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Biomedical subjects

J L Lin

Publications and source records attributed to J L Lin.

At least 37 records · Page 2Linked to original sources

Flow cytometry compared with indirect immunofluorescence for rapid detection of dengue virus type 1 after amplification in tissue culture.

Dengue virus (DV) was detected early in infected mosquito C6/36 cells by using indirect immunofluorescence (IF) in conjunction with flow cytometry. Three fixation-permeabilization methods and three DV serotype 1 (DEN-1)-specific monoclonal antibodies, 8-8 (anti-E), 16-4 (anti-NS1), and 15F3-1 (anti-NS1), were evaluated for the detection of DEN-1 in infected C6/36 cells. We found that these three monoclonal antibodies were capable of detecting DV in C6/36 cells as early as 24 h postinoculation by using a conventional indirect IF stain. Both 8-8 and 16-4 detected DV earlier and showed a greater number of DV-positive cells than 15F3-1. In flow cytometry, 3% paraformaldehyde plus 0.1% Triton X-100 with 16-4, the best fixation-permeabilization method for testing DV, showed higher sensitivity (up to 1 PFU) than indirect IF stain. The higher sensitivity of 16-4 in detecting DEN-1 was found with both IF and flow cytometry. Flow cytometry, which had a sensitivity similar to that of nested reverse transcription-PCR, was more sensitive in detecting DV in the infected mosquito cells 10 h earlier than the conventional IF stain. When clinical specimens were amplified in mosquito C6/36 cells and then assayed for DV using flow cytometry and conventional virus isolation at day 7 postinfection, both methods had 97.22% (35 out of 36) agreement. Moreover, among 12 positive samples which were detected by conventional culture method, the flow cytometry assay could detect DV in 58.33% (7 out of 12) of samples even at day 3 postinfection. In conclusion, both monoclonal antibodies 8-8 and 16-4 can be used for the early detection of DEN-1-infected C6/36 cells, with 16-4 (anti-NS1) being the best choice for the rapid diagnosis of DV by both the IF staining and flow cytometry methods.

Animals↗

[Diagnosis of non-typical myocarditis by applying immunohistochemical method of CD68].

OBJECTIVE: To make a distinction between myocarditis and the reaction to some pathological state of myocardium. METHODS: Myocardium of 26 cases with sudden cardiac death were stained and LM light microscopies with immunohistochemical method 10 cases with normal myocardium were contrasted. RESULTS: A great deal of stained positive monocyte of immunohistochemistry emerged in the parasetions of myocarditis patients with various farms and stacking(> 15). CONCLUSION: The stain of immunohistochemistry can be used as one of the indications for diagnosing non-typical myocarditis.

Adolescent↗

[Computer-assisted acquisition and analysis of high-resolution spectrum].

Based on the unique characteristic of spectral line center in the whole spectrum and noise threshold, a computer approach and program for the determination of spectral line position and relative intensity automatically are presented in this paper. Exploring this approach and computer program, we pre-analyzed the partially overlapped 16 line TuFIR experiment spectra of CHF3. The results of line positions and intensities for these TuFIR spectra are in excellent agreement with the results by least-square fit with heavily manual inference. The accuracy and efficiency of this method and program will ensure their wide application in complex high-resolution molecular spectrum.

Algorithms↗

Creation of "quantum platelets" via strain-controlled self-organization at steps.

We demonstrate, by both theory and experiment, the strain-induced self-organized formation of "quantum platelets," monolayer-thick islands of finite dimensions. They form at the early stage of heteroepitaxial growth on a substrate with regularly spaced steps, and align along the steps. In the direction perpendicular to substrate steps, the island position and spacing can be preselected through substrate miscut. Along the steps, the island size and density are controlled by self-organized growth.

Journal Article↗

Radiofrequency catheter ablation of tachycardia in children with and without congenital heart disease: indications and limitations.

