Waseda University

About: Waseda University is a education organization based out in Tokyo, Japan. It is known for research contribution in the topics: Large Hadron Collider & Catalysis. The organization has 24220 authors who have published 46859 publications receiving 837855 citations. The organization is also known as: Waseda daigaku & Sōdai.

Bacterial adhesion to and viability on positively charged polymer surfaces

Abstract: Secondary and tertiary amino groups were introduced into polymer chains grafted onto a polyethylene flat-sheet membrane to evaluate the effects of surface properties on the adhesion and viability of a strain of the Gram-negative bacterium Escherichia coli and a strain of the Gram-positive bacterium Bacillus subtilis. The characterization of the surfaces containing amino groups, i.e. ethylamino (EA) and diethylamino (DEA) groups, revealed that the membrane potentials are proportional to amino-group densities and contact angle hysteresis. A high bacterial adhesion rate constant k was observed at high membrane potential, which indicates that membrane potential could be used as an indicator for estimating bacterial adhesion to the EA and DEA sheets, especially in B. subtilis. The bacterial adhesion rate constant of E. coli markedly increased at a membrane potential higher than -7.8 mV, whereas that of B. subtilis increased at a membrane potential higher than -8.3 mV, at which the dominant effect on bacterial adhesion is expected to change. The viability experiments revealed that approximately 80% of E. coli cells adhering to the sheets with high membrane potential were inactivated after a contact time of 8 h, whereas 60% of B. subtilis cells were inactivated. Furthermore, E. coli viability significantly decreased at a membrane potential higher than -8 mV, whereas B. subtilis viability decreased as membrane potential increased, which reflects differences in cell wall structure between E. coli and B. subtilis.

The influence of antioxidant supplementation on markers of inflammation and the relationship to oxidative stress after exercise.

Abstract: Interest in the relationship between inflammation and oxidative stress has increased dramatically in recent years, not only within the clinical setting but also in the fields of exercise biochemistry and immunology. Inflammation and oxidative stress share a common role in the etiology of a variety of chronic diseases. During exercise, inflammation and oxidative stress are linked via muscle metabolism and muscle damage. Because oxidative stress and inflammation have traditionally been associated with fatigue and impaired recovery from exercise, research has focused on nutritional strategies aimed at reducing these effects. In this review, we have evaluated the findings of studies involving antioxidant supplementation on alterations in markers of inflammation (e.g., cytokines, C-reactive protein and cortisol). This review focuses predominantly on the role of reactive oxygen and nitrogen species generated from muscle metabolism and muscle damage during exercise and on the modulatory effects of antioxidant supplements. Furthermore, we have analyzed the influence of factors such as the dose, timing, supplementation period and bioavailability of antioxidant nutrients.

Muscle volume compared to cross-sectional area is more appropriate for evaluating muscle strength in young and elderly individuals

Abstract: Objective: the present study examined which of muscle volume (MV) and cross-sectional area (CSA) is appropriate for evaluating the relation with elbow flexor muscle strength in young and elderly individuals. Methods: the subjects were 52 young (20‐34 year; 30 men and 22 women) and 51 elderly individuals (60‐77 year, 19 men and 32 women). The MV and maximal anatomical CSA (ACSA) of elbow flexors were determined by magnetic resonance imaging. The torque developed during maximal voluntary contraction of isometric elbow joint flexion was converted to force by dividing it by the forearm length of each subject. Results: torque was significantly correlated with MV in young and elderly individuals (r = 0.564‐0.926). Similarly, force was also significantly correlated with ACSA in each of them (r = 0.637‐0.906). However, the y-intercepts of the regression lines for the ACSA-force relationship in young men and women were significantly higher than zero. There was no age effect on torque per MV, whereas force per ACSA was significantly higher in young adults than in elderly individuals. Conclusion: for elbow flexors, MV compared to ACSA is appropriate for evaluating the size‐strength relationship and the existence of age-related difference in muscle strength per size.

Chronic activation of the prostaglandin receptor EP4 promotes hyaluronan-mediated neointimal formation in the ductus arteriosus.

Abstract: PGE, a potent vasodilator, plays a primary role in maintaining the patency of the ductus arteriosus (DA). Genetic disruption of the PGE-specific receptor EP4, however, paradoxically results in fatal patent DA (PDA) in mice. Here we demonstrate that EP4-mediated signals promote DA closure by hyaluronic acid–mediated (HA-mediated) intimal cushion formation (ICF). Chronic EP4 stimulation by ONO-AE1-329, a selective EP4 agonist, significantly enhanced migration and HA production in rat DA smooth muscle cells. When HA production was inhibited, EP4-mediated migration was negated. Activation of EP4, adenylyl cyclase, and PKA all increased HA production and the level of HA synthase 2 (HAS2) transcripts. In immature rat DA explants, ICF was promoted by EP4/PKA stimuli. Furthermore, adenovirus-mediated Has2 gene transfer was sufficient to induce ICF in EP4-disrupted DA explants in which the intimal cushion had not formed. Accordingly, signals through EP4 have 2 essential roles in DA development, namely, vascular dilation and ICF. The latter would lead to luminal narrowing, helping adhesive occlusion and permanent closure of the vascular lumen. Our results imply that HA induction serves as an alternative therapeutic strategy for the treatment of PDA to the current one, i.e., inhibition of PGE signaling by cyclooxygenase inhibitors, which might delay PGE-mediated ICF in immature infants.