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Biomedical subjects

J L Lin

Publications and source records attributed to J L Lin.

At least 127 records · Page 7Linked to original sources

No evidence for linkage of long QT syndrome and chromosome 11p15.5 markers in a Chinese family: evidence for genetic heterogeneity.

Recently the defective gene locus in seven Caucasian families with the Romano-Ward form of long QT syndrome (LQT) has been mapped to chromosome 11p. To understand the molecular basis of LQT in Chinese, a three-generation family was investigated. Fourteen family members were studied and five individuals were diagnosed to be affected, according to electrocardiographic criteria. Two genomic DNA probes (c-Ha-ras-3'-HVR and insulin-5'-HVR) and one tetranucleotide repeat polymorphism (THZ) derived from chromosome 11p15.5 loci and previously demonstrated to be closely linked to LQT were used as probes to analyze this family. A lod score of less than -2 was noted for all three polymorphisms. Our data show that there was no evidence of linkage between these three loci and the gene for LQT in this studied family. We believe that this result provides additional evidence for genetic heterogeneity of LQT.

Adolescent↗

Outcomes of severe hyperkalemia in cardiopulmonary resuscitation with concomitant hemodialysis.

OBJECTIVE: To investigate the efficacy of hemodialysis during cardiopulmonary resuscitation as an effective adjunct to the treatment of severe hyperkalemia. DESIGN: A prospective study. SETTING: In hospital dialysis units and intensive care units. PATIENTS: Renal failure patients who developed hyperkalemia induced cardiac arrest and failed to recover from conventional cardiopulmonary resuscitation (CPR) were included. Three patients entered into this study: 2 patients with chronic renal failure maintained on regular hemodialysis and one with acute renal failure who suffered from severe hyperkalemia. INTERVENTIONS: All three patients developed asystolic cardiac arrest with unrecordable blood pressure due to severe hyperkalemia. Aggressive CPR together with intravenous epinephrine, sodium bicarbonate and calcium chloride were instituted. External cardiac massage with cardiac defibrillation was unable to restore spontaneous heart action. After lack or response to intensive resuscitation, hemodialysis was performed concomitant with CPR to eliminate the potassium load. MEASUREMENTS AND RESULTS: Sinus rhythm and blood pressure were restored in all 3 patients but one of them eventually succumbed to her underlying disease. CONCLUSION: Hemodialysis during CPR is probably an effective adjunct to the treatment of severe hyperkalemia in patients with severe hemodynamic compromise and asystolic cardiac arrest.

Adult↗

Significance of left atrial spontaneous echo contrast in rheumatic mitral valve disease as a predictor of systemic arterial embolization: a transesophageal echocardiographic study.

The association between left atrial spontaneous echo contrast (SEC) and a history of systemic arterial embolization was evaluated in 359 consecutive patients with rheumatic mitral valve disease during a 3-year period. All patients underwent transesophageal echocardiographic (TEE) and cardiac catheterization studies. Of these, 207 patients had predominant mitral stenosis, 55 had significant mitral regurgitation, and the remaining 97 with xenograft mitral valve replacement developed valvular dysfunction (32 resulted in predominant mitral stenosis and 65 in significant mitral regurgitation). Left atrial SEC was detected in 108 patients (group A) and was absent in 251 (group B). Group A patients showed a higher frequency of left atrial thrombi or history of previous embolization than those in group B (59.3% vs 7.2%; p < 0.001). Group A patients also had a higher frequency of recent (< or = 1 week before TEE study) and remote (> 1 week before TEE study) embolization than did group B patients (recent: 19.4% vs 2.8% [p < 0.001]; remote: 13.0% vs 4.0% [p < 0.001]). Multivariate analysis showed that left atrial SEC (p = 0.01) was the only independent predictor of systemic arterial embolization. It is concluded that patients with left atrial SEC had a significantly higher risk for thromboembolism, and TEE is a useful modality to identify this subset of patients with rheumatic mitral valve disease.

Adult↗

Regression of left ventricular mass after mitral valve repair of pure mitral regurgitation.

