bluuebunny/crossref_metadata_2025_split huggingface dataset:
Serum growth differentiation factor 15 level is associated with muscle strength and lower extremity function in older patients with cardiometabolic disease
Authors: Oba Kazuhito , Ishikawa Joji , Tamura Yoshiaki , Fujita Yasunori , Ito Masafumi , Iizuka Ai , Fujiwara Yoshinori , Kodera Remi , Toba Ayumi , Toyoshima Kenji , Chiba Yuko , Mori Seijiro , Tanaka Masashi , Ito Hideki , Harada Kazumasa , Araki Atsushi 
Published: September 2020

AimsSarcopenia is a serious problem because of its poor prognosis. Growth differentiation factor 15 (GDF15) is associated with mitochondrial dysfunction, inflammation, insulin resistance and oxidative stress, which may play crucial roles for the development of sarcopenia. We aimed to examine whether serum GDF15 level is associated with muscle mass, strength and lower extremity function in older patients with cardiometabolic disease.MethodsSerum GDF15 levels were measured in 257 patients with cardiometabolic diseases (including 133 patients with diabetes) who had visited the frailty clinic, using a latex turbidimetric immunoassay. Appendicular skeletal muscle index, handgrip strength, timed‐up‐and‐go test and gait speed were evaluated. Power, speed, balance and total scores based on the sit‐to‐stand test were calculated to assess lower extremity function.ResultsThe highest tertile of serum GDF15 was independently associated with low handgrip strength, low gait speed, long timed‐up‐and‐go time and scores of lower extremity function but not an appendicular skeletal muscle index in multiple logistic regression analyses after adjustment for covariates. Patients in the highest tertile of GDF15 were at the risk of having three to nine times lower grip strength, three times lower gait speed, five to six times lower mobility and five to 11 times reduction in lower extremity function as compared with those in the lowest GDF15 tertile dependent on the models.ConclusionsElevated serum GDF15 level was independently associated with low muscle strength and lower extremity function in older patients with cardiometabolic disease. Serum GDF15 could be one of the biomarkers for muscle weakness and low physical performance. Geriatr Gerontol Int 2020; 20: 980–987.
Cut‐offs for calf circumference as a screening tool for low muscle mass: WASEDA'S Health Study
Authors: Kawakami Ryoko , Miyachi Motohiko , Sawada Susumu S. , Torii Suguru , Midorikawa Taishi , Tanisawa Kumpei , Ito Tomoko , Usui Chiyoko , Ishii Kaori , Suzuki Katsuhiko , Sakamoto Shizuo , Higuchi Mitsuru , Muraoka Isao , Oka Koichiro 
Published: September 2020

AimTo re‐evaluate the suitability of calf circumference as a surrogate marker of low muscle mass measured by both bioelectrical impedance analysis (BIA) and dual‐energy X‐ray absorptiometry (DXA). We also examined the effects of obesity and age on low muscle mass screening using calf circumference.MethodsIn total, 1239 adults participated in this cross‐sectional study. We measured the maximum calf circumference in a standing position and appendicular skeletal muscle mass (ASM) using BIA and DXA. We defined low muscle mass based on the Asian Working Group for Sarcopenia 2019 consensus.ResultsCalf circumference was positively correlated with BIA‐measured ASM/height2 (men: r = 0.81, women: r = 0.73) and DXA‐measured ASM/height2 (men: r = 0.78, women: r = 0.76). In the subgroup analyses by obesity and age, calf circumference was also positively correlated with ASM/height2. The optimal calf circumference cut‐offs for low muscle mass screening measured by BIA and DXA were 35 cm (sensitivity 91%, specificity 84%) and 36 cm (sensitivity 82%, specificity 80%) for men, and 33 cm (sensitivity 82%, specificity 84%) and 34 cm (sensitivity 85%, specificity 72%) for women, respectively.ConclusionsCalf circumference is positively correlated with BIA‐ and DXA‐measured muscle mass regardless of obesity and age and is a simple and accurate surrogate marker of muscle mass for diagnosing sarcopenia. Geriatr Gerontol Int 2020; 20: 943–950.
Furosemide as a factor to deteriorate therapeutic efficacy of tolvaptan in patients with decompensated cirrhosis
Authors: Uchida Yoshihito , Inao Mie , Tsuji Shohei , Uemura Hayato , Kouyama Jun‐ichi , Naiki Kayoko , Sugawara Kayoko , Nakao Masamitsu , Nakayama Nobuaki , Imai Yukinori , Tomiya Tomoaki , Mochida Satoshi 
Published: September 2020

