Herpes simplex virus (HSV) stimulates DNA synthesis in mouse spleen cultures prepared from normal, macrophage-depleted, and T-cell-depleted spleen cells, but not from thymocytes. In addition, a polyclonal antibody response is observed in HSV-infected spleen cultures. These findings indicate that the cells stimulated to undergo DNA synthesis after HSV infection appear to be the bone marrow-derived lymphocytes. The newly synthesized DNA is host cell and not of viral origin. Heat treatment and ultraviolet irradiation of HSV before addition to spleen cultures prevents the induction of DNA synthesis. We consider the use of this system as assay for the study of cell transformation by HSV and also for the study of host cell control of the expression of the viral genome.

Animals↗

PubMed1977

Swine vesicular disease: continuing serological surveys of pigs presented for slaughter in the United Kingdom.

Following the first serum survey for swine vesicular disease [SVD] in Great Britain in 1974 (Watson and Hedger 1974), three further surveys have been carried out. In these four surveys an overall total of 9760 sera have been examined, involving pigs from 958 premises in the first three surveys and an unknown number of premises in the fourth survey taken on a national basis. Forty-three farms were visited as sources of origin or possible sources of origin of the pigs from which positive or inconclusive results were obtained. Subsequent to the one clinical case of disease already reported with the results of the first survey, no further clinical cases of SVD have been confirmed, although lesions suggestive of the disease were found in some pigs on four of the premises visited. SVD quarantine restrictions on these four farms were removed subsequent to further serological sampling and when there was no indication that a spreading vesicular condition existed.

Animals↗

PubMed1977

The metabolism of prostaglandins F2alpha and E2 by non-pregnant porcine endometrial and luteal tissue and early pregnant porcine endometrial tissue, luteal tissue and conceptuses in vitro.

Slices of porcine endometrium and corpus luteum from both early pregnant and non-pregnant sows and conceptuses from early pregnant sows were incubated with radioactive PGF2alpha and PGE2 and the degree of metabolism of the prostaglandins measured. Prostaglandins and a metabolites were separated by TLC, radioactive bands located with a Panax scanner and the radioactivity measured in a scintillation counter. Endometrial and luteal tissue from non-pregnant sows gave no significant metabolism at any stage of the oestrous cycle, and while similar tissue from pregnant sows metabolised both prostaglandins slightly, only the conceptuses gave any significant metabolism. The possible physiological significance of these results is discussed.

Animals↗

PubMed1977

The effect of cloprostenol on human luteal steroid and prostaglandin secretion in vitro.

1 Human luteal tissue slices from days 18, 21 and 25 of the menstrual cycle were superfused in vitro with Medium 199 alone or containing cloprostenol (1 microgram/ml). Concentrations of progesterone, oestradiol-17beta and prostaglandins F2alpha and E2 were determined in the superfusate samples. 2 Secretion of steroids and prostaglandins was maintained at an approximately constant level throughout the experiments (21 h in one case) when the tissue was perfused with M199 alone. 3 Superfusion with cloprostenol (1 microgram/ml) resulted in an initial depression of progesterone and oestradiol-17beta but this was not maintained, levels returning to control values or showing an increase, while superfusion with cloprostenol continued. Cloprostenol is not therefore considered to be luteolytic at this dose and under these conditions for human luteal tissue in vitro. 4 Superfusion with cloprostenol (1 microgram/ml) also resulted in a large stimulation of secretion of endogenous prostaglandin F2 alpha following a short lag phase. This stimulation was possibly due to the initial depression of progesterone secretion. A short-lived stimulation of prostaglandin E2 secretion was also observed. 5 The significance of the increase in prostaglandin E2 secretion and the interrelationships between the various changes observed with cloprostenol are difficult to interpret.

Corpus Luteum↗

PubMed1977

Inhibition of Tamoxifen of the stimulatory action of FSH on oestradiol-17beta synthesis by rat ovaries in vitro.

