Increase in serum FSH following unilateral ovariectomy in the rat.
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Biomedical subjects
Publications and source records attributed to B Benson.
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Mouse mononuclear phagocytes cultivated in 50 per cent newborn calf serum medium pinocytize actively and form large numbers of phase-dense granules as well as three hydrolytic enzymes. When such cells are then placed in 1 per cent newborn calf serum they illustrate (a) a low level of pinocytic activity, (b) a shrinkage in granule size, and (c) a loss in cell protein, acid phosphatase, beta-glucuronidase, and cathepsin. Examination of the extracellular medium revealed no detectable hydrolase activity. The reintroduction of cells into high levels of serum again resulted in granule and enzyme formation. Cells rapidly incorporated fluorescein-conjugated calf serum proteins into the phase-dense granules. The fluorescence of labeled granules was lost during an 18 hour period in non-fluorescein-containing medium. Crystalline egg white lysozyme was concentrated in the macrophages. Approximately 80 per cent of the cell-associated enzyme was lost during a 24 hour washout period in either 1 or 50 per cent serum medium. No enzymatic activity could be recovered in the medium. Colloidal gold was taken up and concentrated in macrophage granules. Quantitative assays revealed this particle to be conserved during a 24 hour washout period.
Pulmonary surfactant is a phospholipid-protein complex which serves to lower the surface tension at the air-liquid interface in the alveoli of the mammalian lung and is essential for normal respiration. Inadequate levels of surfactant at birth, a frequent situation in premature infants, results in respiratory failure. In all species examined, surfactant is composed primarily of dipalmitoylphosphatidylcholine and two major protein species of relative molecular mass (Mr) 32,000 (32K) and 10K (refs 2-5). Reconstitution in vitro of purified 32K pulmonary surfactant apoprotein (PSAP) with synthetic lipids forms a lipoprotein complex that lowers surface tension by spreading to create a thin interfacial film. Here we describe the cloning of the human PSAP gene and complementary DNA, and discuss features of the unusual encoded protein.
Pressure ulcers are an immense problem among older and disabled populations. Although there are many studies in the literature about the etiology, interface pressures, natural history, and epidemiology of skin breakdown, there is relatively little information about factors that stimulate the repair of body wall tissues after breakdown. Specifically, there is a paucity of information about the effects of mechanical stress on healing. This is a particularly important consideration for those areas, such as the perineal tissues, that bear large mechanical forces. The purpose of this paper is to discuss the research that addresses skin and tissue repair in response to tension. Two case studies that support the hypothesis that tension stimulates wound healing are presented from the Spinal Cord Injury Center at the Seattle VAMC. After weeks of nonhealing, each of these cases healed within 2 weeks of initiating a range of motion program that applied tension to the nonhealing portion of a myocutaneous flap.
Postmortem human lung tissue was evaluated for its utility in studies of the mRNAs for the surfactant proteins. Data obtained from different analytical procedures indicated that surfactant protein mRNAs are quite stable in these tissues with a half-life of 10 to 12 h. These analyses revealed no major regional differences in the mRNA levels for the surfactant protein A (SP-A) and surfactant protein B (SP-B) although small differences were present in the levels for the surfactant protein C (SP-C). Analysis of adult surgical lung specimens indicated that there is greater individual variation in the mRNA levels for SP-A and SP-B compared to SP-C among individuals. Furthermore, in a given individual the level of SP-A mRNA correlated well with that of SP-B, whereas the level of SP-C mRNA did not correlate with either that of SP-A or SP-B.
Chronic treatment with diethylstilbesterol (DES) induces renal cancer in male Syrian hamsters. This tumor may result from direct carcinogenicity of the estrogen, but extrarenal neuroendocrine effects of DES may also be important in modulating tumor growth in the kidney. Since light deprivation is known to profoundly influence neuroendocrine function in the hamster, we elected to examine the effects of short photoperiod or blinding on the development of the DES-induced renal tumor in this species. Animals were maintained either in long (14 hours of light and 10 hours of dark) or short (10 hours of light and 14 hours of dark) photoperiod or blinded. Groups of six to eight animals were sacrificed after three, six or nine months of treatment with either DES or the vehicle. All animals treated with DES for nine months had evidence of renal tumors, but the rate of growth and final size of the tumors were significantly reduced by either maintenance in short photoperiod or blinding. These data provide unique evidence of the importance of neuroendocrine system in the modulation of the DES-induced renal tumor in hamsters.