To evaluate the effect of mitral valve repair on the regression of left ventricular mass, we studied 50 consecutive patients with severe, pure mitral regurgitation undergoing mitral valve repair. Two-dimensional echocardiograms were recorded a mean 2.5 +/- 2.0 weeks before and 6.5 +/- 2.5 months after valve operation. Postoperative significant mitral regurgitation was present in 3 patients. After mitral valve repair there were significant decreases in left ventricular end-diastolic volume index (133 +/- 39 mL/m2 to 79 +/- 35 mL/m2; p < 0.001), end-systolic volume index (44 +/- 26 mL/m2 to 30 +/- 26 mL/m2; p < 0.001), stroke volume index (89 +/- 29 mL/m2 to 49 +/- 19 mL/m2; p < 0.001), and mass index (211 +/- 82 g/m2 to 134 +/- 52 g/m2; p < 0.001). There also were significant decreases in left atrial dimension (47 +/- 9 mm to 38 +/- 9 mm; p < 0.001), left ventricular end-diastolic dimension (61 +/- 8 mm to 48 +/- 7 mm; p < 0.001), and end-systolic dimension (39 +/- 8 mm to 32 +/- 7 mm; p < 0.001). Left ventricular ejection fraction decreased slightly from 0.69 +/- 0.12 to 0.64 +/- 0.12; p < 0.01) after repair. Thus, correction of pure mitral regurgitation leads to reduction of the cardiac chamber size and left ventricular volumes as well as regression of the left ventricular mass.

Adolescent↗

Anatomic substrate of the slow atrio-ventricular nodal pathway in an experimental atrio-ventricular nodal reentrant tachycardia.

We investigated the anatomic substrate of the slow pathway of the atrio-ventricular (AV) node in a dog with AV nodal reentrant tachycardia. Sustained AV nodal reentrant tachycardia was repeatedly induced in a mongrel dog after putting cryolesions on the anterior atrial septum for 1 month. A posterior perinodal dissection was performed for ablation of the slow pathway and cure of the tachycardia. After the operation, AV nodal reentrant tachycardia and discontinuity of the AV conduction were no longer demonstrated. A histologic examination of the AV junction revealed that the dissection injured mainly in two areas: (1) the superficial atrial fibers of the subendocardium over the compact AV node; and (2) the inferior portion of the posterior atrial inputs near the tricuspid annulus. The compact AV node and its transitional cells remained intact. In conclusion, our results suggested that (1) the anatomic circuit of AV nodal reentrant tachycardia does involve some extranodal atrial tissues; and (2) the superficial right atrial fibers over the AV node and/or the inferior portion of the posterior atrial inputs, contribute to part of the slow AV nodal pathway.

Animals↗

Recovery of atrial function after atrial compartment operation for chronic atrial fibrillation in mitral valve disease.

OBJECTIVES: We prospectively studied the recovery of atrial function after atrial compartment operation and mitral valve surgery in patients with chronic atrial fibrillation caused by mitral valve disease. BACKGROUND: Chronic atrial fibrillation is the most common arrhythmia in mitral valve disease. This arrhythmia is associated with excessive morbidity and mortality. Mitral valve surgery alone rarely eliminates it. METHODS: Twenty-two patients underwent mitral valve surgery and a new surgical method, atrial compartment operation. Doppler echocardiography was performed in all patients before operation and at 1 week and 2 and 6 months after operation in the successful cardioversion group. Peak early diastolic (E) and atrial (A) filling velocities, peak A/E velocity ratio and A/E integral ratio of the mitral and tricuspid valves were measured. RESULTS: Sinus rhythm was restored immediately after operation in 91% of patients and was maintained for > 1 week in 15 (68%) of 22 patients and > 6 months in 14 (64%) of 22. Eleven of 15 patients had left atrial paralysis (A/E integral ratio 0) at 1 week and 6 of 14 patients at 2 months. Nine of 15 patients had right atrial paralysis (A/E integral ratio 0) at 1 week and 1 of 14 patients at 2 months. Both left and right atrial contractile function (presence of an A wave on Doppler findings) was detected at 6 months in 14 patients. Mean (+/- SD) peak atrial filling velocity of the mitral valve was 15 +/- 26 cm/s at 1 week, 38 +/- 39 cm/s at 2 months and 93 +/- 32 cm/s at 6 months (p < 0.001). Mean peak atrial filling velocity of the tricuspid valve was 14 +/- 19 cm/s at 1 week, 33 +/- 19 cm/s at 2 months and 50 +/- 19 cm/s at 6 months (p < 0.001). Peak early diastolic and atrial filling velocities, peak A/E velocity ratio and A/E integral ratio of the mitral and tricuspid valves increased significantly from 1 week to 6 months. CONCLUSIONS: Chronic atrial fibrillation in mitral valve disease can often be eliminated by atrial compartment operation. No surgical mortality or significant complications were encountered. Both left and right atrial function, as manifested by Doppler findings, recover after compartment operation and improve over time. The mechanical function of the right atrium recovers earlier than that of the left.