AimTo optimize the therapeutic strategy for patients with decompensated cirrhosis manifesting hepatic ascites and/or edema, factors affecting the outcome of patients receiving tolvaptan were evaluated.MethodsThe subjects were 165 patients receiving tolvaptan including 116 patients (70%) also treated with furosemide. The therapeutic efficacy of tolvaptan was defined as “effective” when a body weight reduction of 1.5 kg or more was obtained within 1 week. The long‐term outcome was defined as “favorable” when the ascites‐related events‐free duration was prolonged following tolvaptan treatment, compared with that before treatment, or ascites‐related events were absent for at least 120 days during treatment based on the hazard function analysis.ResultsTolvaptan was effective in 115 patients (70%). Among them, the long‐term outcome was evaluated in 99 patients and was favorable in 70 patients (71%). A multivariate analysis revealed that the serum blood urea nitrogen levels at baseline (odds ratio 0.960 per +1 mg/dL, P = 0.021) and the type of tolvaptan initiation (planned vs. emergent; 3.695, P < 0.001) were associated with therapeutic efficacy, while the furosemide dose (0.280 per +20 mg/day, P = 0.014) and previous ascites‐related events (0.074, P < 0.001) were associated with the long‐term outcome. Receiver operating curve analyses identified the optimal cut‐off values for the furosemide dose as 15 mg/day (P < 0.001). Furthermore, the cumulative survival rates in patients receiving furosemide at 15 mg/day or less were significantly higher than those in the remaining patients (P = 0.048).ConclusionFurosemide given at baseline contributed to an unfavorable outcome in patients receiving tolvaptan; consequently, tolvaptan should be given before increasing the furosemide dose.
Effect of the transgenerational exposure to elevated CO2 on low temperature tolerance of winter wheat: Chloroplast ultrastructure and carbohydrate metabolism
Authors: Li Hui , Liu Shengqun , Guo Junhong , Liu Fulai , Song Fengbin , Li Xiangnan 
Published: September 2020

AbstractThe transgenerational effect of elevated atmospheric CO2 concentration (e[CO2]) on low temperature response in wheat is still little investigated, through the interaction of e[CO2], and low‐temperature stress has been reported in a single generation. Here, the low temperature‐induced modifications of chloroplast ultrastructure and carbohydrate metabolism in wheat after four generations continuously grown under ambient CO2 concentration (a[CO2]) and e[CO2] (2014–2018) were investigated. The results indicated that the transgenerational exposure to e[CO2] increased the number of grana lamellae and the amounts of osmiophilic lipid droplets, attenuating the negative effect of low temperature on chloroplast ultrastructure. The transgenerational e[CO2] enhanced the activities of antioxidant enzymes (i.e. SOD, POD and CAT) and concentrations of osmotic substances (i.e. proline and soluble sugar), which alleviated the low temperature‐induced oxidative damage to the chloroplast ultrastructure. In addition, transgenerational exposure of wheat to e[CO2] increased activities of vacInv and cwInv, while decreased fructokinase activity, which affected the sucrose metabolism in wheat leaf. These findings elucidated that transgenerational exposure to e[CO2] could improve low temperature tolerance of winter wheat, which provide novel insights to the response of wheat to future climate change.
Family member eating assistance and food intake in long‐term care: A secondary data analysis of the M3 Study
Authors: Wu Sarah A. , Morrison‐Koechl Jill , Slaughter Susan E. , Middleton Laura E. , Carrier Natalie , McAiney Carrie , Lengyel Christina , Keller Heather 
Published: September 2020

