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Y Iwasa

Publications and source records attributed to Y Iwasa.

At least 109 records · Page 6Linked to original sources
PubMed1991

Optimal growth schedule of pathogens within a host: switching between lytic and latent cycles.

We have studied the optimal growth schedule of a pathogen, which maximizes the total number of transmissions from an infected host to other individuals until host death or recovery. It is assumed that both transmission rate f(N) and host mortality increase with the number of pathogens, N. The model predicts that the optimal growth schedule of pathogens strongly depends on the curvature of f(N): If f(N) increases faster than linearly with N, the pathogens should always reproduce at the maximum speed. By contrast, if f(N) saturates with N, the optimal schedule is composed of (1) a brief initial stage of infection, in which the pathogens proliferate at the maximum speed (productive cycle), (2) followed by the long latent period with the "stationary infection level," N* (latent cycle), (3) which may end when the pathogens start rapid proliferation triggered either by the host's senescence ("programmed break") or by the sudden rise in the host's mortality ("incidental break"). The latter may be caused by the double infection of another strain. We also examine the Nash equilibrium schedule of pathogen growth in the presence of multiple infections.

Age Factors↗
PubMed1991

Transcriptional regulation of ferritin messenger ribonucleic acid levels by insulin in cultured rat glioma cells.

Recent data have shown that ferritin, a ubiquitous protein, has a role as a regulator of cellular differentiation. In the present study we have investigated the expression of ferritin mRNAs in cultured C6 cells, a rat glioma cell line, in response to insulin, which has an important role in cellular growth and differentiation. Insulin stimulated steady state levels of both ferritin heavy chain and ferritin light chain mRNAs. An increase in the level of ferritin heavy or light chain mRNA was detected after 2 h of incubation with insulin, and a plateau was reached after 48 h for heavy chain mRNA and after 72 h for light chain mRNA. The responses were dose-dependent and were maximal at 100 nM for both mRNAs. Treatment of cells with actinomycin-D showed that insulin had no effect on the posttranscriptional stability of these mRNAs. Actinomycin-D inhibited insulin-induced accumulation of both mRNAs, suggesting transcriptional stimulation of ferritin genes by insulin. A nuclear run-on assay showed that the insulin-induced increase in ferritin heavy chain mRNA was due to an increase in the rate of gene transcription. We also demonstrated that insulin-like growth factor-I (IGF-I) increased ferritin heavy and light chain mRNA levels in a dose-dependent fashion, and that the maximum effect was obtained at a concentration of 10 nM on both mRNA levels. IGF-I was not only 10-fold more potent, but the absolute level of maximum stimulation was also about 2-fold greater than that for insulin. The combination of insulin (100 nM) and IGF-I (10 nM) showed no additive effect. The results suggested that the ferritin heavy and light chain genes are transcriptionally regulated by insulin and influenced by IGF-I.

Actins↗
PubMed1990

Transcriptional regulation of ferritin heavy chain messenger RNA expression by thyroid hormone.

The effect of 3,5,3'-triiodo-L-thyronine (T3) on the steady state levels of ferritin heavy chain (ferritin H) mRNA in cultured rat glioma C6 cells and various rat tissues was examined. Addition of T3 to cultured C6 cells showed the time and dose-dependent increase in the steady-state level of ferritin H mRNA. In vitro nuclear run-on assay revealed that the stimulatory effect was due to the increase in the transcription rate of ferritin H gene. T3 had no effect on the half life of ferritin H mRNA. In hyperthyroid rats, the level of ferritin H mRNA in the kidney was elevated. On the contrary, that was decreased in hypothyroid rats. The results suggest the involvement of T3 in the regulation of ferritin H gene expression.

Animals↗
PubMed1990

Transcriptional regulation of messenger RNA for ferritin heavy chain by thyrotropin.

Thyrotropin increased the steady state levels of ferritin heavy chain messenger RNA in cultured Fisher rat thyroid (FRTL5) cells by about 2.5-fold. Thyrotropin also stimulated the transcription rate of ferritin H gene determined by "nuclear run-on" assay by roughly the same extent as mRNA levels. Thyrotropin showed no effect on the stability of the ferritin heavy chain mRNA, which was suggested using actinomycin D. The results suggest that thyrotropin increases ferritin heavy chain mRNA expression in FRTL5 cells by affecting the step of transcription.

Animals↗
PubMed1989

Endotoxin challenge after menhaden oil diet: effects on survival of guinea pigs.

Improvement in survival to endotoxin has been seen after pretreatment with cyclooxygenase inhibitors. Because eicosapentaenoic acid (EPA), found in menhaden oil, competitively inhibits cyclooxygenase, we fed two groups of guinea pigs diets, in which the fat source was either menhaden or safflower oil, for 6 wk. A third group was allowed the safflower oil diet ad libitum. Menhaden oil-fed animals showed enhanced survival compared with safflower oil control animals 20 h after endotoxin (87 vs 63%, p less than 0.05). Ad libitum-fed safflower oil animals survived least well, with 47% alive at 20 h (p less than 0.005 vs menhaden oil group). We conclude that feeding animals a diet whose predominant lipid source is fish oil significantly improves survival after endotoxin. Dietary fat should be viewed not only as a caloric source but as a pharmacologically active substance that can have profound effects on the host's response to toxic insults.

Animals↗