Search PubMed⌕ Search

Biomedical subjects

J W Chen

Publications and source records attributed to J W Chen.

At least 73 records · Page 4Linked to original sources
PubMed1999

Early alteration of coronary hemodynamics in late restenosis after coronary angioplasty.

It is not known whether changes in coronary hemodynamics may antedate the development of restenosis after percutaneous coronary transluminal angioplasty (PTCA). The purpose of this study was to evaluate the early change in coronary microvascular function in patients with late restenosis after PTCA. Coronary hemodynamics were studied in series before, immediately after, 2 weeks and 3 months after successful PTCA in 12 male patients with a single lesion of the left anterior descending coronary artery. In each patient, great cardiac venous flow (GCVF) and oxygen content were measured both at baseline and during hyperemia induced by adenosine infusion. The sequential changes of coronary hemodynamics were compared between patients with and without restenosis at 3 months after PTCA. Basic characteristics did not differ between the patients with (n = 6) and those without restenosis (n = 6). Luminal diameter stenosis (in percentage) was also similar between the two groups both before (79.2 +/- 18.4% vs 83.0 +/- 9.6%, p = NS) and up to 2 weeks after PTCA (25.8 +/- 10.9% vs 28.5 +/- 7.9%, p = NS). In patients without restenosis, basal and hyperemic GCVF was unchanged up to 2 weeks after PTCA. There was a significant increase in CFR 3 months after PTCA. In patients with restenosis, basal GCVF was significantly increased and hyperemic GCVF was unchanged immediately after PTCA. However, 2 weeks after PTCA, basal GCVF was decreased while luminal diameter was still preserved. In comparison with those without restenosis, patients with restenosis had significantly lower CFR before (1.98 +/- 0.42 vs 2.69 +/- 0.46, p = 0.019), immediately after (1.47 +/- 0.27 vs 2.24 +/- 0.47, p = 0.006) and 3 months after PTCA (1.51 +/- 0.32 vs 3.40 +/- 0.54, p = 0.001). In patients without restenosis, the recovery of coronary microvascular function was delayed up to 3 months after PTCA. In patients with late restenosis, basal coronary microvascular tone was altered within 2 weeks after PTCA suggesting early deterioration of coronary microvascular function before the development of angiographic restenosis.

Aged↗
PubMed1999

Coronary flow reserve and ischemic-like electrocardiogram in patients with symptomatic mitral valve prolapse.

The purpose of the present study was to determine whether coronary microvascular function is impaired in patients with symptomatic mitral valve prolapse (MVP) and whether ischemia-like ECG, if present, is related to coronary microvascular dysfunction. Twenty chest pain patients with normal coronary angiograms and MVP proven by echocardiogram were included. Both treadmill exercise test (TET) and coronary hemodynamic study were done in each patient. Coronary flow reserve (CFR) was determined by measuring coronary sinus flow (CSF) or great cardiac venous flow (GCVF) both at baseline and after dipyridamole 0.56 mg/kg IV for 4 minutes (maximum). All patients were divided into 2 groups with either negative (TET-) or positive results of TET (TET+). Another 10 subjects with atypical chest pain, normal coronary angiograms, echocardiogram and TET were used as controls. There were no differences in GCVF, either at baseline or after dipyridamole infusion, among the 3 groups. Calculated CFR using GCVF was similar among the 3 groups. However, baseline CSF was higher in the TET+ group (TET- vs TET+ vs control: 77 +/- 24 vs 96 +/- 31 vs 75 +/- 12 ml/min, p < 0.05) and maximum CSF was lower in the TET- group (TET- vs TET+ vs control: 167 +/- 25 vs 219 +/- 85 vs 238 +/- 80 ml/min, p < 0.05). Calculated CFR using CSF was significantly reduced in both the TET- (2.26 +/- 0.4) and TET+ groups (2.31 +/- 0.7) as compared with the control subjects (3.18 +/- 0.95, p < 0.01). There were no differences in any of the hemodynamic parameters between the TET- and TET+ groups. Coronary microvascular function could be impaired in patients with symptomatic MVP. Such impairment, when presented, was probably regional and outside the territory of the left anterior descending coronary artery. However, it was irrelevant to the presence of ischemic-like ECG during exercise.

Adult↗
PubMed1999

[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↗
PubMed1998

Parasympathetic withdrawal antedates dynamic myocardial ischemia in patients with syndrome X.

