Gene expressions and activities of protein phosphatases PP1 and PP2A in rat liver regeneration after partial hepatectomy.

We have examined the levels of gene expressions and activities of protein phosphatases, PP1 and PP2A, in rat regenerating livers. PP1 alpha mRNA started to increase from 6 h after partial hepatectomy (PH) and showed two peaks at 12 and 48 h. PP2A mRNA level showed two peaks at 6 and 10-12 h. Protein phosphatase activities were determined both in non-nuclear fraction and in nuclei. While spontaneous PP1 activity in non-nuclear fraction was nearly constant, potential PP1 activity revealed by Co(2+)-trypsin treatment showed a small peak between 7 and 12 h. In nuclei, both spontaneous and potential PP1 activity began to increase from 4-7 h after PH, reached a maximum (about 2.5-fold over control levels) at 12 h, the time which corresponds to the G1 to S transition in the cell cycle, and then declined back to control levels by 7 days. PP2A activity in non-nuclear fraction was nearly constant in both spontaneous and potential forms. PP2A activity in both forms in nuclei was very low throughout. These results suggest the possibility that PP1 in nuclei plays some role in the G1 to S transition in the cell cycle of hepatocyte proliferation.     

Effects of BCG (Bacillus Calmette–Guérin) Vaccines on Immune Responses in Mice

The effects of killed and living BCG on antibody production against hamster erythrocytes (HRBC) and the 2, 4, 6-trinitrophenyl (TNP) group were studied in SL mice. Killed and living BCG, each in doses of 0.008 mg, 0.08 mg, 0.8 mg and 8 mg per mouse, were intravenously inoculated 7 days prior to primary immunization with HRBC. Secondary immunization was carried out 28 days later with TNP-HRBC. Anti-HRBC and anti-TNP antibodies were estimated by a hemagglutination test. The results showed that pretreatment with killed or living BCG enhanced the antibody production against both HRBC and TNP. Comparing the effects of these two BCG preparations, it was noted that killed BCG augmented the anti-HRBC antibody production more effectively than living BCG. In regard to the anti-TNP antibody production, living BCG exhibited a greater augmenting effect than killed BCG. This difference in the modes of action of killed and living BCG was remarkable when two groups given 8 mg of killed and living BCG were compared. In addition, it was shown that living BCG at a dose as high as 8 mg was able to augment the anti-TNP antibody production, even in the absence of preceding immunization with HRBC.     

Mechanism of methylmercury release from bound type in bloodstream or tissues.

Reductants involving selenite freed methylmercury from bound protein without breaking the mercury-carbon bond in conjunction with sulfhydryls such as cysteine or homocysteine. The free methylmercury was transfered through an organic layer from the original -SH radicals to the other -SH radicals. The same effect occurred in normal physical reactions resulting from oxidoreductases, alcohol or lactic dehydrogenase. The oxidation-reduction system may play an important role in transfer of methylmercury from blood to tissues, or vice versa.     

An alkaline metallo-proteinase in the human uterine cervix an changes in its activity by cervical ripening

Human uterine cervix at term pregnancy was found to contain an alkaline metallo-proteinase by use of a synthetic substrate, 2,4-dinitrophenyl-L-Pro-L-Gln-Gly-L-Ile-L-Ala-Gly-L-Gln-D-Arg. The enzyme (with a molecular weight of 3.8 . 10(4)) was most active around pH 9.2 toward casein and N alpha-benzoyl-DL-Arg-rho-nitroanilide. [14C]-Gelatin and proteoglycan subunit were also substrates for the enzyme, but [14C]collagen was not. In particular, the enzyme digested gelatin 70-times faster than the novel neutral proteinase in the cervix. Although EDTA was a potent inhibitor, 1,10-phenanthroline, human serum, diisopropylfluorophosphate and elastatinal had no effect on the enzyme. Alkaline proteinase in term pregnant cervices was significantly higher than in non-pregnant ones.     

Planting geometry as a pre‐screening technique for identifying CO2 responsive rice genotypes: a case study of panicle number

Identifying CO₂ responsive genotypes is a major target for enhancing crop productivity under future global elevated atmospheric CO₂ concentration ([CO₂]). However, [CO₂]‐fumigation facilities are extremely expensive and are not easily accessible, and are limited in space for large‐scale screening. Hence, reliable donors for initiating [CO₂]‐responsive breeding programs are not in place for crops, including rice. We propose a simple and novel phenotyping method for identifying [CO₂]‐responsive genotypes, and quantify the responsiveness to low planting density over 4‐year trials across both temperate and tropical conditions. Panicle number per plant is the key determinant of grain yield and hence was the focus trait across all our trials. In temperate climate, a 3‐season field screening using 127 diverse rice genotypes and employing two planting densities (normal and low density) was conducted. Two japonica genotypes were selected based on their higher responsiveness to low planting density as candidates for validating the proposed phenotyping protocol as a pre‐screen for [CO₂]‐responsiveness. The approach using the two selected candidates and three standard genotypes was confirmed using a free‐air CO₂ enrichment facility and temperature gradient chambers under elevated [CO₂]. In tropical climate, we grew three rice cultivars, previously identified for their [CO₂]‐responsiveness, at two planting densities. The experiments provided confirmation that responsiveness to low planting density was correlated with that of [CO₂]‐responsiveness across both the temperate and tropical conditions. The planting density would be useful pre‐screening method for testing large panels of diverse germplasm at low cost complemented by available CO₂‐control facilities for final validation of candidates from the pre‐screens.     

Elevated mitochondrial biogenesis in skeletal muscle is associated with testosterone-induced body weight loss in male mice

Androgen reduces fat mass, although the underlying mechanisms are unknown. Here, we examined the effect of testosterone on heat production and mitochondrial biogenesis. Testosterone-treated mice exhibited elevated heat production. Treatment with testosterone increased the expression level of peroxisome proliferator-activated receptor-γ coactivator-1α (PGC1α), ATP5B and Cox4 in skeletal muscle, but not that in brown adipose tissue and liver. mRNA levels of genes involved in mitochondrial biogenesis were elevated in skeletal muscle isolated from testosterone-treated male mice, but were down-regulated in androgen receptor deficient mice. These results demonstrated that the testosterone-induced increase in energy expenditure is derived from elevated mitochondrial biogenesis in skeletal muscle.