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Androstenedione↗

PubMed1977

Effect of prostaglandin F-2alpha and uterine extracts on progesterone secretion in vitro by superfused pig corpora lutea.

Corpora lutea obtained from sows in the mid-luteal phase of the oestrous cycle were superfused with various doses of PGF-2alpha, uterine flushings or superfusates from endometrial strips. High doses of PGF-2alpha (1-5 microgram/ml) gave transient stimulation of progesterone secretion; lower doses (0.1-1.0 microgram/ml) inhibited secretion of the steroid, but to a maximum of 55% only and the secretion returned to control levels when superfusion with PGF-2alpha stopped. Uterine flushings from sows in the late luteal phase of the cycle were more effective than mid-cycle flushings in inhibiting progesterone secretion by the luteal tissue: maximal inhibition was 65% and progesterone secretion slowly returned to control levels when superfusion with the flushings was stopped. Superfusate from strips of uterine endometrium from sows in the late luteal phase of the cycle proved most effective in inhibiting progesterone secretion (greater than 90%) and gave a long-lasting inhibition which did not appear to be due to stimulation of PGF-2alpha secretion by the endometrium or corpus luteum.

Animals↗

PubMed1977

The evolution of nursing education in the United States: 100 years of a profession for women.

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Curriculum↗

PubMed1977

Primary nursing--nursing care can be patient centred.

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Australia↗

PubMed1977

Differentiation of B lymphocytes in C3H/HeJ mice: the induction of Ia antigens by lipopolysaccharide.

The lipid A moiety of bacterial lipopolysaccharide (LPS) elicits several types of responses in murine B lymphocytes. First, lipid A induces the nonproliferative expression of cell surface antigens in more immature cell types. Second, lipid A induces a mitogenic response in more mature B cell types. Lipid A induces the expression of Ia antigens on bone marrow cells from C3H/DiSn but not C3H/HeJ mice. The Ia-inducible cells possess surface immunoglobulin. Agents that elevate intracellular levels of adenosine 3',5'-cyclic monophosphate (cyclic AMP) induce the appearance of Ia antigens on B lymphocytes from both C3H/HeJ and C3H/DiSn mice, suggesting that lipid A exerts its inductive effects by increasing cyclic AMP levels in cells. In contrast to what is observed by using other strains of mice, mature B lymphocytes from C3H/HeJ mice do not support a mitogenic response to lipid A. The subpopulation of B lymphocytes in C3H/HeJ mice that normally respond mitogenically to LPS not only appear to lack an LPS-response mechanism utilized in the mitogenic pathway, but they lack the LPS-response pathway of the immature B cell types. A lipid A-bound protein (LAP) induces both the expression of Ia and a mitogenic response in the different subpopulations of B lymphocytes from C3H/HeJ and C3H/DiSn mice. The genetic defect in C3H/HeJ mice that limits responses to lipid A may be associated with a receptor that is normally expressed on many different cell types.

Animals↗

PubMed1977

The response of recombinant inbred strains of mice to bacterial lipopolysaccharides.

Fourteen recombinant inbred strains of mice have been produced by the inbreeding of the F2 generation of a cross between C57BL/6J and C3H/HeJ progenitor mice. The responses of these BXH strains to bacterial lipopolysaccharides (LPS) have been characterized. Four BXH strains are high LPS responders and nine strains are low LPS responders. One BXH strain shows intermediate responsiveness which may reflect residual heterozygosity. F1 hybrid mice from low x high responder strains were intermediate in their response to LPS suggesting additive genetic control. The LPS responses in backcross mice from the F1 x low LPS responders showed segregation consistent with LPS responsiveness being determined by a single gene. In 13/14 BXH strains, there was concordant inheritance of LPS responsiveness and the major urinary protein locus Mup-1b. The association of the expression of the Mup-1 alleles with LPS responsiveness in the BXH strains suggests that the defective LPS response gene in C3H/HeJ mice is located on chromosome 4.

Animals↗

PubMed1977