Environmental and Occupational Health Sciences Institute
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Type 1 diabetes mellitus following COVID-19 vaccination: a systematic review and meta-analysis
No full textObjective: The purpose of this systematic review was to describe the clinical-epidemiological characteristics of patients who developed Type 1 Diabetes Mellitus (T1DM) post-COVID-19 (Coronavirus Disease 2019) vaccination and determine the T1DM prevalence among COVID-19 vaccine recipients.
Introduction: COVID-19 vaccines reduce the rate of hospitalizations and death from COVID-19 infection. Emerging evidence of the development of T1DM post-COVID-19 vaccination poses concerns. It is imperative to determine the prevalence of T1DM among vaccinated individuals and describe patient characteristics to help patients and providers make informed shared decisions regarding COVID-19 vaccination.
Inclusion criteria: This systematic review included case reports/series and observational studies that reported the incidence of T1DM following COVID-19 vaccination among participants of all ages and sexes.
Methods: Seven databases were searched to find published and unpublished literature. Two independent reviewers performed the screening of articles, critical appraisal, and the extraction of data. Meta-analysis using the JBI SUMARI (Joanna Briggs System of the Unified Management of the Assessment and Review of Information) was conducted to determine the prevalence of T1DM among COVID-19 vaccine recipients. Clinical-epidemiological characteristics of patients who developed T1DM following COVID-19 vaccination were synthesized narratively.
Results: 27 studies were included in this systematic review. Based on four studies included in the meta-analysis the prevalence of T1DM post-COVID-19 vaccination is 1%. Individuals who developed T1DM exhibited distinct genetic markers, had a history of autoimmune diseases, or were undergoing treatment with biological agents.
Implications for practice: Clinicians should counsel patients that T1DM is rare after COVID-19 vaccination. Clinicians need to monitor people who have autoimmune conditions and/or receiving biological treatments after receiving COVID-19 vaccines for T1DM symptoms.
Conclusion: The prevalence of T1DM following COVID-19 vaccination is low, which should not be a barrier to vaccination. Clinicians and patients with distinct genetic markers or a history of autoimmunity should be aware of this potential complication, enabling them to make informed decisions.D.N.P.Includes bibliographical reference
Chronic stress increases the risk of Alzheimer’s disease
No full textAlzheimer’s Disease (AD) is the most prominent neurodegenerative disorder, affecting the lives of over six million people in the United States alone. This disease is characterized by a sharp decline in cognitive functions and impaired memory. With no known cure, AD is a disorder that is more prevalent as age increases. The pathology of AD is not fully understood, but the key factors are amyloid precursor protein (APP), its proteolytic processing into Aβ peptides (Aβ-40 and Aβ-42) and the formation of neurofibrillary tangles via hyperphosphorylated tau proteins. The molecular mechanism for neurodegeneration is a result of neurotoxic Aβ-42 plaque accumulation in the neurons by the dysregulation of Aβ transporters that excrete Aβ out of the brain into the bloodstream. Many biological, genetic, and psychological risk factors that could contribute to the onset of the disease in late adulthood have been examined. One of these is chronic stress, in which the response involves complex networking between the hypothalamic–pituitary–adrenal axis and the autonomic nervous system. Prolonged stress triggers hyperactivity and exhaustion of these systems, consequently increasing the release of cortisol, which binds to glucocorticoid receptors that enter the nucleus to increase transcription of APP. The mechanisms underlying the connection between stress response and Alzheimer’s Disease indicate that chronic stress increases susceptibility by increasing glucocorticoid receptor activity responsible for transcribing APP, which is then cleaved into neurotoxic Aβ-42.Winner, First Place, 2024 Paul Robeson Library Undergraduate Research Award
Investigation of photocatalytic properties of iron nanoparticles synthesized via pulsed laser ablation in liquids
No full textIron nanoparticles have interesting optical and magnetic properties, making them promising candidates for various applications such as catalysis and nanoelectronics. Pulsed laser ablation in liquids (PLAL) provides a versatile approach for the synthesis of iron-based nanostructures, offering control over size, shape, and composition through manipulation of laser parameters and liquid environment. We focus on the synthesis and characterization of iron-based nanoparticles using PLAL for nanoparticle production along with UV-Vis spectroscopy, atomic force microscopy, and Raman spectroscopy for sample analysis. The optical properties of the synthesized nanoparticles will be investigated through UV-Vis spectroscopy to understand their absorption and transmission behavior in the ultraviolet and visible spectral regions. The composition and structure of the nanoparticles are investigated with Raman spectroscopy and their morphology is determined through atomic force microscopy.Presented at the annual Celebration of Undergraduate Research and Creative Activity while the author was an undergraduate student at Rutgers University-Camden
A strengths-based approach to managing personal information for people with serious mental illness seeking employment
No full textStatement of the Problem: Employer stigma is central to low workforce participation among individuals with serious mental illness (SMI). Because of employer stigma, some job seekers are reluctant to disclose the presence of SMI during the employment application process or once employed, even though disclosure may provide access to needed support and job accommodations and explain any gaps in their work history. A disclosure decision-making discussion, such as the Plan for Managing Personal Information (PMPI), provides a valuable strategy for planned disclosure discussions (Waghorn & Spowart, 2010).
