bluuebunny/crossref_metadata_2025_split huggingface dataset:
Testicular cancer: a 13‐year retrospective review of ethnic disparities in the Waikato region, New Zealand
Authors: Hari Dass Prashanth , B. Jameson Michael 
Published: November 2019

AbstractBackgroundThe testicular cancer incidence in New Zealand is rising. We evaluated if testicular cancer outcomes differed by ethnicity in NZ.AimsTo study if ethnic disparities existed among testicular cancer patients and their outcomes treated at Waikato Regional Cancer Centre.MethodsRetrospective review of testicular cancer cases in the Medical Oncology database, Waikato Hospital, between 2001 and 2013 inclusive.ResultsThree hundred and twenty‐five patients were seen, with median follow up of survivors being 101 (range 13–230) months. 95 (29.2%) were Māori, 210 (64.6%) NZ European and 20 (6.1%) of other ethnicity. One hundred and eighty‐two patients were diagnosed with seminoma and 143 with non‐seminoma. Māori represented 27.5% of seminoma and 31.4% of non‐seminoma patients. Median age at diagnosis was 39 years for seminoma and 30 years for non‐seminoma; Māori were significantly younger than non‐ Māori for both seminoma (median age 35 versus 42 years) and non‐seminoma (median age 28 vs 34 years, respectively). While stage distribution of seminoma at diagnosis was similar for Māori and non‐Māori (chi‐squared P = 0.31), significantly more Māori had higher‐stage non‐seminoma than non‐Māori (stage III in 44% and 22%, respectively, chi‐squared P = 0.014). Survival for seminoma (logrank P = 0.19) and non‐seminoma (logrank P = 0.89) patients did not differ significantly by ethnicity.ConclusionsMāori patients were younger at diagnosis of testicular cancer and presented with more advanced non‐seminoma testicular tumours compared with non‐Māori but survival was comparable.
Quality of care in inflammatory bowel disease: actual health service experiences fall short of the standards
Authors: Mikocka‐Walus Antonina , Massuger Wayne , Knowles Simon R. , Moore Gregory T. , Buckton Stephanie , Connell William , Pavli Paul , Raven Leanne , Andrews Jane M. 
Published: November 2019

AbstractBackgroundQuality of care in inflammatory bowel disease (IBD) has received much attention internationally; however, the available surveys focus on health professionals rather than patients.AimsTo assess the experiences of healthcare for people living with IBD against established Australian IBD Standards.MethodsAn online cross‐sectional survey was conducted with Australians ≥16 years old recruited via Crohn's & Colitis Australia membership, public and private clinics and the Royal Flying Doctor Service. Participants completed a questionnaire incorporating items addressing the Australian IBD Standards 2016, the Picker Patient Experience Questionnaire, IBD Control Survey and the Manitoba Index.ResultsComplete data were provided by 731 respondents (71.5% female, median age 46 years, ranging from 16 to 84 years). While the majority (74.8%) were satisfied with their IBD healthcare, the care reported did not meet the Australian IBD Standards. Overall, 32.4% had access to IBD nurses, 30.9% to a dietician and 12% to a psychologist in their treating team. Participants managed by public IBD clinics were most likely to have access to an IBD nurse (83.7%), helpline (80.7%) and research trials (37%). One third of respondents reported waiting >14 days to see a specialist when their IBD flared. Participants received enough information, mostly from medical specialists (88.8%) and IBD nurses (79.4%). However, 51% wanted to be more involved in their healthcare.ConclusionsThese data show discordance between expectations of patients and national standards with current levels of service provision, which fail to deliver equitable and comprehensive IBD care.
Sub‐acute hyponatraemia more than chronic hyponatraemia is associated with serious falls and hip fractures
Authors: Bhandari Simran K. , Adams Annette L. , Li Bonnie H. , Rhee Connie M. , Sundar Shirin , Krasa Holly , Danforth Kim N. , Kanter Michael H. , Kalantar‐Zadeh Kamyar , Jacobsen Steven J. , Sim John J. 
Published: November 2019

