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Among 30 children with hepatic ductular hypoplasia and normal extrahepatic bile ducts, 15 formed a hemogeneous, readily recognizable group. In addition to chronic cholestasis, they have characteristic facies, a mesosystolic murmur, vertebral arch defects, growth retardation, mental retardation, and hypogonadism. Typical biochemical and histologic features aid in differentiation of this group from patients with other varieties of biliary disease.
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Resistance to insulin-like growth factor I (IGF-1)-induced cardiac contractile response has been reported in diabetes. To evaluate the role of prediabetic insulin resistance to cardiac IGF-1 resistance, whole body insulin resistance was generated with dietary sucrose and contractile function was evaluated in ventricular myocytes. Mechanical properties were evaluated using an IonOptix system and intracellular Ca(2+) transients were measured as changes in fura-2 fluorescence intensity (Delta FFI). After 8 weeks of feeding, sucrose rats displayed euglycemia, hepatomeglay and normal heart size, and glucose intolerance, confirming the presence of insulin resistance. Myocytes from sucrose-fed rats displayed decreased peak shortening (PS), reduced resting FFI, increased intracellular Ca(2+) clearing, associated with normal duration of shortening and relengthening compared to myocytes from starch-fed rats. IGF-1 (10(-10)-10(-6) M) caused a similar concentration-dependent decrease in PS in both groups. Only the highest concentration of IGF-1 elicited an inhibition on Delta FFI in sucrose myocytes. In addition, the IGF-1-induced response was abolished by the IGF-1 receptor antagonist H-1356 in both groups, and by the nitric oxide synthase inhibitor L-NAME in starch but not sucrose myocytes. These results indicated prediabetic insulin resistance alters cardiac contractile function at the myocytes level, but may not be permissive to cardiac contractile resistance to IGF-1.
The study is based on the experimental model of myocardial hypertrophy in rats. Male Sprague-Dawley adult rats were exposed to acute hypoxia in a hypobaric chamber (0.40 atmospheres of air for 24 hours). Myocardial hypertrophy was detected by wet and dry heart weight values when calculated on the basis of total body weight; i.e., ratio heart weight in mg to body weight in 100 g. The behaviour of myocardial hypertrophy was assessed after treatment of intact animals with Puromycin (10 mg/rat i.p.) or Actinomycin-D (100 micrograms/rat i.p.). The experimental results showed the following dry heart weight values (mean +/- SEM): room pressure 60.5 +/- 1.5; hypoxia 69.2 +/- 0.9; Actinomycin-D + hypoxia 63.5 +/- 0.6; Puromycin + hypoxia 62.4 +/- 1.5, (P less than 0.001). From the comparison of data reveals that inhibitors of protein synthesis completely inhibit the myocardial hypertrophy due to hypoxia. Thus it is documented that acute hypobaric hypoxia is able to induce in the rat an actual myocardial hypertrophy condition as expressed of the enhanced protein synthesis.
Multidector-row CT (MDCT) with retrospective ECG gating allows scanning the entire heart with 1.25 mm slice thickness and 250 ms effective exposure time within 35 s investigation time. The resulting images allow for an accurate high-resolution assessment of morphological detail of both the coronary arteries and the cardiac chambers. Performing a contrast-enhanced MDCT angiography (MD-CTA) in addition to a non-enhanced scan for the detection and quantification of coronary calcifications may be indicated in patients with atypical chest pain and in young patients with high cardiovascular risk. This group of patients may show non-calcified plaques as the first sign of their coronary artery disease. As the proximal part of the coronary arteries is well displayed by MD-CTA it also helps to delineate the course in anomalous coronary vessels. Additional information is drawn from the preoperative use of MD-CTA do determine the distance of the left internal mammarian artery to the left anterior descending coronary artery prior to minimal invasive bypass grafting. Additional indications for MD-CTA are the non-invasive follow up after venous bypass grafting, PTCA, and coronary stent interventions. MD-CTA allows following the course of the coronary vessels to the level of third generation coronary segmental arteries. A definite diagonis to rule out coronary artery disease can be reliably made in vessels with a diameter of 1.5 mm or greater. With MDCT a number of different atherosclerotic changes can be observed in diseased coronary arteries. Non-stenotic lesions may show tiny calcifications surrounded by large areas of irregularly distributed soft tissue. Calcifications in this type of atherosclerotic coronary artery wall changes appear as 'the tip of iceberg'. Heavy calcifications usually tend to be non-stenotic because of vessel remodelling resulting in a widening of the coronary vessel lumen. Therefore, heavy calcifications appear to ack like an 'internal stent' for a coronary vessel segment. Humps of soft tissue either with or without calcifications are more likely to cause significant coronary artery disease and correlate with stenoses of >50% on selective coronary catheter. These humps consist of well-defined soft tissue in the coronary artery wall. The density of this soft tissue may vary between 30-70 HU. In cases where a coronary vessel is occluded by thrombotic material, a typical sign is found with enlargement of the coronary vessel, a hypodense center and a hyperdense rim. Vessel occlusion without thrombus may also appear within a collapsed and dense lumen. In addition to the investigation of the coronary arteries, CTA with MDCT is well suited to assess the presence and morphology of myocardial scars and aneurysms, intracardial tumors and thrombi.
Here we describe the cloning and expression pattern of a new bHLH-PAS domain gene, Npas3. Npas3 shares 50.2% amino acid sequence identity with Npas1 and a lesser similarity with other members of the bHLH-PAS domain family of transcription factors. Northern blot analysis detected Npas3 mRNA between 11.5 and 17.5 d.p.c. in embryonic development and exclusively in the adult brain. Whole-mount and section in situ hybridization assays revealed expression of Npas3 between 9.5 and 11.5 d.p.c. in the developing neural tube. In addition, Npas3 mRNA was expressed throughout the neuroepithelium of the developing central nervous system between 10. 5 and 12.5 d.p.c. Interestingly, at 14.5 d.p.c., the expression of Npas3 mRNA became restricted to the neopallial layer of the cortex. At 12.5 d.p.c., Npas3 mRNA was evident in nonneural tissues such as the developing dermis and mesenchyme surrounding the otic and nasal placodes. Expression was also detected in the developing cardiac valves, limb and developing kidney.
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