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Biomedical subjects

E Loh

Publications and source records attributed to E Loh.

At least 73 records · Page 4Linked to original sources
PubMed1994

In vivo measurement of water diffusion in the human heart.

Existing magnetic resonance methods for diffusion imaging, including echo planar, are ineffective in the beating heart due to motion-induced signal attenuation. To overcome this problem, we used a diffusion-weighted stimulated echo-echo planar magnetic resonance imaging sequence. The two lobes of the diffusion-sensitizing gradient were synchronized to the same point in successive cardiac cycles in order to fix the cardiac position and avoid bulk motion effects. The apparent diffusion coefficients (ADCs) of the interventricular septum in 12 healthy subjects for diffusion gradients along the x-, y-, and z-directions were 1.40 +/- 0.27, 1.48 +/- 0.35, and 1.78 +/- 0.27 x 10(-3) mm2/s. The ADCs of the interventricular septum in a second group of 15 healthy subjects for diffusion gradients along the short axis, horizontal and vertical long axes were 0.92 +/- 0.15, 1.50 +/- 0.15, and 1.10 +/- 0.24 x 10(-3) mm2/s. Because the ADCs were less than the measured values for skeletal muscle and their standard deviations were low, it seems unlikely that bulk motion effects made the dominant contribution to the measured myocardial ADC for the interventricular septum, although motion and/or susceptibility artifacts frequently degraded measurements in the free wall of the left ventricle. Additional evidence that ADC was not predominantly determined by wall motion was obtained in a third group of patients with various cardiac abnormalities, in whom there was only a weak correlation between ADC and ejection fraction.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1994

Early cardiac allograft failure after orthotopic heart transplantation.

Early cardiac graft failure has been reported to occur in 4-25% of patients undergoing orthotopic heart transplantation. To further elucidate the characteristics and prognosis of patients with graft failure, we retrospectively identified 10 patients from a series of 212 consecutive recipients with catastrophic graft dysfunction in the absence of acute cellular rejection, right ventricular failure secondary to pulmonary hypertension and technical factors. We present a case report and the experience from one transplant center, a review of the literature and possible strategies for the management of early graft failure. Mean onset of graft failure was 6.5 days (range intraoperative to 23 days). Multivariable analysis revealed a longer total ischemic time in patients with early graft dysfunction (200 +/- 14 vs. 166 +/- 4 min). No episodes of hyperacute rejection were observed. Pathologic changes noted on biopsy or autopsy included ischemia in 9 and vascular rejection in 1. The mortality at 60 days was 50%. Early use of aggressive mechanical and pharmacological support is described and appears to be important for graft salvage.

Adult↗
PubMed1994

Pericardial effusions after cardiac transplantation.

OBJECTIVES: The aim of this study was to determine the etiologic factors in the formation of significant pericardial effusion after orthotopic heart transplantation and to determine the association of pericardial effusion with survival. BACKGROUND: The formation of pericardial effusions has been well described after orthotopic heart transplantation, but the risk factors for development of effusions remain unclear. Rejection and cyclosporine have been cited as possible causes, but anatomic factors have not been studied. METHODS: We conducted a retrospective review of medical records and echocardiograms of 203 consecutive patients at one center, including ischemic time, incidence and severity of rejection, weight difference between donor and recipient and previous cardiac surgical history. Multivariate analysis was performed, and actuarial survival rate curves were calculated according to the Kaplan-Meier method. RESULTS: Eighteen (8.9%) of 203 transplant recipients developed moderate to large pericardial effusions. Forty-four percent of patients required pericardiocentesis, and 28% subsequently required pericardiectomy for management of the effusions. Multivariate analysis identified the presence of a positive weight difference between recipient and donor (recipient weight > donor weight) and the lack of previous median sternotomy as the most powerful predictors of effusion formation. No significant association was found with rejection. There was no difference in actuarial survival rate between patients with and without effusions. CONCLUSIONS: A positive mismatch in weight between recipient and donor and the absence of previous cardiac surgery are associated with the formation of significant pericardial effusions. Closer monitoring of these patients at risk may be warranted.

