women receiving surgery less often (33.5% compared with 48.2%, respectively) and radiation therapy more often (35.3% and 25.2%, respectively) than white women. In a comprehensive model including demographic factors, FIGO stage, other tumor characteristics, and treatment, the adjusted hazard ratio for mortality remained high for black women at 1.30 (95% CI 1.14, 1.48). CONCLUSION: Race remains an independent predictor of cervical cancer survival after accounting for age, stage of disease, treatment patterns, and other factors. Future studies should assess racial differences in clinical severity of disease, comorbidity, and socioeconomic status.

Adult↗

Seborrheic keratosis of conjunctiva simulating a malignant melanoma: an immunocytochemical study with impression cytology.

OBJECTIVE: Seborrheic keratosis on the conjunctiva appears to have never been reported in the literature. The authors report here a well-documented case of seborrheic keratosis of conjunctiva clinically simulating a malignant melanoma. DESIGN: Case report. METHODS: A 66-year-old man presented with a juxtalimbal pigmented tumor involving the temporal conjunctiva of his left eye. Because of the rapid enlargement of the mass within a period of 5 months, a clinical diagnosis of malignant melanoma was made. Cytopathologic examinations were performed by impression cytology before the patient underwent a wide en-block excision of the tumor. MAIN OUTCOME MEASURES: Cytologic features were studied by impression cytology with periodic acid-Schiff-Papanicolaou stain. Immunochemical characteristics of tumor cells were studied by immunochemical stain of cytokeratin and HMB-45. Tumor morphology was observed by histopathologic examination. RESULTS: Impression cytology disclosed basaloid cells intermixing with squamoid cells, and these cells demonstrated positive immunoreactivity to cytokeratin and no reactivity to HMB-45. Histopathologic examination of the tumor specimen established the diagnosis of seborrheic keratosis, and the results of immunohistochemical staining were consistent with those of the impression cytology with immunocytochemical staining. CONCLUSION: The authors describe the first case report of conjunctival seborrheic keratosis and present its immunocytochemical and immunohistochemical characteristics. Such a benign lesion can clinically mimic a malignant melanoma.

Aged↗

Productivity and some properties of immunoglobulin specific against Streptococcus mutans serotype c in chicken egg yolk (IgY).

Hens were immunized on thighs by using whole cells of Streptococcus mutans MT8148 serotype c strain as antigen through intramuscular (im) and subcutaneous (sc) routes to investigate the difference of immunization reactions and the changes in yolk antibody activities against antigen after initial immunization. Several properties of crude IgY were examined to evaluate the stability during food processing. Results showed that the specificity of IgY of im treated hens was nearly 10 times as high as those of sc treated antibody. IgY from the hens immunized with the serotype c strain showed significant cross-reactions against serotypes e and f, while minor reactions against serotypes a, b, d, and g were observed. In thermal stability tests, IgY activity in both yolk and crude IgY decreased with the increasing temperature, from 70 to 80 degrees C, but the thermal denaturation rates between those two samples were not significantly different. The addition of high levels sucrose, maltose, glycerol, or 2% glycine displayed effective protection against thermal denaturation of IgY. Lyophilized yolk-5% gum arabic powder showed better stability against proteases.

Animals↗

Nutritional deficiencies in a patient with glycogen storage disease type Ib.

The current mainstay of treatment in glycogen storage disease type I (GSD I) is dietary management that includes providing a frequent source of glucose to prevent hypoglycaemia. To ensure compliance, routine follow-up by a health care team, including a dietitian, experienced in the treatment of GSD is necessary. We describe an adolescent patient with GSD Ib in good metabolic control who was admitted with a 3-month history of weakness, depression, vomiting, decreased appetite and a 11.4-kg weight loss. He had a recent onset of unsteady gait, inability to write, and sore mouth. After an extensive work-up, the patient was found to have vitamin B12, folate, iron and other nutritional deficiencies, which explained his symptoms. The patient improved within 72 h of initiation of total parenteral nutrition and therapeutic doses of deficient micronutrients, with a complete recovery in 2 months. Dietary restrictions, dependence on non-food products (e.g. cornstarch in GSD I), and social and developmental issues place individuals with metabolic disorders at a high risk for developing an array of nutritional deficiencies. This case highlights the importance of both close follow-up of the metabolic control and close monitoring of growth and nutritional intake in individuals with inborn errors of metabolism. This case also illustrates the importance of daily supplementation with appropriate multivitamins, calcium and other minerals needed to meet the Recommended Dietary Allowances (RDAs) in these patients.

