Loss Of Identity Research Articles

A threat to the natural World Heritage site rarely happens alone

This study contributes an empirical investigation of the likelihood that different external threats to a UNESCO Natural World Heritage Site occur in combination with each other when site characteristics and location are controlled for. For the purpose of the analysis, the World Heritage database and the UNESCO State of Conservation Reports are used and the nine most frequently appearing external threats are identified. These databases include 6852 site-year observations and 3316 threats over the period 1979–2023. The most commonly identified external threats are illegal activities, with eleven percent of all observations and mining with six percent. Transport infrastructure, tourism and visitor pressure are also common threats. Estimation results based on the multivariate Probit (equation system) model demonstrate that there are strong positive correlations between many pairs of the nine external threats. Most apparent are the links between illegal activities and loss of identity, social cohesion, changes in local population and community, water infrastructure (dams) and farming, as well as illegal activities and land conversion. There are also clear links between tourism and infrastructure. This emphasises that the various threats seldom appear in isolation from each other. Results also highlight that the threats have different drivers. Among the determinants, site characteristics and location are the most important ones. The likelihood of threats is highest for Natural Heritage Sites covered by forests or those in marine and coastal areas, Africa as well as the Arab region. It is also possible to identify a general increase in threats over time, although with a diminishing rate of growth towards the period 2015–2019. Contrary to this development and the general downturn in threats during the Covid-19 pandemic period of 2020–2023, pressure from tourism continues to grow. Methodologically, the results emphasize the need for multivariate Probit models when research goes beyond analyses of descriptive statistics and single equation approaches.

Scientific identity and epistemology of movement, exercise, and sport sciences through the analysis of scientific production of Italian full professors

This study addresses the epistemological and identity challenges encountered by Movement, Exercise, and Sport Sciences (MEaSS) in Italy, particularly concerning the organization of scientific knowledge within academic contexts. MEaSS struggles to define its scientific identity and address epistemological concerns due to the concurrent operation of its academic scientific disciplines (ASD) within both biomedical and pedagogical domains. This situation raises questions about the classification of knowledge within MEaSS and its distinctiveness within the Italian academic community. The study aims to analyze the scientific production of Italian full professors in two ASDs of MEaSS and determine its relevance to biomedical, pedagogical, psychological, or sports domains. It also intends to investigate the alignment of Italian academic structures with international standards, particularly the European Research Council (ERC) model. Each full professor’s top 20 scientific products, ranked by the highest number of citations within the Google Scholar database, were analyzed. The analysis of scientific production among Italian full professors in the two ASDs of Movement, Exercise, and Sport Sciences (MEaSS) revealed significant findings. In the ASD of M-EDF/01, 58.5% of publications were attributed to the biomedical domain, followed by 32.7% in the sports domain, 6.9% in the pedagogical domain, and 1.9% in the psychological domain. For the ASD of M-EDF/02, 47.5% of publications were in the biomedical domain, 25% in the sports domain, 18.1% in the pedagogical domain, and 9.4% in the psychological domain. The prevalence of biomedical-focused research within both ASDs of MEaSS highlights a notable deviation from the intended disciplinary boundaries, raising concerns regarding the loss of scientific identity and epistemological coherence. These results emphasize the urgent need for alignment with international standards to ensure clarity of scientific identity and promote interdisciplinary research in MEaSS.

Influence of Retirement Experiences on Psychological Well-Being of Retired Teachers in East Gonja Municipality, Ghana

