This paper explores how we can write about the postcolonial histories of the modern hospital. With the Philippine General Hospital (PGH), Manila, Philippines as a starting point, I locate the colonial hospital in the broader and often separate historiographies of the modern hospital and the postcolonial histories of science, technology, and medicine in Southeast Asia. Broadly, hospital histories focus more on organizational management and less on the socio-material entanglements that emerge within the hospital space. Historical studies explicitly centered on the modern hospital are almost exclusively written from the perspective of architectural histories. While the current literature presents valuable discourse on the interface of medical and architectural ideas on hospital design, these histories may present Eurocentric and Whiggish narratives, largely excluding histories of modern hospitals in colonies. However, emerging intersections between emotional and architectural histories of imperial infrastructures highlight the potential of material-affective approaches for advancing postcolonial studies (MAPS) of the modern hospital. The second historiographical stream traces the formation of increasingly critical and agential postcolonial histories of science, technology, and medicine in Southeast Asia. Critical science studies have generated compelling analyses of modern hospitals as biopolitical sites in the colonial period. Moreover, the colonial hospital persists as fertile ground for revealing autonomous histories and new relations and subjectivities in Southeast Asia's postcolonial reconfigurations. Critical historians of medicine and science in the region also urge more engagement between historical and ethnographic approaches. By weaving these historiographies, I argue that material-affective methods are vital to writing the postcolonial history of modern hospitals and propose a combined MAPS approach to potentially answer the question: how do we write the postcolonial history of colonial hospitals?
In this study, I examine how museums of traditional medicine in Asia construct and present narratives about zootherapy. Through analyzing displays and their contextual framing, I investigate how animal-derived remedies are represented, which species and medical applications are included, and how museums address conservation and ethical concerns. The study is based on fieldwork conducted between 2018 and 2025, including visits to five museums dedicated to traditional medicine. These institutions include the Museum of Traditional Medicine in Isfara, the Museum of Traditional Vietnamese Medicine, the Hu Qing Yu Tang Traditional Chinese Medicine Museum, the Pharmacy Museum in Lisbon, and the Suzhou Museum of Traditional Chinese Medicine. Exhibit documentation, textual analysis, and comparative research methods were used to assess how zootherapy is represented in these museums. The findings reveal that zootherapy exhibits include a wide range of species, from invertebrates such as insects and mollusks to large mammals like bears, elephants, and tigers. Some exhibits provide detailed descriptions of their medicinal uses, while others lack contextualization or critical engagement with conservation issues. The depiction of zootherapy in museums varies significantly, with some institutions presenting it as an enduring medical tradition and others portraying it as an obsolete practice rooted in historical beliefs rather than modern pharmacology. The absence of ethical considerations in museum narratives is a key concern, particularly regarding endangered species. The study also highlights the role of traditional medicine museums in shaping public perceptions of zootherapy, influencing how these practices are understood in both historical and contemporary contexts.
The debates regarding the impact and costs of public and private health, and the responsibility of the State to offer access to healthcare are ongoing discussions in Latin American countries. This paper discusses the relationship between State formation and public health in Latin America, using case studies from Chile and Peru from the late 19th- to mid-20th centuries. In this period, public health was a determining factor in State consolidation. Multiple sectors debated and pushed the State to embrace public health as a national issue and provide healthcare as a citizens' right. We focus on the efforts of an elite group led by doctors, hygienists, and politicians to place the relationships between healthcare, urban living conditions, and demographic crises on the political and media agenda. Following these efforts, in the early 20th century governments in both countries established public health as a major concern, understanding the issue as synonymous with modernity and progress. In the context of urban and industrial growth, the inadequate sanitary conditions of lower-class housing were considered the main factor in the spread of contagious infections. Legislation transformed the nascent issue of worker housing into a State obligation, while access to sanitary housing became a cornerstone of healthcare and, in turn, one of the earliest public health policies. Given this context, we trace the evolution of housing policies in the two countries through primary sources such as presidential speeches and legislative debates, newspapers, and medical essays and reports.
