North Carolina Central University

Sickle cell disease (SCD) is a devastating genetic hematologic disorder affecting approximately 80,000 African Americans. Beyond the well-characterized vaso-occlusive pain crises, patients experience significant psychological morbidity, including kinesiophobia (fear of movement) and depression, which profoundly impact quality of life and functional outcomes. This comprehensive review synthesizes current evidence on the relationship between kinesiophobia and depression in SCD patients, with particular attention to gender differences, underlying pathophysiological mechanisms, and clinical implications for multidisciplinary care. We conducted a systematic examination of the literature on kinesiophobia, depression, and psychosocial factors in SCD, incorporating data from multiple cohort studies totaling 247 adult African American patients. Assessment instruments included the Tampa Scale for Kinesiophobia (TSK), Beck Depression Inventory (BDI), and Center for Epidemiologic Studies Depression Scale-Revised (CESD-r). Kinesiophobia prevalence in SCD patients (mean TSK score = 30.48) was comparable to patients with chronic back pain and fibromyalgia. Significant gender differences emerged, with women demonstrating strong positive correlations between kinesiophobia and depression (BDI r = 0.31, p = 0.045; CESD-r = 0.54, p = 0.009), while no significant relationships were observed in men (BDI r = 0.24, p > 0.05; CESD-r = 0.13, p > 0.05). The relationship appears mediated by psychomotor retardation, somatization, and pain catastrophizing behaviors. Fear of movement represents a clinically significant but underrecognized contributor to depressive symptomatology in women with SCD. These findings highlight the need for gender-specific psychological interventions and integrated care approaches that address both physical and mental health components of this complex genetic disorder.

Healthcare disparities in pain management represent one of the most persistent and pernicious manifestations of systemic bias within medicine. This comprehensive review examines the complex intersection of implicit bias, racial stigmatization, and clinical decision-making in the context of sickle cell disease, a predominantly African descent genetic disorder characterized by severe recurrent acute pain episodes and chronic pain that worsens with age. Through analysis of empirical research spanning psychosocial functioning, pain perception, healthcare utilization patterns, and provider attitudes, we demonstrate how societal-level prejudices become institutionalized within medical practice, resulting in systematic undertreatment of legitimate pain and inappropriate labeling of patients as drug-seeking. The current opioid crisis has paradoxically exacerbated these disparities, as heightened scrutiny of narcotic prescribing disproportionately affects minority patients who already face substantial barriers to adequate pain management. We argue that understanding the biopsychosocial complexity of sickle cell disease within its historical and social context is essential for dismantling discriminatory practices and achieving equitable healthcare delivery. This paper presents a framework for recognizing and addressing implicit bias in clinical settings while maintaining appropriate safeguards against prescription drug diversion. The implications extend beyond sickle cell disease to encompass broader questions about how societal inequities become embedded in medical practice and perpetuated through ostensibly objective clinical assessments.

In an era marked by institutional uncertainty, algorithmic expansion, and contested knowledge systems, this chapter offers a reflective and future-facing exploration of information science through the lens of a Virgo scholar, artificial intelligence (AI) ethicist, and academic leader. Anchored in personal narrative and professional praxis, the chapter moves through critique, reimagination, and actionable strategies for transforming how we engage with classification, archives, metadata, and AI. It calls for research agendas rooted in care, equity, and imagination – and for practices that balance structure with adaptability. Grounded in values like transparency and epistemic justice, this chapter provides a constellation of tools for those navigating a rapidly evolving field. Ultimately, it frames information systems not merely as technical infrastructures, but as cultural artifacts that must be cultivated with purpose, precision, and collective possibility.

