bluuebunny/crossref_metadata_2025_split huggingface dataset:
Relationship between the severity of cerebral white matter hyperintensities and sympathetic nervous activity in older adults
Authors: Obara Toshimasa , Nagai Kumiko , Shibata Shigeki , Hirasawa Ai , Koshiba Hitomi , Hasegawa Hiroshi , Ebihara Takae , Kozaki Koichi 
Published: November 2017

AimWhite matter hyperintensities (WMH), visualized on brain magnetic resonance imaging, represent an abnormality related to the development of geriatric syndromes. Recently, it has been found that low sympathetic nervous activity might be associated with physical and cognitive dysfunction in older adults. Therefore, we investigated the relationship between the severity of cerebral WMH and sympathetic nervous activity, measured by the heart rate variability.MethodsWe carried out a cross‐sectional study of 39 older patients. Holter recording was carried out for 30 min. From the RR intervals on the electrocardiogram, the standard deviation of the normal‐to‐normal intervals, the standard deviation of all normal‐to‐normal intervals in all the five segments of the entire recording, low frequency (LF), high frequency (HF) and LF/HF were calculated. In regard to the WMH, periventricular hyperintensities and deep white matter hyperintensities (DWMH) were rated according to the Fazekas classification. The WMH were also rated semiquantitatively according to the methods developed by Junque (periventricular hyperintensities) and de Groot (DWMH).ResultsThe LF/HF showed significant negative correlations with the total and regional periventricular hyperintensities, as well as DWMH. Multiple regression analysis showed that the negative associations remained significant between the LF/HF and DWMH (total, temporal, occipital). Furthermore, fall risk index significantly correlated with the LF/HF, total and the occipital DWMH.ConclusionsThe severity of the DWMH was associated with the LF/HF and the fall risk, one of the important geriatric syndromes, suggesting that WMH, sympathetic nervous dysfunction and geriatric syndrome are interrelated to each other. Geriatr Gerontol Int 2018; 18: 569–575.
Effects of wilting and lactic acid bacteria inoculation on fermentation and microbial community of elephant grass silage produced in Vietnam
Authors: Tran Thi Minh Tu , Nguyen Mui Thi , Nguyen Huu Van , Nishino Naoki 
Published: November 2017

AbstractDirect‐cut (dry matter [DM] 165 g kg−1) and wilted (DM250 g kg−1) elephant grass silages were prepared in Hue, Vietnam, with and without a mixture ofLactobacillus paracaseiandLactococcus lactis(LP+LC) orLactobacillus buchneri(LB). The silages were stored for 4 months, and fermentation products and aerobic stability were determined. The microbial community was assessed using denaturing gradient gel electrophoresis and quantitative polymerase chain reaction. Acetate was predominantly produced during the fermentation of control andLB‐inoculated silages, whereas the content was not sufficient to inhibit aerobic spoilage for 7 days in control silage. TheLP+LCinoculation greatly enhanced lactate content, suppressed the alcohol content, and did not improve aerobic stability or decrease the total fungal population. The bacterial community andL. buchneripopulations were similar between control andLB‐inoculated silages; however,Kluyveromyces delphensiswas undetectable and the total fungal population was lowered inLB‐inoculated silage.
Effects of exogenous 5‐aminolevulinic acid on seed germination of alfalfa (Medicago varia Martyn.) under drought stress
Authors: Han Ruihong , Gao Guijuan , Li Zhidan , Dong Zhaoxia , Guo Zhenfei 
Published: November 2017

AbstractMedicago varia is a very important legume forage with a high yield and good nutrient quality. It is widely cultivated in the middle‐eastern regions of China. However, drought is one of the major abiotic stresses that reduce Medicago varia growth and production. 5‐aminolevulinic acid (5‐ALA) is a physiologically active substance in plants with the potential to improve agricultural production. Exogenous application of 5‐ALA is able to increase plant resistance to multiple abiotic stresses. In this study, the effects of different concentrations of 5‐ALA (0, 5, 10, 20, 30 mg L−1) on seed germination and seedling growth of Medicago varia under drought stress was investigated. The results showed that seed germination was reduced significantly under drought stress. However, exogenous 5‐ALA significantly increased the final germination percentage (FGP) and reduced mean germination time (MGT), indicating that 5‐ALA promoted seed germination of Medicago varia under drought stress. In addition, the rate of cotyledon protruding seed coat, seedlings biomass, radicle length, chlorophyll content of cotyledon, aperture width of stomata and pore area of stomata were increased significantly and stomatal density of cotyledon was reduced significantly by 5‐ALA under drought stress. Collectively, our data suggest that 5‐ALA can be applied to promote seed germination of M. varia under drought stress.
HOW IMPORTANT ARE TERMS‐OF‐TRADE SHOCKS?
Authors: Schmitt‐Grohé Stephanie , Uribe Martín 
Published: November 2017

