A systems approach to trauma care in Myanmar: from health partnership to academic collaboration.

Experience from a variety of disciplines suggests that improving healthcare, particularly in resource-poor environments, can benefit from a systems approach. However, putting this into practice is challenging, especially in the context of an international institutional health partnership. In this article, we outline how a systems approach to the improvement of trauma care has informed both clinical improvement and academic collaboration as part of an ongoing partnership involving Cambridge University Hospitals NHS Foundation Trust, the University of Cambridge, and Cambridge Global Health Partnerships in the UK, and Yangon General Hospital, University of Medicine 1, and the Tropical Health and Education Trust (THET) in Myanmar.

Biochemical markers of bone turnover - uses and limitations.

Bone turnover markers of resorption and formation are released during the process of bone remodelling. These markers have been extensively studied in a number of therapeutic trials of osteoporosis during the past decade. This has led to better understanding of their physiology, clinical applications and possible ways to optimize analytical techniques.

Novel mutations of ABCA1 transporter in patients with Tangier disease and familial HDL deficiency.

The objective of the study was the characterization of ABCA1 gene mutations in 10 patients with extremely low HDL-cholesterol. Five patients (aged 6 months to 76 years) presented with splenomegaly and thrombocytopenia suggesting the diagnosis of Tangier disease (TD). Three of them were homozygous for novel mutations either in intron (c.

Multicentre trial of weekly risedronate on bone density in adults with cystic fibrosis.

Background: The aim of this study was to assess the efficacy, tolerability and safety of risedronate in adults with CF.

Methods: Patients with a lumbar spine (LS), total hip (TH) or femoral neck (FN) bone mineral density (BMD) Z-score of -1 or less were randomised to receive risedronate 35 mg weekly or placebo, and calcium (1g)+vitamin D(3) (800IU).

Results: At baseline, BMD Z-scores in the risedronate (n=17) and placebo (n=19) groups were similar.

Ablation of triadin causes loss of cardiac Ca2+ release units, impaired excitation-contraction coupling, and cardiac arrhythmias.

Heart muscle excitation-contraction (E-C) coupling is governed by Ca(2+) release units (CRUs) whereby Ca(2+) influx via L-type Ca(2+) channels (Cav1.2) triggers Ca(2+) release from juxtaposed Ca(2+) release channels (RyR2) located in junctional sarcoplasmic reticulum (jSR). Although studies suggest that the jSR protein triadin anchors cardiac calsequestrin (Casq2) to RyR2, its contribution to E-C coupling remains unclear.

Modest reductions of cardiac calsequestrin increase sarcoplasmic reticulum Ca2+ leak independent of luminal Ca2+ and trigger ventricular arrhythmias in mice.

Cardiac calsequestrin-null mice (Casq2-/-) display catecholaminergic ventricular tachycardia akin to humans with CASQ2 mutations. However, the specific contribution of Casq2 deficiency to the arrhythmia phenotype is difficult to assess because Casq2-/- mice also show significant reductions in the sarcoplasmic reticulum (SR) proteins junctin and triadin-1 and increased SR volume. Furthermore, it remains unknown whether Casq2 regulates SR Ca2+ release directly or indirectly by buffering SR luminal Ca2+.

Casq2 deletion causes sarcoplasmic reticulum volume increase, premature Ca2+ release, and catecholaminergic polymorphic ventricular tachycardia.

Cardiac calsequestrin (Casq2) is thought to be the key sarcoplasmic reticulum (SR) Ca2+ storage protein essential for SR Ca2+ release in mammalian heart. Human CASQ2 mutations are associated with catecholaminergic ventricular tachycardia. However, homozygous mutation carriers presumably lacking functional Casq2 display surprisingly normal cardiac contractility.

The QT and Tp-e intervals in left and right chest leads: comparison between patients with systemic and pulmonary hypertension.

Background: Action potential duration in the right ventricle is normally shorter than that in the left. We tested the hypothesis that there may be intrinsic differences in the QT and Tp-e (an interval from the peak to the end of the T wave) intervals between the left and right chest leads that can be exaggerated by systemic hypertension but attenuated by pulmonary hypertension in humans.

Methods: Electrocardiograms in the left (V4L-V6L) and right (V4R-V6R) chest leads were obtained in 40 healthy individuals, 29 patients with systemic hypertension and left ventricular hypertrophy, and 15 patients with pulmonary hypertension.

ECG repolarization waves: their genesis and clinical implications.

The electrocardiographic (ECG) manifestation of ventricular repolarization includes J (Osborn), T, and U waves. On the basis of biophysical principles of ECG recording, any wave on the body surface ECG represents a coincident voltage gradient generated by cellular electrical activity within the heart. The J wave is a deflection with a dome that appears on the ECG after the QRS complex.

Phase 2 reentry as a trigger to initiate ventricular fibrillation during early acute myocardial ischemia.

Background: Phase 2 reentry caused by heterogeneous loss of the transient outward potassium current (I(to))-mediated epicardial action potential (AP) dome can produce a closely coupled R-on-T extrasystole leading to ventricular fibrillation (VF) under conditions of ST-segment elevation unrelated to ischemia. The present study examined the role of phase 2 reentry in the initiation of VF during early myocardial ischemia.

Methods And Results: Regional myocardial ischemia was produced in an isolated, arterially perfused canine right ventricular wedge preparation.