Adolescent↗
PubMed1994

Nitric oxide regulates basal systemic and pulmonary vascular resistance in healthy humans.

BACKGROUND: The endothelium synthesizes and releases a relaxing factor with the physiochemical properties of nitric oxide (NO). However, the role of endothelium-derived NO in the basal regulation of systemic and pulmonary vascular resistance in humans is not known. Our primary objectives were to determine the effects of inhibiting NO synthesis on blood pressure and systemic vascular resistance and to establish the role of endothelium-derived NO in the regulation of normoxic pulmonary vascular tone. METHODS AND RESULTS: We studied the systemic and pulmonary hemodynamic effects of NG-monomethyl-L-arginine (L-NMMA, 0.03 to 1.0 mg.kg-1.min-1 IV), an NO synthase inhibitor, in 11 healthy volunteers, aged 33 +/- 2 years. An arterial cannula and a pulmonary artery catheter were placed in each subject to measure blood pressure, pulmonary artery pressure, and pulmonary capillary wedge pressure. Cardiac output was determined by the Fick technique, and systemic and pulmonary vascular resistances were calculated. Serum NO levels (free and protein bound) were measured by chemiluminescence in 5 subjects. Six of the subjects also received phenylephrine (25 to 100 micrograms/min IV) to compare the cardiac hemodynamic effects of L-NMMA with those of a direct-acting vasoconstrictor. L-NMMA caused dose-dependent increases in both blood pressure and systemic vascular resistance. At the highest dose of L-NMMA, there was a 15.5 +/- 1.3% increase in mean blood pressure and a 63.4 +/- 8.2% increase in systemic vascular resistance (each P < .01). Pulmonary vascular resistance increased 39.8 +/- 9.4% (P < .01), whereas mean pulmonary artery pressure did not change. Administration of L-NMMA also reduced cardiac output by 27.8 +/- 2.9% and stroke volume by 15.4 +/- 3.5% (each P < .01). Serum NO levels decreased 65 +/- 10% from basal values (P < .05), confirming inhibition of endogenous NO production. Phenylephrine increased blood pressure to a level comparable to that observed with L-NMMA. The decline in stroke volume was greater with L-NMMA than with phenylephrine (P < .01). CONCLUSIONS: This study demonstrates that basal release of endothelium-derived NO is directly involved in the determination of systemic vascular resistance and, therefore, blood pressure in healthy humans. In addition, NO regulates basal normoxic pulmonary vascular tone. The complex hemodynamic effects of NO are composite properties of its actions on systemic and pulmonary vascular resistance and cardiac function.

Adult↗
PubMed1994

Cardiovascular effects of inhaled nitric oxide in patients with left ventricular dysfunction.

BACKGROUND: Pulmonary vascular resistance (PVR) is frequently elevated in patients with advanced heart failure. Nitric oxide (NO), which contributes to the activity of endothelium-derived relaxing factor, causes relaxation of pulmonary arteries and veins in vitro. Inhalation of NO gas causes pulmonary vasodilation in patients with primary and secondary forms of pulmonary hypertension. METHODS AND RESULTS: To test the hypothesis that inhalation of NO gas lowers PVR in patients with heart failure, we studied the hemodynamic effects of a 10-minute inhalation of NO (80 ppm) in 19 patients with New York Heart Association class III (n = 5) and class IV (n = 14) heart failure due to left ventricular (LV) dysfunction. Although inhalation of NO had no effect on pulmonary artery pressures, the PVR decreased by 31 +/- 7% (P < .001) due to a 23 +/- 7% increase (P < .001) in pulmonary artery wedge pressure and despite a 4 +/- 2% (P < .05) decrease in cardiac index. The magnitude of the decrease in PVR with inhaled NO was inversely related (r = -.713; P < .001) to the baseline PVR. Inhaled NO had no effect on heart rate, systemic arterial pressure, systemic vascular resistance, or LV peak +dP/dt or -dP/dt. CONCLUSIONS: In patients with heart failure due to LV dysfunction, inhalation of NO causes a decrease in the PVR associated with an increase in LV filling pressure. These findings predict that inhaled NO, if used alone at this dose (80 ppm), may have adverse effects in patients with LV failure.