AbstractAimTo determine if protein and energy intake is significantly associated with a family member providing eating assistance to residents in long‐term care homes as compared with staff providing this assistance, when adjusting for other covariates.BackgroundWho provides eating support has the potential to improve resident food intake. Little is known about family eating assistance and if this is associated with resident food intake in long‐term care.DesignCross‐sectional, secondary data analysis.MethodsBetween October and January 2016, multilevel data were collected from 32 long‐term care homes across four Canadian provinces. Data included 3‐day weighed/observed food intake, mealtime observations, physical dining room assessments, health record review, and staff report of care needs. Residents where family provided eating assistance were compared with residents who received staff‐only assistance. Regression analysis determined the association of energy and protein intake with family eating assistance versus staff assistance while adjusting for covariates.ResultsOf those residents who required any physical eating assistance (N = 147), 38% (N = 56) had family assistance during at least one of nine meals observed. Residents who received family assistance (N = 56) and those who did not (N = 91) were statistically different in several of their physiological eating abilities. When adjusting for covariates, family assistance was associated with significantly higher consumption of protein and energy intake.ConclusionEnergy and protein intake is significantly higher when family provides eating assistance. Family are encouraged to provide this direct care if it is required.ImpactResidents who struggle with independent eating can benefit from dedicated support during mealtimes. Findings from this study provide empirical evidence that family eating assistance is associated with improved resident food intake and provides strong justification to encourage families to be active partners in the care and well‐being of their relatives. Home administrators and nursing staff should support the specialized care that families can provide at mealtimes.
The relationship between insomnia and trait anger and anger expression among adolescents
Authors: Sisman Fatma N. , Basakci Dilan , Ergun Ayse 
Published: September 2020

AbstractProblemSleeplessness and inadequate sleep may cause an adolescent to experience reduced self‐control and behavioral problems that include anger and an inclination toward crime. This study aimed to examine the relationship between insomnia and trait anger and anger expression among adolescents.MethodsThe study was conducted with 749 students from 27 high schools who were selected by using the stratified cluster sampling method. The data were collected with an Individual Characteristics Form, the Trait Anger/Anger Expression Inventory, and the Insomnia Severity Index.FindingsThe insomnia scores of 14.0% of the participants were over the clinical insomnia threshold of 15 points. A positive relationship was found between insomnia and trait anger, anger‐in, anger‐out scores but a negative relationship with anger control scores. It was observed that the determinants of the severity of insomnia were trait anger and anger‐in, dozing off in class, feeling anger after a sleepless night, sleeping <6 h a night during the week and over the weekend.ConclusionIt was found that 14.0% of the participants experienced insomnia and there was a two‐way correlation between insomnia and anger among adolescents.
A mathematic model to reveal delicate cross‐regulation between MAVS/STING, inflammasome and MyD88‐dependent type I interferon signalling
Authors: Cai Chunmei , Yu Xiao 
Published: September 2020

AbstractEarly type I interferon is essential for antagonizing against malaria infection, which remains a significant global infectious disease. After Plasmodium yoelii YM infection, the activation of MAVS‐, STING‐ and inflammasome‐IRF3‐mediated pathway could trigger the Socs1 expression to inhibit the TLR7‐MyD88‐IRF7‐induced type I interferon production. However, the dynamic regulatory mechanisms of type I interferon response to YM infection and delicate cross‐regulation of these signalling are far from clear. In current study, we established a mathematical model to systematically demonstrate that the MAVS‐, STING‐ and inflammasome‐mediated signalling pathways play distinct roles in regulating type I interferon response after YM infection; and the YM dose could significantly affect the difference of resistance to YM infection among MAVS, STING and inflammasome deficiency. Collectively, our study systematically elucidated the precise regulatory mechanisms of type I interferon signalling after YM infection and advanced the research on therapy of plasmodium infection by incorporating multiple signalling pathways at diverse time.
Serum galectin‐3 as a biomarker for screening, early diagnosis, prognosis and therapeutic effect evaluation of pancreatic cancer
Authors: Yi Nan , Zhao Xuying , Ji Jie , Xu Minxue , Jiao Yujie , Qian Tianyang , Zhu Shengze , Jiang Feng , Chen Jianhua , Xiao Mingbing 
Published: September 2020

