Cardiac auscultation training of medical students: a comparison of electronic sensor-based and acoustic stethoscopes

Background  

To determine whether the use of an electronic, sensor based stethoscope affects the cardiac auscultation skills of undergraduate medical students.     

Latent variable discovery in classification models

The naive Bayes model makes the often unrealistic assumption that the feature variables are mutually independent given the class variable. We interpret a violation of this assumption as an indication of the presence of latent variables, and we show how latent variables can be detected. Latent variable discovery is interesting, especially for medical applications, because it can lead to a better understanding of application domains. It can also improve classification accuracy and boost user confidence in classification models.     

Long QT syndrome with a high mortality rate caused by a novel G572R missense mutation in KCNH2

In a four-generation family with long QT syndrome, syncopes and torsades de pointes ventricular tachycardia (TdP) were elicited by abrupt awakening in the early morning hours. The syndrome was associated with a novel KCNH2 missense mutation, G572R, causing the substitution of a glycine residue at position 572, at the end of the S5 transmembrane segment of the HERG K(+)-channel, with an arginine residue. This segment is involved in the channel pore and the mutation may cause a reduction in the rapidly activating delayed rectifier K+ current (Ikr), or changed gating properties of the ion channel, leading to prolonged cardiac repolarization. The electrocardiograms of affected persons showed prolonged QT interval and notched T waves. Despite treatment with atenolol, 200 mg twice daily, the proband still experienced TdP episodes. Three untreated relatives of the proband died suddenly, and unexpectedly, at 18, 32, and 57 years of age. The G572R mutation is thus associated with a high mortality rate, and the clinical presentation illustrates that some mutations may not be controllable by just beta-blockade.     

In vivo measurement of intracellular pH in human brain during different tensions of carbon dioxide in arterial blood. A 31P-NMR study

The effect of changes in carbon dioxide tension in arterial blood upon intracellular pH in brain tissue was studied in seven healthy volunteers, aged 22-45 years. The pH changes were monitored by use of 31P nuclear magnetic resonance spectroscopy, performed on a whole-body 1.5 Tesla Siemens imaging system. The measurements were carried out during hyperventilation and with the subject breathing atmospheric air containing 5 vol. % and 7 vol. % carbon dioxide. Intracellular pH increased significantly during 15 min of hyper-ventilation and decreased significantly during 18 min respiration of air containing 7 vol. % carbon dioxide. The intracellular buffer capacity was estimated. These results suggest that the ventilation response to carbon dioxide is correlated to changes in intracellular fluid pH.     

The renin–angiotensin system in kidney development: role of COX‐2 and adrenal steroids

Recent data from studies in rodents with targeted gene disruption and pharmacological antagonists have shown that the renin–angiotensin–aldosterone system (RAAS) and cyclooxygenase type‐2 (COX‐2) are necessary for late stages of kidney development. The present review summarizes data on the developmental changes of RAAS and COX‐2 and the pathways by which they are activated; their possible interplay and the mechanisms by which they affect kidney development. Intrarenal and circulating renin and angiotensin II (ANG II) are stimulated at birth in most mammals. In rats, renin and ANG II stay significantly elevated in the suckling period while aldosterone stabilizes at an adult level. COX‐2 is stimulated in thick ascending limb of Henle's loop in the suckling period at a time when urine concentrating ability is not developed. Data suggest that this induction is mediated by combined low plasma glucocorticoid concentration and by a low NaCl intake. Studies with selective inhibitors of COX‐2 and COX‐2 null mice show that COX‐2 activity stimulates renin secretion from JG‐cells during postnatal kidney development and that lack of COX‐2 activity leads to pathological change in cortical architecture and eventually to renal failure. In the postnatal period, ANG II initiates and maintains pelvic and ureteric contractions necessary for urine flow. Lack of ANG II in the neonatal period is thought to cause injury by a chronic increase of renal pelvic pressure. Aldosterone is crucial for survival and growth in the neonatal period through its effects on sodium reabsorption and the intrarenal sensitivity to aldosterone is increased in the postnatal period. Final maturation of the kidney occurs through an intimate interplay between a low dietary sodium intake and a non‐responsive HPA‐axis which stimulates cortical COX‐2 activity. COX‐2 supports increased activity of the RAAS and may contribute to a low concentrating ability.