This study was to evaluate the dynamic changes in cardiac autonomic control preceding electrocardiographic (ECG) myocardial ischemia in patients with syndrome X. Twenty-four-hour ambulatory ECG was obtained in 34 consecutive patients in a drug-free state. Fourteen (41%) of them, aged 58.8+/-13.5 years, presented a total of 19 ischemic episodes, mean duration 12.4+/-19.8 min (ranged 1 to 90 min). Heart rate variability was measured for 24 h; for 3 min and 30 min before, and during the 15 min (in five 3-min intervals) immediately antedating ST segment depression; and for another 3 min after ST segment back to normal. There were significant progressive shortenings in sinus cycle lengths over the 30 min preceding myocardial ischemia (-30 vs -3 minute, 822+/-32 ms vs 637+/-23 ins, P<0.05; a decrement of 22.5%). The sinus cycle lengths lengthened after ischemia ceased. High frequency activity, pNNSO and rMSS.D. were significantly reduced from the -30 min baseline to a nidus in the last 3 min before ischemia (P<0.05), whereas low frequency band and low/high frequency ratio did not present significant change. These findings strongly argue that cardiac autonomic control, especially vagal withdrawal, is involved in the pathogenesis of dynamic myocardial ischemia in syndrome X.

Adult↗
PubMed1998

Regulation of cardiomyocyte apoptotic signaling by insulin-like growth factor I.

Apoptosis is regulated by specific intracellular signaling pathways. The development of cardiomyopathy involves the apoptosis of cardiomyocytes; however, the details of their apoptotic signaling are not yet known. Insulin-like growth factor I (IGF I) is an important survival growth factor for myocardium and other tissues, but the effects of IGF I on apoptotic signaling remain largely unknown. To study apoptotic signaling pathways in cardiomyocytes and to understand IGF I actions on the apoptotic signaling of cardiac muscle cells, we have defined the effects of IGF I on Bcl-2, Bax, caspase 3, DNA fragmentation, and cell survival in primary cardiomyocytes. Compared with Bax levels, the levels of Bcl-2 were found to be quite low in these cells. Serum withdrawal and doxorubicin reduced cell viability, increased fragmentation of DNA, increased cellular contents of Bax, and activated caspase 3. IGF I enhanced cell viability, suppressed DNA fragmentation, attenuated Bax induction, and suppressed caspase 3 activation. The levels of Bcl-2-associated Bax were increased after serum withdrawal and incubation with doxorubicin and were reduced by IGF I. Thus, cardiomyocyte apoptosis induced by serum withdrawal and doxorubicin likely results, in part, from the induction of Bax and activation of caspase 3, but IGF I may inhibit cardiomyocyte apoptosis by attenuating Bax induction and caspase 3 activation. These findings provide new insight into the mechanisms of cardiomyocytes apoptosis and may help elucidate how IGF I modulates apoptotic signaling in cardiac muscle.

Animals↗
PubMed1998

Staphylococcal neonatal necrotising fasciitis: survival without radical debridement.

Necrotising fasciitis is a serious infection associated with high morbidity and mortality. The conventional treatment is radical resection of the involved area with antibiotic as well as intensive supportive therapy. We describe a case of extensive truncal necrotising fasciitis in a neonate, secondary to Staphylococcus aureus infection successfully treated with intensive antibiotic therapy and multi-organ support, followed by fasciotomies, drainage and betadine irrigation. The successful outcome without radical resection could be due to the viability of superficial skin, S aureus as the causative organism and the excellent blood supply of cutaneous neonatal tissue.

Anti-Bacterial Agents↗
PubMed1998

A drug-lipid interaction model: atropine induces interdigitated bilayer structure.

X-ray diffraction and fluorescence methods have been carried out to examine the effects of a drug, atropine, on the structure of model membranes: dipalmitoylphosphatidylglycerol(DPPG) multilamella vesicles(MLVs). A structural analysis by small angle x-ray diffraction shows that, with incorporation of atropine, the lamella repeating period of DPPG MLV is decreased from 5.89 nm to 4.52 nm. Using fluorescence probe 1,6-diphenyl-1,3,5-hexatriene(DPH) we find that the fluorescence intensity of DPH reduces largely at a narrow scope of atropine concentration. The experiments of fluorescence polarization of n-(9-anthroyloxyl)-stearic acid (nAS) and 16-(9-anthroyloxyl)-palmiticacid (16AP) discover that the normal polarization gradient almost disappears in DPPG/atropine system. By colligating the above results, we can draw a conclusion that atropine induces the transition from non-interdigitated to interdigitated stricture of DPPG vesicles in gel phase, which provides a sound model of drug-lipid interaction.

