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Y T Chen

Publications and source records attributed to Y T Chen.

At least 55 records · Page 3Linked to original sources
PubMed2001

Molecular cloning of a novel member of the GLUT family of transporters, SLC2a10 (GLUT10), localized on chromosome 20q13.1: a candidate gene for NIDDM susceptibility.

Non-insulin-dependent diabetes mellitus (NIDDM) is a multifactoral disease with both environmental and genetics causes. Genome-wide screening procedures have identified several susceptibility loci for NIDDM within the human genome. We describe the cloning of a putative sugar transporter that has been localized to human chromosome 20q12-q13.1, one of the genomic loci associated with NIDDM. Because of the strong resemblance of this novel protein to members of the mammalian facilitative glucose transporter family (GLUT), we refer to the protein as GLUT10 (HGMW-approved gene symbol SLC2A10). GLUT10 contains 541 amino acids with several glucose transporter sequence motifs and amino acids essential for glucose transport function. In addition, secondary structure analysis of GLUT10 predicts 12 putative transmembrane domains, a hallmark structure of the GLUT family. The tissue distribution of GLUT10 was determined by Northern analysis, which revealed highest levels of expression in the liver and pancreas. From these data, we believe that the chromosomal localization, tissue distribution, and predicted function make GLUT10 an excellent candidate for a susceptibility gene involved in NIDDM.

Amino Acid Sequence↗
PubMed2001

Osteocalcin gene Hind III polymorphism is not correlated with calcium oxalate stone disease.

The formation of urinary stones is presumed to be associated with polymorphism of the osteocalcin gene. The most frequently seen polymorphism is the Hind III type located at the promoter region. This polymorphism has been used as a genetic marker in the search for a correlation between urolithiasis and normal subjects. In our study, a normal control group of 105 healthy people and 102 patients with calcium oxalate stones were examined. The polymorphism was seen following polymerase chain reaction-based restriction analysis. The results revealed no significant differences between normal individuals and stone patients (P = 0.978), and distribution of the TT homozygote in the control group (42.9%) was similar to that in the patient group (42.2%). Further categorization of the stone patients into normocalciuric and hypercalciuric groups also revealed no statistical differences from controls. We conclude that Hind III polymorphism of the osteocalcin gene is not a suitable genetic marker of urinary stone disease. Further searches for other polymorphisms on this gene correlated with stone disease are suggested.

Adult↗
PubMed2001

Magnolol, a potent antioxidant from Magnolia officinalis, attenuates intimal thickening and MCP-1 expression after balloon injury of the aorta in cholesterol-fed rabbits.

BACKGROUND: Restenosis is a common complication after balloon angioplasty. A number of cytokines, chemotactic factors and growth factors may be involved. Several antioxidants have been shown to inhibit intimal thickening after balloon injury in hyperlipidemic animals. OBJECTIVES: The effects of magnolol on the expression of monocyte chemotactic protein-1 (MCP-1) and intimal response in balloon injured aorta of cholesterol-fed rabbits were investigated. METHODS: Male New Zealand white rabbits were fed a 2% high cholesterol (HC) diet together with daily intramuscular injection of either 1 microg/kg B.W. of magnolol (HC-M, n = 10) or vehicle (propylene glycol) as a control (HC-C, n = 10) for a total of 6 weeks. Another 10 rabbits fed a regular diet also served as a control (C) group. A balloon denudation of abdominal aorta was performed in each group at the end of the third week. The aortas were harvested at the end of 6 weeks. RESULTS: Magnolol treatment significantly inhibited Cu2+-induced LDL oxidation in cholesterol-fed rabbits and reduced atheroma formation [atheroma area ratio: 0.10 +/- 0.03 (HC-M) versus 0.33 +/- 0.07 (HC-C), p < 0.05] in thoracic aortas without lowering serum cholesterol. The intimal response was significantly attenuated in the HC-M rabbits when compared to those of the HC-C group [intimal thickness: 88.95 +/- 14.91 microm (HC-M) versus 198.02 +/- 20.35 microm (HC-C), p < 0.05; intimal area: 278.21 +/- 43.16 x 10(3) microm2 (HC-M) versus 642.70 +/- 65.01 x 10(3) microm2 (HC-C), p < 0.05]. The MCP-1 mRNA and protein expression were reduced in the HC-M group compared to the HC-C and C groups. CONCLUSION: The inhibitory effects on intimal hyperplasia and MCP-1 expression might be attributed to the antioxidant capacity of magnolol instead of lowering serum cholesterol. Magnolol may offer some protection against postangioplasty restenosis.