Administration, Inhalation↗
PubMed1993

Competitor mRNA fragments for quantitation of cytokine specific transcripts in cell lysates.

Synthetic RNAs (sRNAs) specific for four human cytokines were constructed and used as an exogenous internal standard in a quantitative reverse transcriptase-polymerase chain reaction (RT-PCR). The sequences of the sRNA and the target mRNA were identical except for a duplication or deletion of approximately 100 nucleotides. The size difference between these two templates permitted easy electrophoretic separation of their PCR products. The sRNA has polyadenylated sequences at the 3' end and can be added directly either to a cell lysate before RNA purification or to a reverse transcription reaction. One pair of primers is used to amplify the internal standard and the target simultaneously, and the ratio of the two PCR products remains constant throughout the amplification. This technique can be applied to quantitate specific mRNA in as few as 10 cells when the exogenous control is added directly to cell lysates. This method is sensitive, accurate and adaptable for quantitation of other transcripts.

Blotting, Northern↗
PubMed1993

Malocclusion prevalence in an ethnic Chinese population.

Population norms derived from one ethnic group may not necessarily be valid and accurate for other ethnic groups. With the increasing number of ethnic Chinese immigrants in Australia, Europe, and America, it would be useful for dental practitioners to be informed about malocclusion prevalence among Chinese. This study was carried out on 1050 Chinese school children (aged 12-14 years) to assess both qualitatively and quantitatively certain occlusal features. The population was found to have a high incidence of Class III malocclusions compared with caucasians. However, the incidence of Class II malocclusions was quite similar to those reported in caucasians. Normal occlusions occurred in about 7 per cent of this population. Although this percentage was much lower than those reported in blacks, it was similar to those reported in caucasians. Crowding occurred in about 50 per cent of cases, which was slightly less than for those reported for caucasians. Increased overbites were also less common in this Chinese population compared with caucasians. Compared with caucasians, crossbites were also less frequent in this Chinese population.

Adolescent↗
PubMed1992

Molecular evidence for the expression of nicotinic acetylcholine receptor alpha-chain in mouse thymus.

The presence and structure of nicotinic acetylcholine receptor (nAChR) in the thymus has been a subject of interest for many years because of its possible role in the pathogenesis of the autoimmune disease myasthenia gravis. Using the polymerase chain reaction with primers specific for the alpha-chain of nAChR (nAChR-alpha), an 880-bp homologous band was found after amplification of cDNA prepared from mouse thymus, thymic medullary and cortical epithelial cell lines, but not from thymocytes or kidney. Sequencing of the polymerase chain reaction product from the thymus and thymic medullary and cortical epithelial lines showed identity with skeletal muscle nAChR-alpha over the region examined. This region includes the domains of the molecule on which B cell and T cell autoantigenic targets have been described. No evidence was found in mouse tissue for the exon 3A, which has been described in human muscle and the human rhabdomyosarcoma cell line TE671. Our results provide evidence at the RNA level for the expression of the nAChR-alpha on stromal cells but not on thymocytes in normal murine thymus and are consistent with a role for intrathymic autoantigen expression in the pathogenesis of myasthenia gravis.

Animals↗
PubMed1992

Myocardial changes in cardiac transplant-associated coronary arteriosclerosis: potential for timely diagnosis.