Adolescent↗

The putative glucose 6-phosphate translocase gene is mutated in essentially all cases of glycogen storage disease type I non-a.

The purpose of this work was to test the hypothesis that mutations in the putative glucose 6-phosphate translocase gene would account for most of the cases of GSD I that are not explained by mutations in the phosphohydrolase gene, ie that are not type Ia. Twenty-three additional families diagnosed as having GSD I non-a (GSDIb, Ic or Id) have now been analysed. The 9exons of the gene were amplified by PCR and mutations searched both by SSCP and heteroduplex analysis. Except for one family in which only one mutation was found, all patients had two allelic mutations in the gene encoding the putative glucose 6-phosphate translocase. Sixteen of the mutations are new and they are all predicted to lead to non-functional proteins. All investigated patients had some degree of neutropenia or neutrophil dysfunction and the clinical phenotype of the four new patients who had been diagnosed as GSD Ic and the one diagnosed as GSD Id was no different from the GSD Ib patients. Since these patients, and the four type Ic patients from two families previously studied, shared several mutations with GSD Ib patients, we conclude that their basic defect is in the putative glucose 6-phosphate translocase and that they should be reclassified as GSD Ib. Isolated defects in microsomal Pi transporter or in microsomal glucose transporter must be very rare or have phenotypes that are not recognised as GSD I, so that in practice there are only two subtypes of GSD I (GSD Ia and GSD Ib).

Alleles↗

Gender differences in relation to leptin concentration and insulin sensitivity in nondiabetic Chinese subjects.

OBJECTIVE: To investigate the relationship between fasting plasma leptin concentrations and insulin resistance in Chinese men and women. DESIGN: Cross-sectional study design. SUBJECTS: Ninety-six nondiabetic Chinese (51 men and 45 women) with body mass index (BMI) between 18.4-35.8 kg/m2 were studied. MEASUREMENTS: Plasma glucose and insulin concentrations were measured every 30 min for 2 h after a 75 g oral glucose load. The degree of insulin resistance was assessed using a modified insulin suppression test. Plasma leptin values were determined by radioimmunoassay. RESULTS: Fasting plasma glucose, glucose areas, fasting insulin, insulin areas, most of the lipoprotein concentrations and steady state plasma glucose (SSPG) concentrations were relatively similar between men and women. Despite the fact that men had higher BMI values (26.1 +/- 0.5 vs 24.7 +/- 0.5 kg/m2, P < 0.05), fasting plasma leptin concentrations were significantly lower in men than in women (4.9 +/- 0.5 vs 9.0 +/- 0.8 ng/ml, P < 0.001). Fasting leptin values were positively related to SSPG concentrations by simple correlation analysis in both sexes. However, this relationship persisted in men (r = 0.513, P < 0.01) but not in women (r = 0.119, P = NS) after adjustment for BMI. Multiple regression analysis showed that SSPG concentrations, BMI, glucose and insulin responses together accounted for 62.5% and 52.2% of the variation in plasma leptin concentrations in Chinese men and women respectively. CONCLUSION: Fasting plasma leptin concentrations were lower in Chinese men than in Chinese women despite the higher BMI observed in men. After adjustment for BMI, plasma leptin values correlated with the degree of insulin resistance in men but not in women.

Asian People↗

High plasma leptin concentrations in hypertensive men but not in hypertensive women.

