bluuebunny/crossref_metadata_2025_split huggingface dataset:
FAMILY SUPPORT-BASED PSYCHOEDUCATION IN CARING SCHIZOPHRENIC PATIENTS: A LITERATURE REVIEW
Authors: Iswanti Dwi Indah , Rumambo Pandin Moses Glorino 
Published: January 2022

AbstractBackgroundThe burden of family in caring a schizophrenia impacts on psychological shock and emotional burden; lack of disease knowledge and care skills; poor patient medication adherence; the difficulty of getting along with patients; conflict in the family or at work; financial burden; and need adequate social support.AimThis study discussed how family support takes care of people with schizophrenia with a psychoeducational approach in mental health service settings.MethodA non-systematic literature review was carried out using the PICO (Population, Intervention, Comparison, Outcome) framework utilizing Scopus, CINAHL, and ProQuest databases in the last 5 years, searching with keywords “Family Support AND Schizophrenia OR Family Psychoeducation”.ResultsFamilies with schizophrenia experience the most potent stressors on the burden of care borne, in addition to stigma and the frequency of relapse of sufferers. Community care providers can involve the family in various ways, such as providing psychoeducation, supporting the family’s physical, emotional and social needs, and behavioral family assessment or family therapy.ConclusionMental health services must develop and imply family psychoeducation training.
No One Is Leaving This Time: Appraisal of Awareness and Knowledge of Port Health Officers on International Health Regulation IHR (2005)
Authors: Adiama Yusuf Babatunde , Adewoye Solomon Olayinka , Olaniyi Opasola Afolabi , Lateefat Habeeb Modupe , Ahmed Abdullahi , Raimi Morufu Olalekan 
Published: January 2022

AbstractBackgroundHistorically, ships have played an important role in transmitting infectious diseases around the world. The spread of cholera pandemics in the 19th century was thought to be linked to trade routes and facilitated by merchant shipping. The international maritime traffic of people and goods has often contributed to the spread of pathogens affecting public health.ObjectivesTo assess level of awareness and knowledge of international Health regulation (IHR 2005) content among port health officerMethodsThe study design was descriptive cross-sectional evaluation, questionnaires were used to capture the respondents’ knowledge, awareness and sanitary condition of ship in accordance with (IHR 2005)ResultsOn awareness and knowledge, Majority of the respondent (77.1 %) demonstrate good awareness of the IHR (2005), while 22.9% had not and some even testified of hearing the said document for the first time. Despite the fact that majority of respondent were aware but only 24.6% of them can actually demonstrate good knowledge of IHR (2005) and its intent to protect and prevent spread of disease along the international route.ConclusionThere is need to improve the knowledge of port health officers by expand training and guidance on application of the IHR’s to frontline officer at point of entries. Also ensure more thorough inspection and avoid influence of ship agent during inspection of ship.
CCPLS reveals cell-type-specific spatial dependence of transcriptomes in single cells
Authors: Tsuchiya Takaho , Hori Hiroki , Ozaki Haruka 
Published: January 2022

