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  • Article
    Jia G, Dong Z, Sun C, Wen F, Wang H, Guo H, Gao X, Xu C, Xu C, Yang C, Sun Y.
    Oncotarget. 2017 Sep 29;8(44):76987-76999.
    The prostate specific antigen (PSA) test is widely used for early diagnosis of prostate cancer (PCa). However, its limited sensitivity has led to over-diagnosis and over-treatment of PCa. Glycosylation alteration is a common phenomenon in cancer development. Different PSA glycan subforms have been proposed as diagnostic markers to better differentiate PCa from benign prostate hyperplasia (BPH). In this study, we purified PSA from expressed prostate secretions (EPS)-urine samples from 32 BPH and 30 PCa patients and provided detailed PSA glycan profiles in Chinese population. We found that most of the PSA glycans from EPS-urine were complex type biantennary glycans. We observed two major patterns in PSA glycan profiles. Overall there was no distinct separation of PSA glycan profiles between BPH and PCa patients. However, we detected a significant increase of glycan FA2 and FM5A2G2S1 in PCa when compared with BPH patients. Furthermore, we observed that the composition of FA2 glycan increased significantly in advanced PCa with Gleason score ≥8, which potentially could be translated to clinic as a marker for aggressive PCa.
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  • Article
    Wang D, Wei T, Zhao F, Huang J.
    BMJ Open. 2024 Feb 08;14(2):e076987.
    OBJECTIVE: This study aimed to explore the impacts of the changing national fertility policy on maternal and fetal characteristics, and birth timing patterns and provide a basis for the management of the obstetric and midwifery workforce.
    DESIGN: Retrospective cohort study.
    SETTING: Data from medical register of a tertiary referral centre in Beijing, China.
    PARTICIPANTS: We included 20 334 births with a gestational age more than 28 weeks during January 2013-September 2023.
    MAIN OUTCOMES: The main outcomes included birth numbers, maternal age, parity, birth modes, premature rates, neonatal birth weight, and birth timings.
    RESULTS: The birth rates showed a general rising trend before 2016. Afterwards, the birth rates kept decreasing and reached the bottom level in 2022. The caesarean section rates showed a declining trend, while the assisted birth rates were progressively rising, especially among primiparous women. From 2013 to 2022, the proportions of multiparous women (increasing from 9.3% to 36.6%) and women with advanced maternal age (increasing from 11.4% to 34.5%) were on the rise, together with increasing rates of premature birth (increasing from 5.7% to 8.5%) and neonatal low birth weight (rising from 4.3% to 7.2%) in this population. This study found a significant peak of births between 14:00 and 15:00, which remained unchanged despite shifts in the fertility policy (p<0.001 and [Formula: see text] values close to 1, respectively).
    CONCLUSION: The 'three-child' policy did not boost the birth rate further 2 years later after its enactment, and the proportion of multiparous women and women with advanced maternal age were on the rise, accompanied by an increase in rates of premature birth and low birth weight. Targeted training should be offered to healthcare professionals to empower them to deal with possible negative pregnancy outcomes and childbirth complications. Prepregnancy and antepartum education should be parity specific. Adequate midwifery staffing during this 14:00-15:00 is vital to promote a safe birth.
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  • Article
    Heron-Milhavet L, Franckhauser C, Fernandez A, Lamb NJ.
    PLoS One. 2013;8(10):e76987.
    The binding of the cdk inhibitor p21cip1 to Akt2 in the nucleus is an essential component in determining the specific role of Akt2 in the cell cycle arrest that precedes myogenic differentiation. Here, through a combination of biochemical and cell biology approaches, we have addressed the molecular basis of this binding. Using amino-terminal truncation of Akt2, we show that p21cip1 binds at the carboxy terminal of Akt2 since deletion of the first 400 amino acids did not affect the interaction between Akt2 and p21cip1. Pull down using carboxy terminal-truncated Akt2 protein revealed the importance of the region between amino acids 400 and 445 for the binding to p21cip1. Since Akt2_400-445 and Akt2_420-445 peptides could both bind p21cip1, this refines the binding domain on Akt2 between amino acids 420 and 445. In order to confirm these data in living cells, we developed a protocol to synchronize myoblasts at the cell cycle exit point when p21cip1 expression is induced by MyoD before myogenic differentiation. When a synthetic Akt2 peptide spanning the region (410-437) was microinjected in p21-expressing myoblasts, p21cip1 no longer localized exclusively in the nucleus, instead being redistributed throughout the cell, thus showing that injected peptide 410-437 acts to compete with the binding of endogenous Akt2 to p21cip1. Taken together, our data suggest that this 27 amino acid sequence on Akt2 is necessary and sufficient to bind p21cip1 both in vitro and in living cells.