Adolescent↗

Flavonoid-induced acute nephropathy.

We report two cases of acute renal failure induced by sciadopitysin, a type of flavonoid, and review related papers of flavonoid-induced acute nephropathy in the literature. A total of eight patients were studied. The purpose of this report is to alert physicians to consider this cause of acute renal failure with hemolysis, because flavonoids are widely used in the world. All patients initially presented with fever and gastrointestinal upset after the ingestion of a single large dose or long-term small doses. Symptoms that followed were cola-colored urine and jaundice. Elevation of blood nitrogen and serum creatinine lasted for 2 to 9 weeks. Hemolysis (100%), cholestatic hepatitis (50%), and disseminated intravascular coagulopathy (50%) were also noted in flavonoid-induced oliguric acute renal failure patients. All of these patients required hemodialysis and all but one who died completely recovered within 2 to 9 weeks. Renal biopsy was performed and showed acute interstitial nephritis with acute tubular necrosis. Moreover, we first demonstrated multiple polymorphous inclusion bodies within tubular epithelial cells in electron microscopic examinations. The definite pathogenetic mechanism of flavonoid-induced acute nephropathy needs further elucidation.

Acute Kidney Injury↗

Overexpression of human fibroblast caldesmon fragment containing actin-, Ca++/calmodulin-, and tropomyosin-binding domains stabilizes endogenous tropomyosin and microfilaments.

Fibroblast caldesmon is a protein postulated to participate in the modulation of the actin cytoskeleton and the regulation of actin-based motility. The cDNAs encoding the NH2-terminal (aa.1-243, CaD40) and COOH-terminal (aa.244-538, CaD39) fragments of human caldesmon were subcloned into expression vectors and we previously reported that bacterially produced CaD39 protein retains its actin-binding properties as well as its ability to enhance low M(r) tropomyosin (TM) binding to actin and to inhibit TM-actin-activated HMM ATPase activity in vitro (Novy, R. E., J. R. Sellers, L.-F. Liu, and J. J.-C. Lin. 1993. Cell Motil. Cytoskeleton. 26:248-261). Bacterially produced CaD40 does not bind actin. To study the in vivo effects of CaD39 expression on the stability of actin filaments in CHO cells, we isolated and characterized stable CHO transfectants which express varying amounts of CaD39. We found that expression of CaD39 in CHO cells stabilized microfilament bundles as well as endogenous TM. CaD39-expressing clones displayed an increased resistance to cytochalasin B and Triton X-100 treatments and yielded increased amounts of TM-containing actin filaments in microfilament isolation procedures. In addition, analysis of these clones with immunoblotting and indirect immunofluorescence microscopy with anti-TM antibody revealed that stabilized endogenous TM and enhanced TM-containing microfilament bundles parallel increased amounts of CaD39 expression. The increased TM observed corresponded to a decrease in TM turnover rate and did not appear to be due to increased synthesis of endogenous TM. Additionally, the phenomenon of stabilized TM did not occur in stable CHO clones expressing CaD40. Therefore, it is likely that CaD39 can enhance TM's binding to F-actin in vivo, thus reducing TM's rate of turnover and stabilizing actin microfilament bundles.

Actin Cytoskeleton↗

Continuous arteriovenous hemoperfusion in acute poisoning.

We have investigated the efficacy of a pumpless hemoperfusion technique, continuous arteriovenous hemoperfusion (CAVHP) in 3 cases of acute intoxications with meprobamate, theophylline and phenobarbital. Dramatic responses were noted in both hemodynamic unstable and comatous patients. With this technique, a blood flow of 120 cm3/min could be achieved in severe hypotension. Moreover, with the restoration of blood pressure, blood flow increased to 150-400 cm3/min. Our preliminary experience has shown that CAVHP allows an exceptionally high solute elimination. Hemoperfusion clearances of meprobamate, phenobarbital and theophylline were 198 +/- 5.6 cm3/min, 290.25 +/- 25.33 cm3/min and 192.79 +/- 55 cm3/min, respectively. Our present results suggest that CAVHP is a simple, safe, effective and less costly alterative of conventional hemoperfusion.

