bluuebunny/crossref_metadata_2025_split huggingface dataset:
Change in impulsivity is prospectively associated with treatment outcomes for binge-eating disorder
Authors: Boswell Rebecca G. , Gueorguieva Ralitza , Grilo Carlos M. 
Published: November 2021

AbstractBackgroundImpulsivity may be a process underlying binge-eating disorder (BED) psychopathology and its treatment. This study examined change in impulsivity during cognitive-behavioral therapy (CBT) and/or pharmacological treatment for BED and associations with treatment outcomes.MethodsIn total, 108 patients with BED (NFEMALE = 84) in a randomized placebo-controlled clinical trial evaluating the efficacy of CBT and/or fluoxetine were assessed before treatment, monthly throughout treatment, at post-treatment (16 weeks), and at 12-month follow-up after completing treatment. Patients completed established measures of impulsivity, eating-disorder psychopathology, and depression, and were measured for height and weight [to calculate body mass index (BMI)] during repeated assessments by trained/monitored doctoral research-clinicians. Mixed-effects models using all available data examined changes in impulsivity and the association of rapid and overall changes in impulsivity on treatment outcomes. Exploratory analyses examined whether baseline impulsivity predicted/moderated outcomes.ResultsImpulsivity declined significantly throughout treatment and follow-up across treatment groups. Rapid change in impulsivity and overall change in impulsivity during treatment were significantly associated with reductions in eating-disorder psychopathology, depression scores, and BMI during treatment and at post-treatment. Overall change in impulsivity during treatment was associated with subsequent reductions in depression scores at 12-month follow-up. Baseline impulsivity did not moderate/predict eating-disorder outcomes or BMI but did predict change in depression scores.ConclusionsRapid and overall reductions in impulsivity during treatment were associated with improvements in specific eating-disorder psychopathology and associated general outcomes. These effects were found for both CBT and pharmacological treatment for BED. Change in impulsivity may be an important process prospectively related to treatment outcome.
Financial abuse of older people by third parties in banking institutions: a qualitative exploration
Authors: Phelan Amanda , O'Donnell Deirdre , McCarthy Sandra 
Published: November 2021

AbstractFinancial abuse is a significant form of elder maltreatment and is frequently ranked in the top two most common forms of abuse perpetration. Despite this, it is under-identified, under-reported and under-prosecuted. Financial institutions, such as banks, are important environments for identifying and responding to the financial abuse of older people. Traditionally, banks have not always been part of inter-sectorial responses to financial abuse, yet are important stakeholders. The aim of this study is to explore perceptions and experiences of financial abuse in five national banks. Data were collected from 20 bank managers and five members of the National Safeguarding Committee in the Republic of Ireland. Using thematic analysis, four themes were identified: defining a vulnerable adult; cases of financial abuse of vulnerable adults; case responses to financial abuse of vulnerable adults; and contextual issues. The data demonstrate the multiplicity of manifestations and the complexity of case investigation and management. Findings point to the need to enhance banks’ responses, through additional education and training, and promote integrated inter-sectorial collaboration. In addition, a change in societal beliefs is needed regarding financial entitlement, responding to ageism, public awareness of the consequences of financial decisions and types of financial abuse, as well as ensuring such crimes are addressed within the legal system.
Women, Violence, and Gender Dynamics during and after the Five Patani-Siam Wars, 1785–1838
Authors: Bradley Francis R. 
Published: November 2021

AbstractThis article examines five wars that occurred on the Malay-Thai Peninsula in the period 1785–1838 and the deep impact they had upon women's lives during and after the conflicts. Constituting the majority of surviving refugees, women rebuilt their lives in the wake of war through business and trade in Malaya, as Islamic teachers in Mecca and Southeast Asia, and as servants and slaves in Bangkok. In each of these settings, women encountered new forms of agency and newfound challenges, shifting cultural values that regulated decisions and actions, and evolving perceptions of the qualifications for leadership. Focused upon the political demise of the Patani Sultanate, a state with a long history of female rule, this study is of particular relevance to scholarly debates concerning women in contemporary warfare because of its transnational focus with keen attention to women in a variety of Islamic spaces and contexts, its aim of dispelling the pervasive notion of Muslim women as lacking agency, and as a point of comparison for the present armed conflict still raging in Southern Thailand that has claimed more than five thousand and continues to impact women and gender dynamics in the region.
Boreal Headwater Catchment as Hot Spot of Carbon Processing From Headwater to Fjord
Authors: Clayer F. , Thrane J.‐E. , Brandt U. , Dörsch P. , de Wit H. A. 
Published: November 2021