Graft arteriosclerosis is the major limitation to long-term survival after heart transplantation. In this study, myocardial pathologic changes, especially those that might permit early diagnosis, were characterized in endomyocardial biopsy specimens and hearts obtained at retransplantation or autopsy from nine orthotopic heart transplant recipients. All had severe diffuse proliferative arterial stenoses without plaque rupture or coronary thrombi. Eight patients died with and one underwent retransplantation because of graft arteriosclerosis less than 12 months (six patients) or greater than 46 months (three patients) after operation. Six patients had antecedent symptoms of congestive heart failure and six had angiographically demonstrated epicardial coronary artery graft arteriosclerosis; four had both. Myocardial ischemic lesions included subendocardial myocyte vacuolization (seven patients) and microfocal to regional coagulation necrosis and granulation tissue or scar, or both (seven patients). Subendocardial myocyte vacuolization (indicative of sublethal ischemic injury) was diagnosed at prior right ventricular biopsy in two patients and was noted at autopsy in areas accessible to right-sided biopsy in three additional patients. Three patients had pathologic changes diagnostic of acute infarction on right or left ventricular biopsy, or both. Thus, all nine patients had lesions, of which five had biopsy-identified myocardial abnormalities caused by graft arteriosclerosis. It is concluded that graft arteriosclerosis yields not only myocardial pathologic changes similar to those associated with typical coronary atherosclerosis, but also lesions resulting from focal or diffuse ischemia caused by small vessel obstructions. This is manifest as subendocardial myocyte vacuolization or microfocal infarction. Recognition of these biopsy-accessible myocardial changes associated with graft arteriosclerosis may allow early recognition and appropriate therapeutic intervention.

Acute Disease↗
PubMed1992

Differential inotropic effects of flosequinan in ventricular muscle from normal ferrets versus patients with end-stage heart failure.

1. In right ventricular papillary muscles from control ferrets, flosequinan (10(-7)-10(-4) M) produced a concentration-dependent positive inotropic effect (10(-5) M = 153 +/- 24, 10(-4) M = 198 +/- 44% increase in isometric tension; control tension = 100%; n = 11) associated with a corresponding increase in amplitude of the intracellular Ca2+ ([Ca2+]i) transient recorded with aequorin (10(-5) M = 133 +/- 11, 10(-4) M = 187 +/- 36% increase in [Ca2+]i transient; n = 11). 2. The positive inotropic effect of flosequinan in control ferret ventricular muscle was neither blocked by propranolol (6 x 10(-7) M), nor associated with the abbreviation of the [Ca2+]i transient and contraction that is typical of catecholamines. 3. Neither flosequinan (n = 12) nor BTS 53 554, its sulphone metabolite (n = 6) produced a positive inotropic effect or altered the time course of contraction in myocardium from the hearts of patients with end-stage failure. 4. In contrast to milrinone, which produces a positive inotropic effect via phosphodiesterase inhibition, the unresponsiveness of myopathic human myocardium to flosequinan was not restored after intracellular adenosine 3':5'-cyclic monophosphate (cyclic AMP) levels were increased by prior treatment with forskolin (n = 13). 5. Taken together, these data indicate that flosequinan has a direct positive inotropic effect that is Ca(2+)-dependent, but independent of changes in intracellular cyclic AMP concentrations. 6. The positive inotropic effect may be species-dependent or altered by the presence of hypertrophy and/or heart failure. However, when used therapeutically in patients with severe heart failure, our data suggest that flosequinan should not adversely affect myocardial oxygen consumption through direct or catecholamine-mediated actions on the heart.

Animals↗
PubMed1989

The XLR sequence family: dispersion on the X and Y chromosomes of a large set of closely related sequences, most of which are pseudogenes.

The XLR sequence family encodes RNA transcripts specific to late-stage T and B cells and their neoplasms. Only one apparently functional mRNA has been identified thus far and this encodes a novel 25 kDa nuclear protein. In this report, we find that the XLR gene family is composed of 50-75 copies per haploid genome which localize to at least two different portions of the mouse X chromosome. Neither of these locations are near the xid mutation that earlier work had correlated with XLR. In addition, some members of this family are also on the Y chromosome. Another surprising finding is that while the fourteen genomic clones examined to date have the same exon-intron structure and are closely related with respect to sequence conservation (90%), all appear (in most cases by multiple criteria) to be non-functional, raising the possibility that all but one of the members of this large semi-dispersed family are pseudogenes.

Animals↗