Lymphatic filariasis (LF) is a long-lasting, debilitating parasitic infection that has remained an immense burden to the endemic areas globally in the realms of physical, psychological, and socioeconomic suffering. LF presents itself in the form of lymphedema, hydrocele, and disfigurement, and limits motor activity, working capabilities, and interaction processes between people, significantly reducing self-esteem and life quality. LF brings significant socio-psychological distress besides the physical one. A decline in self-esteem often results in anxiety and depression; recognizable deformities are stigmatized and avoided. This social isolation and poverty become internalized, also with the misconceptions of contagion and impurity, and further bring about the perpetuation of vulnerability. Gender acts as a multifactor determinant force of the LF experience. It contains multiple layers of discrimination against women, concerning marriage refusal, and the workplace, where men are denied opportunities to earn their living and can become social outcasts. Such inequities, which are gender-based, are expected to be addressed when it comes to managing diseases. Constant obstacles put access to timely treatment and care in the spotlight, including the lack of awareness, financial constraints, and health facilities. The most effective interventions are the extension of the community participation levels and maximization of mass drug administration (MDA), which can considerably decrease the disease and burden of the disease and its burden. The world campaigns towards the abolition should not henceforth be geared towards pharmacological but rather take a rights-based approach. The psychological support, social rehabilitation, and gender-based interventions introduced into the social health systems can increase the inclusion and cost-efficiency of the individuals who have already experienced the widened perceived effects of LF and their dignity.
The Montreal Neurological Institute (MNI) is often framed as a triumph of North American medical innovation, an institution converging research, clinical care, and neurosurgery under the leadership of Wilder Penfield. Such narratives fail to account for Penfield's emotional labor and the networks of expertise that shaped the MNI. Using primary sources that reveal the transnational influences embedded in its design, this paper interrogates the foundation and evolution of the MNI particularly by looking at the early years of Penfield's career. It situates the MNI within the broader historiographies of medical space and scientific mobility drawing from Penfield's letters to illustrate the early influences that led to the establishment of the MNI. It proposes that history of emotions and history of mentalities can be effective methodologies to understand the diverse medical research communities of the early 20th century. Using his letters to his mother, Jean Jefferson Penfield, this paper interprets the emotional states of a young, self-doubting Penfield within a network of renowned neurologists of that period. In a wider context, through the case study of the MNI, this paper demonstrates that international collaboration and the physical mobility of researchers - as in the example of the American-born Penfield's global journey in search of knowledge and his path to becoming a naturalized citizen of Canada - are essential for the advancement of scientific research.
When COVID-19 survivors reported ongoing symptoms or new health concerns following their infections in 2020 and early 2021, many medical practitioners and health agencies questioned the connection between novel viruses and long-term health impacts. Medical historians studying epidemics understand the connection between viral infection and health complications emerging immediately or years or decades later. In this essay, I explore the similarities between the medical fallout of the 1918 influenza and COVID-19 pandemics. Despite the differences between the viruses, these novel strains produced similar medium- and long-term health difficulties, including cardiovascular dysfunction and crushing fatigue. As I demonstrate, a significant difference between these two pandemics is in the response by medical practitioners. Following influenza, practitioners expected new and worsening health issues and took their patients' complaints seriously, offering support through food delivery, convalescent care, specialist oversight, and in-home nursing. Early in the COVID-19 pandemic, many practitioners characterized ongoing or new symptoms as anxiety. Patients led efforts to recognize Long COVID as an authentic medical condition, and today, physicians around the country refer their patients to Long COVID clinics. The value of medical history is apparent in this comparison-if practitioners understand how historical epidemics impacted various populations, they expect that in the epidemic aftermath or the period following an acute epidemic crisis, not all patients get well. Including the history of epidemics in public health education, continuing education programming, and even medical school curricula can resist epidemic erasure and empower medical practitioners to expect the unexpected.