AbstractBoreal headwaters and aquatic sediments are significant transporters, stores and processors of terrestrial carbon (C) as well as emitters of greenhouse gases (GHGs), mainly CO2 and CH4. While terrestrial ecosystems are net sinks of atmospheric C, lateral fluxes of total organic and dissolved inorganic C (TOC, DIC) as well as GHG release can significantly reduce the land C sink. However, the fate of the laterally exported C remains often unresolved. Here, we combine datasets from high‐frequency sensors, monitoring and modeling to produce a C budget for a typical boreal lake and its catchment and examine it in a regional context. We show that lake TOC removal is dominated by microbial metabolism which shows strong seasonal fluctuations following stratification and ice‐cover dynamics. We estimate that 11.5 g C m−2 catchment yr−1 are exported from the catchment soils and wetlands, including 9.5 g of TOC. Only 5.4 g C m−2 catchment yr−1 reach the coast while over 50% is reemitted to the atmosphere (5.7 g C m−2 catchment yr−1). Part of the reemitted C originates from rapid turnover cycles and would not affect atmospheric CO2 and the land C sink. However, we show that the land C sink at Langtjern is reduced by >14% over the whole aquatic continuum, and by >10% within the headwater catchment. Our regional analysis suggests that headwater lake TOC mineralization is the main TOC loss along the aquatic continuum with burial being relatively small, and highlights the significance of small headwaters as intensive and fast‐responding TOC processors.
Neurological complications and infection mechanism of SARS-CoV-2
Authors: Wan Dandan , Du Tingfu , Hong Weiqi , Chen Li , Que Haiying , Lu Shuaiyao , Peng Xiaozhong 
Published: November 2021

AbstractCurrently, SARS-CoV-2 has caused a global pandemic and threatened many lives. Although SARS-CoV-2 mainly causes respiratory diseases, growing data indicate that SARS-CoV-2 can also invade the central nervous system (CNS) and peripheral nervous system (PNS) causing multiple neurological diseases, such as encephalitis, encephalopathy, Guillain-Barré syndrome, meningitis, and skeletal muscular symptoms. Despite the increasing incidences of clinical neurological complications of SARS-CoV-2, the precise neuroinvasion mechanisms of SARS-CoV-2 have not been fully established. In this review, we primarily describe the clinical neurological complications associated with SARS-CoV-2 and discuss the potential mechanisms through which SARS-CoV-2 invades the brain based on the current evidence. Finally, we summarize the experimental models were used to study SARS-CoV-2 neuroinvasion. These data form the basis for studies on the significance of SARS-CoV-2 infection in the brain.
'You had to do something': prescribing antibiotics in Scotland during the COVID-19 pandemic restrictions and remobilisation
Authors: Duncan Eilidh M. , Goulao Beatriz , Clarkson Janet , Young Linda , Ramsay Craig R. 
Published: November 2021

AbstractIntroduction The COVID-19 pandemic brought about seismic change for dentistry including the direction to provide remote advice and prescribe analgesia and antimicrobials. The possibilities for care have widened, but the impact of both restrictions and remobilisation on antibiotic prescribing is not known.Aims To report the impact of COVID-19 restrictions and remobilisation on dental antibiotic prescriptions and explore dentists' intentions and attitudes towards antibiotic prescribing.Design and setting Public Health Scotland national prescribing and claims data are reported alongside an online survey of Scottish general and public health service dentists including closed and open-ended questions.Results Antibiotic prescribing rose by 49% following the suspension of routine dental care, to a peak of 34,993 antibiotics (July 2020). The data also show that since the remobilisation of NHS dental care, antibiotic prescribing remains raised at levels around 28% higher than pre-pandemic. The survey highlights dentists' frustrations and concerns about this increased use of antibiotics. Most dentists intend to reduce their prescribing; however, significant challenges to this being realised were raised.Conclusions The previous success within dentistry to protect against the development of antimicrobial resistance has suffered a knock-back during the pandemic. A renewed focus on reducing unnecessary antibiotics within dentistry is required but, crucially, needs to be approached sensitively alongside the current backdrop of challenges within the service.
At the dawn: cell-free DNA fragmentomics and gene regulation
Authors: Liu Yaping 
Published: November 2021