AbstractAccording to conventional wisdom, terms‐of‐trade shocks represent a major source of business cycles in emerging and poor countries. This view is largely based on the analysis of calibrated business‐cycle models. We argue that the view that emerges from empirical structural vector autoregression (SVAR) models is strikingly different. We estimate country‐specific SVARs using data from 38 countries and find that terms‐of‐trade shocks explain less than 10% of movements in aggregate activity. We then estimate key structural parameters of a three‐sector business‐cycle model country by country and find a disconnect between the importance assigned to terms‐of‐trade shocks by theoretical and SVAR models.
Rise of the zombie institution, the failure of mental health nursing leadership, and mental health nursing as a zombie category
Authors: Lakeman Richard , Molloy Luke 
Published: November 2017

AbstractIn this paper, we propose that mental health nursing has become a zombie category, at least in the Australian context. Mental health nursing is a concept that has lost any real explanatory or conceptual power, yet nevertheless persists in public discourse and the collective imagination. In recent decades, powerful forces have contributed to the zombification of the mental health nursing workforce and the academy. An increase in medical hegemony, the ascendancy of allied health in mental health service provision, the need for uncritical and servile workers, protocol‐driven work practices, and a failure of leadership to mobilize any substantial resistance to these trends have enabled the infection to spread. The recognition of zombification, active resistance against the forces that conspire to cause it, and the cultivation of genuine conscientious critical thought and debate offer the only hope of survival of mental health nursing as a thriving specialty.
“It's good, they're like me; the same but different.” An interpretative phenomenological analysis of the identities of women with down's syndrome
Authors: Groves Emma , Rayner Kelly , Muncer Steven 
Published: November 2017

BackgroundFor people with disabilities, identity formation is based on responses to hierarchical values determined by able populations. Some adopt a disability identity, whereas others may seek to conceal their disability. No research has focused on how women with Down's Syndrome form an identity.DesignEight women with Down's Syndrome took part in semi‐structured interviews designed to find out more about their individual and shared identities. The transcripts were analysed using interpretive phenomenological analysis.FindingsNegative assumptions of others and oppressive, paternalistic care often lead to a lack of ownership over narratives. “Finding a place in society” is an attempt to challenge this and gain a sense of ownership over their lives.ConclusionsThis research uncovered the individual and shared identities that women with Down's Syndrome construct. Services need to be aware of the role they have in supporting these women to develop autonomy and ownership over their lives.
Expression of CPPED1 in human trophoblasts is associated with timing of term birth
Authors: Haapalainen Antti M. , Karjalainen Minna K. , Daddali Ravindra , Ohlmeier Steffen , Anttonen Julia , Määttä Tomi A. , Salminen Annamari , Mahlman Mari , Bergmann Ulrich , Mäkikallio Kaarin , Ojaniemi Marja , Hallman Mikko , Rämet Mika 
Published: November 2017

AbstractUnderstanding of timing of human parturition is incomplete. Therefore, we carried out proteomic analyses of full‐term placentas from uncomplicated pregnancies to identify protein signatures associated with the onset of spontaneous delivery. We found quantitative associations of 10 proteins with spontaneous term birth, evident either in the basal or in the chorionic plates or in both. Additional 18 proteins were associated according to the location within placenta indicating local variations in protein amounts. Calcineurin‐like phosphoesterase domain‐containing 1 (CPPED1), a phosphatase previously suggested dephosphorylating AKT1/PKB, was one of the identified proteins. qRT‐PCR revealed the mRNA level of CPPED1 was higher in elective caesarean deliveries than in spontaneous births, while immunohistochemistry showed CPPED1 in cytotrophoblasts, syncytiotrophoblasts and extravillous trophoblasts. Noteworthy, phosphorylation status of AKT1 did not differ between placentas from elective caesarean and spontaneous deliveries. Additionally, analyses of samples from infants indicated that single‐nucleotide polymorphisms rs11643593 and rs8048866 of CPPED1 were associated with duration of term pregnancy. Finally, post‐transcriptional silencing of CPPED1 in cultured HTR8/SVneo cells by siRNAs affected gene expression in pathways associated with inflammation and blood vessel development. We postulate that functions regulated by CPPED1 in trophoblasts at choriodecidual interphase have a role in the induction of term labour, but it may be independent of AKT1.
The 3p14.2 tumour suppressor ADAMTS9 is inactivated by promoter CpG methylation and inhibits tumour cell growth in breast cancer
Authors: Shao Bianfei , Feng Yixiao , Zhang Hongbin , Yu Fang , Li Qianqian , Tan Cui , Xu Hongying , Ying Jianming , Li Lili , Yang Dejuan , Peng Weiyan , Tang Jun , Li Shuman , Ren Guosheng , Tao Qian , Xiang Tingxiu 
Published: November 2017