Background: Sirtuin 3 (SIRT3), a mitochondrial NAD+-dependent deacetylase, plays a central role in regulating mitochondrial metabolism, oxidative stress, and cell survival. Although SIRT3 has been implicated in angiogenesis, apoptosis, and inflammation, its global proteomic impact on the brain remains unclear. This study aimed to systematically characterize alterations in angiogenesis-, apoptosis-, chemokine-, and cytokine-related proteins in the brains of SIRT3 knockout (SIRT3 KO aka SIRT3−/−) mice compared with wild-type (WT) controls. Methods: Adult male C57BL/6 WT and SIRT3 KO mice were analyzed using proteome profiler antibody microarrays covering 53 angiogenesis factors, 21 apoptosis markers, 28 chemokines, and 111 cytokines. Protein expression changes were quantified by chemiluminescence imaging and densitometric analysis. Results: The results showed a distinct suppression of angiogenic proteins (amphiregulin, angiogenin, DPPIV, GM-CSF, IGFBP-2, IGFBP-3, IL-1β, PDGF-AA, PDGF-BB, proliferin, serpin F1, thrombospeondin-2, TIMP-4, and VEGF-B), activation of both pro-apoptotic (BAD, cytochrome c, Smac/DIABLO, HIF-1α, Fas, TNF R1, and TRAILR2) and anti-apoptotic, stress-related proteins (Bcl-x, catalase, HO/HMOX2, HSP27, HSP70, and MCL1) in the SIRT3 KO animals compared with the WT controls. Notably, SIRT3 deficiency was associated with increased expression of inflammatory mediators linked to glial activation and neurodegeneration (BLC/CCL13, LIX/CXCL5, MIG/CXCL9, chitinase 3-like 1, CCL22/MDC, IL-6, myeloperoxidase, osteopontin, RBP4, Reg3G, and TNF-α), alongside disturbed proteins involved in immune surveillance and vascular remodeling (6Ckine/CCL21, chemerin, DF, EGF, fractalkine/CX3CL1, HGF, IGFBP-6, IL-16, and I-TAC). Conclusions: Collectively, these findings demonstrate that SIRT3 is a key regulator of mitochondrial-dependent vascular, apoptotic, and neuroimmune pathways in the brain, and that its loss creates a molecular environment consistent with heightened vulnerability to neurodegenerative processes.

Abstract The High-latitude Time-domain Survey (HLTDS) for the Nancy Grace Roman Space Telescope (Roman) will discover thousands of high-redshift Type Ia supernovae (SNe Ia) to set generation-defining cosmological constraints on dark energy. To construct the Roman SN Hubble diagram, a strategy to obtain redshifts must be determined. While the nominal HLTDS will use only the Roman prism, in this work, we consider the utility of the Roman grism observations from overlap with the High-latitude Wide-area Survey for SN Ia cosmology. We determine a galaxy grism redshift recovery rate by simulating dispersed grism images and measuring redshifts with the Grizli software, obtaining an H -band 50% redshift recovery at magnitude 20.61 and 90% recovery at magnitude 19.27. To estimate the total number of spectroscopic redshifts expected for Roman SN cosmology, we also consider a Roman prism SN redshift efficiency and a ground-based telescope redshift efficiency for host galaxies. We apply these redshift efficiencies to SN Ia catalog-level simulations and predict that ∼6800 SNe will have an SN or host spectroscopic redshift. Second, we evaluate the size of potential systematics related to modeling the grism redshift efficiency by considering the impact of additional dependences on stellar mass and host-galaxy color. We estimate the largest potential size of this systematic to be 0.0066 ± 0.002 and −0.0266 ± 0.0079, roughly 42.9% and 49.6% of the statistical uncertainty, for w 0 and w a , respectively. Lastly, we consider the effects of assuming different redshift sources on the optimization of the HLTDS survey strategy by measuring relative changes to the dark energy figure of merit.