From 1993 to 1998, a total of 100 consecutive pediatric patients with tachycardia (45 male and 55 female, aged 1 year 10 months to 17 years, 11+/-4 year) who underwent electrophysiological study were reviewed. Eleven of them were younger than 5 years. Two had tachycardia-related cerebrovascular accident. Congenital heart disease was found in 12 patients. After propofol anesthesia, the clinical tachycardia could not be induced in three (two atrial tachycardia and one AV nodal re-entrant tachycardia) and became nonsustained in five (atrial tachycardia). Mechanical ablation occurred in three and two had subsequent recurrences. Among the 85 cases who received radiofrequency ablation, the overall final success rate of RF ablation for all diagnoses was 94% with a diagnosis-specific success rate ranging from 100 to 57%. Tachycardia cardiomyopathy was noted in four (three atrial tachycardia and one junctional ectopic tachycardia) and all regressed after successful ablation. Success in two patients with left posterioseptal accessory pathway could only be achieved by delivering the energy at the middle cardiac vein. Two patients with right atrial isomerism had an 'AV nodal-to-AV nodal tachycardia' which was eliminated by ablation. Total recurrence rate was 13% but final success was achieved in all during re-study except the three patients who refused re-intervention. The atrial tachycardia developed in postoperative congenital heart disease was associated with the lowest success rate (57%) and highest recurrence rate (25%). Procedure-related complications occurred in four; two with transient brachial palsy, one with first-degree AV block and one with blood loss requiring blood transfusion. In conclusion, the experience of this single center confirmed the efficacy and safety of radiofrequency catheter ablation in treating pediatric arrhythmias, but the limitations in postoperative arrhythmias and the effects of propofol on tachycardia induction (especially the atrial tachycardia) need to be improved.

Anesthetics, Intravenous↗

Forced expression of a dominant-negative chimeric tropomyosin causes abnormal motile behavior during cell division.

Forced expression of the chimeric human fibroblast tropomyosin 5/3 (hTM5/3) in CHO cell was previously shown to affect cytokinesis [Warren et al., 1995: J. Cell Biol. 129:697-708]. To further investigate the phenotypic consequences of misexpression, we have compared mitotic spindle organization and dynamic 2D and 3D shape changes during mitosis in normal cells and in a hTM5/3 misexpressing (mutant) cell line. Immunofluorescence microscopy of wild type and mutant cells stained with monoclonal anti-tubulin antibody revealed that the overall structures of mitotic spindles were not significantly different. However, the axis of the mitotic spindle in mutant cells was more frequently misaligned with the long axis of the cell than that of wild type cells. To assess behavioral differences during mitosis, wild type and mutant cells were reconstructed in 2D and 3D and motion analyzed with the computer-assisted 2D and 3D Dynamic Image Analysis Systems (2D-DIAS, 3D-DIAS). Mutant cells abnormally formed large numbers of blebs during the later stages of mitosis and took longer to proceed from the start of anaphase to the start of cytokinesis. Furthermore, each mutant cell undergoing mitosis exhibited greater shape complexity than wild type cells, and in every case lifted one of the two evolving daughter cells off the substratum and abnormally twisted. These results demonstrate that misexpression of hTM5/3 in CHO cells leads to morphological instability during mitosis. Misexpression of hTM5/3 interferes with normal tropomyosin function, suggesting in turn that tropomyosin plays a role through its interaction with actin microfilaments in the regulation of the contractile ring, in the localized suppression of blebbing, in the maintenance of polarity and spatial symmetry during cytokinesis, and in cell spreading after cytokinesis is complete.

Animals↗

Intravenous sotalol decreases transthoracic cardioversion energy requirement for chronic atrial fibrillation in humans: assessment of the electrophysiological effects by biatrial basket electrodes.