AbstractGalectin‐3 plays an important role in cell‐cell adhesion, macrophage activation, angiogenesis, metastasis and apoptosis and is overexpressed in pancreatic cancer. We explored the importance of galectin‐3 in the screening, early diagnosis, prognosis and therapeutic effect evaluation of pancreatic cancer. A time‐resolved fluorescence immunoassay was performed to detect serum galectin‐3 level. Serum samples were collected from healthy controls and patients with pancreatic cancer before and after different treatments, and the relationships between galectin‐3 level and clinical parameters were analysed. Among the healthy controls, one individual with an abnormally high concentration of galectin‐3 (9.85 μg/L) was diagnosed with pancreatic cancer. Compared to the pre‐operative level, galectin‐3 concentration significantly decreased in patients with radical excision 1 month after surgery (P < .05), but showed no obvious change in patients who underwent palliative resection. Additionally, among patients with radical excision, carcinoma recurrence rate was significantly higher in those with increased or unchanged galectin‐3 level. Retrospective analysis revealed the extraordinarily high value and high specificity of galectin‐3 for predicting 3‐year survival (P < .001). Thus, galectin‐3 may serve as a potential biomarker for the screening and early diagnosis of pancreatic cancer and as an independent prognostic indicator in patients with pancreatic cancer.
The matricellular protein CCN5 prevents adverse atrial structural and electrical remodelling
Authors: Lee Min‐Ah , Raad Nour , Song Min Ho , Yoo Jimeen , Lee Miyoung , Jang Seung Pil , Kwak Tae Hwan , Kook Hyun , Choi Eun‐Kyoung , Cha Tae‐Joon , Hajjar Roger J. , Jeong Dongtak , Park Woo Jin 
Published: September 2020

AbstractAtrial structural remodelling including atrial hypertrophy and fibrosis is a key mediator of atrial fibrillation (AF). We previously demonstrated that the matricellular protein CCN5 elicits anti‐fibrotic and anti‐hypertrophic effects in left ventricles under pressure overload. We here determined the utility of CCN5 in ameliorating adverse atrial remodelling and arrhythmias in a murine model of angiotensin II (AngII) infusion. Advanced atrial structural remodelling was induced by AngII infusion in control mice and mice overexpressing CCN5 either through transgenesis (CCN5 Tg) or AAV9‐mediated gene transfer (AAV9‐CCN5). The mRNA levels of pro‐fibrotic and pro‐inflammatory genes were markedly up‐regulated by AngII infusion, which was significantly normalized by CCN5 overexpression. In vitro studies in isolated atrial fibroblasts demonstrated a marked reduction in AngII‐induced fibroblast trans‐differentiation in CCN5‐treated atria. Moreover, while AngII increased the expression of phosphorylated CaMKII and ryanodine receptor 2 levels in HL‐1 cells, these molecular features of AF were prevented by CCN5. Electrophysiological studies in ex vivo perfused hearts revealed a blunted susceptibility of the AAV9‐CCN5–treated hearts to rapid atrial pacing‐induced arrhythmias and concomitant reversal in AngII‐induced atrial action potential prolongation. These data demonstrate the utility of a gene transfer approach targeting CCN5 for reversal of adverse atrial structural and electrophysiological remodelling.
The association between medication use and gait in adults with intellectual disabilities
Authors: Maas S. , Festen D. A. M. , Hilgenkamp T. I. M. , Oppewal A. 
Published: September 2020

AbstractBackgroundAdults with intellectual disabilities (ID) often have polypharmacy and often use antipsychotics. Both polypharmacy and antipsychotics have a negative effect on gait in the general population, but this has not been studied in adults with ID. These negative effects may add to pre‐existing gait disturbances in adults with ID and increase the risk for adverse health outcomes in this population. Therefore, the aim of this study is to investigate the difference in gait parameters between adults with ID with and without polypharmacy and between adults with ID using and not using antipsychotics.MethodThe gait parameters of 31 participants were collected with the GAITRite walkway, a pressure sensitive walkway measuring spatial and temporal gait parameters, in addition to information about personal characteristics, prescribed medication and presence of polypharmacy.ResultsAfter adjustment for sex and body mass index, participants with polypharmacy had a significantly shorter step length [polypharmacy B (SE) = −0.079 (0.034), P = 0.03], shorter stride length [polypharmacy B (SE) = −0.157 (0.069), P = 0.03] and longer double support time [polypharmacy B (SE) = 0.0004 (0.0001), P = 0.047]. Participants using antipsychotics had a significantly longer double support time [antipsychotic use B (SE) = 0.0003 (0.0002), P = 0.019].ConclusionThis study showed for the first time that both polypharmacy and using antipsychotics are associated with gait in adults with ID. The differences seem to resemble a more cautious gait. Further investigation with larger study samples, additional medication types and dosages are needed to acquire more insight in this important topic.
Impact of intimate partner violence and childhood maltreatment on maternal–infant maltreatment: A longitudinal study
Authors: Kita Sachiko , Tobe Hiromi , Umeshita Kaori , Hayashi Mayu , Kamibeppu Kiyoko 
Published: September 2020