AbstractMotivationCell-cell communications regulate internal cellular states, e.g., gene expression and cell functions, and play pivotal roles in normal development and disease states. Furthermore, single-cell RNA sequencing methods have revealed cell-to-cell expression variability of highly variable genes (HVGs), which is also crucial. Nevertheless, the regulation on cell-to-cell expression variability of HVGs via cell-cell communications is still largely unexplored. The recent advent of spatial transcriptome methods has linked gene expression profiles to the spatial context of single cells, which has provided opportunities to reveal those regulations. The existing computational methods extract genes with expression levels influenced by neighboring cell types. However, limitations remain in the quantitativeness and interpretability: they neither focus on HVGs nor consider the effects of multiple neighboring cell types.ResultsHere, we propose CCPLS (Cell-Cell communications analysis by Partial Least Square regression modeling), which is a statistical framework for identifying cell-cell communications as the effects of multiple neighboring cell types on cell-to-cell expression variability of HVGs, based on the spatial transcriptome data. For each cell type, CCPLS performs PLS regression modeling and reports coefficients as the quantitative index of the cell-cell communications. Evaluation using simulated data showed our method accurately estimated the effects of multiple neighboring cell types on HVGs. Furthermore, applications to the two real datasets demonstrate that CCPLS can extract biologically interpretable insights from the inferred cell-cell communications.AvailabilityThe R package is available athttps://github.com/bioinfo-tsukuba/CCPLS. The data are available athttps://github.com/bioinfo-tsukuba/CCPLS_paper.Contactharuka.ozaki@md.tsukuba.ac.jpSupplementary informationSupplementary data are available at Bioinformatics online.
Assessing the clinical severity of the Omicron variant in the Western Cape Province, South Africa, using the diagnostic PCR proxy marker of RdRp target delay to distinguish between Omicron and Delta infections – a survival analysis
Authors: Hussey Hannah , Davies Mary-Ann , Heekes Alexa , Williamson Carolyn , Valley-Omar Ziyaad , Hardie Diana , Korsman Stephen , Doolabh Deelan , Preiser Wolfgang , Maponga Tongai , Iranzadeh Arash , Wasserman Sean , Boloko Linda , Symons Greg , Raubenheimer Peter , Viljoen Abraham , Parker Arifa , Schrueder Neshaad , Solomon Wesley , Rousseau Petro , Wolter Nicole , Jassat Waasila , Cohen Cheryl , Lessells Richard , Wilkinson Robert J , Boulle Andrew , Hsiao Nei-yuan 
Published: January 2022

AbstractBackgroundEmerging data suggest that SARS-CoV-2 Omicron variant of concern (VOC)is associated with reduced risk of severe disease. The extent to which this reflects a difference in the inherent virulence of Omicron, or just higher levels of population immunity, is currently not clear.MethodsRdRp target delay (RTD: a difference in cycle threshold value of RdRp - E > 3.5) in the Seegene Allplex™ 2019-nCoV PCR assay is a proxy marker for the Delta VOC. The absence of this proxy marker in the period of transition to Omicron was used to identify suspected Omicron VOC infections.Cox regression was performed for the outcome of hospital admission in those who tested positive for SARS-CoV-2 on the Seegene Allplex™ assay from 1 November to 14 December 2021 in the Western Cape Province, South Africa, public sector. Vaccination status at time of diagnosis, as well as prior diagnosed infection and comorbidities, were adjusted for.Results150 cases with RTD (proxy for Delta) and 1486 cases without RTD (proxy for Omicron) were included. Cases without RTD had a lower hazard of admission (adjusted Hazard Ratio [aHR] of 0.56, 95% confidence interval [CI] 0.34-0.91). Complete vaccination was protective of admission with an aHR of 0.45 (95%CI 0.26-0.77).ConclusionOmicron has resulted in a lower risk of hospital admission, compared to contemporaneous Delta infection in the Western Cape Province, when using the proxy marker of RTD. Under-ascertainment of reinfections with an immune escape variant like Omicron remains a challenge to accurately assessing variant virulence.
Addressing selection bias in the UK Biobank neurological imaging cohort
Authors: Bradley Valerie , Nichols Thomas E. 
Published: January 2022

AbstractThe UK Biobank is a national prospective study of half a million participants between the ages of 40 and 69 at the time of recruitment between 2006 and 2010, established to facilitate research on diseases of aging. The imaging cohort is a subset of UK Biobank participants who have agreed to undergo extensive additional imaging assessments. However, Fry et al. (2017) finds evidence of “healthy volunteer bias” in the UK Biobank – participants are less likely to smoke, be obese, consume alcohol daily than the target population of UK adults. Here we examine selection bias in the UK Biobank imaging cohort. We address two common misconceptions: first, that study size can compensate for bias in data collection, and second that selection bias does not affect estimates of associations, which are the primary interest of the UK Biobank. We introduce inverse probability weighting (IPW) as an approach commonly used in survey research that can be used to address selection bias in volunteer health studies like the UK Biobank. We discuss 6 such methods – five existing and one novel –, assess relative performance in simulation studies, and apply them to the UK Biobank imaging cohort. We find that our novel method, BART for predicting the probability of selection combined with raking, performs well relative to existing methods, and helps alleviate selection bias in the UK Biobank imaging cohort.
Prom1 and Notch regulate ciliary length and dynamics in multiciliated cells of the airway epithelium
Authors: Serra Carlos F. H. , Liu Helu , Qian Jun , Mori Munemasa , Lu Jining , Cardoso Wellington V. 
Published: January 2022