The community of Heilig Kreuz, outside Mainz, Germany, has long been something of a historiographical enigma. Its first internal records, dating to the mid-15th century, testify to the presence of a canonry "at the church of the Blessed Virgin in the fields outside the walls of Mainz." In the scant scholarship on Heilig Kreuz, it has been characterized as replacing an earlier, informal community of lepers on the same site. In this paper I argue that, rather, the changing institutional form of the community was an attempt to guarantee continuity of care for the vulnerable. The codex containing the "customs and oaths" of the house testifies to a process of formalizing religious observance and affirming religious status that can be seen in other leper hospitals in the region throughout the later 15th century. The oaths for canons and clerks pledging "service to the persons residing there," in a formula resembling that of many hospital rules concerning service of the sick, and the fact that the statutes were recorded "to avoid perils" that might otherwise befall the community, can be understood in the context of the efforts of the archbishops of Mainz to exercise more direct control over the city's hospitals.
There is considerable discussion concerning the recent increase in the prevalence of overweight/obesity in children and adults. Although it is assumed that current diet and sedentary behavior are key contributors, these factors do not seem to be the only characteristics responsible. In this paper we summarize the findings we have obtained when assessing whether exposures in previous generations may have played a part in this change over time. In particular, we show that ancestral smoking may be an important contributor. We used data collected from parents and grandparents by the Avon Longitudinal Study of Parents and Children (ALSPAC), which has followed children born in 1991-1992 to women resident in south-west England. We have shown that ancestral smoking characteristics were associated with fetal growth and with increased measures of adiposity in their children and grandchildren. Here we describe the detailed findings of the ancestral exposure to cigarette smoking of ancestors at various time points using ALSPAC data and indicate the support for the findings in other cohorts. Since body mass index (BMI) can be a measure of lean (muscle) mass as well as fat mass, we concentrate on associations with body composition from dual-energy x-ray absorptiometry (DXA). Few birth cohorts have collected data on smoking of individuals in the male line and few have used details of fat, bone, and lean mass. Findings concerning grandmaternal smoking in pregnancy and pre-pubertal smoking of male ancestors were nevertheless replicated. We consider the likelihood of epigenetic explanations for these findings.
Helicobacter pylori is a spiral bacillus that can also adopt a coccoid form, a morphology associated with antibiotic resistance and the ability to withstand unfavorable environmental conditions. The relationship between coccoid forms, virulence, and the development of gastroduodenal diseases remains unclear. Therefore, this study aimed to determine the association between virulence and the induction of coccoid forms in H. pylori isolates from patients in Antioquia, Colombia. DNA from 30 clinical isolates was extracted, and the vacA and cagA genes were amplified to classify strains into high, intermediate, or low virulence groups. Four methodologies-each with specific modifications-were evaluated to induce coccoid forms. Bacterial morphology was assessed by optical microscopy, and coccoid cells were quantified using ImageJ. The association between virulence level and coccoid induction was analyzed using the Mann-Whitney U test. Before induction, cultures contained more than 90% spiral forms. The solid medium protocol under aerobic conditions was identified as the fastest in promoting coccoid conversion. After induction, high-virulence isolates showed a higher proportion of coccoid forms (72.6%) compared with low-virulence isolates (49.6%). A significant association was observed between virulence level and the induction of coccoid forms (p = 0.014). The findings suggest a relationship between the presence of vacA and cagA genes and the ability of H. pylori to adopt coccoid morphologies as an adaptive response. However, variability among induction protocols may introduce methodological biases and contribute to divergent interpretations of the biological role of coccoid forms. Further studies are needed to determine whether recurrences represent recrudescence or reinfection and to clarify the role of coccoid forms.
