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921.
A. W. Stewart 《Cellular and molecular life sciences : CMLS》1985,41(4):456-458
Summary Fluorometric recordings of NADH (nicotinamide adenine dinucleotide) were made on rabbit papillary muscles. The specimens were placed between the UV light source and a small window of the detection stage. As the muscle was moved over the window in a transverse direction, simultaneous measurement could be taken of transmitted UV light and fluorescent light for various thicknesses of tissue. It is concluded that a muscle thinckness of 0.65 mm, is optimal before absorption of the incident light decreases the fluorescence signal. 相似文献
922.
Summary A communication signal in an African freshwater electric fish, its pulse-like Electric Organ Discharge (EOD), was investigated in order to determine whether inter- or intraindividual variability of the EOD waveform provides a putative cue for communication, in addition to the electric cues already identified. In contrast to an individual's highly stereotyped EODs showing extremely low variation (fig. 1), variability between individuals was considerable (fig. 2). The dependence of an individual's EOD duration on temperature was weak with a Q10 of close to 1.5. In none of four quantitative EOD waveform measures can a sexual dimorphism be discerned (table).Gnathonemus petersii very likely relies on mechanisms other than discrimination of intraspecific EOD waveforms for mate recognition. 相似文献
923.
Molecular characterization and expression of the gene encoding human erythroid-potentiating activity 总被引:11,自引:0,他引:11
J C Gasson D W Golde S E Kaufman C A Westbrook R M Hewick R J Kaufman G G Wong P A Temple A C Leary E L Brown 《Nature》1985,315(6022):768-771
Erythropoietin is the primary physiological regulator of erythropoiesis; however, in vitro studies have identified another class of mediators which appear to be important in stimulating erythroid progenitors. These factors have generally been referred to as burst-promoting activities (BPA), because they stimulate the growth of early erythroid progenitors referred to as burst-forming units-erythroid (BFU-E) which give rise to colonies of up to thousands of haemoglobinized cells. We recently reported purification of a burst-promoting activity from medium conditioned by the Mo T-lymphoblast cell line infected with human T-cell lymphotropic virus type II (HTLV-II). This purified glycoprotein of relative molecular mass (Mr) 28,000 also stimulates colony formation by more mature erythroid precursors (CFU-E) and is therefore referred to as erythroid-potentiating activity (EPA). Purified EPA specifically stimulates human and murine cells of the erythroid lineage, unlike murine interleukin-3 (IL-3) which stimulates precursor cells from all haematopoietic lineages. We report here the isolation of a complementary DNA molecular clone encoding EPA and its use in producing EPA in COS (monkey) cells and CHO (Chinese hamster ovary) cells. We also define the organization of the EPA gene in human DNA. 相似文献
924.
The study of retrovirus-induced leukaemias in mice is a powerful tool for the elucidation of the normal regulation of the haematopoietic system. The acute murine spleen focus-forming viruses (SFFV) can be classified according to the haematopoietic lineage on which they exert their effects in the adult mouse. Here we report a new SFFV isolate, the AF-1 virus, with the novel ability to transform cells of the mononuclear phagocyte lineage. The virus was isolated from sarcomas that were induced on passage of a cloned Friend helper virus (F-MuLV, 643/22F) in newborn BALB/c mice. We have cloned the transforming defective subunit of the AF-1 viral complex in NRK cells and isolated several subclones. Analysis of the proviral genome in two non-producer cell clones reveals that AF-1 virus contains Harvey v-ras-specific sequences (Fig. 1). Thus, AF-1 virus is closely related to Harvey murine sarcoma virus (Ha-MSV), and is, at present, the only tool by which permanent cell lines can be obtained from mononuclear phagocytes in the mouse. 相似文献
925.
Changes in the expression of class II antigens of the major histocompatibility complex (MHC) have an integral role in the regulation of immune responses, and are brought about in vitro by soluble mediators. However, the mechanism that underlies in vivo expression of MHC class II antigens in, for example, endothelial cells in the absence of immunological stimulation has not been studied. We demonstrate here that expression of MHC class II antigens is not a constitutive property of endothelial cells, for MHC class II antigen-positive endothelial cells do not express these antigens during treatment with the immunosuppressive agent cyclosporin A. In vivo MHC class II antigen expression by canine endothelial cells is therefore dependent on factors, probably the lymphokine gamma-interferon produced by the immune system, whose secretion is inhibited by cyclosporin A. 相似文献
926.
Pituitary content and concentration of growth hormone was significantly reduced, and hypothalamic somatostatin content significantly increased, in old constant estrous as compared to young female rats. Increased levels of somatostatin may contribute to the decrease in pituitary growth hormone levels in these animals. 相似文献
927.
Wounding mice shortly before or shortly after lethal 60Co irradiation enhances survival. Survival of wounded-irradiated mice may be due to enhanced hematopoietic recovery as measured by endogenous spleen colony (E-CFU-s) formation. 相似文献
928.
J M Derry E Gormally G D Means W Zhao A Meindl R I Kelley Y Boyd G E Herman 《Nature genetics》1999,22(3):286-290
Tattered (Td) is an X-linked, semi-dominant mouse mutation associated with prenatal male lethality. Heterozygous females are small and at 4-5 days of age develop patches of hyperkeratotic skin where no hair grows, resulting in a striping of the coat in adults. Craniofacial anomalies and twisted toes have also been observed in some affected females. A potential second allele of Td has also been described. The phenotype of Td is similar to that seen in heterozygous females with human X-linked dominant chondrodysplasia punctata (CDPX2, alternatively known as X-linked dominant Conradi-Hünermann-Happle syndrome) as well as another X-linked, semi-dominant mouse mutation, bare patches (Bpa). The Bpa gene has recently been identified and encodes a protein with homology to 3beta-hydroxysteroid dehydrogenases that functions in one of the later steps of cholesterol biosynthesis. CDPX2 patients display skin defects including linear or whorled atrophic and pigmentary lesions, striated hyperkeratosis, coarse lusterless hair and alopecia, cataracts and skeletal abnormalities including short stature, rhizomelic shortening of the limbs, epiphyseal stippling and craniofacial defects (MIM 302960). We have now identified the defect in Td mice as a single amino acid substitution in the delta8-delta7 sterol isomerase emopamil binding protein (Ebp; encoded by Ebp in mouse) and identified alterations in human EBP in seven unrelated CDPX2 patients. 相似文献
929.
Ultrastructural localization of choline acetyltransferase in vascular endothelial cells in rat brain 总被引:3,自引:0,他引:3
Furchgott and Zawadski have shown that acetylcholine (ACh) does not act directly on the smooth muscle of blood vessel walls, but rather via receptors on the endothelial cells lining the lumen, to release an endothelium-derived relaxing factor (EDRF). As it is very unlikely that neurotransmitter released from the periarterial nerves, which are confined to the adventitial-medial border, diffuses all the way through the medial muscle coat before acting on endothelial cells to release EDRF to produce vasodilatation, this discovery has been regarded as an indication of a pathophysiological mechanism, rather than a physiological one (see refs 2, 3). ACh is rapidly degraded in the blood by acetylcholinesterase, so that ACh must be released locally to be effective on endothelial cells. Here we demonstrate the immunocytochemical localization of choline acetyltransferase in endothelial cells of small brain vessels, which is consistent with the view that the ACh originates from endothelial cells that can synthesize and store it. We suggest that release of ACh following damage to endothelial cells during ischaemia contributes to a pathophysiological mechanism of vasodilation which protects that segment of vessel from further damage as well as brain cells from hypoxia. 相似文献