AbstractEpigenetic mechanisms play instrumental roles in gene regulation during embryonic development and disease progression. However, it is challenging to non-invasively monitor the dynamics of epigenomes and related gene regulation at inaccessible human tissues, such as tumours, fetuses and transplanted organs. Circulating cell-free DNA (cfDNA) in peripheral blood provides a promising opportunity to non-invasively monitor the genomes from these inaccessible tissues. The fragmentation patterns of plasma cfDNA are unevenly distributed in the genome and reflect the in vivo gene-regulation status across multiple molecular layers, such as nucleosome positioning and gene expression. In this review, we revisited the computational and experimental approaches that have been recently developed to measure the cfDNA fragmentomics across different resolutions comprehensively. Moreover, cfDNA in peripheral blood is released following cell death, after apoptosis or necrosis, mainly from haematopoietic cells in healthy people and diseased tissues in patients. Several cfDNA-fragmentomics approaches showed the potential to identify the tissues-of-origin in cfDNA from cancer patients and healthy individuals. Overall, these studies paved the road for cfDNA fragmentomics to non-invasively monitor the in vivo gene-regulatory dynamics in both peripheral immune cells and diseased tissues.
Lipid droplets contribute myogenic differentiation in C2C12 by promoting the remodeling of the acstin-filament
Authors: Tan Yanjie , Jin Yi , Zhao Pengxiang , Wu Jian , Ren Zhuqing 
Published: November 2021

AbstractLipid droplet (LD), a multi-functional organelle, is found in most eukaryotic cells. LDs participate in the regulation of many cellular processes including proliferation, stress, and apoptosis. Previous studies showed the athlete’s paradox that trained athletes accumulate LDs in their skeletal muscle. However, the impact of LDs on skeletal muscle and myogenesis is not clear. We discovered that C2C12 myoblast cells containing more LDs formed more multinucleated muscle fibers. We also discovered that LDs promoted cell migration and fusion by promoting actin-filaments remodeling. Mechanistically, two LD-proteins, Acyl-CoA synthetase long chain family member 3 (ACSL3) and lysophosphatidylcholine acyltransferase 1 (LPCAT1), medicated the recruitment of actinin proteins which contributed to actin-filaments formation on the surface of LDs. During remodeling, the actinin proteins on LDs surface translocated to actin-filaments via ARF1/COPI vesicles. Our study demonstrate LDs contribute to cell differentiation, which lead to new insight into the LD function.
Single-cell transcriptome profiling reveals intratumoural heterogeneity and malignant progression in retinoblastoma
Authors: Yang Jie , Li Yongyun , Han Yanping , Feng Yiyi , Zhou Min , Zong Chunyan , He Xiaoyu , Jia Renbing , Xu Xiaofang , Fan Jiayan 
Published: November 2021

AbstractRetinoblastoma is a childhood retinal tumour that is the most common primary malignant intraocular tumour. However, it has been challenging to identify the cell types associated with genetic complexity. Here, we performed single-cell RNA sequencing on 14,739 cells from two retinoblastoma samples to delineate the heterogeneity and the underlying mechanism of retinoblastoma progression. Using a multiresolution network-based analysis, we identified two major cell types in human retinoblastoma. Cell trajectory analysis yielded a total of 5 cell states organized into two main branches, and the cell cycle-associated cone precursors were the cells of origin of retinoblastoma that were required for initiating the differentiation and malignancy process of retinoblastoma. Tumour cells differentiation reprogramming trajectory analysis revealed that cell-type components of multiple tumour-related pathways and predominantly expressed UBE2C were associated with an activation state in the malignant progression of the tumour, providing a potential novel “switch gene” marker during early critical stages in human retinoblastoma development. Thus, our findings improve our current understanding of the mechanism of retinoblastoma progression and are potentially valuable in providing novel prognostic markers for retinoblastoma.
circKDM4C enhances bladder cancer invasion and metastasis through miR-200bc-3p/ZEB1 axis
Authors: Ma Xueyou , Ying Yufan , Sun Jiazhu , Xie Haiyun , Li Jiangfeng , He Liujia , Wang Weiyu , Chen Shiming , Shen Haixiang , Yi Jiahe , Luo Jindan , Wang Xiao , Zheng Xiangyi , Liu Ben , Xie Liping 
Published: November 2021

