Endocrine changes before and after weaning in response to boar exposure and altered suckling in sows

Eighteen sows (6 primiparous and 12 multiparous) were allotted randomly within parity to two lactational treatments: litter separation (LS; 6 h/day) plus boar exposure (BE; 1 h/day; N = 14) beginning 8 days before weaning (4 weeks) and no LS + no BE (controls; N = 4). Blood was collected from all sows via indwelling venous catheters at 20-min intervals for 5 h on Days -1, 0, 1, 2 and 3 from start of treatment. Control sows and those exposed to LS + BE not exhibiting oestrus during lactation were resampled on Days -1, 0, 1 and 2 from weaning. All 10 multiparous sows receiving LS + BE exhibited oestrus during lactation, whereas none of the 4 primiparous sows exposed to LS + BE or the 2 control multiparous and 2 control primiparous sows exhibited lactational oestrus. Overall concentrations of LH in serum were higher (P less than 0.05) in sows receiving LS + BE than in control sows during lactation, whereas overall FSH was higher (P less than 0.05) in primiparous than multiparous sows. Number and amplitude of pulses of LH were greater (P less than 0.05) for treated primiparous than multiparous sows during lactation. Oestradiol-17 beta increased (P less than 0.05) in sows during LS + BE and was higher (P less than 0.01) in multiparous sows of this group than control multiparous or treated primiparous sows. Preweaning concentrations of cortisol and progesterone in serum were higher (P less than 0.05) in treated than control sows for multiparous and primiparous animals. In sows resampled at weaning, the number of pulses of LH was greater (P less than 0.05) in treated primiparous than in control sows. Postweaning concentrations of FSH in serum were unaffected by preweaning treatments. It was concluded that (1) litter separation and boar exposure increased basal and pulsatile secretion of LH in multiparous and primiparous sows; (2) lack of ovarian follicular development and oestradiol secretion may preclude expression of oestrus in primiparous sows during lactation, despite elevated concentrations of FSH and LH in serum; and (3) if elevated concentrations of cortisol and progesterone inhibit the onset of oestrous cycles, in response to litter separation and boar exposure during lactation, the effect is limited to primiparous sows.     

Analysis of the interaction of antibodies with immunoglobulin idiotypes on neoplastic B lymphocytes: implications for immunotherapy

We have examined the reactions of a panel of nine monoclonal anti-idiotype antibodies with the surface immunoglobulin in situ on guinea pig L2C leukemic lymphocytes. Equilibrium binding constants were shown to range between 10(7) and 10(8) M-1 for univalent Fab' gamma fragments and between 10(8) and 10(9) M-1 for intact IgG. Saturation of the cell surface binding sites was achieved with 2.9 X 10(5) Fab' gamma molecules/cell and 1.2 X 10(5) IgG molecules/cell for each antibody, a result that is consistent with a bivalent mode of interaction for the IgG. Despite these overall similarities in binding characteristics antibodies showed striking differences in their ability to clear Ig from the cell surface by antigenic modulation in vitro. This suggested differences in the readiness with which the antibodies cross-linked neighboring surface Ig molecules. Such an interpretation was supported by differences in the times required to achieve bivalent binding at 0 degree C, and in the rates at which labeled antibody dissociated from the cell surface in the presence or absence of an excess of unlabeled antibody. The data are consistent with there being two functionally distinct types of anti-idiotype antibody: those that form predominantly intra-Ig bridges, with each antibody Fab being linked to an Fab on one target molecule ("monogamous" binding) and not favoring modulation; and those that form predominantly inter-Ig bridges ("bigamous" binding) and favor modulation. The nature of interaction is presumably dictated by the orientation of the particular idiotope concerned. This distinction could be of great importance in the therapeutic use of anti-idiotype to ablate B cell neoplasms.     

Reaction of T lymphocytes with anti-T3 induces translocation of C-kinase activity to the membrane and specific substrate phosphorylation

Reaction of the T cell membrane with monoclonal antibodies to T3 can initiate cellular activation, and this is associated with increased intracellular Ca2+ and inositol-trisphosphate (IP3) release. We therefore studied the possible involvement of Ca2+/phospholipid-dependent kinase (C-kinase) in these phenomena. Quantitative assays of exogenous substrate phosphorylation in unstimulated cells showed Ca2+/phospholipid-dependent kinase activity in the cytosol, but no comparable activity in the particulate fractions corresponding to membrane and cytoskeleton material. At concentrations of soluble anti-T3 that partially activate T cells in the absence of macrophages, there was a 50 to 60% decrease in C-kinase activity in the cytosol, with a comparable increase in activity in the membrane fraction. A similar transfer of activity was also induced with the known C-kinase activator, 12-O-tetradecanoyl-phorbol-13-acetate, although redistribution was more rapid in onset, more complete, and more sustained. Redistribution of enzyme activity was additionally confirmed by qualitative assays of endogenous substrate phosphorylation. Labeling of intact cells followed by immunoprecipitation analysis with anti-T3 indicated signal-dependent phosphorylation of two components of the T3 complex and an unidentified 94,000 substrate that was resistant to reduction and alkylation. These findings are consistent with an important role for C-kinase in transduction of membrane events by the T3-Ti complex.     

Concomitant Increases in the Levels of Choline and Free Fatty Acids in Rat Brain: Evidence Supporting the Seizure-Induced Hydrolysis of Phosphatidylcholine

The main objective of this study was to determine whether the excitotoxic cholinesterase inhibitor soman increases the catabolism of phospholipids in rat brain. Injections of soman (70 micrograms/kg, s.c.), at a dose that produced toxic effects, increased the levels of both free fatty acids (175-250% of control) and free choline (250% of control) in rat cerebrum 1 h after administration. All fatty acids contained in brain phosphatidylcholine were elevated significantly including palmitic (16:0), stearic (18:0), oleic (18:1), arachidonic (20:4), and docosahexaenoic (22:6) acids. The changes observed were consistent with those reported to occur following ischemia and the administration of other convulsants. Pretreatment of rats with the anticonvulsant diazepam (4 mg/kg, i.p.) prevented both the signs of soman toxicity and the soman-induced increase of choline and free fatty acids. Diazepam alone did not affect the levels of choline or free fatty acids, cholinesterase activity, or soman-induced cholinesterase inhibition, suggesting that soman toxicity involves a convulsant-mediated increase in phosphatidylcholine catabolism. In addition, administration of the convulsant bicuculline, at a dose that produces seizures and increases the levels of free fatty acids in brain, significantly increased the levels of choline. Results suggest that excitotoxic events enhance the hydrolysis of phosphatidylcholine in brain as evidenced by a concomitant increase in the levels of choline and free fatty acids.