AbstractDifferences in ciliary morphology and dynamics among multiciliated cells of the respiratory tract have been well reported and known to contribute to efficient mucociliary clearance. Nevertheless, little is known about how phenotypic differences among multiciliated cells are established in the mammalian lung. Here we show that Prominin-1 (Prom1), a transmembrane protein widely used as stem cell and tumor-initiating marker, is crucial to this process. During airway differentiation, Prom1 becomes restricted to multiciliated cells, where it is expressed at distinct levels along the proximal-distal axis of the airways and in the adult airway epithelium in vitro. We found that Prom1 is induced by Notch in post-specified multiciliated cells and that Notch inactivation abolishes the gradients of Prom1 in the developing airways and in differentiating organotypic cultures. Prom1 was not required for multicilia formation and when inactivated resulted in longer cilia, which remained functional but beating at a lower frequency. Disruption of Notch resulted in opposite effects and suggested that Notch fine-tunes Prom1 levels to regulate the multiciliated cell phenotype and generate diversity among these cells in the respiratory tract. By controlling these features, this mechanism contributes to the innate defense of the lung against environmental agents and prevent pulmonary disease.Significance StatementMulticiliated cells are integral components of the epithelia from a variety of organs. In the respiratory tract they are crucial for mucociliary clearance, a first line of defense against environmental agents and microorganisms. Regional differences in ciliary morphology and dynamics of multiciliated cells have been well described. However, little is known about the events generating phenotypical and functional differences among these cells in airways. Here we provide evidence of a novel mechanism in post-specified multiciliated progenitors whereby local Notch and Prom1 regulate ciliary length and ciliary beating to generate morphological and functional diversity among the multiciliated cells. The findings provide insights into the impact of these signals in maintaining the integrity and function of the airway epithelium, preventing pulmonary disease.
Time-lapsed proteomics reveals a role for the novel protein, SNED1, in modulating ECM composition and protein folding
Authors: Lee Fred , Shao Xinhao , Gao Yu (Tom) , Naba Alexandra 
Published: January 2022

ABSTRACTThe extracellular matrix (ECM) is a complex and dynamic meshwork of proteins providing structural support to cells. It also provides biochemical signals governing cellular processes including proliferation and migration. Alterations of ECM structure and/or composition has been shown to lead to, or accompany, many pathological processes including cancer and fibrosis. To understand how the ECM contributes to diseases, we first need to obtain a comprehensive characterization of the ECM of tissues and of its changes during disease progression. Over the past decade, mass-spectrometry-based proteomics has become the state-of-the-art method to profile the protein composition of ECMs. However, existing methods do not fully capture the broad dynamic range of protein abundance in the ECM, nor do they permit to achieve the high coverage needed to gain finer biochemical information, including the presence of isoforms or post-translational modifications. In addition, broadly adopted proteomic methods relying on extended trypsin digestion do not provide structural information on ECM proteins, yet, gaining insights into ECM protein structure is critical to better understanding protein functions. Here, we present the optimization of a time-lapsed proteomic method using limited proteolysis of partially denatured samples and the sequential release of peptides to achieve superior sequence coverage as compared to standard ECM proteomic workflow. Exploiting the spatio-temporal resolution of this method, we further demonstrate how 3-dimensional time-lapsed peptide mapping can identify protein regions differentially susceptible to trypsin and can thus identify sites of post-translational modifications, including protein-protein interactions. We further illustrate how this approach can be leveraged to gain insight on the role of the novel ECM protein SNED1 in ECM homeostasis. We found that the expression of SNED1 by mouse embryonic fibroblasts results in the alteration of overall ECM composition and the sequence coverage of certain ECM proteins, raising the possibility that SNED1 could modify accessibility to trypsin by engaging in protein-protein interactions.
LiCl-induced sickness modulates spontaneous activity and response dynamics in rat gustatory cortex
Authors: Stone Bradly T. , Lin Jian-You , Mahmood Abuzar , Sanford Alden J. , Katz Donald B. 
Published: January 2022

