bluuebunny/crossref_metadata_2025_split huggingface dataset:
COG6‐CDG: Expanding the phenotype with emphasis on glycosylation defects involved in the causation of male disorders of sex development
Authors: Mandel Hanna , Cohen Kfir Nehama , Fedida Ayalla , Shuster Biton Efrat , Odeh Marwan , Kalfon Limor , Ben‐Harouch Shani , Fleischer Sheffer Vered , Hoffman Yoav , Goldberg Yael , Dinwiddie April , Dumin Elena , Eran Ayelet , Apel‐Sarid Liat , Tiosano Dov , Falik‐Zaccai Tzipora C. 
Published: July 2020

AbstractCOG6‐congenital disorder of glycosylation (COG6‐CDG) is caused by biallelic mutations in COG6. To‐date, 12 variants causing COG6‐CDG in less than 20 patients have been reported. Using whole exome sequencing we identified two siblings with a novel homozygous deletion of 26 bp in COG6, creating a splicing variant (c.518_540 + 3del) and a shift in the reading frame. The phenotype of COG6‐CDG includes growth and developmental retardation, microcephaly, liver and gastrointestinal disease, hypohydrosis and recurrent infections. We report two patients with novel phenotypic features including bowel malrotation and ambiguous genitalia, directing attention to the role of glycoprotein metabolism in the causation of disorders of sex development (DSD). Searching the glycomic literature, we identified 14 CDGs including males with DSD, a feature not previously accentuated. This study broadens the genetic and phenotypic spectrum of COG6‐CDG and calls for increasing awareness to the central role of glycosylation processes in development of human sex and genitalia.
Optimizing omentoplasty for management of chronic pelvic sepsis by intra‐operative fluorescence angiography: a comparative cohort study
Authors: Slooter M. D. , Blok R. D. , de Krom M. A. , Buskens C. J. , Bemelman W. A. , Tanis P. J. , Hompes R. 
Published: July 2020

AbstractAimPelviperineal wound complications frequently occur after salvage surgery for chronic pelvic sepsis despite using an omentoplasty. Sufficient perfusion of the omentoplasty following mobilization is essential for proper healing. This study investigated the impact on short‐term clinical outcomes of fluorescence angiography (FA) using indocyanine green for assessment of omental perfusion in patients undergoing salvage surgery.MethodThis was a comparative cohort study including consecutive patients who underwent combined abdominal and transanal minimally invasive salvage surgery with omentoplasty at a national referral centre for chronic pelvic sepsis between December 2014 and August 2019. The historical and interventional cohorts were defined based on the date of introduction of FA in April 2018. The primary outcome was pelviperineal non‐healing, defined by the presence of any degree of pelviperineal infection at the final postoperative evaluation.ResultsEighty‐eight patients underwent salvage surgery with omentoplasty for chronic pelvic sepsis, of whom 52 did not have FA and 36 did have FA. The underlying primary disease was Crohn's disease (n = 50) or rectal cancer (n = 38), with even distribution among the cohorts (P = 0.811). FA led to a change in management in 28/36 (78%) patients. After a median of 89 days, pelviperineal non‐healing was observed in 22/52 (42%) patients in the cohort without FA and in 8/36 (22%) patients in the cohort with FA (P = 0.051). Omental necrosis was found during reoperation in 3/52 and 0/36 patients, respectively (P = 0.266).ConclusionAfter introduction of FA to assess perfusion of the omentoplasty, halving of the pelviperineal non‐healing rate was observed in patients undergoing salvage surgery for chronic pelvic sepsis.
Motivating role of type H vessels in bone regeneration
Authors: Zhang Jiankang , Pan Jian , Jing Wei 
Published: July 2020

AbstractCoupling between angiogenesis and osteogenesis has an important role in both normal bone injury repair and successful application of tissue‐engineered bone for bone defect repair. Type H blood vessels are specialized microvascular components that are closely related to the speed of bone healing. Interactions between type H endothelial cells and osteoblasts, and high expression of CD31 and EMCN render the environment surrounding these blood vessels rich in factors conducive to osteogenesis and promote the coupling of angiogenesis and osteogenesis. Type H vessels are mainly distributed in the metaphysis of bone and densely surrounded by Runx2+ and Osterix+ osteoprogenitors. Several other factors, including hypoxia‐inducible factor‐1α, Notch, platelet‐derived growth factor type BB, and slit guidance ligand 3 are involved in the coupling of type H vessel formation and osteogenesis. In this review, we summarize the identification and distribution of type H vessels and describe the mechanism for type H vessel‐mediated modulation of osteogenesis. Type H vessels provide new insights for detection of the molecular and cellular mechanisms that underlie the crosstalk between angiogenesis and osteogenesis. As a result, more feasible therapeutic approaches for treatment of bone defects by targeting type H vessels may be applied in the future.
Effects of exercise programmes on pain, disease activity and function in ankylosing spondylitis: A meta‐analysis of randomized controlled trials
Authors: Hu Xinmiao , Chen Jialing , Tang Wenjuan , Chen Wenjian , Sang Yan , Jia Lina 
Published: July 2020