Angioplasty, Balloon↗
PubMed2001

Endothelial dysfunction in type 2 diabetes mellitus subjects with peripheral artery disease.

We strived to characterize the endothelial function status in type 2 diabetic patients with peripheral artery disease which was detected by ankle-brachial index by utilizing high frequency ultrasounds. Predictors of endothelial dysfunction were investigated. We chose 23 type 2 diabetic patients had ankle-brachial index <0.97 (0.15-0.95; mean=0.74+/-0.20), 31 diabetic patients had ankle-brachial index >/=1.0 and 28 non-diabetic subjects for study. Older age, a longer duration of diabetes, higher systolic blood pressure, higher prevalence of history of hypertension were observed in patients with peripheral vascular disease. Type 2 diabetic patients showed impaired flow-mediated dilatation than non-diabetic and it showed more impaired in patients with peripheral vascular disease. Nitroglyerin-induced dilatation showed a trend of impairment in patients with peripheral vascular disease but did not reach statistical significance. Age (r=-0.259, P=0.019), baseline brachial artery diameter (r=-0.321, P=0.003), ankle-brachial index (r=0.259, P=0.002) and hypertension history (P=0.01) were significantly associated with flow-mediated dilatation. However, after adjusting for age, only baseline diameter and ankle-brachial index were independent predictors of flow-mediated dilatation. In conclusion, we demonstrated flow-mediated dilatation was impaired in type 2 diabetic patients and it was further impaired in patients with peripheral vascular disease. Nitroglycerin-induced dilatation showed a trend of impairment but did not reach statistical significance.

Aged↗
PubMed2001

Predicting one-year mortality among elderly survivors of hospitalization for an acute myocardial infarction: results from the Cooperative Cardiovascular Project.

OBJECTIVES: We sought to develop a model based on information available from the medical record that would accurately stratify elderly patients who survive hospitalization with an acute myocardial infarction (AMI) according to their risk of one-year mortality. BACKGROUND: Prediction of the risk of mortality among older survivors of an AMI has many uses, yet few studies have determined the prognostic importance of demographic, clinical and functional data that are available on discharge in a population-based sample. METHODS: In a cohort of patients aged > or = 65 years who survived hospitalization for a confirmed AMI from 1994 to 1995 at acute care, nongovernmental hospitals in the U.S., we developed a parsimonious model to stratify patients by their risk of one-year mortality. RESULTS: The study sample of 103,164 patients, with a mean age of 76.8 years, had a one-year mortality of 22%. The factors with the strongest association with mortality were older age, urinary incontinence, assisted mobility, presence of heart failure or cardiomegaly any time before discharge, presence of peripheral vascular disease, body mass index <20 kg/m2, renal dysfunction (defined as creatinine >2.5 mg/dl or blood urea nitrogen >40 mg/dl) and left ventricular dysfunction (left ventricular ejection fraction <40%). On the basis of the coefficients in the model, patients were stratified into risk groups ranging from 7% to 49%. CONCLUSIONS: We demonstrate that a simple risk model can stratify older patients well by their risk of death one year after discharge for AMI.

Aged↗
PubMed2001

Copper(II) complexes with N,N'-dialkyl-1,10-phenanthroline-2,9-dimethanamine: synthesis, characterization, DNA-binding thermodynamical and kinetic studies.