Gender-affirming hormone therapy (GAHT) is a necessary treatment for many transgender people, and there is a critical need to further improve treatment experience and mitigate possible risks. Here we investigated whether DNA methylation (DNAm) biomarkers of health and aging are modified during the first year of GAHT and whether these vary by treatment type. Cohort consisted of 13 trans women (TW) and 13 trans men (TM). Sampling occurred at baseline (pre-GAHT), and at 6- and 12-month follow-up. We tracked the longitudinal dynamics of three epigenetic clocks (Horvath, Hannum, PhenoAge), DNA methylation-based telomere length (DNAmTL), and DunedinPACE. At baseline, the Horvath and Hannum showed accelerated epigenetic aging, particularly pronounced among TM, while the PhenoAge and DunedinPACE showed lower pace of aging in both groups. This discrepancy may reflect possible effects of minority stress in an otherwise healthy cohort. While GAHT did not affect the three clocks, DNAmTL and DunedinPACE showed treatment-specific patterns but with notable inter-individual variability in trajectories. TW had increased DunedinPACE (estimate = 0.057, p=0.002) and slight DNAmTL gains (estimate = 0.024, ns); TM exhibited stable to slight decline in DunedinPACE (estimate = -0.013, ns), and reduction in DNAmTL (estimate = -0.057, p=0.037). The marked heterogeneity is indicative of an individualized response to treatment and highlights the potential value of incorporating such biomarkers in comprehensive health monitoring. Our findings emphasize the need for larger, long-term studies to optimize personalized strategies for gender-affirming healthcare.
Trachoma remains a leading cause of preventable blindness that has long persisted in Egypt. Global estimates tend to undervalue the actual national prevalence, and no previous analysis has comprehensively mapped the temporal and regional trends within the country. The present study addresses these gaps to guide elimination efforts and policy planning. To estimate the prevalence of active and chronic trachoma and associated visual impairment and blindness in Egypt through a comprehensive systematic review and meta analysis. We prospectively registered with PROSPERO (CRD420251070078) and adhered to PRISMA 2020 and Cochrane standards. Three independent reviewers searched 10 databases without language restrictions for population-based, cross-sectional surveys that reported WHO-graded trachoma outcomes. Two reviewers independently screened records, extracted data, and assessed bias using the Joanna Briggs Institute (JBI) checklist; Grading of Recommendations, Assessment, Development and Evaluations (GRADE) appraised evidence certainty. We transformed proportions using the Freeman-Tukey double arcsine transformation, pooled estimates using random-effects meta-analysis and directly age-standardized them to Egypt's 2000-2020 population structure. We performed sensitivity, subgroup, and meta-regression analyses to explore heterogeneity. From 16 cross sectional surveys (n = 45 934), the pooled age standardized prevalence estimates were as follows: active trachoma in children (1-9 years) 10.8% (95% CI; 7.0-14.6), visual impairment in those cases 5.3% (95% CI; 3.2-7.5), chronic trachoma in adults (≥ 15 years) 7.2% (95% CI; 4.0-10.4), associated visual impairment 1.6% (95% CI; 1.0-2.2), and blindness 0.7% (95% CI; 0.1-1.9). Sensitivity, subgroup, and meta regression analyses demonstrated consistent estimates and no evidence of small study effects. Despite substantial declines, active and chronic trachoma remain well above elimination thresholds in Egypt. These findings underscore the need for sustained implementation of the SAFE strategy-particularly enhanced water, sanitation, and hygiene (WASH) infrastructure, ongoing surveillance, and targeted surgical outreach-and call for harmonized survey methods to guide and evaluate future control efforts.
The participation of the Rho-associated protein kinases (ROCK1 and 2) in the regulation of actin cytoskeleton organization, cell adhesion, motility, and gene expression has been extensively investigated in many tumors of different histology. However, their pathogenic roles in medulloblastoma (MB) remain understudied, demanding a deeper appreciation of their participation in cancer cell dissemination and tumor progression. Herein, we show that ROCK2 is downregulated in MB tumor samples and functionally increases migration of cell lines belonging to the SHH subgroup. A comprehensive comparative bioinformatic scrutiny of differentially expressed genes within a list of ROCK2 candidate substrates, uncovered a network of 21 dysregulated genes from which DYPSL3 (dihydropyrimidinase-related protein 3) denoted a strong positive correlation. Enrichment analysis revealed SHH/RHOA/ROCK2/DYPSL3 as top hub genes and the intersection between two biological processes of most importance in MB: actin cytoskeleton remodeling and neuron development. Of note, evidence shows that both ROCK2 and DYPSL3, interact with RHOA and in many tumor types they act as tumor suppressors, mitigating cell spreading. Alternatively, their impaired activity leads to undifferentiated phenotypes and inappropriate cytoskeletal dynamics affecting cell shape, attachment to the extracellular matrix, and cell movement. In parallel, cell motility is considered a prototypical non-canonical response to SHH mediated by RHOA. Therefore, we propose a model in which the interplay between these pathways may lead to a perturbation of proper cytoskeletal dynamics that underpins cell migration.