AbstractBackgroundTo evaluate the effects of exercise programmes on pain, function and disease activity in patients with ankylosing spondylitis (AS).Materials and methodsWe searched PubMed, Embase, CNKI and Wanfang from inception to February 2020. Randomized controlled trials comparing exercises with nonexercise interventions in AS patients were applied. Studies that assessed the visual analogue scale (VAS) pain score, the Bath Ankylosing Spondylitis Disease Activity Index (BASDAI), the Bath Ankylosing Spondylitis Functional Index (BASFI), C‐reactive protein (CRP) and erythrocyte sedimentation rate (ESR) were included. Outcomes of home‐based exercise intervention were also reported independently.ResultsTen studies met the inclusion criteria in all, including 534 patients (278 exercise, 256 control). Compared with the nonexercise group, exercise group had statistically significant improvements in pain (weighted mean difference [WMD]: −1.02 [95% CI: −1.50 to −0.55]) (I2: 31%, P <.0001), BASDAI (WMD: −0.85 [95% CI: −1.09 to −0.61]) (I2: 20%, P <.00001), and BASFI (WMD: −0.66 [95% CI: −0.95 to −0.38]) (I2: 0%, P <.00001), but not in CRP and ESR. What's more, home‐based exercise programmes had positive impacts on BASFI, BASDAI and pain.ConclusionsFor patients with AS, exercise programmes improve pain, function and disease activity. To confirm the results, more well‐designed randomized controlled trials with large number of patients are required.
Past, Present and Future of Home video‐electroencephalographic telemetry: A review of the development of in‐home video‐electroencephalographic recordings
Authors: Brunnhuber Franz , Slater Jeremy , Goyal Sushma , Amin Devyani , Thorvardsson Gardar , Freestone Dean R. , Richardson Mark P. 
Published: July 2020

AbstractVideo‐electroencephalographic (EEG) monitoring is an essential tool in epileptology, conventionally carried out in a hospital epilepsy monitoring unit. Due to high costs and long waiting times for hospital admission, coupled with technological advances, several centers have developed and implemented video‐EEG monitoring in the patient's home (home video‐EEG telemetry [HVET]). Here, we review the history and current status of three general approaches to HVET: (1) supervised HVET, which entails setting up video‐EEG in the patient's home with daily visiting technologist support; (2) mobile HVET (also termed ambulatory video‐EEG), which entails attaching electrodes in a health care facility, supplying the patient and carers with the hardware and instructions, and then asking the patient and carer to set up recording at home without technologist support; and (3) cloud‐based HVET, which adds to either of the previous models continuous streaming of video‐EEG from the home to the health care provider, with the option to review data in near real time, troubleshoot hardware remotely, and interact remotely with the patient. Our experience shows that HVET can be highly cost‐effective and is well received by patients. We note limitations related to long‐term electrode attachment and correct camera placing while the patient is unsupervised at home, and concerns related to regulations regarding data privacy for cloud services. We believe that HVET opens significant new opportunities for research, especially in the field of understanding the many influences in seizure occurrence. We speculate that in the future HVET may merge into innovative new multisensor approaches to continuously monitoring people with epilepsy.
Retrospective observational study on hospital readmission for status epilepticus in the United States over 2016
Authors: Amengual‐Gual Marta , Sánchez Fernández Iván , Vasquez Alejandra , Loddenkemper Tobias 
Published: July 2020

