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.

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.

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.

In 1992, the AIDS Task Force of Alabama (AFTA) secured a $1.8 million federal grant from the US Department of Housing and Urban Development (HUD) to open Agape House, Birmingham, Alabama's first community-maintained AIDS boarding house for adults. Although AIDS boarding houses existed all over the country throughout the 1980s and 1990s, they have received little attention from scholars. The goal of this project is to understand the rise of Agape House and resources that were wielded to make it possible. Beyond help from a federal institution, Agape House received considerable support from local religious organizations. This analysis of AIDS boarding houses offers a local look at how the AIDS epidemic was thwarted. Popular queer history often emphasizes the work of national organizations, like AIDS Coalition to Unleash Power (ACT UP) to explain queer resistance to AIDS and responses to the lack of federal intervention. While important, the centrality of larger organizations to our understanding of AIDS resistance has obfuscated the work of local grassroots organizations. Ultimately, this project aims to answer the following, how did changes in knowledge surrounding AIDS impact the evolution of care? What motivated groups, specifically religious ones, to participate? And how did Agape House survive while similar houses closed?

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.

Oocyte or egg donation has been part of the Assisted Reproductive Technology (ART) landscape since the late 1980s. By the early 1990s, ART clinics, agencies, and family law offices began to place advertisements in college newspapers seeking egg donors to build egg banks and for particular couples. Couples themselves also began to seek out specific donors that matched criteria they were looking for. These ads grew from blanket calls for egg donors between particular ages to asking for intelligence defined by SAT scores, specific races, eye and hair colors, and more. Although scholars such as sociologist Rene Almeling and political scientist Erin Heidt-Forsythe have written about the eugenic assumptions at play in egg donations, this has mostly emerged from looking at clinics and agencies who broker eggs. Focusing instead on both clinical and individual advertising in elite university newspapers more easily reveals eugenic afterlives in how potential egg donation recipients talk about the genetic inheritability of intelligence and race. Considering that ads are placed in elite university newspapers, these egg recipients are targeting presumably intelligent students whose genetic material would contain supposedly superior DNA to pass on to potential offspring. Race is also assumed to be a stable biogenetic concept. These ads reveal how egg donation recipients are implicated within larger societal inequalities and power dynamics surrounding race, kinship, ability, and privilege.

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 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 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?

This paper focuses on the rise and fall of the Utica State Hospital, Utica, New York, once known for its pioneering use of moral treatment, as an example of how psychiatric institutionalization shaped ideas about mental illness, disability, and patient rights in America. Through architecture, patient narratives, and managerial reports, the paper explores how the institute ultimately fell out of use and how institutionalization, even with good intentions, could reinforce exclusion and harm toward the mentally ill and the disabled. The paper further traces the resonance between this legacy and today's psychiatric and disability studies, drawing attention to the recurring societal impulse to define and segregate abnormality.

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.

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 , 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.

Despite obstetric violence inflicted upon marginal female bodies by the Indian medical system being well-documented through the decades, the exploration of the historical production of this attitude has received limited attention. However, the present modes of violences are deeply rooted in a history of culturally-transmitted medicolegal anxiety about unwanted bodies on a shared planet, and their unwanted medicosocial behavior - in particular their reproductive choices. This history of anxiety, unwritten but encoded in multiple implicit and explicit ways, has shaped contemporary medical institutions' perception of reproductive-aged cisgendered Indian women as a source of multifaceted risk-a medicolegal risk to the medical institution, an economic risk to the nation's development, a biosecurity risk to the global stability-that can only be mitigated by clinically intervening in their bodies.

Lung cancer remains the malignancy with the highest morbidity and mortality worldwide. There are no effective guiding therapies and prognosis biomarkers, and the overall prognosis of lung cancer remains poor. The cardiomyocyte enhancer factor 2 (MEF-2) family is a highly evolutionarily conserved transcription factor that plays important roles in a variety of diseases, including tumors. Still, the overall bioinformatics function of the MEF-2 gene family in non-small cell lung cancer (NSCLC) has not been systematically reported yet. MEF-2 family members have low expression in NSCLC tissues and are associated with clinicopathological stages. MEF-2B/2D is highly expressed in lung metastatic tissues. MEF-2A, MEF-2B, and MEF-2D have obvious advantages in the diagnosis of NSCLC. Survival analysis of lung adenocarcinoma (LUAD) patients in the Cancer Genome Atlas (TCGA) database shows that MEF-2C is strongly associated with poor overall survival (OS) and disease-specific survival (DSS). Univariate and multivariate Cox analyses demonstrated that MEF-2A independently predicts the progression-free interval (PFI) in NSCLC patients. Gene set enrichment analysis (GSEA) showed that MEF-2 family members are associated with immune cell receptor function and regulation of immunoglobulin complexes. The differentially expressed genes (DEGs) associated with MEF-2 family members were significantly enriched in the cAMP signaling pathway and gastric acid secretion. Gene ontology (GO) analysis revealed DEGs that play critical roles in the cytochrome-c oxidase activity, electron transfer activity, oxidoreduction-driven active transmembrane transporter activity; the Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis shows that they are mainly enriched in oxidative phosphorylation, thermogenesis, and diabetic cardiomyopathy. MEF-2A is a potential diagnostic, prognostic biomarker, and promising therapeutic target for NSCLC. Further studies are needed to verify and clarify the underlying mechanisms.