Purpose: The purpose of the study was to examine the influence of retirement experiences on psychological well-being of retired teachers in the East Gonja Municipality. The study employed a quantitative approach underpinned by analytical cross-sectional design. The target population of the study comprised of retired teachers in the East Gonja Municipality. A total of 320 retired teachers from East Gonja Municipality were purposively selected to constitute the sample for the study. Methodology: Scale of Positive and Negative Experience (SPANE) and Psychological Well-Being Scale were adopted for data collection. Data was analysed using means and standard deviation and linear regression. Findings: The study found that most of the retired teachers in the East Gonja Municipality in the Savannah Region of Ghana experience positive emotions, express optimism, and are satisfied with their lives in their retirement phase of life. Unique contribution to theory, policy and practice: The study concludes that retirement experiences are unique and can be a liberating experience for retired teachers, where they can pursue their interests and hobbies without any restrictions. It is recommended that retirement should be a time for retired teachers to focus on their health and well-being, a time they can pursue activities that promote physical and mental health. This study recommends to education system to provide pre-retirement counselling and post-retirement support programmes, focusing on mental health and well-being. Also, the study recommends to pension and retirement agencies to develop and implement workshops and peer support programmes to promote retired teachers’ psychological well-being, addressing issues of social isolation and identity loss.

Qualitative investigation of disease course, characteristics and lived experience of generalized pustular psoriasis.

Generalized pustular psoriasis (GPP) is a relapsing-remitting chronic disease characterized by painful pustules with systemic symptoms that negatively impacts quality of life. The psychosocial and economic burden of this rare condition is not well characterized. To qualitatively characterize the cumulative burden of generalized pustular psoriasis on patients' quality of life and psychosocial wellbeing. A retrospective chart review of patients with generalized pustular psoriasis was performed to collect demographic information, followed by prospective semi-structured clinical interviews. Interview transcripts were analyzed using thematic analysis. Three major themes were revealed: (1) Burden of having a chronic disease with an unpredictable course, (2) an inability to fulfill societal roles results in a loss of identity, and (3) a physician-patient relationship grounded in trust and transparency can be invaluable in helping patients endure chronic disease. GPP has a negative impact on patients' quality of life and psychosocial wellbeing. Impairments in daily function and mental health primarily affects patients during flares and influences behavior during periods of quiescence. A strong patient-physician relationship may help mitigate the impact of GPP.

Multi deep invariant feature learning for cross-resolution person re-identification

Person re-identification (Re-ID) is focused on identifying and matching the same pedestrian when captured across various surveillance cameras. However, variations in camera performance and the distances between pedestrians and cameras may result in capturing images of the same person at different resolutions. This specific issue, referred to as cross-resolution person re-identification (CRReID), presents considerable difficulties in achieving accurate person Re-ID. To address this issue, we propose a Multi-level and scale Deep Invariant Feature learning Framework (MDIFF), which effectively tackles the problem of cross-resolution person matching. Our MDIFF reconstructs person features at the shallow layers to alleviate information gaps and extracts resolution-invariant features at the deep layers for cross-resolution person matching. First, to mitigate information loss in resolution-invariant features, we propose a Dual Input Feature Reconstruction (DIFR) structure incorporating dual-stream input and a lightweight decoder, constrained by degradation loss and image reconstruction loss. Second, we propose a Multi-level Global–Local feature Interaction and Fusion (MGLIF) module to enhance the invariant features of persons and obtain deep invariant representations, making the final representation more robust to resolution changes and more discriminative. Finally, to make the feature distribution of the same identity more compact across different resolutions, we propose a cross-resolution joint loss optimization strategy, including cross-resolution triplet loss, cross-resolution center loss, and identity loss. Our comprehensive experimental results demonstrate the superior performance and efficacy of our MDIFF, outperforming current state-of-the-art methods across various CRReID benchmark datasets. Our code is available at https://github.com/MiSanl/MDIFF-for-CRReID.

Caspases compromise SLU7 and UPF1 stability and NMD activity during hepatocarcinogenesis