AbstractObjectiveDescribe hospital readmission for status epilepticus (SE) in the United States, and study potential risk factors for readmission.MethodsThis is a retrospective observational study using the Healthcare Cost and Utilization Project's 2016 Nationwide Readmissions Database. We studied patients of all ages admitted to the hospital due to SE.ResultsWe included 32 327 patients admitted for SE in 2016. 8.4% of these patients were readmitted for SE at least one more time within 2016 (cross‐sectional analysis). The incidence rate was 18 readmissions for SE per 1000 patient‐months. Among the survivors of the index admission for SE who had at least 6 months of follow‐up within this database (16 043 patients), the cumulative probability of having a readmission for SE at 1, 3, and 6 months from the index admission was approximately 3.5%, 7.5%, and 11%, respectively (time‐to‐event analysis). Patients with refractory epilepsy were more likely to have a readmission for SE compared to patients without refractory epilepsy (hazard ratio [HR] 1.49, 95% confidence interval [CI] 1.23‐1.82, adjusted P =.0006), and pediatric patients were more likely to have a readmission for SE compared to adult patients (HR 1.53, 95% CI 1.26‐1.87, adjusted P = .0003) during 6‐month follow‐up.SignificanceHospital readmissions for SE in the United States are frequent. Independent factors associated with readmission in this database were refractory epilepsy and pediatric age.
Peri‐ictal hypoxia is related to extent of regional brain volume loss accompanying generalized tonic‐clonic seizures
Authors: Allen Luke A. , Harper Ronald M. , Vos Sjoerd B. , Scott Catherine A. , Lacuey Nuria , Vilella Laura , Winston Joel S. , Whatley Benjamin P. , Kumar Rajesh , Ogren Jennifer , Hampson Jaison S. , Rani Sandhya , Winston Gavin P. , Lemieux Louis , Lhatoo Samden D. , Diehl Beate 
Published: July 2020

AbstractObjectivesHypoxia, or abnormally low blood‐oxygen levels, often accompanies seizures and may elicit brain structural changes in people with epilepsy which contribute to central processes underlying sudden unexpected death in epilepsy (SUDEP). The extent to which hypoxia may be related to brain structural alterations in this patient group remains unexplored.MethodsWe analyzed high‐resolution T1‐weighted magnetic resonance imaging (MRI) to determine brain morphometric and volumetric alterations in people with generalized tonic‐clonic seizures (GTCS) recorded during long‐term video‐electroencephalography (VEEG), recruited from two sites (n = 22), together with data from age‐ and sex‐matched healthy controls (n = 43). Subjects were sub‐divided into those with mild/moderate (GTCS‐hypox‐mild/moderate, n = 12) and severe (GTCS‐hypox‐severe, n = 10) hypoxia, measured by peripheral oxygen saturation (SpO2) during VEEG. Whole‐brain voxel‐based morphometry (VBM) and regional volumetry were used to assess group comparisons and correlations between brain structural measurements as well as the duration and extent of hypoxia during GTCS.ResultsMorphometric and volumetric alterations appeared in association with peri‐GTCS hypoxia, including volume loss in the periaqueductal gray (PAG), thalamus, hypothalamus, vermis, cerebellum, parabrachial pons, and medulla. Thalamic and PAG volume was significantly reduced in GTCS patients with severe hypoxia compared with GTCS patients with mild/moderate hypoxia. Brainstem volume loss appeared in both hypoxia groups, although it was more extensive in those with severe hypoxia. Significant negative partial correlations emerged between thalamic and hippocampal volume and extent of hypoxia, whereas vermis and accumbens volumes declined with increasing hypoxia duration.SignificanceBrain structural alterations in patients with GTCS are related to the extent of hypoxia in brain sites that serve vital functions. Although the changes are associative only, they provide evidence of injury to regulatory brain sites related to respiratory manifestations of seizures.
COMMEMORATIONS AND NATIONAL IDENTITY: THE 1967 CENTENARY OF KÄTHE KOLLWITZ IN THE GDR
Authors: Zell David J. 
Published: July 2020

ABSTRACTThe article examines how the political capital of cultural anniversaries may promote national identity in an authoritarian state. It investigates whether the 1967 centenary of Käthe Kollwitz (1867–1945) helped the GDR to build a distinct national identity in common with the aims of similar commemorations in the GDR. The twin themes of demarcation from the FRG and appropriation of the German cultural heritage dominated the ideological framework for commemorations throughout GDR history. Primary sources on both sides of the Cold War appear to have accepted the work and life of Kollwitz as essentially linked to the GDR. This reduced the need for the GDR authorities to amplify this framework when planning events. Yet a closer analysis of how she was portrayed reveals discrepancies between the theory and practice of this commemoration. The article examines two types of anniversary activity. Firstly, a film in which various narratives proposing a politicised construct of Kollwitz as an anti‐fascist, communist, and pacifist appear to conflict with a domesticated paradigm of Kollwitz as ‘grieving mother’. Secondly, an anniversary exhibition that concentrates rather on framing the narrative of ‘Kämpferin für das Proletariat’. Despite these inconsistencies, Kollwitz's position as an existing socialist role model who contributed to the construct of GDR national identity was confirmed by the commemoration rather than noticeably strengthened.
Intracellular dynamics of polydnavirus innexin homologues
Authors: Hasegawa D. K. , Zhang P. , Turnbull M. W. 
Published: July 2020