Ocular gene therapy has rapidly advanced from proof-of-concept studies to clinical trials by exploiting the unique advantages of the eye, including its easy accessibility, relative immune privilege, and the ability to use the contralateral eye as a control. An important step forward was achieved with the Food and Drug Administration (FDA) approval of voretigene neparvovec (Luxturna) for the treatment of biallelic RPE65-mutation-associated retinal dystrophies in 2017. Gene therapy is a promising field aimed at treating various inherited and acquired eye diseases. Viral vectors such as adeno-associated virus (AAV) are mainly used to efficiently deliver genes. Despite the immune-privileged status of the eye, viral vector-based therapies can induce immune responses, potentially leading to gene therapy-associated uveitis. Future directions include developing strategies to reduce immune responses while maintaining therapeutic efficacy, optimizing vector selection, and improving delivery techniques. Continued advances in the field of viral vectors, particularly AAV, are expanding the potential applications of gene therapy to treat a variety of ocular diseases. To fully realize the potential of ocular gene therapy, more research and clinical trials are needed to improve these methods, ensure safe and efficient treatments, and ultimately overcome existing obstacles.
Plants have evolved elaborate signaling networks, believed to be necessitated by the diversity and complexity of their morphology, developmental and reproductive strategies, and the need to cope with an ever-changing environment from which they are rooted and cannot escape. Their receptor-like kinase superfamilies, with members numbering in the hundreds to more than a thousand, exemplify how plants have evolved their signaling versatility. FERONIA (FER) receptor kinase from model Arabidopsis is a member of the Malectin-domain receptor kinase family conserved among plants. FER has a perplexingly broad functional range, impacting growth to reproduction throughout the plant life cycle, and survival when encountering biotic and abiotic stressors from the environment, such as pathogens and climatic adversity. Efforts to understand FER signaling have brought to light novel signaling strategies at the continuum of the plant cell wall and plasma membrane, and a network of cytoplasmic and nuclear pathways that together support its biological roles. The discussion here focuses on the cell surface mechanisms, including a sugar-peptide interaction-driven liquid-liquid phase separation process along the cell wall-plasma membrane interface and a plasma membrane-linked signaling node comprised of FER, a glycosylphosphatidylinositol-anchored protein, the RHO GTPase molecular switch and a generator for reactive oxygen species (ROS). The emerging recognition of how the broader FER-related receptor kinase family could impact plant wellness and agricultural productivity is also discussed.
Historically, the Democratic Republic of the Congo (DRC) has faced the greatest public health burden from mpox, including more than 70 000 probable cases from 1 January 2024 to 2 February 2025. However, there has been a relative paucity of investigation focused on mpox community engagement in DRC, including assessments of disease knowledge and risk perception. Given the ongoing Clade I mpox public health emergency of international concern, and the linkage between sustained human-to-human transmission and dense sexual networks, we sought to investigate mpox knowledge and sexual behaviours among key populations. Between 20 March 2024 and 25 August 2024, we recruited 2794 participants distributed across Kinshasa, Kwango and North Kivu provinces, with a focus in urban centres where mpox risk was considered high. Most participants were considered other at-risk populations (948; 33.9%), followed by men who have sex with men (MSM, 828; 29.6%) and sex workers (897; 32.1%). Mpox knowledge, including transmission routes as well as sexual and health-seeking behaviours, was evaluated through questionnaires led by peer educators. Overall, only 6.1% of all participants reported prior mpox knowledge. Among this participant subset, zoonosis ('direct contact with infected animals') and 'people living in high-risk areas' were the most frequently selected options in regard to mpox transmission and populations at risk, respectively. When considering at-risk behaviours for mpox, those who identified as sex workers reported significantly higher risk sexual activities, including multiple sexual partners (80.3% of sex work participants), engaging in transactional sex (84.7%) and anonymous sex (80.8%) compared with MSM. However, both sex workers (44.8%) and MSM (56.7%) reported the highest health seeking behaviours for a suspected sexually transmitted infection. Our results highlight the need to evaluate knowledge in high-risk communities, especially in an endemic setting. Community engagement, which incorporates both mpox knowledge and risk perception activities, is inclusive of at-risk populations and is needed for ongoing mpox containment and mitigation efforts.