Copper(II) complexes (Cu-L, L=N,N'-dialkyl-1,10-phenanthroline-2,9-dimethanamine) were synthesized and characterized by elemental analyses, IR spectra and conductance measurement. The interaction of the copper(II) complex with calf thymus DNA was studied by means of UV melting experiments, fluorescence spectra and circular dichroic spectra. Using ethidium bromide as a fluorescence probe, the binding mode of the complexes Cu-L with calf-thymus DNA was studied spectroscopically. The results indicate that the complexes Cu-L perhaps interact with calf-thymus DNA by both intercalative and covalent binding. Kinetics of binding of the cupric complexes to DNA was studied for the first time using ethidium bromide as a fluorescence probe with stopped-flow spectrophotometer under pseudo-first-order condition. The stronger binding of two steps in the process of the complexes Cu-L interacting with DNA was observed, and the probable interaction process was discussed in detail. The corresponding k(obs) and E(a) of binding to DNA (where k(obs) is the observed pseudo-first-order rate constant, E(a) is the observed energy of activation) were obtained.

Amines↗
PubMed2001

Association between betel quid chewing, periodontal status and periodontal pathogens.

The present investigation examined whether an association exists between betel quid chewing and signs of periodontal disease and determined the prevalence of Actinobacillus actinomycetemcomitans and Porphyromonas gingivalis by polymerase chain reaction. The periodontal status of 34 betel quid chewers and 32 non-betel quid chewers were compared. A significantly higher prevalence of bleeding on probing was found in betel quid chewers than non-chewers among the subjects with higher plaque level, greater gingival inflammation, deeper probing depth or greater attachment loss. Also, the results suggested that betel quid chewers may harbor higher levels of infection with A. actinomycetemcomitans and P. gingivalis than non-betel quid chewers. The association persists after adjusting for severity of the clinical parameters. In conclusion, betel quid chewing was associated with a higher prevalence of bleeding on probing where higher clinical levels of disease existed, and with a likelihood of subgingival infection with A. actinomycetemcomitans and P. gingivalis.

Actinobacillus Infections↗
PubMed2001

Molecular genetic basis and prevalence of glycogen storage disease type IIIA in the Faroe Islands.

Glycogen storage disease type IIIA (GSD IIIA) is caused by mutations of the amyloglucosidase gene (AGL). For most populations, none of the AGL mutations described to date is particularly frequent. In this paper, we report that six children with GSD IIIA from the Faroe Islands were found to be homozygous for the novel nonsense mutation c.1222C>T (R408X) of the AGL gene. This mutation is easily detected by restriction enzyme digest with NsiI after mismatch PCR. Investigating five intragenic polymorphisms, we could show that this mutation was always associated with the same haplotype. The c.1222C>T mutation could be detected on two chromosomes of another 50 unselected GSD IIIA patients of other European or North American origin which means that this mutation plays a minor role worldwide. From the fact that we are currently aware of a total of 14 GSD IIIA cases in the Faroese population of 45 000, the observed prevalence is 1 : 3100. While the novel AGL mutation c.1222C>T was not detectable among 198 German newborns, nine out of 272 children from the Faroese neonatal screening program were found to be heterozygous for this mutation. Thus, the calculated prevalence is 1 : 3600 (95% CI 1:700-1:6400). We conclude that due to a founder effect, the Faroe Islands have the highest prevalence of GSD IIIA world-wide. The detection of the molecular defect has facilitated the diagnosis and has offered the opportunity for prenatal diagnosis in this patient group.

Codon, Nonsense↗
PubMed2001

Simvastatin treatment on postprandial hypertriglyceridemia in type 2 diabetes mellitus patients with combined hyperlipidemia.