OBJECTIVES: This study was undertaken to assess the effects of sotalol on the transthoracic cardioversion energy requirement for chronic atrial fibrillation (AF) and on the atrial electrograms during AF recorded by two basket electrodes. BACKGROUND: The effects of sotalol infusion on transthoracic electrical cardioversion for chronic atrial fibrillation in humans have not been well investigated. METHODS: We included 18 patients with persistent AF for more than three months. Atrial electrograms were recorded by two basket electrodes positioned in each atrium respectively. Transthoracic cardioversion was performed before and after sotalol 1.5 mg/kg i.v. infusion. RESULTS: In the 14 patients whose AF could be terminated by cardioversion before sotalol infusion, the atrial defibrillation energy was significantly reduced after sotalol infusion (236 +/- 74 jules [J] vs. 186 +/- 77 J; p < 0.01). Atrial fibrillation was refractory to cardioversion in four patients at baseline and was converted to sinus rhythm by cardioversion after sotalol infusion in two of them. We further divided the patients into two groups. Group A consisted of 10 patients in whom the energy requirement was decreased by sotalol while group B consisted of eight patients in whom the energy requirement was not decreased. The mean A-A (atrial local electrogram) intervals during AF were significantly increased after sotalol infusion in both groups, but the increment of A-A interval was significantly larger in group A than it was in group B patients (36 +/- 13 ms vs. 22 +/- 8 ms for the right atrium; 19 +/- 7 ms vs. 9 +/- 7 ms for the left atrium; both p < 0.05). The spatial and temporal dispersions of A-A intervals were not significantly changed after sotalol infusion in both atria in both groups. CONCLUSIONS: Sotalol decreases the atrial defibrillation energy requirement by increasing atrial refractoriness but not by decreasing the dispersion of refractoriness.

Adult↗

Response of nasopharyngeal carcinoma cells to Epstein-Barr virus infection in vitro.

Many nasopharyngeal carcinoma (NPC) biopsy specimens contain Epstein-Barr virus (EBV). However, the response of NPC cells to EBV infection in vitro and in vivo is not well characterized. In this experiment we infected NPC cells with EBV particles through endocytosis of a complex of EBV immunoglobulin A (IgA) secretory component (SC) protein to observe the response of host cells to the foreign viral infection in vitro. We found that EBV particles were endocytosed and stabilized in NPC nuclei 24 hours after infection; the EBV genomes were then gradually decreased after serial passages within 3 to 4 weeks by the following pathway: the EBV genomes first moved toward the nuclear envelope from the center of the nucleus; after crossing the nuclear envelope, they moved into the cytoplasm and toward the plasma membrane and were discharged by exocytosis. At the 10th day of EBV infection, EBV-latent membrane protein-1 and Epstein-Barr nuclear antigen (EBNA)-1 protein expressions could be detected, but not EBV-viral capsid antigen. Observation of EBNA-1 protein and host growth factor and cytokine gene expressions in the weeks after incubation revealed that the EBNA-1 protein expression was decreased proportionally with decrease of EBV genome. The mRNA expression of epithelial growth factor receptor, transforming growth factor (TGF)-alpha, interleukin (IL)-1beta, IL-6, and granulocyte-macrophage colony-stimulating factor increased within 1 to 2 weeks after infection, and gradually recovered to the original level at 3 to 4 weeks, whereas the mRNAs of TGFbeta1, TGFbeta receptor type I (TGFbetaRI), TGFbetaR type II, IL-8, and tumor necrosis factor-alpha remained unchanged. It is concluded that in vitro EBV infection in NPC cells results in increase of certain growth factor and cytokine gene expressions in host cells. The change in gene expression returns to the original level approximately 3 to 4 weeks after infection because of exocytosis of EBV DNA by the infected cells through an unidentified mechanism.

Base Sequence↗

Decreased autonomic nervous system activity as assessed by heart rate variability in patients with chronic tetraplegia.

OBJECTIVES: To assess the alterations of autonomic nervous functions and sympathovagal balance of the subjects with spinal cord injuries (SCIs) in different levels by heart rate variability analysis. DESIGN: Prospective, observational study. SETTING: All participants were recruited from the outpatient clinic from National Taiwan University Hospital, which is a tertiary referral center. PARTICIPANTS: Thirty-one patients with traumatic chronic complete SCI (more than 6 months): 14 with paraplegia (Group A), and 17 with tetraplegia (Group B). MAIN OUTCOME MEASURES: Heart rate variability assessed by 24-hour Holter monitoring. RESULTS: Two patients in Group A and 1 in Group B were excluded from final data analysis because of poor recording data. Two time domain variables, the standard deviation (SD) of all normal RR intervals (SDNN) and the mean of the SDs of all normal RR intervals for all 5-minute intervals (SDNNi), over 24 hours were decreased in Group B. All time domain variables, SDNN, SDNNi, root mean square of the successive normal RR interval difference (rMSSD), and the percentage of RR intervals differing >50msec from the preceding one (pNN50), were decreased during the nighttime recordings (all p < .05) in Group B. The very-low-frequency, low-frequency (LF), and high-frequency (HF) components of the power spectrum of the RR intervals were also decreased in Group B (p < .05), irrespective of the daytime and nighttime recordings. The LF-to-HF ratio did not differ significantly in these two groups, indicating the maintained sympathovagal balance in the chronic SCI patients. CONCLUSION: These findings suggested that the autonomic nervous system activity was depressed in the patients with chronic tetraplegia, but the autonomic nervous system still maintained homeostasis.

