Trichomonasfetus—Induced abortion

$\text{History}$ and $\text{Clinical}$$\text{Signs}$: Herds infected with $\text{Trichomonas}$$\text{fetus}$ have histories of infertility, occasional abortions, and pyometra.$\text{Gross}$$\text{Lesions}$: There are no specific gross lesions in the fetus. The fetuses are usually aborted in the first half of gestation and may or may not be accompanied by the placenta.$\text{Microscopic}$$\text{Lesions}$: There are no specific microscopic lesions.$\text{Cultural}$$\text{Procedures}$: It is ordinarily not necessary to culture $\text{T.}$$\text{fetus}$ in order to demonstrate its presence in placental fluids and/or abomasal contents.$\text{Serologic}$$\text{Procedures}$: There are no suitable seroligic procedures for diagnosing Trichomoniasis.$\text{Special}$$\text{Procedures}$: Wet mounts of abomasal contents and/or placental fluids are examined microscopically for $\text{T.}$$\text{fetus}$.$\text{Preferred}$$\text{Diagnostic}$$\text{Procedures}$: Demonstrate the presence of $\text{T.}$$\text{fetus}$ by microscopic examination of wet mounts of placental fluids and/or abomasal contents.     

Invivo and invitro studies of 15α-hydroxyprogesterone in the human placenta

Studies were conducted to determine the fate of 15α-hydroxyprogesterone in human placental tissue. Tritiated 15α-hydroxyprogesterone was perfused through normal human placentas $\text{in situ}$ at the time of Cesarean section and incubated with a 10,000x g microsomal supernate of the placenta $\text{in vitro}$. In both systems the substrate, but no additional metabolites were identified. These findings indicate that 15α-hydroxyprogesterone is not metabolized during its passage in the human term placenta, and suggests that because of its fetal origin clinical measurements of 15α-hydroxyprogesterone may provide a valuable index to the status of fetal viability.     

Altered levels of β-endorphin fragments after chronic morphine treatment of guinea-pig ileum invitro and invivo

The isolated myenteric plexus-longitudinal muscle of the guinea-pig ilem (GPI) was used as testsystem to study the influence of chronic morphine treatment on the levels of enkephalins, β-endorphin and some of its fragments. The peptides were assayed by means of a combination of high pressure liquid chromatography and radioimmunoassays. It was found that the levels of methionine- and leucine-enkephalin and β-endorphin were not altered by chronic morphine treatment of guinea-pigs $\text{in}$$\text{vivo}$ nor in GPI exposed to morphine $\text{in}$$\text{vitro}$. However, the levels of some β-endorphin fragments i.c. γ-endorphin and des-tyrosine-γ-endorphin were elevated after morphine treatment $\text{in}$$\text{vitro}$ and $\text{in}$$\text{vivo}$ respectively. It is suggested that β-endorphin and its fragments are involved in homeostatic processes during development of opiate tolerance.     

Control of gonadotropic hormone release in trout: Influence of synthetic LHRH and LHRH analogues invivo and invitro

Studies were conducted to determine the influence of some LHRH analogues on gonadotropic hormone (GtH) secretion in two species of trout. The observations indicated that synthetic LHRH and various stimulatory LHRH analogues are approximately equipotent in these fish. This is an unexpected result considering the superactive properties of these analogues demonstrated in mammals. An inhibitory LHRH analogue was also tested in the trout with the result that powerful inhibition of LHRH induced GtH release was obtained.     

Danazol inhibits human adrenal 21-and 11β-hydroxylation invitro

The effects of danazol on steroidogenesis $\text{in}$$\text{vitro}$ in the 16–20 week old human fetal adrenal were examined by studying: 1) danazol binding to adrenal microsomal and mitochondrial cytochrome P-450, and 2) enzyme kinetics of danazol inhibition of the adrenal microsomal 21-hydroxylase and the mitochondrial llβ-hydroxylase. The addition of danazol to preparations of adrenal microsomes or mitochondria elicited a type I cytochrome P-450 binding spectrum. Danazol bound to microsomal cytochrome P-450 with a high affinity apparent spectral dissociation constant (Kg) of 1 μM and with a lower affinity K's of 10 μM. Danazol bound to mitochondrial cytochrome P-450 with a Kg of 5 μM. In addition, danazol competitively inhibited the microsomal 21-hydroxylase (apparent enzymatic inhibition constant K_I = 0.8 μM) and the mitochondrial 11β-hydroxylase (K_I = 3 μM). These findings demonstrate that low concentrations of danazol directly inhibit steroidogenesis in the human fetal adrenal $\text{in}$$\text{vitro}$.     