Background & AimsThe homeostasis of the cellular transcriptome depends on transcription and splicing mechanisms. Moreover, the fidelity of gene expression, essential to preserve cellular identity and function is secured by different quality control mechanisms including nonsense-mediated RNA decay (NMD). In this context, alternative splicing is coupled to NMD, and several alterations in these mechanisms leading to the accumulation of aberrant gene isoforms have been involved in human disease including cancer. MethodsRNAseq, Westen blot, qPCR, co-IP in multiple silenced culture cell lines (replicates n≥4), primary hepatocytes and samples of animal models (Jo2, APAP, Mdr2-/- mice, n≥3). ResultsHere we describe that in animal models of liver injury and in human HCC (TCGA, NT =50 vs HCC =374), the process of NMD is inhibited. Moreover, we demonstrate that the splicing factor SLU7 interacts with and preserves the levels of the NMD effector UPF1, and that SLU7 is required for a correct NMD. Our previous findings demonstrated that SLU7 expression is reduced in the diseased liver, contributing to hepatocellular de-differentiation and genome instability during disease progression. However, little was known about the mechanisms underlying SLU7 downregulation. Here we provide evidence showing that caspases activated during liver damage would be responsible of the cleavage and degradation of SLU7. ConclusionsHere we identify the downregulation of UPF1 and the inhibition of NMD as a new molecular pathway contributing to the malignant reshaping of the liver transcriptome. Moreover, and importantly, we uncover caspases activation as the mechanism responsible for the downregulation of SLU7 expression during liver disease progression, which is a new link between apoptosis an hepatocarcinogenesis. Impact and implicationsThe mechanisms involved in the reshaping of hepatocellular transcriptome driving the progressive loss of cell identity and function in liver disease are not completely understood. In this context, we provide evidence on the impairment of a key mRNA surveillance mechanism known as nonsense-mediated mRNA decay (NMD). Mechanistically, we uncover a novel role for the splicing factor SLU7 in the regulation of NMD, including its ability to interact and preserve the levels the key NMD factor UPF1. Moreover, we demonstrate that the activation of caspases during liver damage mediates SLU7 and UPF1 proteins degradation and NMD inhibition. Our findings identify potential new markers of liver disease progression, and SLU7 as a novel therapeutic target to prevent the functional decay of the chronically injured organ.

Analysis, Simulation, and Experiments of Dynamics and Control of a Hydrostatic Wind Turbine Under Partial Load

Abstract Kω2 control, also called torque control, is a popular method for maximizing wind turbine power. For hydrostatic wind turbines, torque control becomes pressure control with pc=K'ω2 because pressure is proportional to torque. Inverse Kω2 control is an alternative approach using rotor speed control with pc=(p/K')1/2. This work analyzes the dynamics of hydrostatic wind turbines using forward and inverse Kω2 control with P-, PD-, PI-, and PID-control for feedback. Dimensionless, linearized models are used. Analysis shows that the mechanical rotor dynamics are much slower than the hydrostatic transmission dynamics and that frictional and leakage losses are negligible. Linear perturbation of the nonlinear model reveals that the closed-loop control is not in Evan's form, so that closed-loop poles and zeros both vary with the loop gain. Pole and zero root locus analysis shows how systems responses change with controller gains. Both control approaches require derivative controller action to sufficiently dampen their responses; both are also fundamentally limited in speed of response by a slow stable pole regardless of controller loop gains. Nonlinear system simulation shows that both control approaches track the maximum power point with nearly identical transient behavior and have nearly identical power losses when using suboptimal values of the control law gain, K. Pressure control has a gain margin of infinity and a phase margin of 99.3 degrees, while speed control has a gain margin of 22.4 dB and a phase margin of 73.8 degrees showing that pressure control is more robust than speed control. Experiments using the power regenerative hydrostatic test stand at the University of Minnesota show that the control approaches have different transient responses but capture comparable power under steady and turbulent conditions.

Cross Domain Early Crop Mapping with Label Spaces Discrepancies using MultiCropGAN

Abstract. Mapping target crops before the harvest season for regions lacking crop-specific ground truth is critical for global food security. Utilizing multispectral remote sensing and domain adaptation methods, prior studies strive to produce precise crop maps in these regions (target domain) with the help of the crop-specific labelled remote sensing data from the source regions (source domain). However, existing approaches assume identical label spaces across those domains, a challenge often unmet in reality, necessitating a more adaptable solution. This paper introduces the Multiple Crop Mapping Generative Adversarial Neural Network (MultiCropGAN) model, comprising a generator, discriminator, and classifier. The generator transforms target domain data into the source domain, employing identity losses to retain the characteristics of the target data. The discriminator aims to distinguish them and shares the structure and weights with the classifier, which locates crops in the target domain using the generator’s output. This model’s novel capability lies in locating target crops within the target domain, overcoming differences in crop type label spaces between the target and source domains. In experiments, MultiCropGAN is benchmarked against various baseline methods. Notably, when facing differing label spaces, MultiCropGAN significantly outperforms other baseline methods. The Overall Accuracy is improved by about 10%.