Adult↗

Role of electrophysiological studies and arrhythmia intervention in repairing Ebstein's anomaly.

BACKGROUND: Repairing Ebstein's anomaly without correction of associated arrhythmia may result in sudden death. Catheter or surgical ablation is indicated for various symptomatic tachyarrhythmias in Ebstein's anomaly. METHODS: Between October 1973 and October 1997, 30 patients with Ebstein's anomaly underwent surgical repair in our hospital. Tricuspid valve replacement was performed in 13 patients, tricuspid annuloplasty and valvuloplasty in the remaining 17 patients. Preoperative electrophysiological studies were performed in 11 patients after 1980. Concomitant arrhythmia ablation was done in 10 patients: 4 for Wolff-Parkinson-White syndrome, 2 for atrioventricular (AV) nodal reentrant tachycardia, one for ventricular tachycardia and 3 for paroxysmal atrial flutter and fibrillation. RESULTS: No mortality or major morbidity occurred in those patients undergoing arrhythmia intervention. There were 7 deaths in total; 6 died suddenly, and the other died of purulent mediastinitis. None of the 6 sudden deaths underwent preoperative electrophysiological evaluation. The functional recovery was good in all survivals. CONCLUSIONS: We conclude that detailed preoperative electrophysiological evaluation in patients with Ebstein's anomaly is mandatory. Aggressive surgical intervention of the associated arrhythmias in addition to anatomic correction can reduce the sudden death in Ebstein's anomaly.

Adolescent↗

Carbofuran-induced delayed neuropathy.

BACKGROUND: Although carbamates have been widely used in the world for many years, carbamate-induced delayed neuropathy is rare. We report what appears to be delayed neuropathy caused by poisoning with carbofuran, a cholinesterase-inhibiting carbamate, although the certainty of diagnosis is somewhat limited by the lack of a sural nerve biopsy and spinal fluid examination. CASE REPORT: A 23-year-old man attempted suicide by ingesting 100 mL of carbofuran (2,3-dihydro-2,2-dimethyl-7-benzofuranyl methylcarbamate). After recovering from acute cholinergic toxicity, he had notable paresthesia in his lower limbs and difficulty walking. Electrophysiologic findings revealed sensorimotor neuropathy. Recovery began at 1 week and continued for 4 months. A similar delayed neuropathy has been described with carbamate, 1-naphthyl N-methylcarbamate, and m-tolyl methylcarbamate, but not with carbofuran insecticides.

Adult↗

Distal end of the atrioventricular nodal artery predicts the risk of atrioventricular block during slow pathway catheter ablation of atrioventricular nodal re-entrant tachycardia.