This study investigated the antibacterial activities of Se-Al/Zn layered double hydroxide (LDH) and its polycarbazole (PCz) hybrid against Gram-positive Bacillus subtilis and Gram-negative E. coli cells. Antibacterial performances were evaluated using zone of inhibition assays, viable cell counting, and measurement of metabolic activity based on intracellular ATP levels. The collective results showed that both materials exhibited significant antibacterial activity, with PCz–Se–Al/Zn LDH demonstrating enhanced antibacterial activity compared to Se–Al/Zn LDH. Fluorescent live/dead staining and scanning electron microscopy revealed that treatment with either material resulted in loss of metabolic activity and induction of a non-culturable state in bacterial cells, without observable membrane damage or pronounced morphological changes. Possible antibacterial mechanisms of action associated with LDH and PCz–LDH systems are briefly discussed.

Understanding structure-property relationships is essential for designing multifunctional biopolymer composites that integrate mechanical robustness, barrier performance, and antimicrobial activity in sustainable materials. Chitosan (CS) exhibits excessive hydrophilicity, limited mechanical strength, and poor moisture stability, which restrict its long-term performance in packaging applications. With the aim to enhance the mechanical strength, moisture absorption, and overall performance of CS, an organic aromatic polymer, poly(o-phenylenediamine) (PoPD), was introduced into the matrix through in situ oxidative polymerization. Incorporation of PoPD improved the properties of CS by introducing aromaticity and electron delocalization, thereby limiting water uptake and molecular diffusion without relying on petroleum-derived additives. Remarkably, a low filler concentration (0.15 wt % of PoPD) produced drastic enhancement, in a tensile strength of 27.98 ± 1.40 MPa (as compared to 9.28 ± 0.46 MPa in neat CS) and an elongation at break value of 5.44 ± 0.27%. Moisture absorption studies confirmed a marked reduction at low filler levels, whereas higher PoPD contents generated compact morphologies that further restricted diffusion. Antibacterial evaluations revealed pronounced inhibition of Bacillus subtilis across all filler concentrations. Molecular docking analyses attributed this behavior to π-π-stacking, hydrogen bonding, and electrostatic interactions between PoPD and bacterial residues. The properties can be tuned by adjusting the filler content, producing multifunctional composites suitable for smart, sustainable packaging applications.

IntroductionStereotactic body radiation therapy (SBRT) for clinically localized prostate cancer has been associated with prolonged acute obstructive and irritative lower urinary tract symptoms (LUTS). Prophylactic alpha-adrenergic antagonists have been used therapeutically to prevent obstructive symptoms in patients undergoing prostate SBRT, however irritative symptoms may be better addressed with beta 3-adrenergic receptor agonists, which are shown to be safe and effective in men with overactive bladder (OAB).ObjectiveThis study retrospectively examines the pattern of bothersome urinary frequency associated with SBRT to determine which patients would have potentially benefitted from prophylactic beta 3-adrenergic receptor agonist.MethodsPatients with clinically localized prostate cancer who underwent prostate SBRT (n=1676) were followed for 3 months post-treatment to evaluate for bothersome urinary frequency, which was assessed by question 4E on the EPIC-26. Answers to question 4E and tamsulosin usage were recorded at regular follow-ups to assess, and demographic factors as well as baseline prostate volume, alpha-adrenergic antagonist usage and IPSS score severity were used as modifiers.ResultsUsing the IPSS questionnaire to determine baseline LUTS, most patients reported moderate urinary symptoms (53%), followed by mild (34%) and severe (13%). Patients endorsed increased irritative LUTS at 1-month post-SBRT, with similar rates of frequency at 3 months compared to baseline. Patients with moderate and severe urinary symptoms per the baseline IPSS were more likely to endorse bothersome urinary frequency at one month post SBRT (EPIC-26 Q4E; OR 2.58 and 10.2 respectively) compared to those with mild symptoms. No significant differences were found in urinary frequency between patients who used and did not use an alpha antagonist at baseline.ConclusionsBothersome post-SBRT urinary frequency persists 1-month post-SBRT. Baseline LUTS predicts bothersome post-treatment urinary frequency. Prophylactic alpha-adrenergic antagonists do not protect against bothersome acute urinary frequency. This paper makes the case that urinary frequency may be better addressed with a prophylactic beta-3 agonist, like vibegron, which is designed to treat storage-related LUTS concerns.