AbstractCircular RNAs (circRNAs) play essential roles in human bladder cancer (BCa) development, however, unusual expression patterns and functional dysfunction of circRNAs in BCa have not been evaluated. In this study, we validated that circKDM4C (hsa_circ_0001839), derived from the KDM4C gene, is elevated in BCa cell lines as well as tissues. Functionally, overexpression of circKDM4C significantly enhances, and silencing of circKDM4C suppresses migration and invasion capabilities of BCa cells. Mechanistically, circKDM4C can directly interact with miR-200b-3p and miR-200c-3p as a miRNA sponge, which enhances the expression of ZEB1 and promotes ﻿mesenchymal phenotype. Conclusively, our findings indicate that circKDM4C may act as a pro-oncogenic factor in BCa invasion and metastasis via the circKDM4C/miR-200bc-3p/ZEB1 axis, which is a potential biomarker or therapeutic target for bladder cancer.
Receptor interacting protein 3 kinase, not 1 kinase, through MLKL-mediated necroptosis is involved in UVA-induced corneal endothelium cell death
Authors: Yu Zhen , Efstathiou Nikolaos E. , Correa Victor S. M. C. , Chen Xiaohong , Ishihara Kenji , Iesato Yasuhiro , Narimatsu Toshio , Ntentakis Dimitrios , Chen Yanyun , Vavvas Demetrios G. 
Published: November 2021

AbstractUltraviolet (UV) is one of the most energetic radiations in the solar spectrum that can result in various tissue injury disorders. Previous studies demonstrated that UVA, which represents 95% of incident photovoltaic radiation, induces corneal endothelial cells (CECs) death. Programmed cell death (PCD) has been implicated in numerous ophthalmologic diseases. Here, we investigated receptor-interacting protein 3 kinase (RIPK3), a key signaling molecule of PCD, in UVA-induced injury using a short-term corneal endothelium (CE) culture model. UVA irradiation activated RIPK3 and mediated necroptosis both in mouse CE and primary human CECs (pHCECs). UVA irradiation was associated with upregulation of key necroptotic molecules (DAI, TRIF, and MLKL) that lie downstream of RIPK3. Moreover, RIPK3 inhibition or silencing in primary corneal endothelial cells suppresses UVA-induced cell death, along with downregulation of MLKL in pHCECs. In addition, genetic inhibition or knockout of RIPK3 in mice (RIPK3K51A and RIPK3−/− mice) similarly attenuates cell death and the levels of necroptosis in ex vivo UVA irradiation experiments. In conclusion, these results identify RIPK3, not RIPK1, as a critical regulator of UVA-induced cell death in CE and indicate its potential as a future protective target.
Spatial and temporal intratumour heterogeneity has potential consequences for single biopsy-based neuroblastoma treatment decisions
Authors: Schmelz Karin , Toedling Joern , Huska Matt , Cwikla Maja C. , Kruetzfeldt Louisa-Marie , Proba Jutta , Ambros Peter F. , Ambros Inge M. , Boral Sengül , Lodrini Marco , Chen Celine Y. , Burkert Martin , Guergen Dennis , Szymansky Annabell , Astrahantseff Kathy , Kuenkele Annette , Haase Kerstin , Fischer Matthias , Deubzer Hedwig E. , Hertwig Falk , Hundsdoerfer Patrick , Henssen Anton G. , Schwarz Roland F. , Schulte Johannes H. , Eggert Angelika 
Published: November 2021

AbstractIntratumour heterogeneity is a major cause of treatment failure in cancer. We present in-depth analyses combining transcriptomic and genomic profiling with ultra-deep targeted sequencing of multiregional biopsies in 10 patients with neuroblastoma, a devastating childhood tumour. We observe high spatial and temporal heterogeneity in somatic mutations and somatic copy-number alterations which are reflected on the transcriptomic level. Mutations in some druggable target genes including ALK and FGFR1 are heterogeneous at diagnosis and/or relapse, raising the issue whether current target prioritization and molecular risk stratification procedures in single biopsies are sufficiently reliable for therapy decisions. The genetic heterogeneity in gene mutations and chromosome aberrations observed in deep analyses from patient courses suggest clonal evolution before treatment and under treatment pressure, and support early emergence of metastatic clones and ongoing chromosomal instability during disease evolution. We report continuous clonal evolution on mutational and copy number levels in neuroblastoma, and detail its implications for therapy selection, risk stratification and therapy resistance.
The mechanics of landslide mobility with erosion
Authors: Pudasaini Shiva P. , Krautblatter Michael 
Published: November 2021

