Regulation of beta-endorphin and ACTH in brain by estradiol

The effect of estradiol on the brain concentration of immunoreactive beta-endorphin (beta-EP) and C-terminal ACTH (CLIP) was studied in ovariectomized rats. Dopamine, a known inhibitor of pituitary intermediate lobe pro-opiomelanocortin (POMC), was examined as a possible mediator of the estradiol induced changes in brain POMC. Animals were treated for 1 or 3 weeks with either 1) saline; 2) silastic estradiol implants; or 3) estradiol implants plus haloperidol 1 mg/kg/day. After one week of treatment no significant change in hypothalamic beta-EP content was noted in any group compared to the control level of 4.13 +/- .33 (SEM) pmoles although in the neurointermediate lobe beta-EP increased from 566 +/- 72 to 942 +/- 73 pmoles after haloperidol (p less than .005). After 3 weeks, however, hypothalamic beta-EP decreased from 3.96 +/- .28 to 2.74 +/- .19 pmoles (p less than .005) and C-terminal ACTH decreased from 3.78 +/- .33 to 2.82 +/- .18 pmoles (p less than .02) in the estradiol treated rats. This estradiol induced decrease in the hypothalamic content of beta-EP and C-terminal ACTH was not blocked by haloperidol. We conclude that estradiol lowers the hypothalamic content of beta-EP and CLIP and that this effect does not appear to be mediated by dopamine.     

Cross-linking of histone H5 in hen erythrocyte nuclei

Following treatment of hen erythrocyte nuclei with dimethyl 3,3'-dithiobispropionimidate, dimers between histones H1a, H1b, and H5 were extracted with 5% perchloric acid. They resolved electrophoretically into four sub-bands and these were identified by non-reducing/reducing gel electrophoresis. The H5-H5 homodimer species was purified by gel electrophoresis and was treated sequentially with BrCN and dithiothreitol. The pattern of resulting fragments indicates that cross-links were mainly formed between the COOH-terminal portions and at a significantly lower frequency between the COOH-terminal and the NH2-terminal portions.     

Characterization of a substance P-Gly12 amidating enzyme in human cerebrospinal fluid

Enzyme activity capable of converting the glycine-extended substance P precursor, substance P-Gly12, into substance P was purified from human cerebrospinal fluid. The conversion reaction was monitored by radioimmunoassay measurement of substance P formation. The chemical identity of the product was verified by reversed-phase HPLC. The enzyme reaction was stimulated by Cu(II) ion and ascorbic acid and inhibited by the presence of diethyldithiocarbamate. By HPLC molecular sieving, the major enzyme activity appeared as a protein of 26,000 molecular weight.     

Effect of cortisol, its polymeric derivative and adenylate cyclase activators on the content of cyclic AMP in rat thymocytes

In has been shown that cortisol immobilized on polyvinylpyrrolidone (PVP-GC) affects cyclic AMP production stimulated by adenosine and isoproterenol in rat thymocytes. This effect of PVP-GC is specific for cortisol: antiglucocorticoid progesterone (at a concentration of 10(-5) M) inhibited completely the action of PVP-GC on the intracellular cAMP level. It is suggested that cortisol effect on cAMP production is one of the mechanisms of glucocorticoid hormone action in target cells.     

T Cell Factor-1 Controls the Lifetime of CD4+ CD8+ Thymocytes In Vivo and Distal T Cell Receptor α-Chain Rearrangement Required for NKT Cell Development

Natural killer T (NKT) cells are a component of innate and adaptive immune systems implicated in immune, autoimmune responses and in the control of obesity and cancer. NKT cells develop from common CD4+ CD8+ double positive (DP) thymocyte precursors after the rearrangement and expression of T cell receptor (TCR) Vα14-Jα18 gene. Temporal regulation and late appearance of Vα14-Jα18 rearrangement in immature DP thymocytes has been demonstrated. However, the precise control of lifetime of DP thymocytes in vivo that enables distal rearrangements remains incompletely defined. Here we demonstrate that T cell factor (TCF)-1, encoded by the Tcf7 gene, is critical for the extended lifetime of DP thymocytes. TCF-1-deficient DP thymocytes fail to undergo TCR Vα14-Jα18 rearrangement and produce significantly fewer NKT cells. Ectopic expression of Bcl-x_L permits Vα14-Jα18 rearrangement and rescues NKT cell development. We report that TCF-1 regulates expression of RORγt, which regulates DP thymocyte survival by controlling expression of Bcl-x_L. We posit that TCF-1 along with its cofactors controls the lifetime of DP thymocytes in vivo.     

Microplastics in soil-plant system: effects of nano/microplastics on plant photosynthesis,rhizosphere microbes and soil properties in soil with different residues

Plant and Soil - To investigate the effects of polystyrene microplastics (PS-beads) on the soil properties, photosynthesis of Flowering Chinese cabbage, the rhizosphere microbial community and...     

Single-cell landscape of the ecosystem in early-relapse hepatocellular carcinoma

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