AbstractBackgroundFalls and hip fractures among older people are associated with high morbidity and mortality. Hyponatraemia may be a risk for falls/hip fractures, but the effect of hyponatraemia duration is not well understood.AimsTo evaluate individuals with periods of sub‐acute and chronic hyponatraemia on subsequent risk for serious falls and/or hip fractures.MethodsRetrospective cohort study in the period 1 January 1998 to 14 June 2016 within an integrated health system of individuals aged ≥55 years with ≥2 outpatient serum sodium measurements. Hyponatraemia was defined as sodium <135 mEq/L with sub‐acute (<30 days) and chronic (≥30 days) analysed as a time‐dependent exposure. Multivariable Cox proportional‐hazards modelling was used to estimate hazard ratios (HR) for serious falls/hip fractures based on sodium category.ResultsAmong 1 062 647 individuals totalling 9 762 305 sodium measurements, 96 096 serious falls/hip fracture events occurred. Incidence (per‐1000‐person‐years) of serious falls/hip fractures were 11.5, 27.9 and 19.8 for normonatraemia, sub‐acute and chronic hyponatraemia. Any hyponatraemia duration compared to normonatraemia had a serious falls/hip fractures HR (95%CI) of 1.18 (1.15, 1.22), with sub‐acute and chronic hyponatraemia having HR of 1.38 (1.33, 1.42) and 0.91 (0.87, 0.95), respectively. Examined separately, the serious falls HR was 1.37 (1.32, 1.42) and 0.92 (0.88, 0.96) in sub‐acute and chronic hyponatraemia, respectively. Hip fracture HR were 1.52 (1.42, 1.62) and 1.00 (0.92, 1.08) for sub‐acute and chronic hyponatraemia, respectively, compared to normonatraemia.ConclusionsOur findings suggest that early/sub‐acute hyponatraemia appears more vulnerable and associated with serious falls/hip fractures. Whether hyponatraemia is a marker of frailty or a modifiable risk factor for falls remains to be determined.
Characteristics of H7N9 avian influenza pneumonia: a retrospective analysis of 17 cases
Authors: Yu Wen‐Qing , Ji Ning‐Fei , Ding Ming‐Dong , Gu Cheng‐Jing , Ma Yuan , Wu Zhen‐Zhen , Wang Yan‐Li , Wu Chao‐Jie , Dai Gui‐Hong , Chen Yan , Jin Rong‐Rong , Tan Yi‐Bin , Yang Zhu , Zhou Da‐Ming , Xian Jian‐Chun , Xu Hong‐Tao , Huang Mao 
Published: November 2019

AbstractBackgroundH7N9 avian influenza is an infection of public health concern, in part because of its high mortality rate and pandemic potential.AimsTo describe the clinical features of H7N9 avian influenza and the response to treatment.MethodsClinical, radiological and histopathological data, and treatment‐related of H7N9‐infected patients hospitalised during 2014–2017 were extracted and analysed.ResultsA total of 17 H7N9 patients (three females; mean age, 58.4 ± 13.7 years) was identified; of these six died. All patients presented with fever and productive cough; four patients had haemoptysis and 13 had chest distress and/or shortness of breath. Early subnormal white blood cell count and elevation of serum liver enzymes were common. Multilobar patchy shadows, rapid progression to ground‐glass opacities, air bronchograms and consolidation were the most common imaging findings. Histopathological examination of lung tissue of three patients who died showed severe alveolar epithelial cell damage, with inflammatory exudation into the alveolar space and hyaline membrane formation; widened alveolar septae, prominent inflammatory cell infiltration; and hyperplasia of pneumocytes. Viral inclusions were found in the lung tissue of two patients. All patients received antiviral drugs (oseltamivir ± peramivir). Four patients carried the rs12252‐C/C interferon‐induced transmembrane protein‐3 (IFITM3) genotype, while the others had the C/T genotype.ConclusionsH7N9 virus infection causes human influenza‐like symptoms, but may rapidly progress to severe pneumonia and even death. Clinicians should be alert to the possibility of H7N9 infection in high‐risk patients. The presence of the IFITM3 rs12252‐C genotype may predict severe illness.
Long noncoding RNA TUG1 contributes to cerebral ischaemia/reperfusion injury by sponging mir‐145 to up‐regulate AQP4 expression
Authors: Shan Weifeng , Chen Wei , Zhao Xian , Pei Aijie , Chen Manli , Yu Yang , Zheng Yueying , Zhu Shengmei 
Published: November 2019