AbstractGustatory Cortex (GC), a structure deeply involved in the making of consumption decisions, presumably performs this function by integrating information about taste, experiences, and internal states related to the animal’s health, such as illness. Here, we investigated this assertion, examining whether illness is represented in GC activity, and how this representation impacts taste responses and behavior. We recorded GC single-neuron activity and local field potentials (LFP) from healthy rats and (the same) rats made ill (via LiCl injection). We show (consistent with the extant literature) that the onset of illness-related behaviors arises contemporaneously with alterations in spontaneous 7-12Hz LFP power at ∼11 min following injection. This process was accompanied by reductions in single-neuron taste response magnitudes and discriminability, and with enhancements in palatability-relatedness – a result reflecting the collapse of responses toward a simple “good-bad” code arising in a specific subset of GC neurons. Overall, our data show that a state (illness) that profoundly reduces consumption changes basic properties of the sensory cortical response to tastes, in a manner that can easily explain illness’ impact on consumption.Significance StatementNeural responses in primary sensory cortex are often thought to faithfully represent physical stimuli, and while recent studies (including ours) have challenged this view by documenting enhancements and decrements in stimulus-induced firing related to animals’ internal states, there has been little work setting these changes in any sort of functional, mechanistic context. Here we show that a state (illness) that profoundly reduces consumption changes basic properties of the sensory cortical response to tastes, and then go beyond this to precisely characterize this response plasticity, connecting it to the specific perceptual changes that drive illness’ impact on consumption.
Origin of congenital coronary arterio-ventricular fistulae from anomalous epicardial and myocardial development
Authors: Palmquist-Gomes P , Ruiz-Villalba A , Guadix JA , Romero JP , Bessiéres B , MacGrogan D , Conejo L , Ortiz A , Picazo B , Houyel L , Gómez-Cabrero D , Meilhac SM , de la Pompa JL , Pérez-Pomares JM 
Published: January 2022

AbstractAimsIn this work we investigated the embryonic origin of coronary arterio-ventricular connections, known as coronary artery fistulas (CAF), a congenital heart disease associated to postnatal and adult changes in systemic hemodynamics that may cause cardiac ischemia.Methods and resultswe have used different animal models (mouse and avian embryos) to experimentally model CAF morphogenesis. Conditional Itga4 (alpha 4 integrin) epicardial deletion in mice and cryocauterisation of chick and quail embryonic hearts disrupted epicardial development and ventricular wall growth, two essential events in coronary embryogenesis. Additional transcriptomics and in vitro analyses were performed to better understand how arterio-ventricular connections are originated in the embryonic heart. Our results show myocardial discontinuities in the developing heart of mutant mice presenting epicardial defects and avian embryos submitted to a physical cryodamage of the ventricle. These ventricular discontinuities promote the formation of endocardial pouch-like structures resembling human CAF. The structure of these CAF-like anomalies was compared with histopathological data from a human CAF, showing histomorphological and immunochemical similarities. Both human and mutant mouse hearts showed similar anomalies in the compaction of the ventricular myocardium. In vitro experiments showed the abnormal contact between the epicardium and the endocardium promote the precocious differentiation of epicardial cells to smooth muscle.ConclusionOur work suggests that myocardial discontinuities in the embryonic ventricular wall are a causative of CAF. These discontinuities would promote the early contact of the endocardium with epicardial-derived coronary progenitors at the cardiac surface, leading to ventricular endocardial extrusion, precocious differentiation of coronary smooth muscle cells, and the formation of pouch-like aberrant coronary-like structures in direct connection with the ventricular lumen.Translational perspectiveCongenital coronary artery fistulas (CAFs) lead to complications such as myocardial hypertrophy, endocarditis, heart dilatation and failure. Unfortunately, and despite their clinical relevance, the origins these congenital anomalies remain unknown. In this work, we provide information on the developmental mechanisms involved in the formation of CAFs that is relevant for their early diagnosis and prevention.
In vitro Kinase-to-Phosphosite database (iKiP-DB) predicts kinase activity in phosphoproteomic datasets
Authors: Mari Tommaso , Mösbauer Kirstin , Wyler Emanuel , Landthaler Markus , Drosten Christian , Selbach Matthias 
Published: January 2022