AbstractChromosome region 3p12‐14 is an important tumour suppressor gene (TSG) locus for multiple cancers. ADAMTS9, a member of the metalloprotease large family, has been identified as a candidate 3p14.2 TSG inactivated by aberrant promoter CpG methylation in several carcinomas, but little known about its expression and function in breast cancer. In this report, ADAMTS9 expression and methylation was analysed in breast cancer cell lines and tissue samples. ADAMTS9 RNA was significantly down‐regulated in breast cancer cell lines (6/8). After treating the cells with demethylation agent Aza and TSA, ADAMTS9 expression was dramatically increased. Bisulphite genomic sequencing and methylation‐specific PCR detected promoter methylation, which was associated with decreased ADAMTS9 expression. Hypermethylation was also detected in 130/219 (59.4%) of primary tumours but only in 4.5% (2/44) of paired surgical margin tissues. Ectopic expression of ADAMTS9 in tumor cells induced significant growth suppression, cell cycle arrest at the G0/G1 phase, enhanced apoptosis and reduced cell migration and invasion. Conditioned culture medium from ADAMTS9‐transfected BT549 cells markedly disrupted tube formation ability of human umbilical vein endothelial cell (HUVEC) in Matrigel. Furthermore, ADAMTS9 inhibited AKT signaling and its downstream targets (MDM2, p53, p21, p27, E‐cadherin, VIM, SNAIL, VEGFA, NFκB‐p65 and MMP2). In addition, we demonstrated, for the first time, that ADAMTS9 inhibits AKT signaling, through suppressing its upstream activators EGFR and TGFβ1/TβR(I/II) in breast cancer cells. Our results suggest that ADAMTS9 is a TSG epigenetically inactivated in breast cancer, which functions through blocking EGFR‐ and TGFβ1/TβR(I/II)‐activated AKT signaling.
The long non‐coding RNA PVT1 represses ANGPTL4 transcription through binding with EZH2 in trophoblast cell
Authors: Xu Yetao , Lian Yifan , Zhang Yuanyuan , Huang Shiyun , Zuo Qing , Yang Nana , Chen Yanzi , Wu Dan , Sun Lizhou 
Published: November 2017

AbstractDespite progress in diagnostics and treatment for preeclampsia, it remains the foremost cause of maternal and foetal perinatal morbidity and mortality worldwide. Over recent years, various lines of evidence have emphasized long non‐coding RNAs (lncRNAs) which function as an innovative regulator of biological behaviour, as exemplified by proliferation, apoptosis and metastasis. However, the role of lncRNAs has not been well described in preeclampsia. Here, we identified a lncRNA, PVT1, whose expression was down‐regulated in qRT‐PCR analyses in severe preeclampsia. The effects of PVT1 on development were studied after suppression and overexpression of PVT1 in HTR‐8/SVneo and JEG3 cells. PVT1 knockdown notably inhibited cell proliferation and stimulated cell cycle accumulation and apoptosis. Exogenous PVT1 significantly increased cell proliferation. Based on analysis of RNAseq data, we found that PVT1 could affect the expression of numerous genes, and then investigated the function and regulatory mechanism of PVT1 in trophoblast cells. Further mechanistic analyses implied that the action of PVT1 is moderately attributable to its repression of ANGPTL4 via association with the epigenetic repressor Ezh2. Altogether, our study suggests that PVT1 could play an essential role in preeclampsia progression and probably acts as a latent therapeutic marker; thus, it might be a useful prognostic marker when evaluating new therapies for patients with preeclampsia.
IL‐35 recombinant protein reverses inflammatory bowel disease and psoriasis through regulation of inflammatory cytokines and immune cells
Authors: Wang Yuan , Mao Ying , Zhang Junfeng , Shi Gang , Cheng Lin , Lin Yi , Li Yiming , Zhang Xiaomei , Zhang Yujing , Chen Xiaolei , Deng Jie , Su Xiaolan , Dai Lei , Yang Yang , Zhang Shuang , Yu Dechao , Wei Yuquan , Deng Hongxin 
Published: November 2017