AbstractEmerging studies have shown that long noncoding RNA (lncRNA) TUG1 (taurine‐up‐regulated gene 1) plays critical roles in multiple biological processes. However, the expression and function of lncRNA TUG1 in cerebral ischaemia/reperfusion injury have not been reported yet. In this study, we found that LncRNA TUG1 expression was significantly up‐regulated in cultured MA‐C cells exposed to OGD/R injury, while similar results were also observed in MCAO model. Mechanistically, knockdown of TUG1 decreased lactate dehydrogenase levels and the ratio of apoptotic cells and promoted cell survival in vitro. Moreover, knockdown of TUG1 decreased AQP4 (encoding aquaporin 4) expression to attenuate OGD/R injury. TUG1 could interact directly with miR‐145, and down‐regulation of miR‐145 could efficiently reverse the function of TUG1 siRNA on AQP4 expression. Finally, the TUG1 shRNA reduced the infarction area and cell apoptosis in I/R mouse brains in vivo. In summary, our results suggested that lncRNA TUG1 may function as a competing endogenous RNA (ceRNA) for miR‐145 to induce cell damage, possibly providing a new therapeutic target in cerebral ischaemia/reperfusion injury.
Deficiency of Macf1 in osterix expressing cells decreases bone formation by Bmp2/Smad/Runx2 pathway
Authors: Qiu Wu‐Xia , Ma Xiao‐Li , Lin Xiao , Zhao Fan , Li Di‐Jie , Chen Zhi‐Hao , Zhang Ke‐Wen , Zhang Ru , Wang Pai , Xiao Yun‐Yun , Miao Zhi‐Ping , Dang Kai , Wu Xiao‐Yang , Qian Ai‐Rong 
Published: November 2019

AbstractMicrotubule actin cross‐linking factor 1 (Macf1) is a spectraplakin family member known to regulate cytoskeletal dynamics, cell migration, neuronal growth and cell signal transduction. We previously demonstrated that knockdown of Macf1 inhibited the differentiation of MC3T3‐E1 cell line. However, whether Macf1 could regulate bone formation in vivo is unclear. To study the function and mechanism of Macf1 in bone formation and osteogenic differentiation, we established osteoblast‐specific Osterix (Osx) promoter‐driven Macf1 conditional knockout mice (Macf1f/fOsx‐Cre). The Macf1f/fOsx‐Cre mice displayed delayed ossification and decreased bone mass. Morphological and mechanical studies showed deteriorated trabecular microarchitecture and impaired biomechanical strength of femur in Macf1f/fOsx‐Cre mice. In addition, the differentiation of primary osteoblasts isolated from calvaria was inhibited in Macf1f/fOsx‐Cre mice. Deficiency of Macf1 in primary osteoblasts inhibited the expression of osteogenic marker genes (Col1, Runx2 and Alp) and the number of mineralized nodules. Furthermore, deficiency of Macf1 attenuated Bmp2/Smad/Runx2 signalling in primary osteoblasts of Macf1f/fOsx‐Cre mice. Together, these results indicated that Macf1 plays a significant role in bone formation and osteoblast differentiation by regulating Bmp2/Smad/Runx2 pathway, suggesting that Macf1 might be a therapeutic target for bone disease.
Insights into the pathogenesis of ATP1A1‐related CMT disease using patient‐specific iPSCs
Authors: Manganelli Fiore , Parisi Silvia , Nolano Maria , Miceli Francesco , Tozza Stefano , Pisciotta Chiara , Iodice Rosa , Provitera Vincenzo , Cicatiello Rita , Zuchner Stephan , Taglialatela Maurizio , Russo Tommaso , Santoro Lucio 
Published: November 2019