Epigenetics has described non-DNA sequence-based transgenerational inheritance, in which phenotypic traits acquired over a lifetime by parents are passed to their progeny across several generations. Transgenerational epigenetic inheritance may be achieved by transmitting repressive epigenetic marks such as DNA methylation and histone 3 lysine 27 trimethylation (H3K27me3) in parental chromatin through sexual reproduction. In general, with infrequent exceptions, epigenetically modified architectures in parental chromatin are extensively erased by reprogramming during reproduction, leaving little possibility of being inherited by offspring. In comparison, plants exhibit transgenerational epigenetic inheritance with relatively greater frequency, although the underlying molecular mechanisms have remained unclear. Recent studies with the flowering plant () have identified plant-specific mechanisms enabling the transgenerational transmission of epigenetic marks during reproduction. achieves chromatin methylation through the small interfering RNA (siRNA)-directed DNA methylation (RdDM) pathways. In addition, Polycomb repressive complex 2 (PRC2) catalyzes H3K27me3 deposition on exchangeable histone variants during reproduction in a plant-specific manner. This review describes recent progress in research of transgenerational epigenetic inheritance, focusing on transmitting epigenetic marks through reproduction steps: meiosis, gametogenesis, and embryogenesis.

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.

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.

Investigating aging has become a subject of intense biomedical focus. This has coincided with an unprecedented rise in epigenetic research. DNA methylation (DNAm) is the most comprehensively investigated epigenetic process. Epigenetic clocks are capable of statistically correlating DNAm changes with chronological age. DNAm changes are also proving to be a worthwhile biomarker of age-related disease, while emerging evidence suggests this epigenetic mechanism could be an effective diagnostic tool for disease detection. Such investigative progress has significant implications for health care. In this brief review we examine some recent findings in this area. The overarching aim and scope of the work is to address the relationship between aging, DNAm, and health. We commence by briefly introducing aging. Next, DNAm and age-related disease are discussed. Thirdly, we critically examine epigenetic clocks. We conclude by exploring recent advances in the use of biosensors for measuring DNAm and disease detection.

Breast cancer (BC) is a highly prevalent malignancy in women and is often resistant to available therapies, calling for urgent investigation of the molecular mechanisms underlying its pathogenesis and progression. BC is thought to result from a complex interplay between genetic and environmental factors. Among key factors, chronic stress has been associated with worse cancer outcomes and can profoundly impact the epigenome. However, both stress and BC phenotypes are complex and heterogeneous, making studies that examine their molecular links challenging. Despite their heterogeneity, stressors trigger a neuroendocrine response that in humans culminates in the release of cortisol, a highly lipophilic hormone that traverses essentially every cell and induces widespread genomic effects. Modeling such effects at the epigenetic level, here we examine whether cellular DNA methylation (DNAm) markers of chronic stress - derived from human fibroblasts undergoing prolonged exposure to physiological stress cortisol levels - distinguish BC phenotypes in two independent human cohorts. Our results show that methylomic signatures of stress are consistently higher in tumor samples as compared to normal samples and in more advanced tumor stages and grades. Follow-up analyses further identify specific DNAm sites driving these associations, which are significantly enriched for cell adhesion pathways in both cohorts. These findings provide insights into the molecular mechanisms linking stress with BC and a proof-of-concept for utilizing cell model-derived disease biomarkers in environmental epigenetics.

Epigenetic alterations are cell type-specific and require methods like single cell sequencing and cell type sorting by flow cytometry. These methods often rely on the availability of fresh tissue, yet postmortem frozen tissue is typically the only material available from non-experimental subjects, including humans and other nonhuman primates (NHP). Many insights can be gained from analysis of these precious samples. To this end, we developed a protocol for isolating intact nuclei from small starting amounts of postmortem frozen chimpanzee () cerebral cortex tissue. Isolated nuclei can be input directly into single cell epigenomics protocols like ATAC-seq or can be immunostained for enrichment of neuronal nuclei via fluorescent-activated nuclei sorting (FANS) followed by bulk epigenetic methods like methylome sequencing. We adapted and optimized this protocol based on existing human brain tissue protocols. Our protocol specifically addresses challenges presented by postmortem frozen NHP brain tissue, including high levels of myelin debris and reduced RNA integrity. We include key steps and troubleshooting guidance to improve nuclei quality and sorting outcomes, and we also discuss limitations and considerations for researchers interested in using these methods.

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 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.