Comparisons of physique, body composition, and somatotype by weight division between male and female collegiate taekwondo athletes

The aim of the study was to compare the physique, body composition and somatotype between male and female collegiate taekwondo athletes and specially focus on differences by weight division. 60 collegiate taekwondo athletes (male: 29, female: 31) voluntarily participated in the study. They were divided into four Olympic weight divisions (male for -58 kg, -68 kg, -80 kg, +80 kg, female for -49 kg, -57 kg, -67 kg, +67 kg). Anthropometric measurements included body weight, height, sitting height, body circumferences (relaxed arm, flexed arm, chest, waist, hip, thigh, and calf), bone widths (humerus and femur), and skinfold thicknesses (triceps, subscapular, suprailiac, thigh, and calf) were measured. The three somatotype components were assessed by Heath-Carter anthropometric method (Carter & Heath, 1990). Independent t-test and one-way ANOVA were applied to analyze difference of dependent variables. Significant level was set at .05. Male athletes were taller and heavier than female athletes. However, sum of skinfold thickness was significantly higher in female athletes than male athletes. The three somatotype components for male athletes were 3.4-3.5-3.1 and characterized with balanced mesomorphy. On the other hand, the somatotype of female athletes were 6.1-3.4-2.6 and characterized with mesomorphic endomorph. In male athletes -80 kg and +80 kg weight divisions were higher mesomorphy, but lower ectomorphy than -58 kg and -68 kg weight divisions. In female, -57 kg, -67 kg and +67 kg weight divisions were higher endomorphy and mesomorphy, but lower ectomorphy than -49 kg weight divisions. In conclusion, male athletes had higher anthropometric characteristics than female athletes except for the skinfold thickness. Female athletes had higher endomorphy, whereas male athletes had higher ectomorphy. Physique and somatotype were different between weight divisions both male and female athletes. This study provides a reference data of morphological characteristics of collegiate elite taekwondo athletes

Catalpol Modulates Lifespan via DAF-16/FOXO and SKN-1/Nrf2 Activation in

Catalpol is an effective component of rehmannia root and known to possess various pharmacological properties. The present study was aimed at investigating the potential effects of catalpol on the lifespan and stress tolerance using C. elegans model system. Herein, catalpol showed potent lifespan extension of wild-type nematode under normal culture condition. In addition, survival rate of catalpol-fed nematodes was significantly elevated compared to untreated control under heat and oxidative stress but not under hyperosmolality conditions. We also found that elevated antioxidant enzyme activities and expressions of stress resistance proteins were attributed to catalpol-mediated increased stress tolerance of nematode. We further investigated whether catalpol’s longevity effect is related to aging-related factors including reproduction, food intake, and growth. Interestingly, catalpol exposure could attenuate pharyngeal pumping rate, indicating that catalpol may induce dietary restriction of nematode. Moreover, locomotory ability of aged nematode was significantly improved by catalpol treatment, while lipofuscin levels were attenuated, suggesting that catalpol may affect age-associated changes of nematode. Our mechanistic studies revealed that mek-1, daf-2, age-1, daf-16, and skn-1 are involved in catalpol-mediated longevity. These results indicate that catalpol extends lifespan and increases stress tolerance of C. elegans via DAF-16/FOXO and SKN-1/Nrf activation dependent on insulin/IGF signaling and JNK signaling

A mutual activation loop between breast cancer cells and myeloid-derived suppressor cells facilitates spontaneous metastasis through IL-6 trans-signaling in a murine model

Introduction : Tumor cell interactions with the microenvironment, especially those of bone-marrow-derived myeloid cells, are important in various aspects of tumor metastasis. Myeloid-derived suppressor cells (MDSCs) have been suggested to constitute tumor-favoring microenvironments. In this study, we elucidated a novel mechanism by which the MDSCs can mediate spontaneous distant metastasis of breast cancer cells. Methods : Murine breast cancer cells, 4T1 and EMT6, were orthotopically grafted into the mammary fat pads of syngeneic BALB/c mice. CD11b+Gr-1+ MDSCs in the spleen, liver, lung and primary tumor mass were analyzed. To evaluate the role of MDSCs in the distant metastasis, MDSCs were depleted or reconstituted in tumor-bearing mice. To evaluate whether MDSCs in the metastasizing tumor microenvironment affect breast cancer cell behavior, MDSCs and cancer cells were co-cultivated. To investigate the role of MDSCs in in vivo metastasis, we blocked the interactions between MDSCs and cancer cells. Results : Using a murine breast cancer cell model, we showed that murine breast cancer cells with high IL-6 expression recruited more MDSCs and that the metastasizing capacity of cancer cells paralleled MDSC recruitment in tumor-bearing mice. Metastasizing, but not non-metastasizing, tumor-derived factors induced MDSCs to increase IL-6 production and full activation of recruited MDSCs occurred in the primary tumor site and metastatic organ in the vicinity of metastasizing cancer cells, but not in lymphoid organs. In addition, tumor-expanded MDSCs expressed Adam-family proteases, which facilitated shedding of IL-6 receptor, thereby contributing to breast cancer cell invasiveness and distant metastasis through IL-6 trans-signaling. The critical role of IL-6 trans-signaling was confirmed in both the afferent and efferent pathways of metastasis. Conclusion : In this study, we showed that metastasizing cancer cells induced higher MDSCs infiltration and prompted them to secret exaggerated IL-6 as well as soluble IL-6Rα, which, in turn, triggered a persistent increase of pSTAT3 in tumor cells. This potential tumor-MDSC axis involving IL-6 trans-signaling directly affected breast cancer cell aggressiveness, leading to spontaneous metastasis.This work was supported by grants from the National R&D Program for Cancer Control, Ministry of Health & Welfare (12202001), Basic Science Research Program through the National Research Foundation of Korea (NRF) funded by the Ministry of Education, Science and Technology (2012008122), and the National Research Foundation of Korea (NRF) grant funded by the Korea government (MEST) (2012014152).Peer Reviewe