AbstractThe development of patient‐specific induced pluripotent stem cells (iPSCs) offered interesting insights in modeling the pathogenesis of Charcot‐Marie‐Tooth (CMT) disease and thus we decided to explore the phenotypes of iPSCs derived from a single CMT patient carrying a mutant ATP1A1 allele (p.Pro600Ala). iPSCs clones generated from CMT and control fibroblasts, were induced to differentiate into neural precursors and then into post‐mitotic neurons. Control iPSCs differentiated into neuronal precursors and then into post‐mitotic neurons within 6‐8 days. On the contrary, the differentiation of CMT iPSCs was clearly defective. Electrophysiological properties confirmed that post‐mitotic neurons were less mature compared to the normal counterpart. The impairment of in vitro differentiation of CMT iPSCs only concerned with the neuronal pathway, because they were able to differentiate into mesendodermal cells and other ectodermal derivatives. ATP1A1 was undetectable in the few neuronal cells derived from CMT iPSCs. ATP1A1 gene mutation (p.Pro600Ala), responsible for a form of axonal CMT disease, is associated in vitro with a dramatic alteration of the differentiation of patient‐derived iPSCs into post‐mitotic neurons. Thus, the defect in neuronal cell development might lead in vivo to a decreased number of mature neurons in ATP1A1‐CMT disease.
Protective effects of L‐arginine on the intestinal epithelial barrier under heat stress conditions in rats and IEC‐6 cell line
Authors: Huang Liqing , Yin Peng , Liu Fenghua , Liu Yilin , Liu Yanhan , Xia Zhaofei 
Published: November 2019

AbstractHeat stress (HS) and the associated restricted blood flow to the intestine have been proven to destroy intestinal integrity. Considering the beneficial properties of L‐arginine on gut function, we investigated the protective effects of L‐arginine on the intestine under HS conditions. In vivo, the serum cortisol level and the rectal temperature increased in response to HS. Under HS, the intestinal damage showed obvious morphological changes. Furthermore, HS decreased the mRNA and protein expression levels of Nurr1, ZO‐1, occludin, claudin‐6 and E‐cadherin, increased the mRNA expression of NF‐κB and IL‐1β, and increased the protein expression of cleaved caspase‐3. In contrast, L‐arginine supplementation maintained intestinal integrity and increased the villus/crypt ratio. L‐arginine also suppressed the expression of inflammation‐related genes and the protein expression of cleaved caspase‐3, whereas it upregulated the mRNA and protein expression of tight junction proteins and LC3B protein expression. In vitro, L‐arginine attenuated HS‐induced apoptosis as demonstrated by flow cytometry and decreased cleaved caspase‐3 protein expression. L‐arginine induced autophagy, which was demonstrated by decreased expression of p62 and p‐mTOR/mTOR, and increased expression of LC3B. The protein expression levels of TJ proteins also enhanced by L‐arginine in IEC‐6 cells. Taken together, these results suggest that L‐arginine can alleviate intestinal damage and protect the intestinal integrity by suppressing local inflammation response, promoting the production of TJs and facilitating autophagy under HS conditions.
Asymmetric patterns of global diversity among plants and mycorrhizal fungi
Authors: Toussaint Aurele , Bueno Guillermo , Davison John , Moora Mari , Tedersoo Leho , Zobel Martin , Öpik Maarja , Pärtel Meelis 
Published: November 2019