AbstractPolydnaviruses associated with ichneumonid parasitoid wasps (Ichnoviruses) encode large numbers of genes, often in multigene families. The Ichnovirus Vinnexin gene family, which is expressed in parasitized lepidopteran larvae, encodes homologues of Innexins, the structural components of insect gap junctions. Here, we have examined intracellular behaviours of the Campoletis sonorensis Ichnovirus (CsIV) Vinnexins, alone and in combination with a host Innexin orthologue, Innexin2 (Inx2). QRT‐PCR verified that transcription of CsIV vinnexins occurs contemporaneously with inx2, implying co‐occurrence of Vinnexin and Inx2 proteins. Confocal microscopy demonstrated that epitope‐tagged VinnexinG (VnxG) and VinnexinQ2 (VnxQ2) exhibit similar subcellular localization as Spodoptera frugiperda Inx2 (Sf‐Inx2). Surface biotinylation assays verified that all three proteins localize to the cell surface, and cytochalasin B and nocodazole that they rely on actin and microtubule cytoskeletal networks for localization. Immunomicroscopy following co‐transfection of constructs indicates extensive co‐localization of Vinnexins with each other and Sf‐Inx2, and live‐cell imaging of mCherry‐labelled Inx2 supports that Vinnexins may affect Sf‐Inx2 distribution in a Vinnexin‐specific fashion. Our findings support that the Vinnexins may disrupt host cell physiology in a protein‐specific manner through altering gap junctional intercellular channel communication, as well as indirectly by affecting multicellular junction characteristics.
Sub‐epidermal moisture measurement: an evidence‐based approach to the assessment for early evidence of pressure ulcer presence
Authors: Budri Aglecia Moda Vitoriano , Moore Zena , Patton Declan , O'Connor Tom , Nugent Linda , Avsar Pinar 
Published: July 2020

AbstractThis paper aims to discuss the literature pertaining to early pressure‐shear induced tissue damage detection, with emphasis on sub‐epidermal moisture measurement (SEM). The current method for pressure detection is visual skin assessment (VSA); however, this method is fraught with challenges. Advances in early detection of pressure ulcers are reported in the literature and mainly involve measuring inflammation markers on weight‐bearing anatomical areas in order to capture the first signs of tissue damage. One novel technique currently in use is SEM measurement. This biophysical marker is the product of plasma that leaks as a response to local inflammation arising due to pressure‐shear induced damage over bony prominences. The early detection of tissue damage is beneficial in two different ways. First, it enables early intervention when the damage is still microscopic and reversible and, therefore, has the potential to prevent further aggravation of healthy surrounding tissue. This arises by avoiding the causation of the problem and stopping the knock‐on effect of inflammation, especially when the rapid pressure ulceration pathway of deformation is in place. Second, when the slow ischaemic‐reperfusion related mechanism is undergoing, cell death can be avoided when the problem is identified before the cell reaches the “death threshold,” completely averting a pressure ulcer.
Vertically Stacked 2H‐1T Dual‐Phase MoS2 Microstructures during Lithium Intercalation: A First Principles Study
Authors: Parida Shayani , Mishra Avanish , Chen Jie , Wang Jin , Dobley Arthur , Carter C. Barry , Dongare Avinash M. 
Published: July 2020