Beneficial Effect of Efonidipine, an L- and T-Type Dual Calcium Channel Blocker, on Heart Rate and Blood Pressure in Patients With Mild-to-Moderate Essential Hypertension

Background and Objectives: Efonidipine hydrochloride, an L- and T-type dual calcium channel blocker, is suggested to have a heart rate (HR)-slowing action in addition to a blood pressure (BP)-lowering effect. The aim of this study was to determine the effect of efonidipine on HR and BP in patients with mild-to-moderate hypertension. Subjects and Methods: In a multi-center, prospective, open-labeled, single-armed study, we enrolled 53 patients who had mild-to-moderate hypertension {sitting diastolic BP (SiDBP) 90-110 mmHg}. After a 2-week washout, eligible patients were treated with efonidipine (40 mg once daily for 12 weeks). The primary end point was the change in HR from baseline to week 12. The secondary end-point included the change in trough sitting BP and 24-hour mean BP between baseline and week 12. Laboratory and clinical adverse events were monitored at each study visit (4, 8, and 12 weeks). Results: Fifty-two patients were included in the intention-to-treat analysis. After 12 weeks of treatment with efonidipine, the resting HR decreased significantly from baseline to week 12 (from 81.5??5.3 to 71.8??9.9 beats/minute (difference, -9.9??9.0 beats/minute), p<0.0001}. The trough BP {sitting systolic blood pressure (SiSBP) and SiDBP} and 24-hour mean BP also decreased significantly (SiSBP: from 144.6??8.2 to 132.9??13.5 mmHg, p<0.0001; SiDBP: from 96.9??5.4 to 88.3??8.6 mmHg, p<0.0001, 24-hour mean systolic BP: from 140.4??13.5 to 133.8??11.6 mmHg, p<0.0001; 24-hour mean diastolic BP: from 91.7??8.7 to 87.5??9.5 mmHg, p<0.0001). Conclusion: Efonidipine was effective in controlling both HR and BP in patients with mild-to-moderate hypertension. Copyright ?? 2010 The Korean Society of Cardiology

Airway epithelial cells initiate the allergen response through transglutaminase 2 by inducing IL-33 expression and a subsequent Th2 response

Transglutaminase 2 (TG2) is a post-translational protein-modifying enzyme that catalyzes the transamidation reaction, producing crosslinked or polyaminated proteins. Increased TG2 expression and activity have been reported in various inflammatory conditions, such as rheumatoid arthritis, inflammation-associated pulmonary fibrosis, and autoimmune encephalitis. In particular, TG2 from epithelial cells is important during the initial inflammatory response in the lung. In this study, we evaluated the role of TG2 in the pathogenesis of allergic asthma, particularly whether TG2 affects initial activation signaling leading to Th2 differentiation against antigens. Methods We induced allergic asthma by ovalbumin sensitization and intranasal challenge in wild-type (WT) BALB/c and TG2-deficient mice. Broncheoalveolar lavage fluid cells and intracellular cytokine production were analyzed by flow cytometry. Interleukin (IL)-33 and TG2 expression in lung epithelial cells was detected by confocal microscopy. Results Airway responsiveness was attenuated in TG2-deficient mice compared to that in the WT control. In addition, recruitment of eosinophils and Th2 and Th17 differentiation decreased in TG2-deficient mice. Treatment with cysteamine, a transglutaminase inhibitor, also reduced airway hypersensitivity, inflammatory cell recruitment, and T helper cell differentiation. TG2-deficient mice showed reduced IL-33 expression following induction of allergic asthma compared to those in the WT control. Conclusions We found that pulmonary epithelial cells damaged by allergens triggered TG2-mediated IL-33 expression leading to type 2 responses by recruiting both innate and adaptive arms of the immune system.Peer Reviewe