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Simultaneous observations of atmospheric potential oxygen (APO=O 2 +1.1×CO 2 ) and air–sea O 2 flux, derived from dissolved oxygen in surface seawater, were carried out onboard the research vessel MIRAI in the northern North Pacific and the Arctic Ocean in the autumns of 2012–2014. A simulation of the APO was also carried out using a three-dimensional atmospheric transport model that incorporated a monthly air–sea O 2 flux climatology. By comparing the observed and simulated APO, as well as the observed and climatological air–sea O 2 fluxes, it was found that the large day-to-day variation in the observed APO can be attributed to the day-to-day variation in the local air–sea O 2 fluxes around the observation sites. It was also found that the average value of the observed air–sea O 2 fluxes was systematically higher than that of the climatological O 2 flux. This could explain the discrepancy between the observed and simulated seasonal APO cycles widely seen at various northern hemispheric observational sites in the fall season. Keywords: atmospheric potential oxygen, air-sea O 2 flux, ship observation (Published: 21 June 2016) Citation: Tellus B 2016, 68, 29972, http://dx.doi.org/10.3402/tellusb.v68.29972

Two dipeptides, glycyl-L-leucine (G-L) and L-leucyl-glycine (L-G), the concentrations of which were 10 mmol/L, were degraded in subcritical water in order to understand fully the phenomena occurring during treatment. Treatment was administered in a stainless steel tubular reactor, which was connected to an HPLC pump and immersed in an oil bath at 200-240 °C, with residence times of 10-180 s. When G-L and L-G were treated, L-G and G-L significantly formed, respectively, and then they gradually decreased at every temperature. Irrespective of the kind of substrate, ring formation occurred, and cyclo-(glycyl-L-leucine) was one of the final products. The reaction rate constants related to degradation were estimated under the assumption that all the reactions obeyed first-order kinetics, and the simulated results corresponded well with the experimental ones in every case.

The main purpose of the present study was to investigate the role(s) of 25-kDa heat shock protein (HSP25) in the regulation and integration of myofibrillar Z-disc structure during down- or upregulation of the size in rat soleus muscle fibers. Hindlimb unloading by tail suspension was performed in adult rats for 7 days, and reloading was allowed for 5 days after the termination of suspension. Interaction of HSP25 and Z-disc proteins, phosphorylation status, distribution, and complex formation of HSP25 were investigated. Non- and single-phosphorylated HSP25s were generally expressed in the cytoplasmic fraction of normal muscle. The level of total HSP25, as well as the phosphorylation ratio, did not change significantly in response to atrophy. Increased expressions of HSP25, phosphorylated at serine 15 (p-Ser15) and dual-phosphorylated form, were noted, when atrophied muscles were reloaded. Myofibrillar HSP25 was also noted in reloaded muscle. Histochemical analysis further indicated the localization of p-Ser15 in the regions with disorganization of Z-disc structure in reloaded muscle fibers. HSP25 formed a large molecular complex in the cytoplasmic fraction of normal muscle, whereas dissociation of free HSP25 with Ser15 phosphorylation was noted in reloaded muscle. The interaction of p-Ser15 with desmin and actinin was detected in Z-discs by proximity ligation assay. Strong interaction between p-Ser15 and desmin, but not actinin, was noted in the disorganized areas. These results indicated that HSP25 contributed to the desmin cytoskeletal organization following the phosphorylation at Ser15 during reloading and regrowing of soleus muscle.

Effects of hindlimb suspension (HS) and ambulation recovery on hippocampal neurogenesis of newly weaned rats were studied by using immunohistochemical techniques. The number of proliferating cell nuclear antigen-positive (PCNA(+)) cells in the subgranular zone (SGZ) markedly decreased during normal growth. However, neither HS nor subsequent recovery caused additional changes in the number of PCNA(+) cells. The number of doublecortin-positive (DCX(+)) neurons decreased gradually during normal growth. HS resulted in a further decrease in these neurons. However, DCX(+) cell numbers became identical to the levels in age-matched controls after 14 days of recovery. PCNA and DCX-double positive cells in the SGZ were also observed, and their cell numbers were not affected by HS and 14-day ambulation. Thus, HS suppressed the generation of DCX(+) neurons without affecting PCNA(+) cells in the SGZ of weaned rats. Taken together, hippocampal neurogenesis in weaned rats was not severely affected by HS while it decreased significantly as they had grown.

A 36GB SSD controller enabling write endurance of 2 PB and 32K internal IOPS under random 4 KB page write workload is presented that offers 10 years of lifetime for random writes of 600GB/day. We point out that minimizing unnecessary data relocation is the single fundamental solution to maximizing effective write endurance and effective write performance. We propose a novel full page-associative block recycling mechanism combined with a feature for retrieving blocks that have the least amount of valid pages. A logically partitioned structure enhances the mechanism further by exploiting spatial locality.

A powdered diet containing 100 or 3 ppm Fe was fed to rats starting at the age of 3 weeks. The voluntary activity level was checked using a wheel in the cage during the 17th week after the beginning of supplementation. Significantly less activity was seen in the 3 ppm Fe group during both light and dark periods. After 20 weeks, the blood and diencephalon were sampled from both groups. Lower hematocrit and blood hemoglobin content was observed in the 3 ppm Fe group. The level of 70 kDa heat shock cognate (HSC70) expression was greater in the diencephalon of the 3 ppm Fe group. In addition, the distribution of HSC70 was determined by proximity ligation assay. More HSC70-positive as well as total cells were noted in several areas of the diencephalon of the iron-deficient rats. The altered expression and distribution of HSC70 might play some role in the neurological changes.