Abstract 1146: Metabolic Regulation Of Induced Pluripotent Stem Cell Derived Endothelial Cells Regenerative Capacity

Introduction: Induced pluripotent stem cells (iPSCs) derived endothelial cells (ECs) have emerged as a novel treatment strategy to restore limb perfusion in a murine model of peripheral artery disease (PAD). However, our lab has demonstrated that iPSC-EC in culture experience a failure of mitophagy and loss of cellular identity, limiting therapeutic implementation. Metabolic regulation of this mechanism is unknown. Methods: y6 human iPSCs were differentiated as previously described (Patsch Nat Cell Bio 2015) to generate ECs. Resulting iPSC-ECs were cultured under varying oxygen conditions (standard 21% vs. physoxic 4%). Markers of cellular identity and metabolic profile were analyzed. Results: iPSC-ECs lost cellular identity markers VE-Cadherin (55% positive in physoxic vs. 29% positive in standard) and PECAM1 (46% positive in physoxic vs. 39% positive in standard) over a period of two weeks (p<0.01). Single-cell RNA sequencing demonstrated the loss of cellular identity coincided with upregulation of endothelial-to-mesenchymal transition (EndMT), including COL1A1/2 and TGF-β. Physoxia significantly altered key metabolic proteins compared with standard conditions. Neuropilin 1 (Nrp1), an angiogenic related protein, was significantly increased in standard conditions (40% increased, p<0.01). PFKFB3, pathological upregulation of which correlates with increased EMT, was favorably downregulated in physoxic (52% lower, p<0.05) compared to standard conditions. Conclusion: iPSC-ECs under standard culture conditions demonstrated loss of EC identity with EndMT transition by single-cell transcriptomic analysis and by Western blot analysis of key metabolic proteins. Physoxia favorably impacted retention of key iPSC-EC identity markers. While increased Nrp1, as seen under standard conditions, can be associated with angiogenesis, the concomitant increase in PFKFB3 suggests an unfavorable metabolic activation and shift towards EndMT. Overactivation of PFKFB3 can results in net loss of energy in iPSC-ECs which leads to uncontrolled EndMT, and impaired regenerative capacity. Our results demonstrate iPSC-ECs effectively maintain metabolic control when grown in physoxic conditions.

Abstract 3142: Pik3c3 Safeguards Smooth Muscle Identity By Promoting Lysosome-mediated Yap1 Degradation

Background: Mature vascular smooth muscle cells (VSMCs) are quiescent and geared for maintaining vascular homeostasis by expressing a unique repertoire of contractile genes. However, key factors in controlling the contractile phenotype of VSMCs are poorly defined. Class III PI3K, PIK3C3 (Phosphatidylinositol 3-Kinase Catalytic Subunit Type 3) is a critical regulator of vesicular trafficking. Although PIK3C3 is known to play an essential role in cardiac homeostasis, its role in VSMCs remains elusive. Methods: To elucidate the role of Pik3c3 in regulating SMC fate and plasticity, we generated smooth muscle-specific Pik3c3 inducible knock out (KO) mice with SMC-lineage tracing. Proteomic mass spectrometry, next-generation RNA sequencing, SMC fate mapping coupled with single-cell RNA sequencing were applied to determine the phenotype and trajectories of SMCs after Pik3c3 ablation. Results: Specific ablation of Pik3c3 in SMCs results in severe gastrointestinal pseudo-obstruction and premature death. Analysis of aorta from the KO mice revealed dramatic vascular remodeling including dilatation, thickening of the vascular wall, spontaneous neointimal formation that was largely contributed by cells of SMC origin, and complete loss of contractility. Proteomics, bulk RNA-seq, and scRNA-seq studies of SMC-restricted Pik3c3 KO mouse aorta showed near complete loss of smooth muscle identity and the acquisition of an intermediate smooth muscle progenitor-like cell phenotype that underwent re-programming into multiple cell types including macrophages, T cells and osteoblasts. Mechanistically, we found that Pik3c3 deletion in VSMCs induces the accumulation of YAP1 (Yes associated protein 1) and its downstream target genes; this elevated YAP1 program appears to result from a blockade of autophagic lysosome-mediated degradation of YAP1, leading to phenotypic modulation of SMCs. Importantly, pharmacological inhibition of YAP by Verteporfin or genetic deletion of Yap1 rescues the vascular phenotype of Pik3c3 SM-specific KO mice. Conclusion: Our study reveals PIK3C3 as a master regulator safeguarding VSMC identity, and perturbation of the PIK3C3-YAP axis may be a novel mechanism underlying VSMC-driven vascular diseases in humans.

