Systematic collection of air samples was made using commercial jet airliners between Tokyo, Japan and Anchorage, Alaska and between Tokyo and Sydney, Australia in 1984 and 1985. The amplitude of the seasonal CO2 cycle in the upper troposphere was found to be largest in high latitudes of the northern hemisphere but decreased and lagged in phase as the equator was approached. The cycle was still clearly observable in the southern hemisphere, due to southward transport of the northern hemispheric air through the upper troposphere by a monsoon circulation. The yearly mean value of the upper tropospheric CO2 was high in the equatorial region and decreased poleward. The seasonal cycle of the lower stratospheric CO2 in northern high latitudes showed a minimum concentration early in May and a maximum concentration early in September, with a peak‐to‐peak amplitude of 2.2 ppmv. Yearly mean CO2 concentrations were lower by 1.4‐2.2 ppmv than those in the upper troposphere. The difference in yearly mean CO2 concentrations between 1984 and 1985 was about 1.1 ppmv at all locations covered by this measurement.

This paper considers a connected Markov chain for sampling 3×3×K contingency tables having fixed two-dimensional marginal totals. Such sampling arises in performing various tests of the hypothesis of no three-factor interactions. A Markov chain algorithm is a valuable tool for evaluating P -values, especially for sparse datasets where large-sample theory does not work well. To construct a connected Markov chain over high-dimensional contingency tables with fixed marginals, algebraic algorithms have been proposed. These algorithms involve computations in polynomial rings using Gröbner bases. However, algorithms based on Gröbner bases do not incorporate symmetry among variables and are very time-consuming when the contingency tables are large. We construct a minimal basis for a connected Markov chain over 3×3×K contingency tables. The minimal basis is unique.Some numerical examples illustrate the practicality of our algorithms.

No abstract

No abstract

No abstract

Myostatin, an endogenous negative regulator of skeletal muscle mass, is a therapeutic target for muscle atrophic disorders. Here, we identified minimum peptides 2 and 7 to effectively inhibit myostatin activity, which consist of 24 and 23 amino acids, respectively, derived from mouse myostatin prodomain. These peptides, which had the propensity to form α-helix structure, interacted to myostatin with KD values of 30-36 nM. Moreover, peptide 2 significantly increased muscle mass in Duchenne muscular dystrophy model mice.

CO2 samples collected in the troposphere over Japan during the period from April 1984 to November 1990 were analyzed for δ13C with a precision of better than 0.03 ‰. The amplitudes of the seasonal cycles of δ13C and CO2 concentration decreased with increasing height, with a phase delay of about 1 month between the lower and upper troposphere. From a comparison of the observed seasonal variation of the CO2 with that of δ13C, it was found that the rate of change in δ13C with respect to the CO2 concentration is about −0.05 ‰/ppmv. This suggests that the seasonal CO2 cycle over Japan is mainly produced by seasonally‐dependent biospheric activities. However, air transport from different latitudes is also important for the seasonal CO2 cycle, particularly in the upper troposphere. δ13C decreased secularly at an average rate of about −0.04 ‰/year, due mainly to combustion of fossil fuel with isotopically light CO2. Interannual variations of δ13C, superimposed on the long‐term trend, were also observed, which were approximately opposite in phase with those of the CO2 concentration. The comparison of both interannual variations suggested that the cause could be primarily attributed to an imbalance in the CO2 exchange between the atmosphere and the biosphere rather than between the atmosphere and the oceans.

Senescent cells develop a pro-inflammatory response termed the senescence-associated secretory phenotype (SASP). As many SASP components affect surrounding cells and alter their microenvironment, SASP may be a key phenomenon in linking cellular senesence with individual aging and age-related diseases. We herein demonstrated that the expression of Sirtuin1 (SIRT1) was decreased and the expression of SASP components was reciprocally increased during cellular senescence. The mRNAs and proteins of SASP components, such as IL-6 and IL-8, quickly accumulated in SIRT1-depleted cells, and the levels of these factors were also higher than those in control cells, indicating that SIRT1 negatively regulated the expression of SASP factors at the transcriptional level. SIRT1 bound to the promoter regions of IL-8 and IL-6, but dissociated from them during cellular senescence. The acetylation of Histone H3 (K9) and H4 (K16) of the IL-8 and IL-6 promoter regions gradually increased during cellular senescence. In SIRT1-depleted cells, the acetylation levels of these regions were already higher than those in control cells in the pre-senescent stage. Moreover, these acetylation levels in SIRT1-depleted cells were significantly higher than those in control cells during cellular senescence. These results suggest that SIRT1 repressed the expression of SASP factors through the deacetylation of histones in their promoter regions.