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  • Book
    edited by Dominique Meynial-Denis.
    Summary: "Maintaining adequate muscle mass is crucial to healthy aging. Numerous diseases as well as deterioration of motor nerves and muscle repair mechanisms cause risks to developing sarcopenia. Sedentary lifestyles coupled with excess caloric intake among senior citizens compound the problem by creating a condition of limited muscle strength overwhelmed with body weight. This book presents biochemical, nutritional, and metabolic implications related to sarcopenia. It provides information on mechanisms regulating age-related loss of muscle mass and function as well as nutritional anti-aging strategies to fight against atrophy and support healthy aging"-- Provided by publisher.

    Contents:
    Definitions of sarcopenia / Heike Bischoff-Ferrari and Bess Dawson-Hughes
    Models of accelerated sarcopenia / Andrew S. Layne, Lisa M. Roberts and Thomas W. Buford
    Sarcopenia in physical frailty / Maturin Tabue-Teguo, Emanuele Marzetti, Riccardo Calvani, Bruno Vellas, Matteo Cesari
    The role of imaging techniques in the diagnosis of sarcopenia / Thiago Gonzalez Barbosa-Silva and Carla Prado
    Nutrient sensing and mTORC1 regulation in sarcopenia / Ted G. Graber and Blake B. Rasmussen
    Different adaptation of ubiquitin-proteasome and lysosome-autophagy signaling in sarcopenic muscle / Kunihiro Sakuma, Hidetaka Wakabayashi
    Myokines in aging muscle / Katie Brown, Aaron Persinger, and Melissa Puppa
    The contribution of satellite cells to skeletal muscle aging / Christopher Fry
    Muscle stem cell microenvironment in sarcopenia / Neia Naldaiz-Gastesi and Ander Izeta
    Sarcopenia and oxidative stress : from the bench to therapeutical strategies / Coralie Arc-Chagnaud, Allan F. Pagano, Thomas Brioche
    Muscle protein turnover and sarcopenia in the elderly : the effects of nutrition / Paolo Tessari
    The relationship between muscle mitochondrial turnover and sarcopenia / Heather N. Carter, Nashwa Cheema and David A. Hood
    Skeletal muscle fat infiltration with aging : an important factor of sarcopenia / Allan F. Pagano, Coralie Arc-Chagnaud, Thomas Brioche, Angèle Chopard, Guillaume Py
    Nutritional modulation of mitochondrial-associated death signaling in sarcopenia / Stephen E. Alway
    Beneficial effects and limitations of strategies (nutritional or other) to limit muscle wasting due to normal aging / Dominique Meynial-Denis
    Declines in whole muscle function with aging : the role of age-related alterations in contractile properties of single skeletal muscle fibres / Nicole Mazara and Geoffrey A. Power
    Sarcopenic dysphagia, presbyphagia and rehabilitation nutrition / Hidetaka Wakabayashi and Kunihiro Sakuma
    Wasting and cachexia in chronic kidney disease / Giacomo Garibotto, Daniela Picciotto, Daniela Verzola
    Sarcopenia and Parkinson's disease : molecular mechanisms and clinical management / Manlio Vinciguerra
    Sarcopenic obesity in the elderly / Michael Tieland, Inez Trouwborst, Amely Verreijen, Robert Memelink and Peter J.M. Weijs
    Sum up and future research / Dominique Meynial-Denis.
    Digital Access TandFonline 2019