Recent studies have shown that statins are effective in reducing fasting low-density lipoprotein-cholesterol (LDL-C) and triglyceride levels. However, it remains unknown if treatment with statins also lowers daily postprandial triglyceride concentrations, which may promote atherogenesis in type 2 diabetes subjects. Forty-one subjects with type 2 diabetes and combined hyperlipidemia who had stable glycemic control were randomly assigned to take simvastatin 20 mg (n = 27) or a placebo (n = 14) once daily for 12 weeks. The medication dosage was doubled after 4 weeks if a subject's LDL-C was not less than 130 mg/dL. Among these participants, 24 subjects (15 on simvastatin and 9 on placebo) agreed to take a meal tolerance test with isocaloric mixed meals (carbohydrate, 52%; fat, 33%, and protein, 15% of the daily caloric intake) and daytime hourly blood sampling from 8 AM to 4 PM. Simvastatin treatment reduced the fasting total cholesterol level from 237 +/- 5 to 178 +/- 6 mg/dL (-25%), the LDL cholesterol level from 150 +/- 6 to 87 +/- 5 mg/dL (-40%), and raised high-density lipoprotein-cholesterol (HDL-C) level from 36 +/- 2 to 40 +/- 2 mg/dL (+11%) (all P <.001). Fasting and daily ambient triglyceride concentrations from 8 AM to 4 PM decreased significantly in response to simvastatin administration (P <.001), but not to the placebo (P =.305). Simvastatin treatment not only decreased total cholesterol and LDL-C levels and increased HDL-C levels effectively, it also decreased fasting, as well as daily postprandial triglyceride concentrations, but had no effect on glycemic control in type 2 diabetes subjects with combined hyperlipidemia.

Cholesterol↗
PubMed2001

Tumor necrosis factor alpha -238 and -308 polymorphisms do not associate with insulin resistance in hypertensive subjects.

It is well established that, as a group, patients with essential hypertension are characterized by insulin resistance. Previous studies have shown that a biallelic polymorphism in the tumor necrosis factor (TNF)alpha promoter position -308 and -238 might be involved in the insulin resistance state in diabetic and/or nondiabetic subjects. We determined these polymorphisms in 235 nondiabetic hypertensive subjects and 246 unrelated normotensive controls. Fasting plasma glucose, insulin, lipoprotein, leptin, and TNFalpha concentrations were measured, in addition to plasma glucose and insulin responses to a 75-g oral glucose tolerance test (OGTT). Insulin sensitivity was also determined by an insulin suppression test in 69 hypertensive and 76 normotensive individuals. The results showed no association of these genotypic distributions between hypertensive and normotensive individuals both at -308 (GG, GA, and AA were 80.9%, 17.9%, and 1.3% in hypertensives, 84.2%, 15.4%, and 0.4% in normotensives, chi(2) = 1.68, P =.432) and at -238 (GG, GA, and AA were 98.3%, 1.7%, and 0% in hypertensives, 96.7%, 3.3%, and 0% in normotensives, chi(2) = 1.19, P =.276) sites. These results did not change even after adjustment for values of age and body mass index (BMI). Anthropometric measurements, fasting plasma glucose, insulin, lipoprotein concentrations, glucose, and insulin responses to OGTT, TNFalpha, and leptin concentrations were similar between the genotype at the -308 site both in hypertensive and normotensive groups. Insulin sensitivity, either measured by an insulin suppression test or homeostasis model assessment (HOMA) index, did not differ between the genotype at the -308 site in subjects with hypertension or normotension. Fasting plasma TNFalpha (10.2 alpha 0.5 pg/mL v 10.1 +/- 0.5 pg/mL, P =.928) concentrations did not differ between hypertensive and normotensive subjects even after adjustment for body fat and BMI values. We conclude that TNFalpha promoter gene polymorphisms at position -238 and -308 do not play a major role in the pathogenesis of insulin resistance in Chinese subjects with or without hypertension.

Alleles↗
PubMed2001

Angiotensin-converting enzyme inhibitor dosages in elderly patients with heart failure.

BACKGROUND: We sought to describe the dosages of angiotensin-converting enzyme (ACE) inhibitor prescribed to elderly patients with heart failure at hospital discharge, the factors associated with dosing level, and the association of these dosages with 1-year outcomes. METHODS: Demographic, procedural, and medication data were collected retrospectively from medical records at 18 Connecticut hospitals. Information on mortality and readmission was obtained from the Health Care Financing Administration administrative databases. Dosages of ACE inhibitor were grouped into 3 categories: dosages recommended in practice guidelines or higher (target dose), dosages used in clinical trials but lower than guideline recommendations (subtarget dose), and dosages lower than those used in clinical trials (low dose). RESULTS: A total of 554 patients, 65 years old or less with confirmed heart failure and systolic dysfunction, were prescribed an ACE inhibitor at discharge. Target, subtarget, and low doses were given in 19%, 63%, and 18% of the patients, respectively. Few demographic or clinical factors were related to lower dosages. Both subtarget and target doses of ACE inhibitors were associated with a significantly lower adjusted 1-year mortality (relative risk 0.67, P =.04; relative risk 0.51, P =.02, respectively) compared with low doses of ACE inhibitors. CONCLUSIONS: In a representative elderly cohort of patients with heart failure with systolic dysfunction, the majority (82%) were discharged on doses of ACE inhibitors consistent with those used in clinical trials. We observed a dose-response relationship between higher doses and lower mortality. Future studies will need to determine whether this association is causal.