OBJECTIVE: To search for a reliable anatomical landmark within Koch's triangle to predict the risk of atrioventricular (AV) block during radiofrequency slow pathway catheter ablation of AV nodal re-entrant tachycardia (AVNRT). PATIENTS AND METHODS: To test the hypothesis that the distal end of the AV nodal artery represents the anatomical location of the AV node, and thus could be a useful landmark for predicting the risk of AV block, 128 consecutive patients with AVNRT receiving slow pathway catheter ablation were prospectively studied in two phases. In phase I (77 patients), angiographic demonstration of the AV nodal artery and its ending was performed at the end of the ablation procedure, whereas in the subsequent phase II study (51 patients), the angiography was performed immediately before catheter ablation to assess the value of identifying this new landmark in reducing the risk of AV block. Multiple electrophysiologic and anatomical parameters were analysed. The former included the atrial activation sequence between the His bundle recording site (HBE) and the coronary sinus orifice or the catheter ablation site, either during AVNRT or during sinus rhythm. The latter included the spatial distances between the distal end of the AV nodal artery and the HBE and the final catheter ablation site, and the distance between the HBE and the tricuspid border at the coronary sinus orifice floor. RESULTS: In phase I, nine of the 77 patients had complications of transient (seven patients) or permanent (two patients) complete AV block during stepwise, anatomy guided slow pathway catheter ablation. These nine patients had a wider distance between the HBE and the distal end of the AV nodal artery, and a closer approximation of the catheter ablation site to the distal end of the AV nodal artery, which independently predicted the risk of AV block. In contrast, none of the available electrophysiologic parameters were shown to be reliable. When the distance between the distal end of the AV nodal artery and the ablation target site was more than 2 mm, the complication of AV block virtually never occurred. In phase II, all 51 patients had successful elimination of the slow pathways without complication when the ablation procedure was guided by preceding angiography with identification of the distal end of the AV nodal artery. CONCLUSIONS: The distal end of the AV nodal artery shown by angiography serves as a useful landmark for the prediction of the risk of AV block during slow pathway catheter ablation of AVNRT.

Adolescent↗

Glucose-6-phosphatase mutation G188R confers an atypical glycogen storage disease type 1b phenotype.

Glycogen storage disease type 1a (GSD 1a) is caused by a deficiency in microsomal glucose-6-phosphatase (G6Pase). A variant (GSD 1b) is caused by a defect in the transport of glucose-6-phosphate (G6P) into the microsome and is associated with chronic neutropenia and neutrophil dysfunction. Mutually exclusive mutations in the G6Pase gene and the G6P transport gene establish GSD la and GSD 1b as independent molecular processes and are consistent with a multicomponent translocase catalytic model. A modified translocase/catalytic unit model based on biochemical data in a G6Pase knockout mouse has also been proposed for G6Pase catalysis. This model suggests coupling of G6Pase activity and G6P transport. A 5-mo-old girl with hypoglycemia, hepatomegaly, and lactic acidemia was diagnosed with GSD 1a. She also developed neutropenia, neutrophil dysfunction, and recurrent infections characteristic of GSD 1b. Homozygous G188R mutations of the G6Pase gene were identified, but no mutations in the G6P translocase gene were found. We have subsequently identified a sibling and two unrelated patients with similar genotypic/phenotypic characteristics. The unusual association of neutrophil abnormalities in patients with homozygous G188R mutations in the G6Pase gene supports a modified translocase/catalytic unit model.

Animals↗

Control of idiopathic ventricular fibrillation by implantable cardioverter-defibrillator in a child who survived sudden death.

Idiopathic ventricular fibrillation (VF) is extremely rare in children who have not previously undergone cardiac surgery. Patients resuscitated from idiopathic VF remain at risk for recurrence. The use of an implantable cardioverter-defibrillator (ICD) effectively prevents such recurrences. We report the case of a 12-year-old girl who had a history of recurrent syncope and had survived an episode of VF. Serial studies after prolonged but successful resuscitation, including echocardiography, an electrocardiogram (ECG), and coronary angiography failed to reveal abnormal cardiac structures responsible for VF. No abnormal conduction pathways or abnormal early or late after depolarization were found on electrophysiologic study. The ST segments of the 12-lead ECG remained normal after procainamide challenge. The patient underwent ICD implantation 2 weeks after admission and syncope did not recur during a follow-up of 14 months. This report emphasizes that idiopathic VF may be responsible for syncope in children. ICD therapy prevents the recurrence of idiopathic VF and the associated risk of sudden death.

Child↗

Extrauterine pelvic arteriovenous malformation mimicking the clinical presentation of structural heart disease.

