Structure of tomato busy stunt virus IV. The virus particle at 2.9 A resolution

The structure of tomato bushy stunt virus has been determined crystallographically to 2.9 A resolution. Details are presented of both the molecular structure and the methods by which it has been solved. The icosahedrally symmetric viral shell is composed of 180 protein subunits (Mr 43,000), with three similar but distinct modes of subunit bonding. This capacity for alternative packing is due to localized flexibility in the folded polypeptide (hinges between domains) and to multiple conformations for surface side-chains. The polypeptide backbone has an essentially invariant fold within a compact domain. A mechanism for correct positioning of the different modes of subunit interaction is evident from the structure of the TBSV particle. Thirty-five residues of the polypeptide chain fold in an ordered way on 60 of the 180 subunits, forming an internal framework. Interaction of folded domains with this framework permits accuracy of long-range geometry (correct curvature and closure) to be determined by unambiguous switching between alternative local contact angles. RNA packs tightly into the particle interior. Protein-RNA interactions occur through parts of the subunit that are flexibly linked to the well-ordered domains of the shell. This variable interaction imposes minimum restrictions on the folding of the RNA chain.     

Stimulation of ovine myometrial activity by 6-keto prostaglandin E1

6-keto prostaglandin E1 (6KE) is a metabolite of PGI2, which we have shown previously inhibits spontaneous myometrial activity. In the present study we examined the effects of 6KE on uterine electrical and mechanical activity in non-pregnant ovariectomized sheep. 6KE stimulated uterine activity in a dose-dependent fashion. The effect was enhanced by pre-treatment with estradiol (E2). It was not influenced by pre-treatment with meclofenamic acid and was not associated with significant changes in the concentrations of 13,14 dihydro 15-keto PGF2 alpha in vena cava plasma. After E2 treatment, 6KE had 0.2-0.3 of the stimulatory activity of PGF2 alpha. In the absence of E2, the uterine response to both 6KE and PGF2 alpha was decreased. In animals in which spontaneous myometrial activity was inhibited by PGI2, the uterus remained responsive to 6KE. We conclude that in the ovariectomized non-pregnant sheep 6KE stimulates uterine activity, and that the effect is independent of endogenous PG production.     

Serum progesterone concentration in pyometritic and normal postpartum dairy cows

Two studies were conducted to evaluate the concentration of serum progesterone in pyometritic cows and relate it to palpation of ovarian structures per rectum . In Trial 1, serum samples from 34 pyometritic cows were assayed for progesterone. Mean serum progesterone concentrations were 6.8 +/- 0.7 ng/ml. In Trial 2, each of 54 pyometritic cows was paired with a control cow on the basis of days post partum (18-50 days). Mean concentration of progesterone was 9.7 +/- 1.0 ng/ml for the pyometritic cows and 5.7 +/- 0.8 ng/ml in control cows (P<0.005). Progesterone concentration was greater (P<0.005) in both groups of cows with palpable corpora lutea (CLs). Ninety-six percent of the pyometritic cows had palpable CLs compared to 57% of the control group. Comparing serum progesterone only in cows with a palpable CL, the mean concentration was still greater (P<0.005) in the pyometritic group (10.6 +/- 1.0 ng/ml) than the control group (6.6 +/- 1.0 ng/ml). Compatability of rectal palpation findings and concentrations of serum progesterone were 92.6% for the pyometritic group and 72.2% for the control group. Progesterone concentration increased (P<0.05) by increased days post partum in Trial 2 (n=54) but not in Trial 1 (n=23). In both Trials 1 and 2, uterine size due to pyometra increased (P<0.05) with increased days post partum. No other associations were found.     

Alterations in cholesterol and fatty acid biosynthesis in rat liver homogenates by aryloxy acids (Short Communication)

2,4-Dichlorophenoxyacetic acid and 2,4,5-trichlorophenoxyacetic acid inhibited the incorporation of [2-(14)C]mevalonate into cholesterol and non-saponifiable lipids. Both compounds inhibited the conversion of [1-(14)C]isopentenyl pyrophosphate into cholesterol and the synthesis of cholesterol and fatty acids from [2-(14)C]acetate. There was no inhibition of the conversion of [1-(14)C]mevalonate into CO(2). At low concentrations (0.5mm) of the compounds there was a stimulation of acetate incorporation into fatty acids.