OBJECTIVE: Previous studies on humans have reported higher leptin levels in women than in men, independent of body fat, and leptin has been correlated with insulin resistance in men but not in women. Since insulin resistance is thought to play a role in raising blood pressure, we investigated sex differences in leptin concentrations between hypertensive and normotensive individuals. METHODS: Ninety-two nondiabetic hypertensive patients (48 men and 44 women) and 92 age, body mass index (BMI)-matched normotensive control individuals were studied. Fasting plasma glucose, insulin, leptin and lipoprotein concentrations, glucose and insulin responses to 75 g oral glucose tolerance test (OGTT) and insulin suppression tests were determined. RESULTS: Fasting plasma leptin concentrations were higher in hypertensive men than in normotensive men (5.1 +/- 0.5 versus 3.9 +/- 0.4 ng/ml, P = 0.015). However, fasting plasma leptin concentrations were not significantly different between hypertensive and normotensive women (11.8 +/- 1.0 versus 10.9 +/- 1.0 ng/ml, P = 0.440). Fasting plasma leptin concentrations showed good correlation with BMI, body fat, fasting plasma insulin concentrations, and insulin area to OGTT in both men and women (all P < 0.001). However, fasting plasma leptin concentrations were related to steady-state plasma glucose (SSPG) concentrations, a measure of insulin sensitivity by insulin suppression test, in men only (P < 0.001). After adjustment for body fat amount, age and duration of hypertension, fasting plasma leptin levels still correlated significantly with SSPG concentrations in men. These four variables together accounted for a 67.9% variation in fasting plasma leptin levels in men. In women, body fat amount was the only significant determinant for plasma leptin levels. These four variables accounted for a 78.2% variation in plasma leptin levels in women. CONCLUSIONS: Our study confirmed a sex difference in leptin levels both in hypertensive and normotensive subjects. Higher plasma leptin concentrations in hypertensive men but not in hypertensive women when compared with normotensive control individuals was also demonstrated. These observations are consistent with the findings that plasma leptin is correlated with insulin sensitivity in men but not in women. Further studies are needed to understand the causes and consequences of sex effects on leptin in blood pressure regulation.

Adipose Tissue↗

Cadherin function in junctional complex rearrangement and posttranslational control of cadherin expression.

The role of E-cadherin, a calcium-dependent adhesion protein, in organizing and maintaining epithelial junctions was examined in detail by expressing a fusion protein (GP2-Cad1) composed of the extracellular domain of a nonadherent glycoprotein (GP2) and the transmembrane and cytoplasmic domains of E-cadherin. All studies shown were also replicated using an analogous cell line that expresses a mutant cadherin construct (T151) under the control of tet repressor. Mutant cadherin was expressed at approximately 10% of the endogenous E-cadherin level and had no apparent effect on tight junction function or on distributions of adherens junction, tight junction, or desmosomal marker proteins in established Madin-Darby canine kidney cell monolayers. However, GP2-Cad1 accelerated the disassembly of epithelial junctional complexes and delayed their reassembly in calcium switch experiments. Inducing expression of GP2-Cad1 to levels approximately threefold greater than endogenous E-cadherin expression levels in control cells resulted in a decrease in endogenous E-cadherin levels. This was due in part to increased protein turnover, indicating a cellular mechanism for sensing and controlling E-cadherin levels. Cadherin association with catenins is necessary for strong cadherin-mediated cell-cell adhesion. In cells expressing low levels of GP2-Cad1, protein levels and stoichiometry of the endogenous cadherin-catenin complex were unaffected. Thus effects of GP2-Cad1 on epithelial junctional complex assembly and stability were not due to competition with endogenous E-cadherin for catenin binding. Rather, we suggest that GP2-Cad1 interferes with the packing of endogenous cadherin-catenin complexes into higher-order structures in junctional complexes that results in junction destabilization.

Amino Acid Sequence↗

Histamine alters cadherin-mediated sites of endothelial adhesion.

We tested the hypothesis that histamine alters the focal apposition of endothelial cells by acting on sites of cadherin-mediated cell-cell adhesion. Focal apposition was measured as the impedance of a cell-covered electrode, which was partitioned into a cell-matrix resistance, a cell-cell resistance, and membrane capacitance. Histamine causes an immediate, short-lived decrease in the impedance of an electrode covered with human umbilical vein endothelial (HUVE) cells. ECV304 cells are a line of spontaneously transformed HUVE cells that do not express the endothelial cadherin, cadherin-5. Histamine increased ECV304 cell calcium to 600 nM. Histamine did not increase myosin light chain phosphorylation of control or transfected ECV304 cells. ECV304 cells transfected with either E-cadherin or cadherin-5 on a dexamethasone-responsive plasmid (pLKneo) increased their cell-cell resistance when stimulated with dexamethasone, whereas ECV304 cells transfected with pLKneo-lacZ did not. Histamine did not affect the impedance of ECV304 cells transfected with pLKneo-lacZ. In contrast, histamine decreased the cell-cell resistance of ECV304 cells transfected with either pLKneo-E-cadherin or pLKneo-cadherin-5. From these data, we conclude that histamine acts on sites of cadherin-mediated cell-cell apposition.

Animals↗

Trp64Arg polymorphism of the beta 3-adrenergic receptor gene is associated with increased plasma leptin levels in obese Chinese women.