It has been proposed that mechanically induced tension is the critical factor in the induction of muscle hypertrophy. However, the molecular mechanisms involved in this process are still under investigation. In the present study, the effect of mechanical stretch on intracellular signaling for protein translation initiation and elongation was studied in C2C12 myoblasts. Cells were grown on a silicone elastomer chamber and subjected to 30-min of 5 or 15% constant static or cyclic (60 cycles/min) uniaxial stretch. Western blot analyses revealed that p70 S6 kinase (p70S6K) and eukaryotic elongation factor 2 (eEF2), which are the markers for translation initiation and peptide chain elongation, respectively, were activated by both static and cyclic stretch. The magnitude of activation was greater in response to the 15% cyclic stretch. Cyclic stretch also increased the phosphorylation of MAP kinases (p38 MAPK, ERK1/2 and JNK). However, the pharmacological inhibition of MAP kinases did not block the stretch-induced activation of p70S6K and eEF2. An inhibitor of the mammalian target of rapamycin (mTOR) blocked the stretch-induced phosphorylation of p70S6K but did not affect the eEF2 activation. A broad-range tyrosine kinase inhibitor, genistein, blocked the stretch-induced activation of p70S6K and eEF2, whereas Src tyrosine kinase and Janus kinase (JAK) inhibitors did not. These results suggest that the stretch-induced activation of protein translation initiation and elongation in mouse myoblast cell lines is mediated by tyrosine kinase(s), except for Src kinase or JAK.

A New digital signature scheme based on Stepwise Triangular Scheme (STS) is proposed. The proposed trapdoor has resolved the vulnerability of STS and secure against both Grobner Bases and Rank Attacks. In addition, as a basic trapdoor, it is more efficient than the existing systems. With the efficient implementation, the Multivariate Public Key Cryptosystems (MPKC) signature public key has the signature longer than the message by less than 25 %, for example.

In a weighted undirected graph, a matching is said to be α-robust if for all p, the total weight of its heaviest p edges is at least α times the maximum weight of a p-matching in the graph. Here a p-matching is a matching with at most p edges. In 2002, Hassin and Rubinstein [4] showed that every graph has a 1/√2-robust matching and it can be found by k-th power algorithm in polynomial time. In this paper, we show that it can be extended to the matroid intersection problem, i.e., there always exists a 1/√2-robust matroid intersection, which is polynomially computable. We also study the time complexity of the robust matching problem. We show that a 1-robust matching can be computed in polynomial time (if exists), and for any fixed number α with 1/√2 0, there exists a weighted graph such that no k-th power algorithm outputs a (1/√2+ e)-approximation for computing the most robust matching.

The potential contamination of human blood or plasma with prions, such as variant Creuftzfelt-Jacob disease (vCJD), is becoming a serious problem. In this study, we established a Western blot-based detection method for PrP Sc (263K) spiked in plasma. Although plasma contains a large amount of protein, specific detection of a small amount of 263K in plasma could be specifically detected only after ultra-centrifugation followed by heat-denaturation of plasma proteins included in the resulting precipitate, before the digestion with proteinase K.

Expansion of triplet repeat sequences such as (CTG)n, (CGG)n, and (GAA)n causes human genetic diseases. Since DNA is packaged into arrays of nucleosomes in eukaryotic cells, chromatin may be involved in the mechanism of triplet repeat diseases. To elucidate this issue, we have examined effects of triplet repeat sequences on the chromatin organization in vivo using well defined yeast minichromosomes. We show here that (CGG)-|2 disrupts an array of positioned nucleosomes, whereas (CTG)i2 promotes the nucleosome formation. Thus, triplet repeat sequences can affect the chromatin organization in vivo, which may contribute to the triplet repeat expansion or alterations in the expression of genes associated with triplet repeat diseases.

This paper deals with the transit of a neutrophil through narrow capillary segments. In the segments are modeled by arc-shaped constrictions arranged in a straight pipeline. Initially the spherical cell deforms in transit through the first constriction. We focus on the transit time to the deformed cell through the second constriction. We investigate the effects of segment geometry on the transit time. Finally, it is shown that the transit time is independent of the shape of the first segment so long as it is organized by the entrance cell radius.Copyright © 2003 by ASME

Robotic camera positioners are now accepted and expected as assisting devices for solo surgery among endoscopic surgeons. However, camera guidance is an additional task for the operating surgeon, which may result in frustration, fatigue and longer surgery time. To cope with this problem, automatic camera guidance based on the visual tracking of surgical instruments may be effective, although it does not always provide an optimal view. We investigated the effectiveness of the selective use of automatic/manual control of a robotic laparoscope positioner.

Triplet repeat sequences that cause human hereditary diseases can form a variety of DNA conformations. Since DNA structures act as determinants of chromatin structure, chromatin may be involved in mechanisms of these diseases. To address this issue, we examined effects of triplet repeat sequences on chromatin structure and gene expression in Saccharomyces cerevisiae. We show here that (1) (CTG)12 promotes nucleosome formation, (2) (CGG)12 disrupts an array of positioned nucleosomes, and (3) (GAA)12 has little effect on nucleosome formation. Also, we show that insertion of (CGG)12 increases gene expression of a UAS-less promoter about 10-fold, while (CTG)12 and (GAA)12 have no effect. Thus, expansion of triplet repeat sequences may cause improper expression of disease related genes, through their effects on chromatin structure.