Method: This study used a field correspondence audit design to observe the impact of disability status and the inclusion of elements of the PMPI on callbacks from employers hiring for line/prep cook positions. Cover letters and resumes, matched in their qualifications and skills but differed on the reason for an employment gap, were sent to 750 hiring managers of restaurants throughout the United States. Hypothetical applicants were either out of work due to receiving treatment for a mental health condition, a serious physical injury, or no disability. Half of the cover letters included elements of the PMPI.
Results: Using binary logistic regression to predict callback based on disability status and inclusion of elements of the PMPI, results supported the prediction that job seekers with a mental health condition would be less likely to be called back compared to job seekers with a serious physical injury, or no stated disability. However, the data did not support the prediction that including elements of the PMPI would improve the likelihood of receiving a callback for any hypothetical applicants.
Conclusion: The stigma around mental illness continues to persist among employers. Hiring managers in the restaurant industry were less likely to call back applicants who disclosed an MHC. Although no effect was found for including elements of the PMPI during the application stage, job seekers and employees can still benefit from planning discussions with service providers on managing personal information in employment. Educating businesses and dispelling myths associated with mental illness is necessary to continue to address mental health stigma in hiring.Ph.D.Includes bibliographical reference
The role of cypin in the regulation of the ubiquitin-proteasome system
No full textProteome homeostasis is crucial for the proper functioning of the neurons. Disruptions in homeostasis lead to dysregulation in cellular functions, affecting neuronal functions and synaptic plasticity and ultimately leading to cell death. Protein homeostasis depends on efficient transcription, translation, and subsequent removal by protein degradation systems. Two major degradation systems, the Ubiquitin proteasome system, and the Autophagy lysosome pathway, play crucial roles in removing short-lived and damaged or dysfunctional proteins and membrane-bound proteins and organelles, respectively. Post-translational modifications of proteins with ubiquitin (Ub), a key regulator in the protein degradation systems, are implicated in neuronal development by regulating synapse formation and maturation, signal transduction, and synaptic plasticity through proteasome-dependent and independent mechanisms. Despite the mounting evidence identifying the role of ubiquitin in neuronal homeostasis and function, not much is known about the mechanism through which these substrates are targeted. In this dissertation, we explored a novel role of cypin (cytosolic PSD-95 interactor) in promoting the ubiquitination of proteins while negatively affecting proteasome activity when overexpressed. We further explored the role of cypin in promoting proteasome-independent ubiquitin linkages (K63-Ub), which is known to play a crucial role in synaptic plasticity, via UBE4A (a key player in promoting K63-Ub linkages). We found cypin overexpression led to an increase in the levels of synaptic proteins, K63-polyubiquitination of PSD-95, a major scaffolding protein at the postsynaptic density, and intracellular Ca+2 levels. Proteome-wide studies revealed cypin overexpression altered the protein ubiquitination pathway and promoted synaptogenesis in in vitro studies. Further analysis of proteome changes at the synapses identified cypin overexpression playing a major role in pre and postsynaptic functions, postsynaptic being predominant. Taken together, data presented here identified a novel role for cypin in regulating the proteasome activity and proteasome-independent post-translational modifications (PTM) to regulate the synaptic architecture.Ph.D.Includes bibliographical reference
Ceramic stereolithography debinding: an analysis of resin formulation, degradation, and thermal decomposition kinetics
No full textCeramic stereolithography is one of the most popular processing technologies for creating intricate ceramic parts. Ceramic stereolithography offers high-resolution, high-speed part creation and the ability to make one-off parts for rapid prototyping. Despite stereolithography's advantages in forming ceramic parts, thermal binder removal (TBR) remains a complex, slow, and time-consuming process. Various processing parameters, including resin curing parameters, resin formulation, and debinding atmospheres, can heavily influence this process. Chapter 1 of this thesis examines the influence of various resin and ceramic suspension compositions on the properties of printed samples. Chapter 2 is dedicated to evaluating the impact of polyethylene glycol (PEG) addition to resin on thermal degradation behavior, curing enthalpy, and degree of polymerization. The development of a model to accurately describe the thermal degradation kinetics of the resin is addressed in Chapter 3. Finally, Chapter 4 