AbstractQuestionsAlthough the roles of mycorrhizal fungi in different vegetation types are widely acknowledged, it is still largely unknown how the diversity and frequency of different symbiotic partners vary among plant assemblages globally. We asked (1) how the global distribution of vascular plants correlates with the diversity (i.e. number of species) and frequency (i.e. relative abundance) of different plant mycorrhizal types (i.e. arbuscular mycorrhizal [AM], ectomycorrhizal [ECM], ericoid mycorrhizal [ERM], orchid mycorrhizal [ORM] and non‐mycorrhizal [NM]); and (2) how the diversities of the most dominant plant mycorrhizal types (AM and ECM) correlate with those of their respective mycorrhizal fungal partners.LocationWorldwide.MethodsWe retrieved all vascular plant occurrences available in the Global Biodiversity Information Facility database from sites worldwide where AM and ECM fungal diversity has been examined. Plant mycorrhizal types were assigned to plant species using expert‐based imputation. Diversity and frequency indices were calculated using extrapolation and bootstrapping procedures in order to account for the heterogeneity and uncertainty of the datasets.ResultsEach plant mycorrhizal type correlated differently with the global diversity pattern of vascular plants, with higher total plant diversity in AM‐dominated vegetation, compared with vegetation containing a larger share of ECM, ERM or NM plant species. The diversities of AM and ECM fungi were positively correlated with the frequency, but not diversity, of their respective plant mycorrhizal types; and weakly correlated with the frequency and diversity of other plant mycorrhizal types.ConclusionsAt the global scale, vascular plant distribution correlates, among other factors, with the frequency, and to a lesser extent diversity, of different mycorrhizal types of plants and fungi. Recognizing these relationships may help to predict changes in the frequency of ECM and AM plant mycorrhizal types under the different ongoing global changes.
The nation against the State: The Irish question and Britain‐based anarchists in the Age of Empire
Authors: Gutiérrez José Antonio , Ferretti Federico 
Published: November 2019

AbstractThis paper discusses the relationship between early anarchism and republican/nationalist ideas. We will focus on the case of British‐based activists grouped around the journal Freedom and their engagement with Irish nationalism during the Age of the Empire. Freedom, founded in 1886, was the most important anarchist journal of the English‐speaking anarchist–communist networks at the time and was the main editorial reference for the worldwide community of anarchist activists, mostly exiled, who resided in London at that time. Extending current interdisciplinary literature on transnational anarchism, we argue that anarchist views of nations, while rejecting the novel notion of the nation‐state, were associated with anti‐colonial struggles and with republican anti‐monarchical and egalitarian notions. Based on primary sources, we discuss the intersections between these Britain‐based anarchists and anti‐colonial Irish radicals, by engaging both with their writings and their international networks of solidarity, thus exploring the complex intermingling of anarchism, anti‐colonialism, and republicanism.
Proteomics of human glomerulonephritis by laser microdissection and liquid chromatography‐tandem mass spectrometry
Authors: Kawata Naoto , Kang Dedong , Aiuchi Toshihiro , Obama Takashi , Yoshitake Osamu , Shibata Takanori , Takimoto Masafumi , Itabe Hiroyuki , Honda Kazuho 
Published: November 2019