AbstractLayered transition‐metal dichalcogenides (TMDs) have shown promise to replace carbon‐based compounds as suitable anode materials for Lithium‐ion batteries (LIBs) owing to facile intercalation and de‐intercalation of lithium (Li) during charging and discharging, respectively. While the intercalation mechanism of Li in mono‐ and bi‐layer TMDs has’ been thoroughly examined, mechanistic understanding of Li intercalation‐induced phase transformation in bulk or films of TMDs is still largely unexplored. This study investigates possible scenarios during sequential Li intercalation and aims to gain a mechanistic understanding of the phase transformation in bulk MoS2 using density functional theory (DFT) calculations. The manuscript examines the role of concentration and distribution of Li‐ions on the formation of dual‐phase 2H‐1T microstructures that have been observed experimentally. The study demonstrates that lithiation would proceed in a systematic layer‐by‐layer manner wherein Li‐ions diffuse into successive interlayer spacings to render local phase transformation of the adjacent MoS2 layers from 2H‐to‐1T phase in the multilayered MoS2. This local phase transition is attributed to partial ionization of Li and charge redistribution around the metal atoms and is followed by subsequent lattice straining. In addition, the stability of single‐phase vs. multiphase intercalated microstructures, and the origins of structural changes accompanying Li‐ion insertion are investigated at atomic scales.
SIRT2, a direct target of miR‐212‐5p, suppresses the proliferation and metastasis of colorectal cancer cells
Authors: Du Feng , Li Zhijun , Zhang Guohua , Shaoyan Si , Geng Dejun , Tao Zhougen , Qiu Kunhua , Liu Silei , Zhou Yu , Zhang Yichao , Gu Jianwen , Wang Gang , Li Lianyong , Wu Wei 
Published: July 2020

AbstractThe aberrant expression of human sirtuin 2 (SIRT2) has been detected in various types of cancer; however, the biological roles, underlying mechanisms and clinical significance of SIRT2 dysregulation in human colorectal cancer (CRC) remain unclear. The results of this study demonstrate that compared with paired normal tissues, SIRT2 expression is significantly decreased in CRC tissues. SIRT2 loss has been correlated with clinicopathological characteristics, including distant metastasis, lymph node metastasis and American Joint Committee on Cancer (AJCC) stage; this loss serves as an independent factor that indicates a poor prognosis for patients with CRC. Further gain‐ and loss‐of‐function analyses have demonstrated that SIRT2 suppresses CRC cell proliferation and metastasis both in vivo and in vitro. Mechanistically, miR‐212‐5p was identified to directly target the SIRT2 3′‐untranslated region (3′‐UTR), leading to SIRT2 down‐regulation. The ectopic expression of SIRT2 reverses the effect of miR‐212‐5p overexpression on CRC cell colony formation, invasion, migration and proliferation. Clinically, an inverse correlation was found between miR‐212‐5p and SIRT2 expression. High miR‐212‐5p expression has been found to result in a poor prognosis and aggressive clinicopathological characteristics in patients with CRC. Taken together, these results suggest that SIRT2, targeted by miR‐212‐5p, acts as a tumour suppressor in CRC and that the miR‐212‐5p/SIRT2 axis is a promising prognostic factor and potential therapeutic target in CRC.
Apatinib attenuates phenotypic switching of arterial smooth muscle cells in vascular remodelling by targeting the PDGF Receptor‐β
Authors: Shao Wenchao , Li Xiaoguang , Peng Jiangtong , Fan Siyuan , Liang Minglu , Huang Kai 
Published: July 2020

AbstractApatinib (YN968D1) is a small‐molecule tyrosine kinase inhibitor（TKI）which can inhibit the activity of vascular endothelial growth factor receptor‐2 (VEGFR‐2). It has been reported that apatinib has anti‐tumour effect of inhibiting proliferation and inducing apoptosis of a variety of solid tumour cells, whereas its effect on vascular smooth muscle cells (VSMC) remains unclear. This study investigated the effect of apatinib on phenotypic switching of arterial smooth muscle cells in vascular remodelling. Compared to the vehicle groups, mice that were performed carotid artery ligation injury and treated with apatinib produced a reduction in abnormal neointimal area. For in vitro experiment, apatinib administration inhibited VSMC proliferation, migration and reversed VSMC dedifferentiation with the stimulation of platelet‐derived growth factor type BB (PDGF‐BB).In terms of mechanism, with the preincubation of apatinib, the activations of PDGF receptor‐β (PDGFR‐β) and phosphoinositide‐specific phospholipase C‐γ1 (PLC‐γ1) induced by PDGF‐BB were inhibited in VSMCs. With the preincubation of apatinib, the phosphorylation of PDGFR‐β, extracellular signal‐related kinases (ERK1/2) and Jun amino‐terminal kinases (JNK) induced by PDGF‐BB were also inhibited in rat vascular smooth muscle cell line A7r5. Herein, we found that apatinib attenuates phenotypic switching of arterial smooth muscle cells induced by PDGF‐BB in vitro and vascular remodelling in vivo. Therefore, apatinib is a potential candidate to treat vascular proliferative diseases.