AbstractInterleukin‐35 (IL‐35), a member of the IL‐12 family, functions as a new anti‐inflammatory factor involved in arthritis, psoriasis, inflammatory bowel disease (IBD) and other immune diseases. Although IL‐35 can significantly prevent the development of inflammation in many diseases, there have been no early studies accounting for the role of IL‐35 recombinant protein in IBD and psoriasis. In this study, we assessed the therapeutic potential of IL‐35 recombinant protein in three well‐known mouse models: the dextransulfate sodium (DSS)‐induced colitis mouse model, the keratin14 (K14)‐vascular endothelial growth factor A (VEGF‐A)‐transgenic (Tg) psoriasis mouse model and the imiquimod (IMQ)‐induced psoriasis mouse model. Our results indicated that IL‐35 recombinant protein can slow down the pathologic process in DSS‐induced acute colitis mouse model by decreasing the infiltrations of macrophages, CD4+T and CD8+T cells and by promoting the infiltration of Treg cells. Further analysis demonstrated that IL‐35 recombinant protein may regulate inflammation through promoting the secretion of IL‐10 and inhibiting the expression of pro‐inflammatory cytokines such as IL‐6, TNF‐α and IL‐17 in acute colitis model. In addition, lower dose of IL‐35 recombinant protein could achieve long‐term treatment effects as TNF‐α monoclonal antibody did in the psoriasis mouse. In summary, the remarkable therapeutic effects of IL‐35 recombinant protein in acute colitis and psoriasis mouse models indicated that IL‐35 recombinant protein had a variety of anti‐inflammatory effects and was expected to become an effective candidate drug for the treatment of inflammatory diseases.
Identification of a novel RPGRIP1 mutation in an Iranian family with leber congenital amaurosis by exome sequencing
Authors: Imani Saber , Cheng Jingliang , Mobasher‐Jannat Abdolkarim , Wei Chunli , Fu Shangyi , Yang Lisha , Jadidi Khosrow , Khosravi Mohammad Hossein , Mohazzab‐Torabi Saman , Shasaltaneh Marzieh Dehghan , Li Yumei , Chen Rui , Fu Junjiang 
Published: November 2017

AbstractLeber congenital amaurosis (LCA) is a heterogeneous, early‐onset inherited retinal dystrophy, which is associated with severe visual impairment. We aimed to determine the disease‐causing variants in Iranian LCA and evaluate the clinical implications. Clinically, a possible LCA disease was found through diagnostic imaging, such as fundus photography, autofluorescence and optical coherence tomography. All affected patients showed typical eye symptoms associated with LCA including narrow arterioles, blindness, pigmentary changes and nystagmus. Target exome sequencing was performed to analyse the proband DNA. A homozygous novel c. 2889delT (p.P963 fs) mutation in the RPGRIP1 gene was identified, which was likely the deleterious and pathogenic mutation in the proband. Structurally, this mutation lost a retinitis pigmentosa GTPase regulator (RPGR)‐interacting domain at the C‐terminus which most likely impaired stability in the RPGRIP1 with the distribution of polarised proteins in the cilium connecting process. Sanger sequencing showed complete co‐segregation in this pedigree. This study provides compelling evidence that the c. 2889delT (p.P963 fs) mutation in the RPGRIP1 gene works as a pathogenic mutation that contributes to the progression of LCA.
Empagliflozin decreases remnant‐like particle cholesterol in type 2 diabetes patients with insulin resistance
Authors: Hattori Sachiko 
Published: November 2017