BACKGROUND: beta 3-Adrenergic receptors are predominantly expressed in the fat cells of visceral adipose tissue in humans. They mediate catecholamine-induced lipolysis and thermogenesis of adipose tissue, which are important for the regulation of energy expenditure and, therefore, body weight. Recently, a Trp64Arg polymorphism of the beta 3-adrenergic receptor gene was reported to be associated with obesity and obesity-related metabolic complications in some ethnic populations. Leptin, a protein secreted by adipocytes, is proposed as a signal linkage between the central nervous system and peripheral fat storage. It has been shown in rodents that leptin may activate the sympathetic nervous system and, thus, beta 3-adrenergic receptors in adipose tissue. However, little is known about the relationship between the Trp64Arg polymorphism and plasma leptin in humans. METHODS: To determine the effects of the beta 3-adrenergic receptor gene Trp64Arg mutation on anthropometric measures, metabolic parameters and plasma leptin levels, 188 premenopausal Chinese women (mean age +/- standard deviation, 32 +/- 10 years) with body mass index (BMI) between 16.1 and 59.8 kg/m2 were investigated. Trp64Arg polymorphism was determined by DNA analysis, body fat mass by bioelectric impedance analysis and plasma leptin by radioimmunoassay. RESULTS: Trp64Arg allele frequency was 15% in this population and there was no homozygous Arg64Arg mutant. When the subjects were divided into three groups based on BMI values (BMI < 22.2, n = 60; 22.2 < or = BMI < or = 29.5, n = 63; BMI > 29.5 kg/m2, n = 65), there was no difference in Trp64Arg allele frequency (16% vs 11% vs 18%, p = 0.149). Across the three groups, plasma leptin correlated positively with BMI (r = 0.843, p < 0.0001) and total fat mass (r = 0.824, p < 0.0001). Within each BMI tertile, the waist to hip ratio, fat mass, plasma lipids, glucose and insulin were relatively similar between Trp64Trp homozygotes and Trp64Arg heterozygotes. However, Trp64Arg heterozygotes had higher plasma leptin levels than Trp64Trp homozygotes (35.9 +/- 11.0 vs 30.0 +/- 12.8 ng/ml, p = 0.0023) in those with BMI above 29.5 kg/m2, a difference which remained after adjustment for body fat mass (p = 0.024). CONCLUSIONS: Trp64Arg polymorphism of the beta 3-adrenergic receptor gene is not associated with obesity in Chinese women. Plasma leptin concentrations correlate well with BMI and total fat mass. For obese Chinese women, the Trp64Arg genotype of the beta 3-adrenergic receptor gene may contribute to an increased plasma leptin level.

Adult↗

Evaluation of arterial compliance in patients with carotid arterial atherosclerosis.

BACKGROUND: High-resolution peripheral vascular sonography has the capability to determine vessel compliance. A number of factors affect compliance in humans, including age, hypertension and atherosclerosis. However, compliance in patients with coronary artery disease (CAD) combined with carotid artery lesions has not been well studied. The objectives of this study were: 1) to determine whether carotid artery compliance is reduced in patients with CAD and carotid artery lesions, and 2) to determine whether decreased arterial compliance is related to an abnormality in vascular wall structure. METHODS: The study participants included 12 patients with CAD and carotid artery disease (group III), 13 patients with CAD only (group II) and 13 age-matched normal subjects who served as controls (group I). High-resolution peripheral vascular ultrasonography was performed to directly visualize the common carotid artery and to measure its diameter and wall thickness. Carotid artery elastic properties were determined relative to arterial diameter and pressure generated within the heart. RESULTS: Carotid artery walls were thicker in Group II and III patients than in normal subjects (1.49 +/- 0.03 mm, 1.98 +/- 0.04 mm, vs 1.22 +/- 0.03 mm, p < 0.05 and p < 0.01). There were significant differences in wall thickness between subgroups of CAD patients (p < 0.01). Carotid distensibility was lower (21.8 +/- 1.2 x 10(-6).N-1.m2, 14.8 +/- 1.7 x 10(-6).N-1.m2, vs 25.6 +/- 1.5 x 10(-6).N-1.m2; p < 0.05 and p < 0.01) and Young's modulus of elasticity was higher (3.12 +/- 0.43 x 10(5).Nm-2, 4.18 +/- 0.30 x 10(5).Nm-2, vs 2.34 +/- 0.23 x 10(5).Nm-2; p < 0.05 and p < 0.01) in group II and III patients than in normal subjects. These two indices of carotid artery compliance also differed between subgroups of CAD (p < 0.01). Increased wall thickness may occur secondary to changes in the architectural structure of the vessel wall, and these atherosclerotic changes lead to decreased compliance of arteries. CONCLUSION: The mechanical properties of the carotid arteries provide reliable information regarding changes caused by atherosclerosis.