Atropine↗
PubMed1998

Serine protease of hepatitis C virus expressed in insect cells as the NS3/4A complex.

Hepatitis C virus (HCV) protease NS3 and its protein activator NS4A participate in the processing of the viral polyprotein into its constituent nonstructural proteins. The NS3/4A complex is thus an attractive target for antiviral therapy against HCV. We expressed the full-length NS3 and NS4A in insect cells as a soluble fusion protein with an N-terminal polyhistidine tag and purified the two proteins to homogeneity. Cleavage at the junction between HisNS3 and NS4A occurs during expression, producing a noncovalent complex between HisNS3 and NS4A with a subnanomolar dissociation constant. We purified the HisNS3/4A complex by detergent extraction of cell lysate and by metal chelate chromatography. We removed the His tag by thrombin cleavage and then further purified the complex by gel filtration. The purified NS3/4A complex is active in a protease assay using a synthetic peptide substrate derived from the NS5A-NS5B junction, with kcat/K(m) of 3700 (+/- 600) M-1 s-1, an order of magnitude above those previously reported for NS3 expressed by other strategies. This high protease activity implies that the full-length sequences of NS3 and NS4A are required for optimal activity of the NS3 protease domain. We examined the dependence of the NS3/4A protease activity on buffer conditions, temperature, and the presence of detergents. We find that, under most conditions, NS3 protease activity is dependent on the aggregation state of the NS3/4A complex. The monodisperse, soluble form of the NS3/4A complex is associated with the highest protease activity.

Adenosine Triphosphatases↗
PubMed1998

Cloning the chicken leptin gene.

Chicken is characterized by a relative insulin resistance and a physiological hyperglycemia (2g/L) and is also subjected to fattening. Fat deposits in chicken, as in mammals, are regulated by environmental and genetic factors. In mammals, leptin, an adipose cell-specific secreted protein has been characterized that is encoded by ob gene. Leptin regulates satiety through hypothalamic specific receptors, energy balance, energy efficiency and contributes to adaptation to starvation. The leptin gene has been characterized in various mammalian species, and the cloning and sequencing of the chicken leptin gene (ob gene) are reported. Using RT-PCR and primers flanking the coding region of the leptin gene selected from known mammalian sequences, we have successfully amplified a 600-bp fragment from chicken liver and adipose tissue total ARNs. The amplified fragment exhibits a similar size to that of the coding region of the mammalian leptin gene. The sequences of the coding region of chicken liver and adipose tissue are identical and presented 97%, 96% and 83% similarity to the mouse, rat and human sequences, respectively. Finally, this is the first report showing that leptin gene expression in chicken is not exclusively localized in adipose tissue but is also expressed in liver. The expression of leptin in liver may be associated with a key role of this organ in avian species in controlling lipogenesis.

Adipose Tissue↗
PubMed1998

Cognitive improvement despite minimal arachnoid cyst decompression.

There are relatively few reports that evaluate the cognitive functions of patients with arachnoid cysts. Presumably, these 'silent cysts' are regarded as incidental findings with no functional significance. Although postoperative clinical improvement is well documented in patients with significant reduction in cystic volume, the current report describes a patient who underwent cystoperitoneal shunting due to mass effect, with minimal postoperative decompression. Neuropsychological testing indicated significant cognitive improvement in verbal learning, memory, visual-perceptual abilities, constructional skills, conceptual shifting, and psychomotor speed after shunt placement, despite marginal evidence of decompression. These findings suggest that (1) significant cognitive changes can occur in these patients, despite minimal postoperative regression of the lesion, (2) cognitive measures may provide an alternative, functional index of outcome efficacy, and (3) reliance on traditional outcome measures (i.e. anatomical decompression or resolution of clinical symptoms) may underestimate the efficacy of surgical intervention for these patients.

Adult↗
PubMed1998

Molecular cloning and nucleotide sequence of 3'-terminal region of classical swine fever virus LPC vaccine strain.

A cDNA of the 3'-terminus of classical swine fever virus (LPC vaccine strain) was cloned and sequenced. The 3431 nucleotides and deduced amino acid sequences were compared with those of other pestiviruses, and the similarity of nucleotide sequences and deduced amino acid sequences were found to be 84-95% and 95-98%, respectively. Similar to other isolates of classical swine fever virus, the sequenced region included the non-structural gene p58 (NS5A) and part of p76 (NS5B) gene. The p76 gene of LPC vaccine strain also contained a highly conserved motif G-D-D (Gly-Asp-Asp) that is present in the RNA replicase of positive-stranded RNA viruses. With the sequence data currently available, we carried out a phylogenetic analysis and obtained a genealogical relationship among members of the classical swine fever virus.