AbstractAimThis study identifies the impact of intimate partner violence (IPV) during pregnancy, and childhood maltreatment on mothers’ perpetration of child maltreatment on 1‐month postnatal infants.MethodsA longitudinal study was conducted on women in the third trimester of pregnancy in two obstetric hospitals in Tokyo, Japan, from June 2016 to September 2017. Participants were asked to complete online self‐reported questionnaires during their pregnancy period and at 1 month postnatal. The relationship between suffering from IPV during pregnancy, experiencing childhood maltreatment before the age of 18 years, and perpetration of child maltreatment toward infants was measured among mothers using the Violence Against Women Screen and a survey of four and 14 ad hoc questions. To identify the impact of poly‐victimizations of IPV and childhood maltreatment on maternal–infant maltreatment, the study implemented logistic regression models.ResultsThe data from 533 respondents to the first and second surveys were analyzed. Maternal–infant maltreatment at 1 month postnatal was strongly associated with poly‐victimizations of IPV during pregnancy and childhood maltreatment (adjusted odds ratio [AOR] = 5.17; p < .001; 95% CI = 2.39–11.20), single victimization of IPV (AOR = 3.43, p < .001, 95% CI = 1.76–6.72), and single victimization of childhood maltreatment (AOR = 1.75, p = .03, 95% CI = 1.04–2.93; neither = reference).ConclusionThe results emphasize the importance of individuating pregnant women with poly‐victimizations of IPV during pregnancy and childhood maltreatment and providing intensive and continuous support for such women to prevent maternal–infant maltreatment after childbirth.
Oncostatin M induces hyperalgesic priming and amplifies signaling of cAMP to ERK by RapGEF2 and PKA
Authors: Garza Carbajal Anibal , Ebersberger Andrea , Thiel Alina , Ferrari Luiz , Acuna Jeremy , Brosig Stephanie , Isensee Joerg , Moeller Katharina , Siobal Maike , Rose‐John Stefan , Levine Jon , Schaible Hans‐Georg , Hucho Tim 
Published: September 2020

AbstractHyperalgesic priming is characterized by enhanced nociceptor sensitization by pronociceptive mediators, prototypically PGE2. Priming has gained interest as a mechanism underlying the transition to chronic pain. Which stimuli induce priming and what cellular mechanisms are employed remains incompletely understood. In adult male rats, we present the cytokine Oncostatin M (OSM), a member of the IL‐6 family, as an inducer of priming by a novel mechanism. We used a high content microscopy based approach to quantify the activation of endogenous PKA‐II and ERK of thousands sensory neurons in culture. Incubation with OSM increased and prolonged ERK activation by agents that increase cAMP production such as PGE2, forskolin, and cAMP analogs. These changes were specific to IB4/CaMKIIα positive neurons, required protein translation, and increased cAMP‐to‐ERK signaling. In both, control and OSM‐treated neurons, cAMP/ERK signaling involved RapGEF2 and PKA but not Epac. Similar enhancement of cAMP‐to‐ERK signaling could be induced by GDNF, which acts mostly on IB4/CaMKIIα‐positive neurons, but not by NGF, which acts mostly on IB4/CaMKIIα‐negative neurons. In vitro, OSM pretreatment rendered baseline TTX‐R currents ERK‐dependent and switched forskolin‐increased currents from partial to full ERK‐dependence in small/medium sized neurons. In summary, priming induced by OSM uses a novel mechanism to enhance and prolong coupling of cAMP/PKA to ERK1/2 signaling without changing the overall pathway structure.
image