Aged↗
PubMed2001

Hepatic storage of glycogen in Niemann-Pick disease type B.

We report 2 patients with confirmed Niemann-Pick disease, type B, with previous diagnoses of glycogen storage disease based on excessive glycogen on liver biopsy specimens. These cases emphasize the importance of a complete evaluation, including biochemical confirmation, for patients with suspected metabolic storage diseases.

Child, Preschool↗
PubMed2001

Impression cytology study of conjunctival epithelial phenotypes on the healing ocular surface after pterygium excision.

PURPOSE: To compare the process of conjunctival epithelial regeneration after three types of pterygium excision procedures. METHODS: Thirty-eight patients (45 eyes) with primary pterygium were randomly assigned to a bare-sclera procedure (group 1, 15 eyes of 12 patients), bare-sclera with intraoperative mitomycin C (MMC 0.02% for 30 seconds; group 2, 15 eyes of 14 patients), or pterygium excision with conjunctival autografting (group 3, 15 eyes of 12 patients). Controls were healthy fellow eyes and seven eyes of age- and sex-matched subjects. Impression cytology was performed preoperatively, at 1 and 2 weeks, and at 1, 3, 6, and 12 months after surgery. The nucleus-to-cytoplasm (N/C) ratio of nongoblet epithelial cells and goblet cell density (GCD) in the pterygial area were calculated and compared over time across treatment groups. RESULTS: Pterygium excision wounds healed in a similar four-stage process in all groups, but at different rates and with different final results. The N/C ratio was highest at about 1 month postoperatively in groups 1 and 2 and at 2 weeks in group 3, before gradually returning to control levels. Preoperatively, the GCD in treated eyes was almost twice that in control eyes (p = 0.001) but fell to zero immediately postoperatively. Goblet cells first appeared (with the most rapidly increased density) in group 3, followed by group 1. At 12 months, the mean GCD in groups 1 and 3 were not significantly different from those in controls, whereas the mean GCD in group 2 was still less than that of control (p = 0.02). CONCLUSIONS: Healing of conjunctiva is delayed by MMC and is promoted by autografting. Even 1 year after surgery, the ocular surface remains abnormal with respect to epithelial phenotypes in eyes treated by any of the three techniques.

Adult↗
PubMed2001

Canine model and genomic structural organization of glycogen storage disease type Ia (GSD Ia).

A canine model of glycogen storage disease Ia (GSD Ia), similar clinically, biochemically, and pathologically to the human disease, was established by crossbreeding Maltese and Beagle dogs carrying a mutated, defective glucose-6-phosphatase (G-6-Pase) gene. Ten puppies were born in three litters from these crossbreedings. Six were homozygous for the previously described M121I GSD Ia mutation. Of these six affecteds, two were stillborn, and one died at 2, 32, and 60 days of life, respectively (puppies A, B, C, D, E), while one is alive at age 15 months (puppy F). Affected puppies exhibited tremors, weakness, and neurologic signs when hypoglycemic. They had postnatal growth retardation and progressive hepatomegaly. Biochemical abnormalities included fasting hypoglycemia, hyperlactacidemia, hypercholesterolemia, hypertriglyceridemia, and hyperuricemia. Microscopic examination of tissues from affected puppies showed diffuse, marked hepatocellular vacuolation, with distended clear hepatocytes and central to marginally located rounded nuclei. In the kidneys of puppies D and E, there was segmental glomerular sclerosis and vacuolation of proximal convoluted tubular epithelium. Biochemical analysis revealed increased liver glycogen content and isolated markedly reduced G-6-Pase enzyme activity in liver and kidney. The canine G-6-Pase gene was characterized by screening a canine genomic library. It spans approximately 11.8 kb and consists of five exons with >90% amino acid sequence homology to the derived human sequence. The first 1.5 kb of the 5' region was sequenced and contains several putative response element motifs homologous to the human 5' region. Establishment of this canine colony of GSD Ia that closely resembles human disease and isolation of the canine genomic gene provides an excellent model for studying pathophysiology and long-term complications and an opportunity to develop novel therapeutic approaches such as drug and gene therapy.