investigates the effects of resin compositions and debinding environments on the Thermal Binder Removal (TBR) process. It was found that adding PEG 400 or urethane acrylate changes the cure depth, lateral growth, surface roughness, and layer height of the samples when the energy dose is constant. Resin modification with PEG also altered the degradation temperature, curing enthalpy, and degree of polymerization of formulated resins. The developed thermal degradation kinetic model accurately captured critical experimental reaction rate peaks when predicting resin degradation. Lastly, modifying the resin composition by adding PEG significantly suppressed cracking during TBR, and the choice of gas atmosphere was found to be of secondary importance compared to the resin formulation.Ph.D.Includes bibliographical reference
Structural peculiarities in Rachmaninoff’s piano concerto no. 4, op. 40
No full textRachmaninoff (1873–1943) was one of the greatest composers and pianists of his time. He left a significant legacy in classical music, including works for piano, chamber music, symphonies, operas, and choral music. His four piano concertos are rightfully considered some of his most significant, distinguished, and popular works. Rachmaninoff’s first three concertos were written in pre-revolutionary Russia and achieved broad success. The fourth was written after his emigration to the United States following almost 10 years of silence and left both Rachmaninoff and his audiences dissatisfied. This dissertation uses Rachmaninoff’s fourth concerto as a medium to more deeply understand the crucial influence of this genius composer’s life circumstances on the continuous evolution of the concerto’s structure and the multiple attempts at its revision, which were triggered by Rachmaninoff’s painful dependence on the opinions of his audiences and critics. In various attempts to improve the reception and understanding of the piece by the public, Rachmaninoff made elaborate changes to the masterpiece’s form but succeeded only in rendering its message progressively less clear. Here, I use Hepokoski–Darcy theory and its flexible concept of the sonata form to analyze the variations in Rachmaninoff’s sonata form. I adopt a new, critical, combined version of the concerto to reinvigorate interest in this work.Ph.D.Includes bibliographical reference
Novel pathological mechanisms of B lymphoma development and progression
No full textB lymphomas are significant health issues both in the US and worldwide. Advances in new targeted therapy and immunotherapy, together with traditional chemotherapy, radiotherapy, surgery, and bone marrow or stem cell transplant, have significantly improved patient survival, but many subtypes of B lymphomas remain incurable. Thus, a better understanding of the pathological mechanisms is required. Various intrinsic signaling pathways of oncogenic mutations in genes such as MYC or TRAF3 drive B cell malignant transformation and lymphoma development. Interestingly, our laboratory recently reported that specific ablation of the adaptor protein TRAF3 from myeloid cells also leads to spontaneous B lymphoma development in mice, suggesting the existence of B cell-extrinsic pathological mechanisms. In an effort to elucidate such novel mechanisms, we found that depletion of commensal bacteria with broad-spectrum antibiotic treatment effectively prevented or substantially inhibited the development and metastasis of spontaneous B lymphomas in two different mouse models. These models include the myeloid cell-specific Traf3-deficient (M-Traf3-/-) mice with diffuse large B cell lymphoma (DLBCL) or follicular lymphoma (FL) and B cell-specific Traf3-deficient (B-Traf3-/-) mice with splenic marginal zone lymphoma (MZL) or B1 lymphoma. Interestingly, we detected commensal bacteria transmigration to the liver in M-Traf3-/- mice but no evidence of transmigration or infection in B- Traf3-/- mice, suggesting that commensal bacteria can promote B lymphoma development and progression even in the absence of transmigration and systemic infection. Although commensal bacteria have been implicated in the carcinogenesis of other human cancers (such as colon, pancreatic, liver, and breast cancers), B lymphocytes are the only cell type of the mammalian body that expresses specific antigen receptors (BCR) and can produce specific antibodies in response to commensal bacterial antigens. Notably, almost all human B lymphomas that demonstrate active BCR signaling and inhibition of this pathway by BTK inhibitors have recently achieved clinical success. In this context, our findings obtained from the two mouse models with B lymphomas led us to test a novel hypothesis that in the absence of infection, commensal bacteria-derived antigens can engage BCR signaling to induce B cell survival, proliferation, or activation, thereby promoting B lymphoma development and progression in genetically predisposed individuals. Indeed, my dissertation research has provided multiple lines of evidence to support this hypothesis, including both in vitro and in vivo data obtained from complementary mouse models and human malignant B cell lines as well as patient samples. Overall, my dissertation research provides novel insights to better understand the pathological mechanisms of B lymphoma development and progression. Importantly, our findings obtained from this study bear significant implications for the development of novel diagnostics and therapeutics to improve early detection, prevention, and treatment for patients with various B lymphomas.Ph.D.Includes bibliographical reference
