Spontaneous reduction of intussusception: verification with US

PURPOSE: To report cases of spontaneous reduction of intussusception. MATERIALS AND METHODS: The authors reviewed the clinical and imaging findings in four patients with intussusception. Patients ranged in age from 3 to 7 months and were seen over a 12-year period. RESULTS: Intussusception was diagnosed with ultrasound (US) in all four patients; however, when enema studies were performed, intussusception was not identified. Repeat US also failed to demonstrate the presence of an intussusception, and all four patients showed concomitant rapid resolution of symptoms. CONCLUSION: Spontaneous reduction of intussusception is probably more common than is generally thought, and its documentation was facilitated with US. It is likely that spontaneously reduced intussusception will be documented more frequently in the future.     

Current and future status of ovulation induction in polycystic ovary syndrome

Great progress had been achieved during the last 20 years in the field of ovulation induction in patients with polycystic ovary syndrome (PCOS). Clomiphene citrate remains the first line of treatment for all anovulatory women with PCOS, since in properly selected patients the cumulative pregnancy rate approaches that in normal women. Human urinary gonadotrophins have been used extensively for ovulation induction, but the development of low-dose regimens has opened a new era in the management of anovulation related to PCOS. This article discusses the main advantages and disadvantages of the principal methods and regimens currently used for ovulation induction in patients with PCOS including clomiphene citrate, gonadotrophins, pulsatile gonadotrophin-releasing hormone (GnRH) and GnRH agonists. It also discusses new drugs discovered recently, particularly recombinant gonadotrophins and GnRH antagonists, and provides some thoughts regarding their use in future protocols. Finally, based on the discovery of new ovarian substances which specifically control luteinizing hormone (LH) secretion, this article develops assumptions on possible implications of these substances in the pathophysiology of PCOS and their potential use in the management of the syndrome.     

Sympathomimetic enantiomers and asthma

Airways of asthma patients can become hyperresponsive to airway spasmogens following regular use of isoprenaline or beta 2-selective sympathomimetics. Hyper-reactivity that results from acute exposure of animals to these drugs is pre-empted by vagal section (a procedure which does not influence spasmolytic efficacy of sympathomimetics), is not diminished by antagonism of beta 2-adrenoceptors and is not associated with loss of responsivity of beta 2-adrenoceptors in the airways. Since activation, modulation, or blockade of beta 2-adrenoceptors does not determine this form of hyperreactivity, the possibility that distomers may induce hyperreactivity must be considered. Ocular and vascular responses to distomers of sympathomimetics have long been recognised and, more recently, comparable observations have been made for the airways. Thus, reactivity of guinea-pig airways to spasmogens was increased following exposure to S-isoprenaline, S-salbutamol, or S-terbutaline and exposure to S-isoprenaline or S-salbutamol can intensify symptoms in asthmatics. Regular exposure to the racemate, especially during or following an allergic reaction, predisposes to expression of hyper-reactivity, which is nullified, acutely, by the eutomer. These observations imply that biological effects of sympathomimetic distomers may contribute to morbidity and mortality in asthma patients.     

The benefit of appropriate empirical antibiotic treatment in patients with bloodstream infection

Sudden cardiac deaths of young athletes, which are usually associated with physical exertion, continue to achieve high public visibility and generate considerable concern. Despite broad community participation in sports, such catastrophes are uncommon, occurring in about 1/200000 high school athletes per academic year. Various unsuspected congenital cardiovascular diseases are usually responsible; the most common lesions are hypertrophic cardiomyopathy and several congenital coronary artery anomalies. Selected reports suggest that arrhythmogenic right ventricular dysplasia may be a more common cause of these deaths than previously suspected. In some trained athletes with borderline increases in thickness of the left ventricular wall, mild morphologic expression of hypertrophic cardiomyopathy can often be distinguished from the physiologic consequences of athlete's heart by noninvasive clinical assessment and testing. In addition, the recognized cardiovascular risks of the athletic field are now extended to include cardiac arrest resulting from relatively modest, nonpenetrating chest blows produced by projectiles (such as baseballs) or bodily contact in the absence of underlying cardiac disease and without structural injury to the chest wall or heart. These uncommon but usually fatal events seem to result when chest impact occurs precisely during the vulnerable phase of repolarization, and they may be reduced by use of softer baseballs. Preparticipation screening for cardiovascular disease, consisting of standard history and physical examination, is customary practice for most high school and college athletes in the United States. Evidence suggests, however, that the present screening process for cardiovascular disease in high school athletes may be largely inadequate, given the content of the approved screening questionnaires (which serve as guidelines for the process) and the use of examiners with little cardiovascular training. This emphasizes the need for national standardization of preparticipation screening. The recommendations of the 26th Bethesda Conference for disqualification from competitive athletics are now a standard for management decisions when cardiovascular abnormalities are identified in trained athletes.     

Inactivation and stabilization of urokinase fibrinolytic activity in vitro

The first and second internal transcribed spacers (ITS1, ITS2) as well as the intervening 5.8S coding region of the rRNA gene were characterized in eight Babesia canis isolates of differing geographic origin, vector specificity, and pathogenicity to dogs. The genotypes determined by sequencing segregated into three clearly separated groups close to or near the species level and correspond to the previously proposed subspecies B. canis canis, B. canis vogeli, and B. canis rossi. The three genotypes can be distinguished by Sau96I digestion of the polymerase chain reaction (PCR)-amplified rDNA target.     

The orphan receptor CRF2-4 is an essential subunit of the interleukin 10 receptor

BACKGROUND/AIMS: Models of hepatopulmonary syndrome require both hepatic injury and portal hypertension to develop pulmonary microvascular and gas exchange abnormalities. Recently, increased endothelin-1 levels associated with vasodilatation, have been observed in cirrhosis. We investigated endothelin-1 production in common bile duct ligated animals with hepatopulmonary syndrome in comparison to partial portal vein ligated animals that do not develop hepatopulmonary syndrome. METHODS: Organ and plasma endothelin-1 were measured in sham, bile duct ligated and portal vein ligated rats, and Northern analysis and immunohistochemistry were performed in liver. Plasma endothelin-1 levels were correlated with pulmonary endothelial nitric oxide synthase levels and alveolar-arterial oxygen gradients. RESULTS: Hepatic and plasma endothelin-1 increased only after bile duct ligation, and were accompanied by increased hepatic endothelin-1 mRNA and increased endothelin-1 protein in biliary epithelium. Plasma endothelin-1 levels correlated directly with both pulmonary endothelial nitric oxide synthase levels and alveolar-arterial gradients. CONCLUSIONS: Enhanced hepatic production and increased plasma levels of endothelin-1 occur after bile duct ligation, but not after portal vein ligation, and correlate with associated molecular and gas exchange alterations in the lung. Endothelin-1 may contribute to the pathogenesis of hepatopulmonary syndrome.