Dinoflagellate sterols IV: Isolation and structure of 4α,23ξ,24ξ-trimethylcholestanol from the dinoflagellate Glenodiniumhallii

The dinoflagellate $\text{Glenodinium}$$\text{hallii}$ was investigated for its sterol composition. Five of the six sterols were isolated and identified as cholest-5-en-3β-ol, (24ξ)-24-methylcholest-5-en-3β-ol, stigmasta-5,22-dien-3β-ol, (22E,24R)-4α,23,24-trimethyl-5α-cholest-22-en-3β-ol, and 4α,23ξ,24ξ-trimethyl-5α-cholestan-3β-ol.     

A comparison of the substrate specificities of endo-β-N-acetylglucosaminidases from Streptomyces griseus and Diplococcus pneumoniae

The substrate specificities of the endo-β-N-acetylglucosaminidases from $\text{Diplococcus pneumoniae}$ and $\text{Streptomyces griseus}$ were compared and found to differ considerably. The enzyme from $\text{D. pneumoniae}$ released Asn-GlcNAc-Fuc-containing glycopeptides from exoglycosidase-treated acidic IgM glycopeptides but was limited in its capacity to hydrolyze ovalbumin glycopeptides larger than Asn(GlcNAc)₂(Man)₅. In contrast, the enzyme from $\text{S. griseus}$ hydrolyzed this and larger neutral oligosaccharides but could not hydrolyze the above fucose-containing IgM glycopeptides. Removal of the fucose residue, however, converted the latter to an active substrate for the $\text{S. griseus}$ enzyme, thus broadening its substrate range to encompass most of those substrates hydrolyzed by the $\text{D. pneumoniae}$ endoglycosidase.     

Estradiol-17β effects on lipid and carbohydrate metabolism and on the induction of a yolk precursor in goldfish, CarassiusAuratus

The effects of estradiol-17β treatment on plasma lipid levels, liver lipid and glycogen reserves were examined during different phases of the reproductive cycle in goldfish, $\text{Carassius}$$\text{auratus}$. Estrogen therapy resulted in increased plasma and hepatic lipid levels except during the spawning season. Hepatic glycogen deposits were depleted by estradiol injections during all seasons. Treatment of fish with the estrogen antagonist, CI-628, during the spawning season caused a reduction in plasma and liver lipid levels. Electrophoretic studies conducted during the post-spawning season showed that estrogen induces the appearance of a specific lipoprotein, probably a yolk precursor, in the serum and liver of goldfish.     

L-Leucinthiol — A potent inhibitor of leucine aminopeptidase

L-leucinthiol (2-amino-4-methyl-1-pentanethiol) was designed as an inhibitor of leucine aminopeptidase by analogy with sulfhydryl inhibitors of other zinc-containing peptidases. It was synthesized from L-leucinol and shown to be a potent competitive inhibitor of the microsomal aminopeptidase from porcine kidney (K_i = 2.2 × 10^?8M). The results suggest that the mechanism of aminopeptidase may be similar to that of other metalloproteases.     

Effects of 4-methyl-α-ethyl-tyramine, 4, α-dimethyl-tyramine and tetrabenazine on the release and uptake of 5-hydroxytryptamine by human blood platelets invitro

4-Methyl-α-ethyl-tyramine and its 4, α-dimethyl analogue release 5-HT from human blood platelets $\text{in}$$\text{vitro}$. At lower concentrations they inhibit the uptake of 5-HT into platelets. Tricyclic antidepressant drugs do not block 5-HT release by these compounds. On removal of the depletor, platelets recover their ability to take up 5-HT; platelets preloaded with exogenous 5-HT lose the same proportion of amine as those containing only endogenous 5-HT. Tetrabenazine behaves similarly, but its actions are partial, whereas those of the tyramines are more complete. The temperature dependence of spontaneous and drug-induced 5-HT release has been measured. The results are discussed in terms of the action of these drugs and with special reference to the use of human blood platelet as a model of a 5-HT-containing nerve ending.     

