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Biomedical subjects

J L Lin

Publications and source records attributed to J L Lin.

At least 145 records · Page 8Linked to original sources
PubMed1993

Human fibroblast tropomyosin isoforms: characterization of cDNA clones and analysis of tropomyosin isoform expression in human tissues and in normal and transformed cells.

A tropomyosin-specific oligonucleotide probe (REN29) designed to hybridize to all known human tropomyosin isoforms was used to study tropomyosin mRNA levels in normal and transformed human cells. At least four different sizes of RNAs were detected in normal human fibroblast KD cells by Northern blot analysis. The major bands of 1.1 kb RNA for hTM1 and 3.0 kb RNA for hTM4 were decreased substantially in various transformed cell lines. One of the minor RNA bands (2.0 kb for hTM2 and hTM3) appeared to be absent in a human pancreatic carcinoma cell line. The level of the other minor RNA band (2.5 kb for hTM5) was found to be unchanged or slightly decreased in transformed cells. This differential expression of tropomyosin isoforms at the RNA level was not totally in agreement with the difference in the protein amounts found in normal and transformed cells, suggesting that translational control may also play an important role in the expression of some tropomyosin isoforms. The REN29 probe was further used to screen lambda gt10 and lambda gt11 cDNA libraries, which were constructed from poly(A)+ RNAs of human fibroblast cell lines HuT-14 and WI-38, respectively. In addition to cDNA clones encoding known isoforms, we obtained three classes of new cDNA clones that encode two low M(r) isoforms (hTM5a and hTM5b), and a high M(r) isoform (hTMsm alpha). Sequence comparison revealed that hTM5a and hTM5b are alternatively spliced products derived from the same gene that encodes hTM2 and hTM3. Northern blot analysis and amino acid sequence comparison suggested that the hTMsm alpha represents a smooth muscle tropomyosin which is also expressed in human fibroblasts. The exon specific for, and common to, hTM5a and hTM5b was found to be highly expressed in small intestine. However, there was no detectable expression of this exon in stomach and skeletal muscle. The difference in tissue-specific expression suggests that different isoforms may perform distinct functions in different tissues.

Amino Acid Sequence↗
PubMed1993

Activation of protein kinase C potentiates postsynaptic acetylcholine response at developing neuromuscular synapses.

1. Phorbol 12-myristate 13-acetate (TPA, 1 microM) and phorbol 12,13-dibutyrate (PDBu, 2 microM), activators of protein kinase C (PKC), increased the mean amplitude and decay time of the spontaneous synaptic currents of Xenopus nerve-muscle coculture, whereas, 4 alpha-phorbol (2 microM) which is an inactive phorbol analogue had no effect. 2. Staurosporine (0.5 microM) and H-7 (10 microM), inhibitors of PKC, inhibited the potentiation effects of TPA on the spontaneous synaptic currents. 3. Effects of TPA on the postsynaptic acetylcholine (ACh) sensitivity were examined by iontophoresis of ACh to the surface of embryonic muscle cells of 1-day-old Xenopus cultures. TPA increased both the amplitude and decay time of ACh-induced whole-cell currents in isolated myocytes. 4. TPA concentration-dependently increased the mean open time of low-conductance ACh channels but did not affect those of high-conductance ACh channels. PDBu but not 4 alpha-phorbol exhibited similar effects to TPA. Staurosporine and H-7 inhibited the increasing effects of TPA. 5. These results suggest that activation of PKC might be involved in synaptogenesis at developing neuromuscular synapses by the postsynaptic potentiation of ACh sensitivity.

Acetylcholine↗
PubMed1993

Expression of GLUT-4 glucose transporter in unweighted soleus muscle of normal and STZ-induced diabetic rats.

Effects of 6 days of hindlimb suspension on expression of glucose transporters were studied in the skeletal muscle of nondiabetic and streptozotocin-induced diabetic rats. Although total membrane protein recovered from soleus muscles tended to decrease with suspension, GLUT-4 protein concentration (amount per gram membrane protein) was increased by 66 and 91% compared with weight-bearing control in nondiabetic and diabetic rats, respectively. Therefore, the amount of GLUT-4 protein in whole soleus muscle did not decrease with the hindlimb suspension in normal and diabetic rats. In contrast, hindlimb suspension decreased GLUT-4 mRNA amount in whole soleus muscle by 47 and 27% in nondiabetic and diabetic rats, respectively. Thus the GLUT-4 protein-to-GLUT-4 mRNA ratio was increased 2.1-fold in nondiabetic and 1.4-fold in diabetic rats. The extensor digitorum longus muscle, which generally shows little response to unweighting, exhibited no such changes. These results suggest that the amount of GLUT-4 glucose transporter in the unweighted soleus muscle was maintained via a translational and/or posttranslational mechanism in nondiabetic rats as well as in streptozotocin-induced diabetic rats under the condition of reduced weight-bearing activity.