Adult↗

Left atrial appendage function determined by transesophageal echocardiography in patients with rheumatic mitral valve disease.

Left atrial thrombi have been considered to be the major source of systemic arterial embolization in patients with rheumatic mitral valve disease. Almost half of the left atrial thrombi are found in the left atrial appendage (LAA). To investigate LAA size and LAA contractile function in patients with rheumatic mitral valve disease, transesophageal echocardiographic and Doppler studies were performed in 61 patients. Among them, 46 patients were in atrial fibrillation (group 1), while the other 15 were in sinus rhythm (group 2). Thirty-six patients with nonrheumatic atrial fibrillation were chosen as control to group 1. Another 22 patients with various cardiovascular diseases and sinus rhythm served as control to group 2. When compared to the patients with nonrheumatic atrial fibrillation (control group), group 1 patients tended to have a larger LAA maximal area (9.7 +/- 5.2 vs. 5.9 +/- 2.8 cm2; p < 0.001). LAA ejection fraction and LAA peak emptying velocity were also lower. A significantly higher incidence of LAA spontaneous echo contrast (SEC) and thrombus formation was also found in these patients. Group 2 patients were also found to have a larger LAA maximal area when compared to the control group (8.8 +/- 3.7 vs. 5.2 +/- 3.0 cm2; p < 0.001). LAA ejection fraction and LAA peak emptying velocity were lower in this group, too. A higher incidence of LAA SEC formation was found in these patients with rheumatic mitral valve disease (4/15 vs. 0/22; p = 0.021). There was no significant difference, however, in LAA thrombus formation between group 2 and its control group (1/15 vs. 1/22; p = NS).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

Change in left ventricular diastolic filling patterns in patients with supraventricular tachycardia treated by radiofrequency ablation: a Doppler echocardiographic study.

To evaluate changes in left ventricular diastolic filling patterns resulting from radiofrequency ablation for supraventricular tachycardia (SVT), 44 patients with SVT undergoing radiofrequency ablation (study group), and 16 patients with SVT undergoing electrophysiologic study without ablation (control group) were studied by pulsed Doppler echocardiography. Peak early diastolic filling velocity (E), peak atrial filling velocity (A), and an E/A ratio were obtained from the transmitral flow velocity pattern before and 24-48 h after ablation or electrophysiologic study. In the study group, E and E/A ratio decreased from 67 +/- 16 and 1.26 +/- 0.42 to 61 +/- 16 cm/s and 1.09 +/- 0.39 (p < 0.001), respectively. In the control group, only E/A ratio decreased from 1.40 +/- 0.47 to 1.26 +/- 0.44 (p < 0.001). Heart rate increased from 71 +/- 10 to 80 +/- 10 beats/min (p < 0.001) in the study group and from 67 +/- 8 to 72 +/- 10 beats/min (p < 0.05) in the control group. E and E/A ratio decreased significantly from 73 +/- 17 and 1.35 +/- 0.49 to 60 +/- 18 cm/s and 0.96 +/- 0.40 (p < 0.001) in patients with heart rate change of > 20% after ablation. E, A, and E/A ratio did not change significantly in patients with heart rate change of < 10% and of between 10 and 20% after ablation. Blood pressure and left ventricular ejection fraction did not change in either the study or control groups. It was concluded that left ventricular ejection fraction and Doppler diastolic filling patterns are unaffected by radiofrequency ablation.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

Probability of supraventricular tachycardia recurrence in pediatric patients.