We reviewed the role of miRNAs in the regulation of T cell differentiation and function in cardiometabolic inflammatory diseases, such as obesity, type 2 diabetes, atherosclerosis, and autoimmune diseases, such as type 1 diabetes, rheumatoid arthritis, asthma, and cancer. Cardiometabolic diseases, type 1 diabetes, and rheumatoid arthritis are characterized by miRNA expression profiles that favor the differentiation of T helper 1 and 17 cells and cytotoxic cells and a decrease in T helper 2 cells, regulatory T cells, and myeloid-derived suppressor cells. Asthma is characterized by changes in miRNAs that favor the differentiation of T helper 2 cells. Finally, cancer is characterized by miRNA profiles that cause a decrease in T helper 1 and 17 cells and cytotoxic cells and an increase in T helper 2 cells, regulatory T cells, and myeloid-derived suppressor cells. In particular, differences in the expression of miR-155 and a cluster containing Let-7, miR-10a, miR-17-92, miR-34a, miR-142, and miR-150 may determine whether the balance flips towards cytotoxicity or immunosuppression. High levels of miR-21 and miR-29 and low levels of miR-150 are associated with T cell profiles that protect against inflammatory and autoimmune diseases associated with tissue damage but also induce tumor growth. All these miRNAs were found to be associated with disease progression and/or response to therapy in one or more of the diseases under study. Therefore, studies on the value of the identified miRNA clusters in predicting disease progression and selecting therapies that may yield gains in treatment costs are warranted.
Adverse childhood experiences (ACE) can lead to diverse outcomes, ranging from resilience to an increased risk of psychiatric disorders such as anxiety, depression, and posttraumatic stress disorder (PTSD). In mammals, most multiexon genes encode an average of 3.9 protein-coding isoforms, which amplify transcriptomic diversity and potentially exhibit distinct functional characteristics. Recent research has shown long-lasting transcriptomic changes associated with ACE, particularly in immune-related genes. However, differential isoform usage may not be captured when analyses are confined to gene-level expression. To date, no studies have explored isoform-level dysregulation in postmortem brains of individuals exposed to ACEs. Our study investigated transcriptomic dynamics across four prefrontal regions-the dorsolateral (dlPFC), dorsal Anterior Cingulate (dACC), orbitofrontal (OFC), and subgenual prefrontal (sgPFC) cortices-in a cohort of 22 donors with PTSD, comprising 11 with and 11 without ACE history. The OFC exhibited the highest number of differentially expressed genes (DEGs), followed by the sgPFC. Correspondingly, these regions also showed the most pronounced differential isoform usage, or "isoform switching". Notably, our integrated transcriptomic analysis revealed that while PAQR6 was downregulated in the sgPFC among ACE-exposed individuals, its principal isoform (PAQR6-201) showed increased usage. Several genes exhibiting significant isoform switching did not display substantial differential gene expression. Functional pathway analysis revealed that genes with altered expression or isoform usage converged on neurogenesis regulation, with isoform-switching genes specifically enriched in gliogenesis. This study demonstrates that examining differential isoform usage unveils previously unrecognized genes potentially implicated in ACE. Future research should focus on characterizing the functional consequences of isoform-specific up- or downregulation to comprehensively understand transcriptomic dysregulation in complex psychiatric disorders.
