Patient Health Literacy and Communication with Providers Among Women Living with HIV: A Mixed Methods Study

AIDS and Behavior - In this mixed-methods study, we examine the relationship between provider communication and patient health literacy on HIV continuum of care outcomes among women living with HIV...     

Magnetic field interactions between current consumer electronics and cardiac implantable electronic devices

Journal of Interventional Cardiac Electrophysiology - Ablation index (AI) is a radiofrequency lesion quality marker. The AI value that allows effective and safe pulmonary vein isolation (PVI) is...     

Binding of 125I-labelled thyrotrophin to transfected human thyrocytes (SGHTL-34 cells)

The binding of 125I-labelled bovine TSH to a human thyroid cell line (SGHTL-34) has been studied. Binding to hormonally responsive cells was time dependent, specific and reversible. Scatchard analysis of the binding data indicated the presence of a single binding site with high affinity (intrinsic dissociation constant (Kd) = 0.25 +/- 0.08 nmol/l; mean +/- S.E.M.; n = 4) and low capacity (maximum binding (Bmax) = 104 +/- 29 fmol/mg protein; mean +/- S.E.M.; n = 4). Hill plots confirmed the presence of a single site. Kinetic data demonstrated close agreement between the Kd and Bmax obtained from the competition data (Kd = 0.23 +/- 0.35 nmol/l; Bmax = 161 +/- 83 fmol/mg protein; n = 6).     

Risk of venous thromboembolism associated with the common hereditary haemochromatosis Hfe gene (C282Y) mutation

A high prevalence of a common mutation in the Hfe gene (C282Y) has recently been reported in patients with the factor V Leiden mutation and a history of thrombosis. The aim of this study was to estimate the relative risk of venous thromboembolism in a large case-control study. 56/481 patients (11.6%) and 57/497 controls (11.5%) were heterozygous for the C282Y allele giving an odds ratio of 1.02 (95%CI 0.69-1.51). 12/81 patients with the factor V Leiden mutation were heterozygous for the C282Y allele compared to 1/13 controls, odds ratio 2.09 (95%CI 0.25-17.6). An analysis of a further group of patients and controls selected for the factor V Leiden mutation did not indicate a higher prevalence of the C282Y allele in symptomatic patients, odds ratio 0.17 (95%CI 0.34-0.81). This study does not support the hypothesis that the C282Y allele is an additional risk factor for venous thrombosis in patients with the factor V Leiden mutation.     

Light chain 2 profile and activity of human ventricular myosin during dilated cardiomyopathy. Identification of a causal agent for impaired myocardial function.

BACKGROUND. A number of parameters reflecting the effects of idiopathic dilated cardiomyopathy (IDC) on the structure and function of myosin from the human myocardium were analyzed. METHODS AND RESULTS. The content of the regulatory light chain, LC2, was reduced in myopathic heart myosin in contrast to the controls in which it was present in stoichiometric amounts relative to the essential light chain, LC1. In IDC hearts, the absence or significant reduction in amount of LC2 was related to the presence of an active protease, which was isolated and purified about 130-fold. The protease exhibited a significant degree of specificity: It cleaved LC2 almost totally (but not the heavy chains) in human control heart myosin but only partially cleaved LC2 in canine heart or in rabbit skeletal muscle myosins. The protease was present at a very low level or was inactive in control heart tissue. When the LC1/LC2 molar ratio was calculated, it was found to be 1:1.0 in control heart myosin and remained constant in various samples analyzed, whereas in myopathic myosin from different individuals, this ratio varied from 1:0.1 to 1:0.69. The rates of ATP binding to control and myopathic myosins were similar, whereas the Vm of actin-activated ATPase of myopathic myosin was about 25% less than that of the control. However, ATP binding and its hydrolysis by control S1, i.e., the myosin head, were faster by a factor of 2 than that of the myopathic S1. In addition, control myosin synthetic thick filament length as well as turbidity in solution, measured by light scattering, were twice as large as those of the myopathic heart myosin. These effects induced by myopathy in both filament assembly and turbidity were reversed upon reassociation of IDC myosin with LC2. CONCLUSIONS. The changes in myosin structure and function were linked to a protease-mediated cleavage of LC2 in myosin; a possible role for the protease in the degenerative effects of idiopathic dilated cardiomyopathy is thus defined.     

Pulmonary vascular disease in neonates with transposition of the great arteries and intact ventricular septum.