Supraventricular tachycardia (SVT) in pediatric patients is usually associated with a better prognosis than that in adults. However, late recurrence of SVT has been recently described. A total of 90 patients who had their initial SVT episode before 15 years of age were retrospectively studied (2-228 follow-up months; median, 215 months). Concomitantly congestive heart failure was present in 14 (16%) patients, and a cerebrovascular accident occurred in 1 patient. Intravenous verapamil was most frequently used to convert the initial SVT episodes without adverse effects, even in those younger than 1 year of age (9 patients). Older children could also be converted spontaneously or by vagal maneuvers. Patients with SVT recurrence were associated with an older age at initial SVT episodes (p < 0.001). By Kaplan-Meier actuarial analysis, the chance of remaining SVT-free during the follow-up was much lower in patients with initial SVT after 5 years of age than in patients with initial attacks before the age of 1 and between the age of 1 and 5 (p = 0.02 and 0.04, respectively). Even though, about 40% of the patients whose initial attacks occurred during infancy had recurrences 5 years later. Only those who had the initial attacks during the prenatal period remained free from SVT recurrences. Patients with initial SVT episodes during infancy have a longer period without SVT attacks and a lower chance of recurrences; nonetheless, a substantial number of them had recurrence at later childhood except those with initial SVT attacks during the prenatal period.(ABSTRACT TRUNCATED AT 250 WORDS)

Actuarial Analysis↗

Heroin lung: report of two cases.

Heroin lung is the most frequent complication of heroin intoxication. In September 1991 and January 1993, two young men aged 19 and 22 years presented with a sudden loss of consciousness and cyanosis after injecting heroin. They were both brought to our emergency department in the night and were immediately intubated and given 100% oxygen. Following intravenous naloxone, they both regained consciousness. The first patient's chest X ray revealed increased bilateral perihilar lung markings and mild patchy alveolar edema while the second patient showed a bat's wing shaped confluent alveolar edema. The blood gases in both cases revealed hypoxemia and hypercapnia. Follow-up chest roentgenograms on the second hospital day in case 1 and the third hospital day in case 2 revealed partial clearing of the lung fields. Fever developed on the second hospital day and they both received two weeks of antibiotics prior to discharge. Case 1 had normal pulmonary function testing, but case 2 developed mild restrictive lung changes. Review of the literature shows that heroin can cause a fulminant but rapidly reversible form of pulmonary edema. The treatment for this noncardiogenic pulmonary edema is adequate ventilation, good pulmonary toilet, and naloxone to reverse the respiratory and central nervous system depression. Diuretics, digitalis and morphine are not recommended in the treatment of heroin lung.

Adult↗

Does lead play a role in the development of renal insufficiency in some patients with essential hypertension?

The association of excessive lead burden and essential hypertension has been a subject of much dispute. In particular, the potential detrimental effect of low level environmental exposure on BP has caused considerable concern. We studied the urinary excretion of lead following the infusion of EDTA (1 g of calcium disodium edetate) in 12 healthy controls (group I), 10 subjects with essential hypertension alone (Group II) and in 36 subjects with chronic renal insufficiency. Those subjects with renal insufficiency were further divided into three groups: group III, 12 patients with a history of 7-19 years of essential hypertension who subsequently developed into renal failure; group IV, patients with chronic renal failure alone; and group V, patients with chronic renal failure due to causes other than hypertensive nephropathy and associated with secondary hypertension. In comparison with other groups, subjects with hypertensive nephropathy (group III) had significantly elevated lead body burden. In addition, we found that five of the 12 subjects with hypertensive nephropathy had histories of acute gouty attacks after the development of renal function impairment. In conclusion, our observation of a higher EDTA postinfusional urinary lead excretion among some patients with essential hypertension with renal function impairment indicates that lead may play a crucial role in a subgroup of patients with hypertensive nephropathy.

Adult↗

Body lead stores and urate excretion in men with chronic renal disease.

OBJECTIVE: To determine the relationship of urate excretion to body lead stores in patients with chronic renal disease without previous lead exposure. METHODS: We compared 40 male subjects in 3 groups, on the basis of their serum creatinine and histories of gout, with serum urate, creatinine clearance, urate clearance, daily urate excretion, fractional urate excretion, and body lead stores. Group 1 consisted of 10 patients with normal serum creatinine levels and no evidence of gout. Group 2 contained 10 men with gout and abnormal serum creatinine levels. Group 3 included 20 subjects with abnormal serum creatinine levels and no evidence of gout. All patients received EDTA mobilization tests and 72 h urine collections. The total amount of lead excreted over 72 h was estimated as the body lead stores. An ANOVA test with Fisher pairwise least significant difference, correlation coefficients, and multiple linear regression test were used to measure any statistical significance among these variables. A p value < 0.05 was considered significant. RESULTS: Lead stores and serum urate were significantly higher in gouty patients with renal insufficiency than those of other groups, but the urate excretion of gouty patients was not relatively increased. Not only was there a significant correlation between creatinine clearance and urate excretion, but body lead stores also appeared to be negatively related to urate excretion in our patients, even though body lead stores in these subjects were within the normal range. CONCLUSION: Our findings suggest that lead may play a role in gouty patients with impaired renal function and chronic low level environmental lead exposure may subtly affect urate excretion in patients with chronic renal disease.