Abstract 1041: Loss Of The ETS Transcription Factor ERG Disrupts Fate-defining Programs In The Aortic Endothelium And Promotes Expansion Of Endothelial Lineage Cells In Atherosclerotic Plaque

Aim: The ETS transcription factor ERG has been identified as a principal regulator of endothelial function through its ability to repress inflammation in endothelial cells (ECs), and loss of ERG induces endothelial to mesenchymal transition (EndMT) in fibrotic disease. To investigate ERG function in atherosclerosis, we employed an EC-specific Erg knockout ( Erg EC - KO ) in PCSK9-overexpression and apoE-deficient murine atherosclerosis models. Methods: Atherosclerosis was induced in 10-week-old Erg EC - KO mice or wild-type counterparts that had a Cre-inducible EC lineage tag ( Cdh5 CreER ; R26-CAG-LSL-Sun1-sfGFP ). Atherosclerosis was modeled by Apoe deletion or AAV8-PCSK9 with 12 weeks of high-cholesterol diet (1.25%). Aortic intimal cells were assessed with flow cytometry. Plaque burden, morphology, and cellularity were characterized with brightfield, Oil Red O, H&E, Movat, and immunofluorescence imaging. Results: Erg EC-KO in PCSK9-overexpression mice led to a 1.6-fold increase in aortic plaque burden and plaque formation in regions that are usually protected (e.g., greater curvature; p≤0.03; n=9-10). Loss of ERG increased elastin breaks (1.7-fold; p=0.02; n=9) and decreased fibrous cap thickness (0.76-fold; p=0.02; n=9-10) in aortic arch cross sections. Aortic intimal digests from Erg EC- KO mice contained increased Sun1-sfGFP + EC lineage cells (1.9-fold; p=0.01; n=4), which had reduced CD31 positivity (0.79-fold; p=0.03; n=4). Notably, a 5.3-fold increase in EC lineage cells was observed in plaques from brachiocephalic artery cross sections (p=0.0001; n=6-15), which had hallmarks of EndMT (e.g., 31.5-fold increase in GFP + ACTA2 + cells, p=0.02, n=3-5). Increased aortic plaque burden was recapitulated in apoE-deficient E rg EC- KO mice (2.1-fold; p=0.02; n=4-8). Conclusion: Endothelial Erg KO results in increased plaque burden and altered plaque topography in murine atherosclerosis. Loss of ERG induces EndMT and marked ingression of ECs from the luminal endothelium to the plaque interior. These findings highlight loss of ERG as a novel mechanism by which intimal ECs acquire mesenchymal identity in atherosclerosis and implicate EC identity loss as a driver of EC migration into plaques, which is associated with a vulnerable morphology.

