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Ventricular Lumen (ventricular + lumen)
Selected AbstractsRegulation of development of oligodendrocytesJOURNAL OF NEUROCHEMISTRY, Issue 2002K. Ikenaka Oligodendrocyte (OL) is the myelin-forming glial cell in the central nervous system. In the spinal cord, molecular markers for OL precursor cells (OPCs), such as PDGF a-receptor (PDGFR a), are first expressed in a strictly restricted focus of the ventral ventricular lumen at E12.5 in mouse and later spread throughout the cord. To investigate how they originate from these specific regions, we used an explant culture system of E12 mouse cervical spinal cord. When we cultured the ventral and dorsal spinal cords separately, a robust increase in the number of O4+ cells was observed in the ventral fragment. This phenomenon suggests the presence of factors inhibiting OL development from dorsal spinal cord. BMP4 is secreted from dorsal spinal cord and is a strong candidate for this factor; however, it did not affect OL development in our system. Here we show that Wnt-1 and Wnt-3a, in contrast, may have a role in OL maturation. The developmental profile of wnt-1/3a gene expressions in the dorsal spinal cord showed a significant correlation with that of the dorsal activity, which was very strong at E11, and then reduced to an undetectable level by E14. When Wnt-3a was added to the dissociation culture prepared from E14 mouse ventral cervical cords, the numbers of OL decreased. b-Catenin and LEF family proteins are known to form a transcription factor complex at the down stream of Wnt signalling. OL,like differentiation of CG4 cells was inhibited by constitutively active LEF-b-Catenin, supporting the idea that Wnt signalling directly inhibits OL differentiation. [source] Control of the release of digestive enzymes in the larvae of the fall armyworm, Spodoptera frugiperdaARCHIVES OF INSECT BIOCHEMISTRY AND PHYSIOLOGY (ELECTRONIC), Issue 1 2010Digali Lwalaba Abstract There is a basal level of enzyme activity for trypsin, aminopeptidase, amylase, and lipase in the gut of unfed larval (L6) Spodoptera frugiperda. Trypsin activity does not decrease with non-feeding, possibly because of the low protein levels in plants along with high amino acid requirements for growth and storage (for later reproduction in adults). Therefore, trypsin must always be present so that only a minimal protein loss via egestion occurs. Larvae, however, adjust amylase activity to carbohydrate ingestion, and indeed amylase activity is five-fold higher in fed larvae compared to unfed larvae. Gut lipase activity is low, typical of insects with a high carbohydrate diet. A flat-sheet preparation of the ventriculus was used to measure the release of enzymes in response to specific nutrients and known brain/gut hormones in S. frugiperda. Sugars greatly increase (>300%) amylase release, but starch has no effect. Proteins and amino acids have little or no effect on trypsin or aminopeptidase release. The control of enzyme release in response to food is likely mediated through neurohormones. Indeed, an allatostatin (Spofr-AS A5) inhibits amylase and trypsin, and allatotropin (Manse- AT) stimulates amylase and trypsin release. Spofr-AS A5 also inhibits ileum myoactivity and Manse-AT stimulates myoactivity. The epithelial secretion rate of amylase and trypsin was about 20% of the amount of enzyme present in the ventricular lumen, which, considering the efficient counter-current recycling of enzymes, suggests that the secretion rate is adequate to replace egested enzymes. © 2009 Wiley Periodicals, Inc. [source] Syncope associated with hypertrophic cardiomyopathy in a dromedary camelAUSTRALIAN VETERINARY JOURNAL, Issue 8 2000C GUTIERREZ A case of hypertrophic cardiomyopathy in a dromedary camel (Camelus dromedarius) is described for the first time. The patient, a castrated 9-year-old animal, presented with a 6-month history of several episodes of syncope after moderate exercise and later at rest. The syncope had a sudden onset and a duration of 30 to 45 seconds. After clinical, electro-cardiographical and echocardiographical examination, a tentative diagnosis of hypertrophic cardiomyopathy was made. At necropsy, the heart had a globose shape and was firm on palpation. The left ventricular free wall and the inter-ventricular septum were thickened in cross-section and the left ventricular lumen was small. The clinical diagnosis was confirmed by histologic examination of heart tissue that demonstrated hypertrophy of myocardial fibres with vesicular nuclei and the presence of diffuse interstitial fibrosis. [source] Congestive heart failure caused by intracardiac tumours in two dogsJOURNAL OF SMALL ANIMAL PRACTICE, Issue 8 2006S. M. Warman Congestive heart failure is a common presentation in small animal practice. Cardiac tumours are an unusual cause of congestive heart failure and, when they occur, usually cause clinical signs associated with pericardial effusion and cardiac tamponade. This case report outlines the clinical and histological findings in two dogs presented with clinical signs of congestive heart failure caused by obstruction of blood flow by intracavitary cardiac tumours. Case 1 showed signs of left-sided heart failure caused by osteosarcoma within the left atrial lumen, and case 2 presented with clinical signs of right-sided heart failure due to haemangiosarcoma occupying the right atrial and ventricular lumens. This case report provides further evidence for the inclusion of intracardiac neoplasia in the differential diagnosis for dogs with clinical signs of congestive heart failure. [source] | ||||||||||