Animals↗
PubMed1993

Acute nephropathy of organotin compounds.

Three patients who developed acute nephropathy following ingestion of triphenyltin acetate (TPTA) are described. All of them had significant proteinuria, azotemia, and polyuria. Mild neurological manifestations in all patients were also noted. Hematuria and pyuria were noted in 1 severely poisoned patient. Evidence for hepatitis was present in 2 patients, and for pancreatitis in 1. Renal biopsy showed focal fusion of glomerular cell processes and proximal tubular damage with cellular necrosis. Two patients survived with complete recovery of renal functions. One old patient died of aspiration pneumonia. Acute nephropathy following organotin intoxication appears to result mainly from proximal renal tubular damage with a benign and reversible clinical course.

Adult↗
PubMed1993

Urinary N-acetyl-glucosaminidase excretion and environmental lead exposure. Green Cross Health Service Association Study Group.

To understand the relationship between chronic low-level lead exposure and renal function, residents living nearby a lead battery factory for more than 10 years were selected and entered in this cross-section study. The residents living in the 1st village, within 500 m from the factory, were grouped in group 1; those in the 2nd village, within 1,000-1,500 m, in group 2, and those in the 3rd village, far from any lead-contaminated sources, in group 3. Twenty-four-hour urinary N-acetyl-glucosaminidase (NAG) was detected as early indicator of renal damage, and an ethylenediamine-tetraacetic acid mobilization test was performed to estimate total body lead burden of lead-exposed persons. Blood lead level (BLL) showed a significant difference among the three study groups. The further the distance between the group and the factory, the higher BLL. The results showed a significant high prevalence of abnormal urine NAG excretion in the chronic lead-exposed group, although BLL and body lead burden of these persons were within the 'normal' range. A significant correlation between body lead burden less than 200 micrograms and 24-hour urine NAG excretion and a dose-response relationship between them were found. These observations suggested that lead was the possible cause of abnormal renal tubular function in persons with chronic low-level lead exposure, but this effect became blunt when body lead burden was more than 200 micrograms. The possible explanation may be that high body lead burden from long-term exposure will deplete the kidney of NAG or render it insensitive to the effects of lead exposure.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetylglucosaminidase↗
PubMed1993

Infective endocarditis in the transesophageal echocardiographic era.

During a 45-month period, 50 consecutive patients with infective endocarditis were evaluated at the National Taiwan University Hospital with emphasis on the role of transesophageal echocardiography (TEE) in the management of these patients. Among them, rheumatic heart disease was still the most common underlying cardiac disorder (10/50, 20%), while mitral valve prolapse (8/50, 16%) and congenital heart disease (8/50, 16%) were also frequently encountered. More than one third (19/50, 38%) had no underlying heart disease. Four intravenous drug abusers, quite rare previously in Taiwan, were found during the study period. Native valves involved were mostly mitral valve (n = 18), aortic valve (n = 15), and both mitral and aortic valves (n = 3). Tricuspid valve and pulmonic valve were involved in 3 and 2 patients, respectively. Streptococcus viridans was the leading microorganism isolated (21/50, 42%). Staphylococci and enterococci were found in 9 (18%) and 5 (10%) patients, respectively. Twelve patients (24%) were culture-negative in this series. Embolic complications occurred in 13 patients (26%), with a total of 17 episodes. No significant correlation was found between the occurrence of embolization and the vegetation size or the location of the vegetation, if patients with right-sided valvular vegetation and no identifiable vegetation were excluded. Surgery was needed by 25 patients (50%), and mortality occurred in 6 (12%). TEE was superior to transthoracic echocardiography in the detection of vegetations at the mitral or prosthetic valves. Concerning the associated complications with infective endocarditis, TEE was also superior in estimating the severity of mitral regurgitation, recognizing ruptured chordae tendineae and detecting subaortic complications such as valve ring abscess and mitral valve perforation.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1993

Acute renal failure due to ingestion of the gallbladder of grass carp: report of 3 cases with review of literature.