“Healthy women, healthy lives”: the Nurses’ health study and American women’s health research, 1960s-2000s
No full textLaunched by Harvard epidemiologists in 1976, the Nurses’ Health Study (NHS) is the largest and longest running study of women’s health in the world. Hundreds of thousands of nurse participants fill out biennial questionnaires covering almost all aspects of their health, from mental illness to diet. NHS findings helped shape public health policy, clinical practice, and individual behavior as the study—frequently discussed in the popular press—reached general audiences. This dissertation uses the NHS to examine the evolution of women’s health research in the United States from the 1960s-2000s, reevaluating how researchers produced medical knowledge about women’s bodies and how female research subjects experienced their participation. Despite the medical establishment’s general lack of interest in women’s health and the traditional hierarchies between physician researchers and the nurse participants, the nurses who answered the questionnaire year after year exercised an unusual degree of agency and helped to shape the study’s priorities. I draw on oral histories, medical and popular publications, and nurse activists’ writings to raise new questions about the development of American women’s health research—a process that has shaped not only the field’s priorities, but also women’s everyday experiences and healthcare.Ph.D.Includes bibliographical reference
Sickle cells to super cells: the alluring genetic cure for sickle cell disease
No full textSickle Cells to Super Cells: The Alluring Genetic Cure for Sickle Cell Disease investigates how scientists and physicians are harnessing the cellular material of people living with sickle cell disease to engineer new biotechnological advancements to serve the bioeconomy. In the postgenomic era, a curative and genetic hegemony has emerged that makes an alluring promise to cure sickle cell disease. While existing and emerging disease-modifying therapies are available, these groups prioritize biological innovations that cause permanent biological change to literally and figuratively transform sickle cells into super cells to aid in neoliberal goals of a reduction in seeking care, public spending, and disability policies. Centered around the phenomenological concept of cure, which I argue is also an ontological concept, I examine how people living with sickle cell disease understand their illness, therapeutic options, and what it means to live well as various healthcare spaces are taken up with curative and genetic therapies. I employ in-depth interviews with people living with sickle cell disease who have and have not undergone curative and genetic therapies and their families, providers, researchers, and funders of novel research and ethnographic observation at a major healthcare research institution where first-in-human gene therapy trials and other clinical trials for sickle cell disease are occurring. The first section of the dissertation discusses the driving forces central to the development of biotechnological advances for sickle cell disease. I reveal how therapeutic development has become a matter of bioeconomic concern in the postgenomic era given the hegemonic power of cure and genes that is emerging. I advance a theory of the politics of desperation: the process of using a form of desperation that extends beyond the physical or emotional suffering characteristic of an illness into persistent, structural neglect in order to advance biotechnological development and the bioeconomy. This theory emerges from evidence from participants who described the pursuit of gene therapy as a way to be freed from pain crises and as a way to limit future occurrences of racialized healthcare experiences. The second section closely follows the days of several individuals who participated in disease-modifying and curative therapies for sickle cell disease to illuminate the varying contextual forces that shape how they understand what it means to live with sickle cell disease and their perceptions of emerging therapies. The third section presents how various stakeholders understand the concept of cure. In it, I theorize the sociological mechanism that can counter the politics of desperation, that of parachutes: a continued need for social and technological advancements that can come in different forms beyond cure that would allow people with illnesses, especially racialized illnesses, to descend from an unsafe height. I argue that to achieve the very real possibility of living well with illness, the biomedical research and healthcare industry will need to recognize that care will always be needed before cure, after cure, and, most forgotten, alongside cure.Ph.D.Includes bibliographical reference