Abstract 3067: Chronic Knockout Of The ETS Transcription Factor ERG Promotes Loss Of Endothelial Cell Identity And Endothelial Cell Dysfunction In An Aortic Endothelial Cell Model Relevant For Atherosclerosis

Background: The ETS transcription factor ERG is a key endothelial cell (EC) transcription factor. ERG represses vascular inflammation and is downregulated in chronic inflammatory diseases (e.g. liver fibrogenesis, atherosclerosis). Previously, transient ERG knock-down has been associated with endothelial-mesenchymal transition (EndMT) and EC dysfunction; however, the mechanisms underlying EndMT and the EC dysfunction associated with chronic ERG loss have not been elucidated in an atherosclerosis-relevant model. We hypothesize that chronic ERG knockout (KO) in telomerase-immortalized human aortic ECs (teloHAECs) induces EndMT and contributes to EC dysfunction underlying vascular dysregulation in atherosclerosis. Methods: TeloHAECs with CRIPSR/Cas9-mediated deletion of ERG were used. Chromatin accessibility and gene expression in ERG KO and wildtype (WT) teloHAECs were assessed using ATAC-seq (n=2) and RNA-seq (n=5-6). TOBIAS and diffTF were used to identify enriched motifs by footprinting (P<0.05) and to profile TF activity (FDR<0.05), respectively. ERG-mediated EC dysfunction was investigated using immunofluorescence (IF; n=3), western blot (WB; n=3), and a timelapse migration assay (n=3). Results: There were ~ 21,000 differentially accessible chromatin peaks between ERG KO and WT ECs. Integrated analysis of chromatin accessibility and gene expression demonstrated increased activity of TGFβ-SMAD and IL-1β signaling constituents and classical EndMT transcription factors. Loss of ERG downregulated EC genes (e.g., CLDN5 , TIE1 ) and protein expression (e.g., CDH5, vWF) and upregulated mesenchymal genes (e.g., ACTA2 , FSP1 ) and protein distribution (e.g., FN1, COL1A1). Investigation of EC-dysfunction phenotypes revealed increased migration and proliferation in ERG KO teloHAEC - with the percentage of Ki67 positive ECs increasing from 14% to 49% (P<0.05, n=3). Conclusion: ERG KO in cultured aortic ECs markedly impacts chromatin accessibility and gene expression and induces EC identity loss, migration, and proliferation, providing mechanistic insight into the role of ERG in vascular dysfunction in atherosclerosis.

THREAT – DAMAGE – PROTECTION: ANTHROPOLOGICAL ASPECTS OF RHIZOMORPHOUS REALITY

This study contains an ontological analysis of the subject’s existence in the realities of an open, unstable, heterogeneous space, requiring from him new abilities and qualities that will allow him to survive and adapt. The traumatic social experience of the present generation is reflected in the triad of anthropological aspects of its hybrid existence: threat - damage - protection. The threat appears as permanent. The damage is expressed in a person's loss of identity, sociality and subjectivity. Protection correlates with physicality, mobility and nomadism.

A Study of Donne's Poetry in Postcolonial Feminist Perspective: To His Mistress Going to Bed

To His Mistress Going to Bed is a love poem by John Donne, a British metaphysical poet. The poem describes the process in which the male protagonist seduces the female protagonist. Most critics focus on the mystical metaphor of Donne as a poet, but lack attention to the underlying significance of this poem. This article analyzes the female subject in poetry based on the theory of postcolonial feminism, revealing that the female subject in the poem is in a state of being banned by mainstream Western society, suppressed by patriarchal society, and colonized. It studies the issue of identity loss and identity construction of female subjects; This article also explores the social background and cultural colonization of the Elizabethan and James I eras in which the poet lived, and the subtle influence of colonial consciousness on the poet and his poetry. Ultimately, it is concluded that John Donne constructed a textual world of "others" through the poetic text in the process of creating this poem. This paper provides a new perspective for the study of postcolonial feminism and helps to drive people to engage in new reflections.

Single-cell analyses reveal transient retinal progenitor cells in the ciliary margin of developing human retina

The emergence of retinal progenitor cells and differentiation to various retinal cell types represent fundamental processes during retinal development. Herein, we provide a comprehensive single cell characterisation of transcriptional and chromatin accessibility changes that underline retinal progenitor cell specification and differentiation over the course of human retinal development up to midgestation. Our lineage trajectory data demonstrate the presence of early retinal progenitors, which transit to late, and further to transient neurogenic progenitors, that give rise to all the retinal neurons. Combining single cell RNA-Seq with spatial transcriptomics of early eye samples, we demonstrate the transient presence of early retinal progenitors in the ciliary margin zone with decreasing occurrence from 8 post-conception week of human development. In retinal progenitor cells, we identified a significant enrichment for transcriptional enhanced associate domain transcription factor binding motifs, which when inhibited led to loss of cycling progenitors and retinal identity in pluripotent stem cell derived organoids.