Gallbladder toxin of the grass carp (Ctenopharyngodon idella) is a less well-known cause of acute renal failure. Three cases are reported and the diagnosis is primarily clinical. All our patients presented initially with gastrointestinal upset including nausea, vomiting, diarrhea, and abdominal fullness. These symptoms usually occurred with 10 min to 18 h after the ingestion the raw gallbladder of the grass carp. All our cases developed acute renal failure and in two of them toxic hepatitises were noted. An acute tubular necrosis was demonstrated on renal biopsy in one of our patients. The treatment is mainly supportive and two of them received hemodialysis. All three cases recovered, with normal renal and liver functions 2-4 weeks after the incident. A review of the cases previously reported in the English literature is presented.

Acute Kidney Injury↗
PubMed1993

Acute sodium chlorite poisoning associated with renal failure.

A 25-year-old Chinese male presented with generalized cyanosis and respiratory distress. The patient was known to have ingested 10 g of sodium chlorite in a suicide attempt. Methemoglobinemia was found and intravenous methylene blue was given repeatedly. However, the therapy could not prevent an acute hemolytic crisis. Methemoglobinemia remained profound (43.1%) and disseminated intravascular coagulation ensued. He was put on CAVHD to correct the fluid overload and probably to remove the active metabolites of the chlorite. After 24 h, the methemoglobin was reduced to 16.9%. However, the development of acute renal failure further complicated the clinical course. Percutaneous renal biopsy suggested a picture of acute tubulointerstitial nephropathy. In addition, hemodialysis was continued for 4 weeks. After 3 months, renal function normalized. To our knowledge, there has been no clinical report of human intoxication with sodium chlorite.

Acute Kidney Injury↗
PubMed1993

Massive oral ingestion of elemental mercury.

A 42 year old male, while repairing a sphygmomanometer, intentionally ingested an estimated 3 kg (220 mL) of metallic mercury. During admission, only tremor, irritability, forgetfulness and fatigue were noted. There were no obvious gastrointestinal or hepatic complications. Blood and urine mercury levels were significantly elevated. Most of the metallic mercury was cleared from the gut within 10 days. A few months later, hepatic dysfunction with jaundice developed. Serial investigations did not suggest a viral etiology or alcoholism. Liver function tests and blood and urine mercury levels returned to normal over the next 10 months. The observation suggests that massive and prolonged retention of metallic mercury may facilitate the conversion of metallic, elemental mercury to divalent mercury and its subsequent absorption with development of hepatic dysfunction.

Administration, Oral↗
PubMed1993

Continuous arteriovenous hemoperfusion in meprobamate poisoning.

A patient with severe meprobamate poisoning presented within 4 h after suicidal ingestion of an unknown amount of the drug. The patient was unconscious, unresponsive, and hypotensive. Continuous arteriovenous hemoperfusion with coated activated charcoal resulted in a clearance of 198.8 +/- 15.6 mL/min with an extraction ratio of 0.66 +/- 0.05 (n = 3). There was almost complete elimination of the drug from the blood by 16 h. Continuous arteriovenous hemoperfusion, which can be performed in areas where dialysis facilities are not available, may be an effective adjunct to the treatment of acute meprobamate intoxication, particularly in patients with profound hypotension.

Adult↗
PubMed1993

Acute renal failure after open heart surgery: clinical experience with continuous arteriovenous hemodialysis.

Continuous arteriovenous hemodialysis (CAVHD) was employed in five patients who suffered from acute renal failure (ARF) after open heart surgery during the period from July 1991 to February 1992. All patients had a urine output of less than 400 mL/24h and clinical evidence of fluid overload. Most of the patients needed respiratory support for respiratory insufficiency and required vasopressor infusions. They could not tolerate conventional hemodialysis due to severe hemodynamic instability, and the concurrent thoracic surgery precluded the application of peritoneal dialysis. All patients tolerated the CAVHD well, despite persistent hypotension. The mean age of the five patients was 53.6 +/- 15.3 years. The duration of CAVHD treatment ranged from 1.5 to 22 days. Whole blood clearances for urea, creatinine and phosphate were 13.27 +/- 1.86 mL/min, 13.05 +/- 3.12 mL/min, and 13.99 +/- 2.61 mL/min, respectively. According to the clinical condition, ultrafiltration averaged 100-200 mL/h; up to 1 L/h could be obtained without difficulty. In these situations, large concurrent amounts of vasopressors and nutritional fluids could be easily prescribed without fear of fluid overload. The introduction of CAVHD allowed a more stabilized environment for gradual recovery of the temporarily compromised ventricular function after open heart surgery. Later, the hemodynamic status was stabilized without or with only minimal infusions of vasopressors in all five patients. Renal function recovered in four patients and one was shifted to conventional hemodialysis. All five patients survived under CAVHD treatment. There were no significant complications related to the application of CAVHD.(ABSTRACT TRUNCATED AT 250 WORDS)