ABSTRACTPhosphoproteomics routinely quantifies changes in the levels of thousands of phosphorylation sites, but functional analysis of such data remains a major challenge. While databases like PhosphoSitePlus contain information about many phosphorylation sites, the vast majority of known sites are not assigned to any protein kinase. Assigning changes in the phosphoproteome to the activity of individual kinases therefore remains a key challenge.. A recent large-scale study systematically identified in vitro substrates for most human protein kinases. Here, we reprocessed and filtered these data to generate an in vitro Kinase-to-Phosphosite database (iKiP-DB). We show that iKiP-DB can accurately predict changes in kinase activity in published phosphoproteomic datasets for both well-studied and poorly characterized kinases. We apply iKiP-DB to a newly generated phosphoproteomic analysis of SARS-CoV-2 infected human lung epithelial cells and provide evidence for coronavirus-induced changes in host cell kinase activity. In summary, we show that iKiP-DB is widely applicable to facilitate the functional analysis of phosphoproteomic datasets.
An essential function for autocrine Hedgehog signaling in epithelial proliferation and differentiation in the trachea
Authors: Yin Wenguang , Liontos Andreas , Koepke Janine , Ghoul Maroua , Mazzocchi Luciana , Liu Xinyuan , Lu Chunyan , Wu Haoyu , Fysikopoulos Athanasios , Sountoulidis Alexandros , Seeger Werner , Ruppert Clemens , Günther Andreas , Stainier Didier Y.R. , Samakovlis Christos 
Published: January 2022

AbstractThe tracheal epithelium is a primary target for pulmonary diseases as it provides a conduit for air flow between the environment and the lung lobes. The cellular and molecular mechanisms underlying airway epithelial cell proliferation and differentiation remain poorly understood. Hedgehog (Hh) signaling orchestrates communication between epithelial and mesenchymal cells in the lung, where it modulates stromal cell proliferation, differentiation and signaling back to the epithelium. Here, we reveal a new, autocrine function of Hh signaling in airway epithelial cells. Epithelial cell depletion of the ligand Sonic hedgehog (SHH) or its effector Smoothened (SMO) causes defects in both epithelial cell proliferation and differentiation. In cultured primary human airway epithelial cells, Hh signaling inhibition also hampers cell proliferation and differentiation. Epithelial Hh function is mediated, at least in part, through transcriptional activation as Hh signaling inhibition leads to downregulation of cell-type specific transcription factor genes in both the mouse trachea and human airway epithelial cells. These results provide new insights into the role of Hh signaling in epithelial cell proliferation and differentiation during airway development.
Nicotinic signaling is required for motor learning but not rehabilitation after spinal cord injury
Authors: Li Yue , Hollis Edmund R 
Published: January 2022

AbstractCurrently, therapeutic intervention for spinal cord injury is limited. Many approaches rely on strengthening the remaining substrate and driving recovery through rehabilitative training. As compared to learning novel compensatory strategies, rehabilitation focuses on restoring movements lost to injury. Whether rehabilitation of previously learned movements after spinal cord injury requires the molecular mechanisms of motor learning, or if it engages previously trained motor circuits without requiring novel learning. Our findings implicate the latter mechanism, as we demonstrate that nicotinic acetylcholine signaling is required for motor learning but is dispensable for the recovery of previously trained motor behavior after cervical spinal cord injury.