AbstractAimLaser microdissection (LMD) and liquid chromatography‐tandem mass spectrometry (LC‐MS/MS) enable clinicians to analyse proteins from tissue sections. In nephrology, these methods are used to diagnose diseases of abnormal protein deposition, such as amyloidosis, but they are seldom applied to the diagnosis and pathophysiological understanding of human glomerular diseases.MethodsRenal biopsy specimens were obtained from five patients with IgA nephropathy (IgAN), five patients with membranous nephropathy (MN) and five kidney transplant donors (as controls). From 10‐μm‐thick sections of formalin‐fixed, paraffin‐embedded specimens, 0.3‐mm2 samples of glomerular tissue were subjected to LMD. The samples were analysed by LC‐MS/MS and investigated clinically and histologically.ResultsFrom the control glomeruli, we identified more than 300 types of proteins. In patients with IgAN, we detected significant increases not only in IgA1 and in C3, but also in the factors related to oxidative stress and cell proliferation in comparison to the controls. In patients with MN, levels of IgG1, IgG4, C3, C4a and phospholipase‐A2‐receptor were significantly elevated in comparison to the controls, as were the aforementioned factors related to oxidative stress and cell proliferations detected in IgAN.ConclusionApplication of LMD and LC‐MS/MS to renal biopsy specimens enabled us to identify not only pathognomonic proteins for the diagnosis, but also several factors possibly involved in the pathogenesis of human glomerular diseases.
Identification of the most clinically useful skeletal muscle mass indices pertinent to sarcopenia and physical performance in chronic kidney disease
Authors: Wilkinson Thomas J. , Nixon Daniel G. D. , Richler‐Potts Danielle , Neale Jill , Song Yan , Smith Alice C. 
Published: November 2019

AbstractAimPatients with chronic kidney disease (CKD) are characterised by low skeletal muscle mass that negatively impacts physical performance. Operational definitions of ‘low muscle mass’ are inconsistent, and it is unknown how different skeletal muscle mass indices affect the relationship between muscle mass and physical function.MethodsAppendicular skeletal muscle mass (ASM) was measured by dual‐energy X‐ray absorptiometry in 72 CKD patients. Along with crude ASM, alternative muscle indices were calculated adjusting for height, height‐squared, body mass, and BMI. Physical performance was assessed by handgrip strength, sit‐to‐stand tests, gait speed, the incremental shuttle walk test and ‘Short Physical Performance Battery’.ResultsPrevalence of ‘low muscle mass’ ranged from 26% to 35% of patients depending on the criteria used. The relationship between muscle mass indices and physical function differed for each criteria. Using average coefficients, the association with overall physical function and muscle indices were as follows: crude ASM (r = .258), ASM/height (r = .249), ASM/height‐squared (r = .332), ASM/body mass (r = .249) and ASM/BMI (r = .206). Muscle adjusted for markers of adiposity (ASM/body fat %, r = .266; ASM/fat mass, r = .338) provided the best overall associations with physical function.ConclusionThe use of alternative muscle mass indices provide different estimates of ‘low muscle mass’ prevalence, and the strongest (and most useful definition in regard to functional status) involves adjustment for either total or relative body fat. ASM adjusted for adiposity may be physiologically and clinically more relevant in patients with renal disease.
The genetics of exapted resistance to two exotic pathogens in pedunculate oak
Authors: Bartholomé Jérôme , Brachi Benjamin , Marçais Benoit , Mougou‐Hamdane Amira , Bodénès Catherine , Plomion Christophe , Robin Cécile , Desprez‐Loustau Marie‐Laure 
Published: November 2019

Summary

Exotic pathogens cause severe damage in natural populations in the absence of coevolutionary dynamics with their hosts. However, some resistance to such pathogens may occur in naive populations. The objective of this study was to investigate the genetics of this so‐called ‘exapted’ resistance to two pathogens of Asian origin (Erysiphe alphitoides and Phytophthora cinnamomi) in European oak.

Host–pathogen compatibility was assessed by recording infection success and pathogen growth in a full‐sib family of Quercus robur under controlled and natural conditions. Two high‐resolution genetic maps anchored on the reference genome were used to study the genetic architecture of resistance and to identify positional candidate genes.

Two genomic regions, each containing six strong and stable quantitative trait loci (QTLs) accounting for 12–19% of the phenotypic variation, were mainly associated with E. alphitoides infection. Candidate genes, especially genes encoding receptor‐like‐kinases and galactinol synthases, were identified in these regions. The three QTLs associated with P. cinnamomi infection did not colocate with QTLs found for E. alphitoides.

These findings provide evidence that exapted resistance to E. alphitoides and P. cinnamomi is present in Q. robur and suggest that the underlying molecular mechanisms involve genes encoding proteins with extracellular signaling functions.