Acute Kidney Injury↗
PubMed1993

Acute iron intoxication: a case report with ferric chloride ingestion.

A 24 y/o male, after attempting suicide by ingesting liquid ferric chloride, presented with protracted vomiting and epigastric pain. He was noted to have leukocytosis, a metabolic acidosis and an elevated serum iron level. Hemorrhagic gastritis, coagulation defects and an increase in urine beta 2-microglobulin, indicating renal tubular damages were found in the following day. He later recovered after treatment with deferoxamine and good supportive care. This is Taiwan's first reported case of acute iron intoxication in an attempted suicide. We discussed the characteristics of this liquid form of iron intoxication, the limitations of local laboratories in providing support and how to diagnose and treat acute iron intoxication without waiting for serum iron and total iron binding capacity levels. In conclusion, to evaluate the severity of iron intoxication, a deferoxamine challenge test and the severity of symptoms and signs should be assessed without relying only on serum iron and total iron binding capacity levels. Deferoxamine and good supportive care should be given to all serious iron intoxications.

Acute Disease↗
PubMed1992

Characterization of GLUT3 protein expressed in Chinese hamster ovary cells.

We have expressed GLUT3 protein, an isoform of a facilitative glucose transporter, in Chinese hamster ovary cells by transfection of its cDNA using an expression vector. The expressed GLUT3 protein was detected by Western-blot analysis as a broad band of 45-65 kDa, indicating intensive glycosylation of the protein. The expressed GLUT3 protein was observed, by immunofluorescence staining, to be located mainly at the plasma membrane, and its expression was associated with a marked increase in glucose-transport activity. Kinetic analysis revealed that the Km value of GLUT3 protein for 3-O-methylglucose uptake was approx. 35% of that of GLUT1 protein, whereas the Km value of GLUT3 protein for 2-deoxy-D-glucose uptake was very similar to that of GLUT1 protein. The Vmax. value of GLUT3 protein for 3-O-methylglucose and 2-deoxyglucose uptake was approx. 20-50% of that of GLUT1 protein. GLUT3 protein was well photolabelled with [3H]cytochalasin B or a mannose derivative, 2-N-4-[3H](1-azi-2,2,2-trifluoroethyl)benzoyl-1,3-bis-(D-mannos -4-yloxy)-2- propylamine. Thus GLUT3 protein has very similar characteristics to GLUT1 protein including its subcellular localization, but exhibits lower Km and Vmax. values for 3-O-methylglucose uptake.

3-O-Methylglucose↗
PubMed1992

Replacement of intracellular C-terminal domain of GLUT1 glucose transporter with that of GLUT2 increases Vmax and Km of transport activity.

The intracellular C-terminal domain is diverse in size and amino acid sequence among facilitative glucose transporter isoforms. The characteristics of glucose transport are also divergent, and GLUT2 has far higher Km and Vmax values compared with GLUT1. To investigate the role of the intracellular C-terminal domain in glucose transport, we expressed in Chinese hamster ovary cells the mutated GLUT1 protein whose intracellular C-terminal domain was replaced with that of GLUT2 by means of engineering the chimeric cDNA. Cytochalasin B, for which GLUT2 protein has much lower affinity, bound to this chimeric protein in a fashion similar to GLUT1. In contrast, greater transport activity was observed in this chimeric glucose transporter compared with the wild-type GLUT1 at 10 mM 2-deoxy-D-glucose concentration. The kinetic studies on 2-deoxy-D-glucose uptake revealed a 3.8-fold increase in Km and a 4.3-fold increase in Vmax in this chimeric glucose transporter compared with the wild-type GLUT1. Thus, replacement of the intracellular C-terminal domain confers the GLUT2-like property on the glucose transporter. These results strongly suggest that the diversity of intracellular C-terminal domain contributes to the diversity of glucose transport characteristics among isoforms.