Animals↗
PubMed2001

The incidence of coronary artery disease in patients with symptomatic bradyarrhythmias.

Symptomatic bradyarrhythmia occurs most often in aged patients. Most of these patients have multiple coronary risk factors and present with angina-like symptoms. The coexistence of CAD not only has major effects on their prognosis but also influences the long-term care. This study was designed to evaluate the incidence of coexistent CAD in patients with symptomatic bradyarrhythmias and its relationship to conventional coronary risk factors in Chinese people. From May 1996 to April 1998, we prospectively studied all consecutive patients admitted to our institution for symptomatic bradyarrhythmias requiring permanent pacemaker implantation. Coronary angiographies were performed non-selectively at the same session of pacemaker implantation. Based on the presence or absence of CAD, patients were divided into two groups for analysis. Multivariate logistic regression analysis was performed to determine independent predictors of CAD including sex, age, diabetes mellitus (DM), hypertension, hypercholesterolemia, and smoking. The odds-ratio (OR) and 95% confidence interval (CI) were determined. A total of 113 patients [68 males and 45 females, mean age 70.4+/-8.2 years old (range 45-86)] were included in our study. The diagnosis was sick sinus syndrome in 69 patients (61%) and atrioventricular block in 44 patients (39%). The incidence of CAD based on coronary angiography was 20%. The nodal-related artery was seldom involved among patients with coexistent CAD and symptomatic bradyarrhythmias (9%), and most patients had significant stenosis over LAD (74%). The baseline characteristics and presenting symptoms were not different statistically between patients with or without CAD. Hypercholesterolemia (OR 6.6, 95% CI 2.0-22.2, p=0.002) and DM (OR 4.7, 95% CI 1.3-17.2, p=0.020) were the two most significant independent predictors of CAD. In our patients with symptomatic bradyarrhythmias requiring permanent cardiac pacing, the incidence of CAD was 20% as determined by coronary angiography (CAG). Hypercholesterolemia and DM were the two most significant independent predictors for CAD in these patients. The nodal artery was seldom involved in patients with coexistent CAD and symptomatic bradyarrhythmias.

Aged↗
PubMed2001

Immunohistochemical and reverse transcription-polymerase chain reaction expression analysis of tyrosinase and microphthalmia-associated transcription factor in angiomyolipomas.

Angiomyolipomas (AMLs) show a characteristic immunoreactivity with melanocyte differentiation markers such as monoclonal antibody (mAb) HMB45, which detects melanocyte differentiation antigen gp100 and mAb A103 reacting with Melan-A/MART-1. Monoclonal antibody T311 to tyrosinase (a key enzyme of melanogenesis) and mAb D5 to the microphthalmia (Mitf) antigen are two newly available markers of melanocytic differentiation. The authors tested 15 AMLs with T311 and D5 by immunohistochemistry and a subset of 3 cases by reverse transcription-polymerase chain reaction for their expression of tyrosinase and Mitf mRNA. T311 showed poor sensitivity in AMLs because only focal staining was seen in 1 out of 15 cases, although tyrosinase mRNA was found in all tested cases. Mitf mRNA was present in 3 of 3 tested cases, and D5 was positive in 15 of 15 AMLs. However, D5 immunostaining often was focal and not as homogeneous as A103, which was analyzed in a previous study. D5 staining also could be seen in other cell types such as normal renal tubular cells, macrophages, and renal cell carcinoma. The current results show that in contrast with HMB45 and A103, T311 has little or no value in the diagnosis of AMLs. D5 may be useful in a panel of antibodies in the diagnosis of AMLs.

Angiomyolipoma↗