In 1993, geneticist Dean Hamer and his colleagues published a groundbreaking study suggesting that a region on the X chromosome-Xq28-might be linked to male homosexuality. Widely covered in the press and championed by LGBTQ rights advocates, the study lent scientific weight to the argument that sexual orientation is biologically rooted rather than solely the product of psychosexual developmental failure. This posed a significant threat to the cultural authority of conversion therapists, who had long relied on psychoanalytic frameworks that pathologized same-sex desire as a "curable" condition. In response, conversion therapists launched a coordinated counteroffensive, rejecting the emerging biological evidence about homosexuality and doubling down on psychodynamic theories about same-sex desire developed in the mid-20th century. This article argues that the publication of Hamer's research drew conversion therapists into the heart of the United States' culture wars, where they forged interfaith political coalitions and constructed alternative knowledge-production networks to preserve the plausibility of sexual reorientation. Their opposition to genetic research was more than scientific skepticism; it was a strategic political effort to defend heteronormativity, enforce rigid gender roles, and delegitimize queer and trans identities. By tracing how conversion therapists selectively engaged with emerging scientific discourses around LGBTQ individuals being "born that way," this article reveals how marginalized actors helped shape-and distort-the boundaries of scientific authority in service of a broader anti-queer agenda.
Objective: Activating transcription factor 3 (ATF3) has attracted recent scientific attention as a novel mediator of tumor suppression, particularly within the context of cervical cancer (CC). Our prior research demonstrated that ATF3 overexpression induces cell cycle arrest and apoptosis in human papillomavirus (HPV)16- and HPV18-positive CC cells. The present study aims to examine the impact of ATF3 overexpression on the expression levels of p16 and NF-κB, two proteins with pro-tumorigenic roles in HPV-induced CC. Methods: Ca Ski and HeLa cells underwent transfection with pCMV6-AC-IRES-GFP plasmids containing the ATF3 gene. To establish the optimal plasmid DNA quantities for transfection, MTT assay was conducted. Furthermore, fluorescence microscopy and flow cytometric analysis were employed to assess the efficiency of transfection. The expression levels of p16 and NF-κB were evaluated by RT-qPCR and western blotting prior and subsequent to ATF3 overexpression. Results: The overexpression of ATF3 induced a decrease in p16 mRNA levels in both Ca Ski and HeLa cells (p<0.04), along with the concomitant reduction of p16 protein expression within both cellular populations (p<0.005). Additionally, it led to a reduction in NF-κB p65 protein levels in both cell lines (p<0.005), with no discernible impact on its mRNA expression. Conclusion: Given ATF3's demonstrated capability to downregulate p16 and NF-κB, both of which play important pro-tumorigenic roles in HPV-related CC, ATF3 emerges as a promising therapeutic candidate with the potential for application in the treatment of CC.
This article examines the historical roots of medical neglect experienced by Black women, focusing on the 18th- and 19th-century British West Indies. During this period, White male physicians constructed racialized and gendered frameworks of disease that excluded enslaved Black women from diagnosis, care, and medical legitimacy. Positioned not as patients but as reproducers and laborers, their suffering was either pathologized or dismissed. Drawing on medical treatises and plantation manuals, this article argues that enslaved Black women were relegated to a space of medical liminality: recognized as reproductive laborers but denied clinical legitimacy or voice. It advances three key arguments. First, it explores how physicians framed Black women as morally deficient and biologically inferior, blaming their behavior for illness. Second, it shows how reproductive outcomes like miscarriage and abortion were weaponized to portray Black women as lacking maternal instinct. Third, it examines how female-only diagnoses, such as Chlorosis, excluded Black enslaved women, even when they presented similar symptoms. Instead, they were assigned stigmatized conditions, like "dirt-eating," reinforcing assumptions of biological difference and unworthiness of care. By tracing this history, the article reveals the foundations of contemporary racial disparities in women's healthcare. It concludes by linking these colonial ideologies to current maternal health outcomes, where Black women in the United States still face disproportionate rates of medical dismissal and death. This legacy underscores the urgent need to confront the historical frameworks that continue to shape how Black women are treated in medicine today.