Pancreatic β-Cell Identity Change through the Lens of Single-Cell Omics Research.

The main hallmark in the development of both type 1 and type 2 diabetes is a decline in functional β-cell mass. This decline is predominantly attributed to β-cell death, although recent findings suggest that the loss of β-cell identity may also contribute to β-cell dysfunction. This phenomenon is characterized by a reduced expression of key markers associated with β-cell identity. This review delves into the insights gained from single-cell omics research specifically focused on β-cell identity. It highlights how single-cell omics based studies have uncovered an unexpected level of heterogeneity among β-cells and have facilitated the identification of distinct β-cell subpopulations through the discovery of cell surface markers, transcriptional regulators, the upregulation of stress-related genes, and alterations in chromatin activity. Furthermore, specific subsets of β-cells have been identified in diabetes, such as displaying an immature, dedifferentiated gene signature, expressing significantly lower insulin mRNA levels, and expressing increased β-cell precursor markers. Additionally, single-cell omics has increased insight into the detrimental effects of diabetes-associated conditions, including endoplasmic reticulum stress, oxidative stress, and inflammation, on β-cell identity. Lastly, this review outlines the factors that may influence the identification of β-cell subpopulations when designing and performing a single-cell omics experiment.

Transcriptomics Analysis Identifies the Decline in the Alveolar Type II Stem Cell Niche in Aged Human Lungs.

Aging poses a global public health challenge, which is linked to the rise of age-related lung diseases. The precise understanding of the molecular and genetic changes in the aging lung that elevate the risk of acute and chronic lung diseases remains incomplete. Alveolar type II (AT2) cells are stem cells that maintain epithelial homeostasis and repair the lung after injury. AT2 progenitor function decreases with aging. The maintenance of AT2 function requires niche support from other cell types, but little has been done to characterize alveolar alterations with aging in the AT2 niche. To systematically profile the genetic changes associated with age, we present a single-cell transcriptional atlas comprising nearly half a million cells from the healthy lungs of human subjects spanning various ages, sexes, and smoking statuses. Most annotated cell lineages in aged lungs exhibit dysregulated genetic programs. Specifically, the aged AT2 cells demonstrate loss of epithelial identities, heightened inflammaging characterized by increased expression of AP-1 (Activator Protein-1) transcription factor and chemokine genes, and significantly increased cellular senescence. Furthermore, the aged mesenchymal cells display a remarkable decrease in collagen and elastin transcription and a loss of support to epithelial cell stemness. The decline of the AT2 niche is further exacerbated by a dysregulated genetic program in macrophages and dysregulated communications between AT2 and macrophages in aged human lungs. These findings highlight the dysregulations observed in both AT2 stem cells and their supportive niche cells, potentially contributing to the increased susceptibility of aged populations to lung diseases.

Creation of a ‘New Species’: A Decolonial Reading of Frantz Fanon and B.R Ambedkar

This paper argues that Fanon’s critique of colonisation and Ambedkar’s evaluation of the caste system share similarities because they collectively present a psycho-social understanding of the oppressed human condition. Both Fanon and Ambedkar argue that colonial and caste oppression has introduced a loss of cultural legacy, identity and capacity for self-determination. This loss is imprinted so deeply in the minds of the colonised and stakeholders of the caste system that a new species with a different social, political and economic consciousness is needed to transform and facilitate the formation of radical new social beliefs. For such a decolonisation of the mind to occur, Fanon proposes that violence—the capacity to resist and question—is fundamental, which I argue is also the foundation of Ambedkar’s solution to annihilate caste. However, violence in terms of Fanon and Ambedkar does not translate to physical harm. It is the intellectual capacity and desire for self-reflection that ruptures existing hierarchical power structures and renews the meaning of being human in democratic civilisations.