Amino Acid Sequence↗
PubMed1998

Effects of La3+ on lipid fluidity and structural transitions in human erythrocyte membranes.

The effects of La3+ on the structure and function of human erythrocyte membranes were investigated by fluorescence polarization, spin-labeled electron spin resonance (ESR) and differential scanning calorimetry (DSC). The results showed that increasing concentrations of La3+ inhibited (Na(+) + K+)-ATPase and Mg(2+)-ATPase activities. La3+ lowered the lipid fluidity of erythrocyte membranes and induced structural transitions in erythrocyte membranes.

Ca(2+) Mg(2+)-ATPase↗
PubMed1998

Differentiating syndrome X from coronary artery disease by treadmill exercise test in patients with chest pain and exercise-induced myocardial ischemia.

Even though the underlying mechanisms of myocardial ischemia may be different, it is difficult to differentiate syndrome X from coronary artery disease (CAD) by means of the treadmill exercise test in elderly patients with chest pain and exercise-induced myocardial ischemia. One hundred sex- and age-matched patients-42 with syndrome X and 58 with CAD-were studied. Another 10 subjects with atypical chest pain, negative treadmill exercise test, and normal-appearing coronary angiograms served as controls. We evaluated the difference in exercise performance between patients with syndrome X and CAD, and the treadmill exercise test was undertaken with modified Bruce protocol within 2 weeks before coronary angiography. Parameters including time to 1 mm ST segment depression (STD), exercise duration (ED), heart rate (HR), systolic blood pressure, rate-pressure product (RPP), and percentage of age-predicted maximum HR (% HR) at different stages of the test were measured and then compared among the three groups of patients. Compared with CAD patients, syndrome X patients had significantly higher HR, % HR, and RPP at the time of 1 mm STD and at peak exercise. The time to 1 mm STD and ED were longer in syndrome X than in CAD patients. However, ED was shorter and HR, % HR, and RPP at peak exercise were similar in syndrome X patients as compared with control subjects. The new criterion of combined ED (> or =315 seconds) and RPP at peak exercise (> or =24,000 beats x mmHg/min) was found to be highly specific (86%) and moderately sensitive (64%) in differentiating syndrome X from CAD patients. The positive likelihood ratio for this criterion was 4.57 and negative likelihood ratio was 0.42. In conclusion, syndrome X patients had better exercise performance than CAD patients, but less ED and similar workload when compared with control subjects. The new criterion proposed in this study may provide a quick and simple way to differentiate syndrome X from CAD in a group of aged and predominantly male patients with chest pain and positive treadmill exercise test.

Adult↗
PubMed1998

Differential glucose tolerance in dipper and nondipper essential hypertension: the implications of circadian blood pressure regulation on glucose tolerance in hypertension.

OBJECTIVE: The goals of this study were to compare glucose tolerance in dipper and nondipper hypertensive patients and to explore the cause of glucose intolerance in essential hypertension. RESEARCH DESIGN AND METHODS: A total of 50 patients <45 years old who had essential hypertension were recruited and studied by 24-h blood pressure monitoring and an oral glucose tolerance test (OGTT). Autonomic function was assessed with spectral analysis of heart rate variability RESULTS: Dipper hypertensive patients (n=25) had lower nocturnal blood pressure than nondipper (n=25) patients. During OGTT, postprandial glucose levels were higher in the nondippers at 0, 90, and 120 min (all P < 0.05). Nondippers had a higher fasting insulin/glucose ratio than was apparent in normal control subjects. Despite higher postprandial glucose levels, nondippers had lower postprandial insulin levels. These results suggest that nondippers were insulin resistant and that their pancreatic beta-cell function was impaired. For all patients, nocturnal reduction of blood pressure was inversely related to total glucose levels under the OGTT curve and was positively related to postprandial insulin levels. Daytime heart rate did not differ between the dippers and nondippers, but nocturnal heart rate was higher in the nondippers, suggesting that nocturnal sympathetic activities were higher among the nondippers. Spectral analysis of heart rate variability suggests that the nondippers had lower parasympathetic activities and unbalanced sympathetic/parasympathetic outflow. CONCLUSIONS: These findings indicate that nondipper hypertensive patients are more glucose intolerant than are dipper patients. The abnormalities of glucose metabolism in nondippers could be explained by insulin resistance and beta-cell dysfunction. The results of spectral analysis suggest that abnormal autonomic outflow may represent a possible link between hypertension and associated metabolic dysfunction.

Adult↗