AbstractErosion can significantly increase the destructive power of a landslide by amplifying its volume, mobility and impact force. The threat posed by an erosive landslide is linked to its mobility. No mechanical condition has yet been presented for when, how and how much energy erosive landslides gain or lose. Here, we pioneer a mechanical model for the energy budget of erosive landslides that controls enhanced or reduced mobility. Inertia is related to an entrainment velocity, is a fundamentally new understanding. This ascertains the true inertia of erosive landslides, making a breakthrough in correctly determining the landslide mobility. Erosion velocity, which regulates the energy budget, determines the enhanced or reduced mobility. Newly developed energy generator offers the first-ever mechanical quantification of erosional energy and a precise description of mobility. This addresses the long-standing question of why many erosive landslides generate higher mobility, while others reduce mobility. We demonstrate that erosion and entrainment are different processes. Landslides gain energy and enhance mobility if the erosion velocity exceeds the entrainment velocity. Energy velocity delineates distinct excess energy regimes. Newly introduced mobility scaling and erosion number deliver the explicit measure of mobility. Presented dynamical equations correctly include erosion induced net momentum production.
ACE2-like carboxypeptidase B38-CAP protects from SARS-CoV-2-induced lung injury
Authors: Yamaguchi Tomokazu , Hoshizaki Midori , Minato Takafumi , Nirasawa Satoru , Asaka Masamitsu N. , Niiyama Mayumi , Imai Masaki , Uda Akihiko , Chan Jasper Fuk-Woo , Takahashi Saori , An Jianbo , Saku Akari , Nukiwa Ryota , Utsumi Daichi , Kiso Maki , Yasuhara Atsuhiro , Poon Vincent Kwok-Man , Chan Chris Chung-Sing , Fujino Yuji , Motoyama Satoru , Nagata Satoshi , Penninger Josef M. , Kamada Haruhiko , Yuen Kwok-Yung , Kamitani Wataru , Maeda Ken , Kawaoka Yoshihiro , Yasutomi Yasuhiro , Imai Yumiko , Kuba Keiji 
Published: November 2021

AbstractAngiotensin-converting enzyme 2 (ACE2) is a receptor for cell entry of SARS-CoV-2, and recombinant soluble ACE2 protein inhibits SARS-CoV-2 infection as a decoy. ACE2 is a carboxypeptidase that degrades angiotensin II, thereby improving the pathologies of cardiovascular disease or acute lung injury. Here we show that B38-CAP, an ACE2-like enzyme, is protective against SARS-CoV-2-induced lung injury. Endogenous ACE2 expression is downregulated in the lungs of SARS-CoV-2-infected hamsters, leading to elevation of angiotensin II levels. Recombinant Spike also downregulates ACE2 expression and worsens the symptoms of acid-induced lung injury. B38-CAP does not neutralize cell entry of SARS-CoV-2. However, B38-CAP treatment improves the pathologies of Spike-augmented acid-induced lung injury. In SARS-CoV-2-infected hamsters or human ACE2 transgenic mice, B38-CAP significantly improves lung edema and pathologies of lung injury. These results provide the first in vivo evidence that increasing ACE2-like enzymatic activity is a potential therapeutic strategy to alleviate lung pathologies in COVID-19 patients.
Developmental decrease of entorhinal-hippocampal communication in immune-challenged DISC1 knockdown mice
Authors: Xu Xiaxia , Song Lingzhen , Kringel Rebecca , Hanganu-Opatz Ileana L. 
Published: November 2021

AbstractThe prefrontal-hippocampal dysfunction that underlies cognitive deficits in mental disorders emerges during early development. The lateral entorhinal cortex (LEC) is tightly interconnected with both prefrontal cortex (PFC) and hippocampus (HP), yet its contribution to the early dysfunction is fully unknown. Here we show that mice that mimic the dual genetic (G) -environmental (E) etiology (GE mice) of psychiatric risk have poor LEC-dependent recognition memory at pre-juvenile age and abnormal communication within LEC-HP-PFC networks throughout development. These functional and behavioral deficits relate to sparser projections from LEC to CA1 and decreased efficiency of axonal terminals to activate the hippocampal circuits in neonatal GE mice. In contrast, the direct entorhinal drive to PFC is not affected, yet the PFC is indirectly compromised, as target of the under-activated HP. Thus, the entorhinal-hippocampal circuit is already impaired from neonatal age on in GE mice.