Arteriosclerosis↗

Variations in and correlates of length of stay in academic hospitals among patients with heart failure resulting from systolic dysfunction.

OBJECTIVE: Given the high cost of caring for patients with congestive heart failure, there are strong incentives to decrease hospital costs by shortening length of hospital stay. We sought to identify factors associated with length of stay among patients admitted for the treatment of heart failure resulting from systolic dysfunction. STUDY DESIGN: Retrospective cohort study. METHODS: We examined data from patients with a principal discharge diagnosis of congestive heart failure who had been admitted to 1 of the 49 academic hospitals across the United States that participated in the CHF Benchmark Project, a large collaborative quality improvement project coordinated by the University HealthSystem Consortium. Patients were discharged between January 1 and June 30, 1996. We obtained patient characteristics and hospitalization data by retrospectively reviewing medical records. We used linear regression models to identify major determinants of length of stay. RESULTS: Among the 1046 patients eligible for the study, 59% were women, 55% were white, and 58% were aged 65 years or older. Adjusting for patient demographic and admission clinical characteristics, the mean length of stay was 4.9 +/- 0.9 days. Length of stay varied significantly among hospitals, even after adjusting for differences in patient characteristics. In multivariate regression models, factors that were independently associated with a significantly longer length of stay were prior renal failure, peripheral edema, atrial fibrillation, hyponatremia, urinary catheter on admission, initiation of an antiarrhythmic or warfarin, and major complications. Patient characteristics and hospital events combined explained 16% of the variation in the length of stay. Adjusting for the individual hospitals explained an additional 10% of the variation in the length of stay. CONCLUSIONS: Although a number of patient and hospitalization factors were associated with length of stay in patients with congestive heart failure resulting from systolic dysfunction, much unexplained variation remained. Clinical factors alone explained about 50% more variation than did factors specific to the individual hospitals.

Academic Medical Centers↗

Antagonistic effect of l-stepholidine on striatal ischemic injury in rat.

AIM: To elucidate the protection of l-stepholidine (SPD) on neuronal morphology and function against the striatal ischemic injury in rat. METHODS: The forebrain ishemia to Sprague Dawley rats was induced with four-vessel occlusion. Histological examination was performed on the dorsolateral striatum with cresylviolet stain. In striatal slices of rat as an in vitro ischemic model, the activity of calcium/calmodulin-dependent protein kinase II (CCDPK) and lactate dehydrogenase (LDH) was examined by the method of 32P-incorporation and colorimetry, respectively. RESULTS: In the SPD-treated groups, most of the neurons in the striatum kept the normal morphological appearance after 30-min ischemia followed by 6-h or 12-h reperfusion. The number of neurons was much more in SPD groups than that in vehicle group. The sparse and abnormal neurons were observed in the vehicle group. SPD attenuated the ischemic effect on the CCDPK activity in striatal slices. In addition, SPD inhibited the leakage of LDH from neurons induced by ischemia in incubated striatal slices. CONCLUSION: SPD protected striatal neurons against ischemic injury and antagonized the inhibitory action on CCDPK activity induced by ischemia. SPD reduced the leakage of LDH from striatal neurons induced by ischemia.

Animals↗

[Reconstruction of elbow flexion and shoulder abduction with transfer of pectoralis major].

OBJECTIVE: To evaluate the clinical application of primary transfer of pectoralis major to reconstruct the elbow flexion and shoulder abduction. METHODS: 12 cases of old injury of branchial plexus with dysfunction of both elbow and shoulder joints were received surgical operation to reconstruct the palsy joints by primary transfer of pectoralis major, shoulder abduction was reconstructed by clavicular head and elbow flexion by sternal head respectively. All cases were followed up for 5 to 18 months. RESULTS: The function of both joints recovered obviously, the total superior rate is 91.7%. CONCLUSION: Only if the palsy joints, shoulder or elbow, remained normal or almost normal passive motion, and the muscle power of pectoralis major over 4 degrees, the primary transfer of pectoralis major should be a simple, reliable and convenient technique to reconstruct the palsy joints.

Adolescent↗