In vitro and in vivo effects on brain GABA metabolism of (S)-4-amino-5-fluoropentanoic acid,a mechanism-based inactivator of γ-aminobutyric acid transaminase

The effects of intraperitoneal administration of (S)-4-amino-5-fluoropentanoic acid, a mechanism-based covalent inactivator of γ-aminobutyric acid transaminase (GABA-T), on whole brain GABA metabolism in mice were investigated. A dose-dependent and time-dependent irreversible inactivation of GABA-T was observed with a concomitant increase in whole brain GABA levels. The compound exhibited no $\text{in vitro}$ nor $\text{in vivo}$ time-dependent inhibition of glutamate decarboxylase (GAD), alanine transaminase, or aspartate transaminase (Asp-T). It was, however, a potent competitive reversible inhibitor of GAD and a weak competitive inhibitor of Asp-T. The chloro analogue, (S)-4-amino-5-chloropentanoic acid, was ineffective.     

A synthesis of 3′,4-́dideoxykanamycin B

3′,4′-Dideoxykanamycin B, the kanamycin B derivative that is active against resistant bacteria, was prepared from kanamycin B viaN-tosylation, 3′,4′-O-sulphonylation, 3′,4′-unsaturation, and hydrogenation. The unsaturated intermediate was obtained from the 3′,4′-di-O-sulphonyl derivatives by the action of sodium iodide in N,N-dimethylformamide; if zinc dust was added in this reaction, aziridine derivatives were formed, Removal of the tosyl group was successfully performed by using sodium in ammonia-ethylamine.     

Binding of steroids to P.testosteroniΔ5-3-ketosteroid isomerase: Measurement of the number of binding sites by equilibrium dialysis

The binding of progesterone, 17β-estradiol and 19-nortestosterone acetate to the Δ⁵-3-ketosteroid isomerase from $\text{Pseudomonas}$$\text{testosteroni}$ has been investigated by the technique of equilibrium dialysis. Under the conditions used, all three steroids formed 2:1 complexes with each molecule of enzyme dimer (M.W. = 26,788). No evidence of any cooperative binding phenomena was obtained. The dissociation constants of the enzyme steroid complexes at 25°C were: progesterone, 2.2 μ$\text{M}$; estradiol, 2.5 μ$\text{M}$; 19-nortestosterone acetate, 9.2 μ$\text{M}$.     

Androgen on the estrogen receptor I — Binding and in vivo nuclear translocation

In the immature rat uterus, high concentrations of androgens competed specifically with estradiol on the estrogen receptor (RE). This competition was stereospecific for C₁₉ steroids bearing a 17β and/or 3 hydroxyl group. Very low affinity ligands, such as testosterone, could not compete with estradiol at equilibrium but decreased the association rate of estradiol on its receptor. High doses (> 0.4mg) of 5 α aihydrotestosterone provoked $\text{in vivo}$ as $\text{in vitro}$ the nuclear translocation of RE. The nuclear receptor thus formed displayed the same 5.2 S sedimentation constant as that induced by estradiol. We conclude that the weak affinity binding of androgens to the estrogen receptor is sufficient to induce its nuclear translocation $\text{in vivo}$ provided androgen concentration is high enough in uterus to occupy the estradiol binding site. Conversely, progesterone which does not bind RE could not provoke its nuclear translocation.     

Purification and partial characterization of a new,sporulation specific,exo-β-glucanase from Saccharomyces cerevisiae

A new exo-β-glucanase, sporulation-specific, was purified from sporulating $\text{S. cerevisiae}$ ($\text{AP}\text{1}\text{,}\text{a}\text{α}$). Characterization of this new activity shows that the enzyme is a glycoprotein with substrate specificities, kinetic parameters and aminoacid composition clearly different from those of its vegetative counterpart.