Adult↗

Developmental change in the modulation of acetylcholine receptor channel by protein kinase C activation in Xenopus embryonic muscle cells.

Protein phosphorylation is important in synaptic transmission and plasticity. We report here that phorbol 12-myristate 13-acetate (TPA), a protein kinase C (PKC) activator, enhances the postsynaptic response at developing neuromuscular junctions by increasing the open time of embryonic acetylcholine (ACh) channels at earlier stages of cultured myocytes. Compared with day-1 cultures, the effects of TPA declined or disappeared on day-3 cultures. Adenosine 5'-triphosphate (ATP) which is co-stored and co-released with ACh at motor nerve terminals and is reported to enhance spontaneous synaptic currents by the activation of PKC, also shows similar developmental changes in the modulation of embryonic ACh channels in Xenopus embryonic myocytes.

Adenosine Triphosphate↗

Usefulness of pulmonary venous flow pattern and maximal mosaic jet area detected by transesophageal echocardiography in assessing the severity of mitral regurgitation.

Pulmonary venous flow pattern detected by transesophageal echocardiography (TEE) has been reported to be a good marker of mitral regurgitation (MR) severity. In 89 patients with MR detected by TEE, both pulmonary venous flow pattern and maximal mosaic jet area were recorded for evaluating the severity of MR. Cardiac catheterization was performed in all patients for grading the severity of MR. Systolic reversed flow in pulmonary veins was a good marker for angiographic grade 3 or 4 MR with a sensitivity of 97% (33 of 34) and specificity of 95% (52 of 55). Maximal mosaic jet area had a good correlation with the grading of MR (r = 0.79). When a maximal mosaic jet area of > 6 cm2 was used to detect grade 3 or 4 MR, the sensitivity and specificity were lower than those of the systolic reversed flow (sensitivity 82 vs 97%, p = 0.073; specificity 80 vs 95%, p = 0.013). The accuracy of systolic reversed flow was not influenced by the cardiac rhythm or jet eccentricity. However, the sensitivity of maximal mosaic jet area was lower in patients with an eccentric jet than in patients with a central jet (67 vs 95%, p = 0.046). In conclusion, systolic reversed flow in pulmonary veins detected by TEE is better than the maximal mosaic jet area in detecting grade 3 or 4 MR, especially in patients with eccentric jet.

Adolescent↗

Role of tryptophan-388 of GLUT1 glucose transporter in glucose-transport activity and photoaffinity-labelling with forskolin.

GLUT1 glucose-transporter cDNA was modified to substitute leucine for Trp-388 and transfected into Chinese hamster ovary cells using the expression vector termed pMTHneo. This tryptophan residue is conserved among most of the facilitative glucose-transporter isoforms and has been proposed to be the photolabelling site of forskolin, a competitive inhibitor of glucose transport. In addition, this residue is located on membrane-spanning helix 10 which is suggested to contain the dynamic segment of the transporter. The mutated glucose transporter was expressed and inserted into the plasma membrane in a fashion similar to the wild-type. Unexpectedly, this mutation did not abolish photolabelling with forskolin. However, the mutation induced a marked decrease in 2-deoxyglucose uptake with a 4-fold decrease in turnover number and a 1.25-fold increase in Km compared with the wild-type GLUT1. A similar decrease in zero-trans influx activity was also observed for 3-O-methylglucose. In contrast, no apparent decrease was observed in zero trans efflux activity for 3-O-methylglucose. The mutation decreased the turnover number of the glucose transporter in equilibrium exchange influx for 3-O-methylglucose by 33% without any change in Km. These results indicate that (1) Trp-388 is not the photolabelling site for forskolin, if we assume that the labelling occurs at a single site and (2) Trp-388 is more likely to be involved in interconversion between the inward-facing and outward-facing conformers of GLUT1 than binding of glucose, and thus, substitution of leucine for Trp-388 in this dynamic segment would decrease the rate of alternating conformation, which would preferentially affect the influx activity.

3-O-Methylglucose↗