Applications of Grounded Theory Methodology to Investigate Hearing Loss: A Methodological Qualitative Systematic Review With Developed Guidelines.

Qualitative methodologies are commonly adopted in hearing loss research. Grounded theory methodology is increasingly used to establish novel theories explaining experiences related to hearing loss. Establishing and improving the quality of grounded theory studies has been emphasized as critical to ensuring theoretical trustworthiness. Thus, the primary aim of the present study was to systematically review hearing loss research studies that have applied grounded theory methodology and assess the methodological quality of those grounded theory applications. Secondarily aims were to (i) explore how grounded theory methodology has been applied to investigate hearing loss, and (ii) use the findings of the review to develop a set of guidelines to aid the future high-quality application of grounded theory methodology to hearing loss research. Original peer-reviewed studies applying grounded theory methodology and published in English were identified through systematic searches in 10 databases; Applied Social Sciences Index and Abstracts, British Nursing Index, Cumulative Index to Nursing and Allied Health Literature, EBSCO, Global Health, MEDLINE (OvidSP), PsycINFO, PubMed, Scopus, and Web of Science. The quality of studies was assessed according to 12 grounded theory principles using the Guideline for Reporting, Evaluating, and applying the core principles of Grounded Theory studies (GUREGT) tool. Data were analyzed using qualitative inductive thematic analysis. After the removal of duplicates, 155 articles were retrieved. Of those, 39 met the criteria for inclusion in the systematic review. An increase in the adoption of grounded theory methodology to investigate hearing loss was identified with the number of published studies tripling in the last 5 years. Critical appraisal using the GUREGT tool identified four studies as high-quality. Most included studies were of moderate study quality (n = 25), and 10 were classified as being of low study quality. Using inductive thematic analysis, the included studies investigated one of four areas relating to hearing loss: (a) Living with hearing loss, (b) Identity and hearing loss, (c) Coping strategies for hearing loss, and (d) Audiological counseling and rehabilitation. Analysis also identified four main grounded theory factors frequently overlooked in hearing loss research: the different schools of grounded theory, sampling strategy, sample size, and the depth of grounded theory application. Use of grounded theory methodology is increasing at a rapid rate in hearing loss research. Despite this, studies conducted in the field to date do not meet and apply the full spectrum of grounded theory principles, as outlined by the GUREGT tool. To improve methodological rigor in future studies using grounded theory, we propose a set of guidelines that address the most commonly overlooked methodological considerations in hearing loss studies to date. The guidelines are designed to aid researchers to achieve high methodological quality in any field, improve qualitative rigor, and promote theoretical credibility.

The Undeserved Indignity: Making a Case for Muslim Dignity

A simple definition of Human dignity describes it as a worth attached to every human being, by virtue of being born as a human. But is the situation really so simple? Several instances reveal that the notion, nature and operation of dignity evade such simplistic definitions. As we delve deeper, an important question surfaces: how is it that dignity remains most elusive for the Muslim populations? The so-defined age of Terror further justifies such loss of dignity for the Muslim populations. It must be stressed however, that while terror events like 9/11 (the USA) or 7/7 (London, UK) or 9/7 (New Delhi, India), have served to resuscitate the fear of the radical other (that is, the Muslims) these attitudes go back a long time in history. It is reflected in the general outlook towards Muslims. Undoubtedly, there remain a section of terrorists, who borrow from a particular interpretation of Islam. But is this cause enough for the wholesale othering of the Muslim community? Having to live as second- rate people despite being citizens, being saddled with assumed linkages to terrorism; these are just a few dimensions of the otherising discourse. Islam comes into the picture not only because the ‘terrorists’, in some cases, have been Muslims, but also because these radical sections forward Islam as the source of their actions. We need to question the uncritical homogenizing that follows such revelations, viz. all Muslims are terrorists, Islam is a violent religion, Muslims are disloyal and radical, so on and so forth. The perpetual tagging as the potential terrorists causes not only an irretrievable loss of identity, but also a fatal blow to one’s dignity. Here, Kant’s notion of dignity becomes useful for understanding the problem of Muslim indignity.