BACKGROUND--Progressive pulmonary vascular disease in surgically unrepaired transposition of the great arteries with or without ventricular septal defect had been frequently described in the past. Occurrence of progressive pulmonary vascular disease has been reported even after atrial switch procedure done at three months of age. With the advent of neonatal surgical repair, this problem is virtually non-existent. There is a small subgroup of infants with transposition of the great arteries who show pulmonary vascular disease in the neonatal period that can adversely affect the surgical outcome. The clinico-pathological correlation in this group of patients was studied. OBSERVATIONS--Three patients, with transposition of the great arteries and intact ventricular septum, who showed histological evidence of pulmonary vascular disease in the neonatal period or early infancy are described. Two of these patients, continued to have poor systemic oxygenation despite adequate atrial communication. One patient had a close ductus arteriosus within the first two hours of birth while on prostaglandin E1 infusion. CONCLUSIONS--In the absence of left ventricular outflow tract obstruction, a poor response to atrial septostomy suggests pulmonary hypertension and pulmonary vascular disease. Antenatal constriction of the ductus arteriosus may contribute to such changes in pulmonary vasculature.     

Total anomalous pulmonary venous drainage in infancy.

Between May 1971 and December 1975, 39 infants had operations for correction of total anomalous pulmonary venous drainage. Fourteen of the 39 patients were under 1 month of age at the time of operation. Twenty-four patients had supracardiac, 7 intracardiac, and 6 infracardiac total anomalous pulmonary venous drainage, and 2 had a mixed type. The overall hospital mortality was 36 per cent. There have been no late deaths. The improvement in survival rate in this series is attributed to: (1) earlier recognition and prompt referral, (2) an aggressive approach to diagnosis involving complete cardiac catheterisation and angiocardiography, (3) vigorous preoperative care, (4) early complete correction including construction of a large anastomosis and enlargement of the left atrium when indicated, and (5) intensive postoperative management paying particular attention to fluid balance and treatment of pulmonary complications. Operative mortality was highest in patients with total anomalous pulmonary venous drainage directly to the superior vena cava, and in those with infradiaphragmatic drainage of whom all had pulmonary venous obstruction. Mortality was not closely related to age, body weight, or severity of pulmonary hypertension.     

Vitamin D receptor gene polymorphism associates with graft-versus-host disease and survival in HLA-matched sibling allogeneic bone marrow transplantation

We investigated the role of polymorphism of the vitamin D receptor (VDR) gene in HLA-matched sibling BMT for polymorphisms previously associated with human disease pathology. In intron 8 of the VDR gene, the B and A alleles of the BsmI and ApaI RFLPs were found to associate with reduced aGVHD when present in the patient's genotype. Logistic regression analysis demonstrated that patient VDR genotype, along with previously identified IL-10(-1064) and IFN-gamma genotype to be risk factors for severe acute GVHD. The A allele also associates with increased likelihood of death when present in the donor genotype (AA vs Aa or aa, hazard ratio 2.03, P = 0.0232). In patients who received increased prophylaxis with multi-agent therapy, patients whose graft was from a donor with an AA genotype had a substantially worse survival than patients whose graft was from a donor with a non-AA genotype (hazard ratio 12.93, P < 0.0001). Analysis of VDR genotype in prospective BMT recipients could indicate patients at risk of severe aGVHD. Analysis of VDR genotype in prospective BMT donors may identify individuals who have greater transplant-related mortality, and also allow appropriately restricted use of increased immunosuppressive prophylaxis.     

Rest and exercise hemodynamic effects of sequential alpha-1-adrenoceptor (trimazosin) and beta-adrenoceptor (propranolol) antagonism in essential hypertension

The efficacy of acute beta blockade in essential hypertension is limited by reflex vasoconstriction. The aim of this study was to determine whether the latter response was modified by prior selective alpha-1-adrenoceptor blockade. A single-blind, within-patient, placebo-controlled evaluation of the immediate hemodynamic effects of sequential alpha-1 (trimazosin)- and beta (propranolol)-adrenoceptor blockade was undertaken in 10 men (34 to 58 years) with previously untreated essential hypertension. The study commenced with a 4-minute control period of constant-load (600 to 900 kpm/min) upright bicycle exercise, and measurements were made before (control) and 30 minutes after intravenous trimazosin (2 mg/kg) and exercise was then repeated; measurements at rest were again made 4 minutes after intravenous propranolol (0.2 mg/kg) before a final exercise period. Trimazosin at rest reduced systolic and diastolic arterial pressure and systemic vascular resistance without change in heart rate, cardiac output, or left ventricular (LV) filling pressure. During upright bicycle exercise the reductions in blood pressure were sustained without change in their rest-to-exercise increments. Other circulatory variables did not differ from control values. At rest the addition of propranolol further reduced systolic arterial pressure. Heart rate and cardiac output fell and systemic vascular resistance increased to its pretreatment control value. During exercise the changes at rest were sustained and the rest-to-exercise increments in blood pressure, heart rate, and cardiac output were reduced. LV filling pressure was significantly increased. In conclusion, alpha-1-adrenoceptor blockade modified the adverse effects of acute beta blockade at rest but not during exercise.