AbstractAims/IntroductionRemnant lipoproteins are thought to be atherogenic. Remnant‐like particle cholesterol (RLP‐C), which reflects the levels of various kinds of remnant lipoproteins in the blood, has a significant correlation with insulin resistance.Materials and MethodsIn the present study, we measured the effect of empagliflozin (EMPA) on the levels of RLP‐C, and investigated whether EMPA‐mediated change in RLP‐C is associated with a change in insulin resistance in type 2 diabetes patients who have insulin resistance.ResultsPatients were allocated to receive a placebo (n = 51) or EMPA (n = 58) as an add‐on treatment. Fasting blood samples were collected before and 12 weeks after this intervention. EMPA significantly decreased glycated hemoglobin, bodyweight, systolic blood pressure, plasma triglycerides, liver transaminases and estimated glomerular filtration rate, and increased high‐density lipoprotein cholesterol. Furthermore, EMPA decreased RLP‐C and homeostatic model assessment of insulin resistance. In the placebo group, there were no significant changes in these factors except for slight increases in liver transaminases. Multiple regression analysis showed that the change in homeostatic model assessment of insulin resistance (P = 0.0102) and the change in alanine aminotransferase (P = 0.0301) were significantly associated with the change in RLP‐C in the EMPA group. The change in RLP‐C significantly correlated with the change in homeostatic model assessment of insulin resistance (Pearson correlation coefficient 0.503, 95% confidence interval 0.199–0.719; P = 0.00241).ConclusionEMPA decreases RLP‐C levels, which is closely associated with amelioration of insulin sensitivity in diabetes patients who have insulin resistance.
In vitro and in vivo characterization of the antibacterial activity and membrane damage mechanism of quinic acid against Staphylococcus aureus
Authors: Bai Jinrong , Wu Yanping , Wang Xiaoyan , Liu Xiaoyan , Zhong Kai , Huang Yina , Chen Yiting , Gao Hong 
Published: November 2017

AbstractIn this study, we investigated the antibacterial activity of quinic acid (QA) and elucidated its membrane action mechanism against Staphylococcus aureus. In vitro antibacterial assay showed that QA effectively inhibited the growth of test bacteria. In model food systems of cabbage suspension and barley soup, QA possessed a great antibacterial capacity. The membrane hyperpolarization and a decrease of membrane fluidity demonstrated a significant effect of QA on damaging the normal functions of cell membrane, which was further validated by the observation of the transmission electron microscope. The interaction of QA with Phe residues in the membrane protein was revealed by fluorescence quenching. Overall, the present study illustrates QA as a potent antibacterial agent and its inhibition action on S. aureus by damaging the cell membrane.Practical applicationsIn model food systems of cabbage suspension and barley soup, QA possessed a great antibacterial capacity to control the total counts of viable bacteria. This study provided the theoretical foundations for the application of QA in foods to prevent the growth of foodborne pathogens.
Enteroendocrine and adipokine associations with type 2 diabetes: Phenotypic risk scoring approaches
Authors: Cox Amanda J , Zhang Ping , Bowden Donald W , Devereaux Benedict , Davoren Peter M , Cripps Allan W , West Nicholas P 
Published: November 2017

AbstractBackground and AimThe contribution of gut‐derived factors to the mechanisms linking obesity and metabolic disease remains under‐investigated. The aim of the current study was to examine the associations between glucagon and enteroendocrine signaling and type 2 diabetes (T2D) using a derived risk score approach. To compare the relative importance of the enteroendocrine system, associations between adipokine measures and T2D were also investigated.MethodsA total of 130 individuals with T2D and 161 individuals without T2D were included in the study. Circulating concentrations of enteroendocrine (glucagon, ghrelin, glucagon‐like peptide‐1, and gastric inhibitory peptide) and adipokine mediators (adiponectin, leptin, resistin, visfatin, and adipsin) were measured. Standard scores (Z‐scores) were determined for each measure and enteroendocrine risk scores (ERS) and adipokine risk scores (ARS) calculated based on summation of the component measures. Associations between both the ERS and ARS and T2D status were assessed using logistic regression models.ResultsThe ERS was significantly associated with T2D status in an adjusted model (odds ratio: 1.36; 95% confidence interval [CI]: 1.08–1.72; P = 0.009). Associations between the ARS and T2D status were not independent of age, sex, and body mass index (odds ratio: 1.21; 95%CI: 0.99–1.47; P = 0.06). Quantification of risk across ERS tertiles revealed that individuals with an ERS in the upper tertile were 10 times more likely (CI: 3.23–32.73; P < 0.001) to have T2D.ConclusionsThese data support an association between enteroendocrine signaling and T2D. Use of the ERS as a potential tool for classifying individuals with metabolic syndrome as high or low risk for T2D development is being considered.