Amino Acid Sequence↗
PubMed1992

Domains responsible for the differential targeting of glucose transporter isoforms.

Facilitative glucose transporter isoforms, GLUT1 and GLUT4, have different intracellular distributions despite their very similar structure. In insulin-responsive tissues such as adipose tissues and muscle, GLUT4 protein resides mainly in the intracellular region in a basal condition and is translocated to the plasma membrane upon stimulation of insulin. In contrast, GLUT1 protein was distributed about equally between plasma membranes and low density microsomal membranes in 3T3-L1 adipocytes. Furthermore, GLUT1 and GLUT4 were reported to be differentially targeted to the plasma membrane and intracellular region, respectively, when expressed in Chinese hamster ovary cells and HepG2 cells. To elucidate the differential intracellular targeting mechanisms, several chimeric glucose transporters in which portions of GLUT4 are replaced with corresponding portions of GLUT1 have been stably expressed in Chinese hamster ovary cells. Immunofluorescence and immunoelectron microscopy as well as measurement of glucose transport activity revealed that two domains of GLUT4, which are not the NH2- or COOH-terminal domain, determine its targeting to the intracellular vesicles. The first domain contains the consensus sequence of the leucine zipper structure, suggesting that a dimer-forming structure of the glucose transporter might be required for its proper targeting. The other domain contains 28 amino acids, nine of which are different between GLUT1 and GLUT4. Immunoelectron microscopy revealed that the chimeric transporters containing both of these two domains of GLUT1, only the first domain of GLUT1, and none of the domains, exhibited a different cellular distribution with approximately 65, 30, and 15% of the transporters apparently on the plasma membrane, respectively. The addition of insulin did not alter the apparent cellular distributions of these chimeric transporters. These domains would be specifically recognized by intracellular targeting mechanisms in Chinese hamster ovary cells.

Animals↗
PubMed1992

Reappraisal by transesophageal echocardiography of the significance of left atrial thrombi in the prediction of systemic arterial embolization in rheumatic mitral valve disease.

Systemic arterial embolization imparts a significant risk of serious complications throughout the lives of patients with rheumatic heart disease. Left atrial (LA) thrombi have been thought to be the major source of emboli. A transesophageal echocardiography (TEE) study of 260 consecutive patients with rheumatic mitral valve disease was performed during a period of 24 months, with particular reference to understanding the association between LA thrombi and embolic complications. Of these patients, 155 had predominant mitral stenosis, 24 had significant mitral regurgitation, and the remaining 81 with xenograft mitral valve replacement developed valvular dysfunction (25 resulted in predominant mitral stenosis and 56 in significant mitral regurgitation). LA thrombi were detected in 38 patients (group A) and absent in 222 (group B). Group A patients had a higher frequency of recent (less than or equal to 1 week before TEE study) and remote (greater than 1 week before) embolization than did group B patients (recent: 26.3 vs 5.4% [p less than 0.001]; remote: 18.4 vs 5.0% [p less than 0.01]). The frequency of atrial fibrillation was also greater in group A patients (100 vs 74.3%; p less than 0.001). The exclusion of patients with significant mitral regurgitation and sinus rhythm had no effect on the association between LA thrombi and evidence of previous embolization. It is concluded that TEE is a convenient diagnostic modality that can be used to identify a subset of patients with rheumatic mitral valve disease at high risk for systemic embolization. Consequently, preventive anticoagulation for possible embolic complications should be more vigorously adhered to in patients with rheumatic mitral valve disease and LA thrombi.

Echocardiography↗
PubMed1992

Deletion of C-terminal 12 amino acids of GLUT1 protein does not abolish the transport activity.

We engineered the GLUT1 cDNA to delete C-terminal 12 amino acids of encoded GLUT1 protein. This mutated GLUT1 protein expressed in CHO cells by transfection of its cDNA was demonstrated to reside on the plasma membrane by cell surface labeling technique, and retain the transport activity, similar to that of the wild-type GLUT1. In addition, metabolic labeling of the intact cells with 35S indicated that the half-life of the mutated GLUT1 was not significantly different from that of the wild-type GLUT1. These results suggest that C-terminal 12 amino acids of GLUT1 are not important for the transport activity and the stability of the protein. Taken together with our previous results on the mutant without C-terminal 37 amino acids, the amino acids between the 37th and the 13th from the C-terminus appear to be essential for the transport activity.

Animals↗