A case is reported of an extrauterine pelvic arteriovenous malformation involving branches of the internal iliac arteries. Cardiomegaly and a rough cardiac murmur were the clinical presentations mimicking a structural heart disease. A continuous bruit could only be detected by the diaphragm of the stethoscope applied firmly to the left lower abdomen. Multiple blood samplings from inferior vena cava, and iliac and femoral veins for determination of oxygen saturation may be necessary for suspected cases. However, selective arteriography remains the best method for diagnosing the presence, extent, and multiplicity of the lesions before surgery or percutaneous arterial embolization.

Arteriovenous Malformations↗

Chelation therapy for patients with elevated body lead burden and progressive renal insufficiency. A randomized, controlled trial.

BACKGROUND: Nephropathy is known to occur in persons exposed to high levels of lead, but the question of whether long-term exposure to low levels of environmental lead is associated with impaired renal function remains controversial. OBJECTIVE: To examine whether chelation therapy slows the progression of renal insufficiency in patients with mildly elevated body lead burden. DESIGN: Randomized, controlled trial. SETTING: Academic medical center in Taiwan. PATIENTS: 32 patients with chronic renal insufficiency (serum creatinine level > 132.6 micromol/L [1.5 mg/dL] and < 353.8 micromol/L [4.0 mg/dL]), mildly elevated body lead burden (> 0.72 micromol [150 microg] of lead per 72-hour urine collection and < 2.90 micromol [600 microg] of lead per 72-hour urine collection [EDTA mobilization tests]), and no history of heavy lead exposure. INTERVENTION: The treatment group received 2 months of chelation therapy; the control group received no therapy. MEASUREMENTS: The reciprocal of serum creatinine (1/Cr) was used as an index of progressive renal insufficiency. RESULTS: Rates of progression of renal insufficiency were similar in the treatment group and the control group during a 12-month baseline observation period (1/Cr, 0.000054 L/micromol per month compared with 0.000046 L/micromol per month; P > 0.2). After the 2-month treatment period, improvement in renal function was greater in the treatment group than in the control group. In the 12 months after the treatment period, renal insufficiency progressed more slowly in the treatment group than in the control group (1/Cr, 0.000033 +/- 0.00038 L/micromol per month compared with 0.000045 +/- 0.000038 L/micromol per month; P = 0.0030). CONCLUSION: Chelation therapy seems to slow the progression of renal insufficiency in patients with mildly elevated body lead burden. This implies that long-term exposure to low levels of environmental lead may be associated with impaired renal function in patients with chronic renal disease.

Adult↗

Long-term beta-blocker therapy improves autonomic nervous regulation in advanced congestive heart failure: a longitudinal heart rate variability study.

BACKGROUND: beta-Blocker therapy is believed to modulate the detrimental effect of overcompensating neurohormonal activation in chronic heart failure. However, clinical doubts remain, particularly the physiologic sympathovagal balance. METHODS: To respond to clinical concern about worsening autonomic nervous perturbation in beta-blocker therapy of advanced congestive heart failure, 15 consecutive patients were longitudinally studied to elucidate the evolution of cardiac function versus 24-hour heart rate variability (HRV) before and after 1, 3, and 6 to 9 months of atenolol-combined therapy. RESULTS: Two patients died prematurely within 1 month. All 13 surviving patients showed improvement in New York Heart Association functional class, with decrease in left ventricular end-systolic and end-diastolic dimensions and increase in fraction shortening and ejection fraction by echocardiography after at least 3 months of atenolol use. The retarded therapeutic effect was accompanied by a general rise of total, very low, low-, and high-frequency components (9.0 +/- 0.5, 8.8 +/- 0.5, 6.2 +/- 0.6, and 6.1 +/- 0.5 vs 10.9 +/- 0.3, 10.7 +/- 0.4, 8.6 +/- 0.3, and 7.8 +/- 0.3; all P <.02) of daily HRV. This implied recovery of parasympathetic and baroreceptor function. Return of sympathovagal interaction was further supported by the suppression of Cheyne-Stokes type HRV as detected by Wigner-Ville distribution. CONCLUSIONS: Long-term beta-blocker therapy for advanced congestive heart failure upwardly regulates the autonomic nervous interaction in synchrony with the evolution of cardiac function performance.

Adrenergic beta-Antagonists↗