In a compelling study published in Cell on September 17, 2025, Stanford researchers have shifted the spotlight to an abnormal type of fat, colloquially termed “creeping fat,” which aggressively envelops the intestines in Crohn’s patients. Unlike benign adiposity, this pathological fat contributes directly to the formation of intestinal fibrosis, a scarring process that stiffens and narrows the bowel in what are known clinically as strictures. This insight reframes creeping fat from a mere symptom of disease to an active player exacerbating the progression of Crohn’s, offering novel molecular targets for intervention that were previously unconsidered.

Crohn’s disease, a perplexing and chronic inflammatory condition of the gastrointestinal tract, generally emerges in adolescence or early adulthood. Patients suffer from a cascade of symptoms—including relentless abdominal pain, diarrhea, malnutrition, and profound fatigue—that deeply impact quality of life. While anti-inflammatory treatments can sometimes achieve remission, a significant subset of patients inevitably progress to develop strictures, a severely fibrotic thickening that impairs intestinal function. Surgical excision remains the primary recourse for strictures; however, this approach is far from ideal, given its invasive nature and the high rate of recurrence.

The challenge in managing strictures lies not only in their physical toll but in their biological complexity. Prior investigations noted the consistent presence of creeping fat adjacent to these scarred intestinal segments, but the mechanistic links remained elusive. This new study, led by pediatric surgeon Jeong Hyun and surgeon-scientist Michael Longaker, probes these mechanisms with unprecedented rigor, combining human tissue analysis and sophisticated animal modeling. Their work reveals that creeping fat houses specialized fibroblasts that are highly responsive to mechanical stress—a factor previously underappreciated in Crohn’s pathogenesis.

Detailed genetic and molecular profiling of fibroblasts within creeping fat tissue discloses a fascinating mechanosensitivity: these cells detect and respond to mechanical strain emanating from the tense, inflamed intestine. This response includes the production of extracellular matrix components, the fundamental constituents of fibrotic scar tissue. Crucially, these activated fibroblasts concentrate at the interface where fat meets intestine, suggesting a localized, dynamic interplay that intensifies tissue stiffening. This insight overturns the conventional mucosa-centric view of Crohn’s, which has historically focused on immune-driven inflammation within the innermost bowel layers.

Equally groundbreaking is the development of an animal model that faithfully recapitulates the human Crohn’s phenotype, including hallmark creeping fat and stricture formation. In this model, mechanical tension of the intestine synergizes with chronic inflammation to activate the fibroblasts in adjacent fat, thereby fueling fibrosis. Such a paradigm foregrounds the role of biomechanical forces alongside immune dysregulation—an integrative perspective that better explains the complex progression of the disease.

The molecular pathways elucidated in this process include the highly conserved YAP/TAZ signaling cascade, known to mediate cellular responses to mechanical stimuli across diverse tissues. Longaker’s laboratory, previously engaged in exploring scar formation in skin, identified that inhibiting YAP/TAZ signaling in fat-resident fibroblasts drastically reduces the fibrotic response in the intestines of diseased mice. This discovery not only implicates a specific, druggable target but also aligns intestinal fibrosis with broader principles of mechanically induced scarring, revealing a potential therapeutic avenue previously untapped in Crohn’s management.

These insights carry profound clinical implications. Current anti-inflammatory regimens address only one facet of Crohn’s pathophysiology—immune activation—while ignoring the potent feedback loop established by creeping fat and mechanosensitive fibrosis. Patients who experience escalating fibrosis despite medication highlight this gap in treatment strategies. The identification of fat-derived fibroblasts as drivers of strictures points toward therapies that could intercept scarring processes before surgery becomes necessary, potentially transforming patient outcomes.

The emotional and physical burden borne by Crohn’s patients is immense. Jeong Hyun, who regularly performs surgeries to excise fibrotic strictures, describes the experience of his patients as one marked by unpredictability and chronic suffering. The inability to control symptom flare-ups or disease progression inflicts a dual hardship—bodily and psychological. This research not only illuminates a path forward scientifically but also holds promise for ameliorating a disease that, until now, offered limited avenues beyond invasive interventions.

Furthermore, the notion of “outside-in” signaling introduced by this study—that inflammation and mechanical forces permeate the full thickness of the bowel wall and the surrounding fat—is a significant conceptual advance. It challenges the prevailing “inside-out” dogma, which confined pathogenetic considerations to layers closest to the intestinal lumen. Recognizing the mesentery and creeping fat as bioactive sites reshapes the therapeutic landscape and necessitates a broader approach to drug development.

This finely detailed exploration also underscores the power of multidisciplinary collaboration. Contributions from institutions beyond Stanford, including Case Western Reserve University and the Icahn School of Medicine at Mt. Sinai, as well as support from a spectrum of funding agencies, illustrate the collective effort required to tackle complex diseases like Crohn’s. Such synergy between surgical insight, molecular biology, and translational research is key to accelerating progress in difficult clinical arenas.

In conclusion, the Stanford-led study reinvents our understanding of fat’s role in Crohn’s disease, transforming creeping fat from a passive marker of disease into a mechanosensitive culprit driving fibrosis. The revelation that biomechanical forces and associated signaling pathways contribute crucially to intestinal scarring underscores the urgency of developing targeted anti-fibrotic therapies. If successful, these could revolutionize care, reducing the need for repeated surgeries and profoundly improving the lives of millions affected by this relentless disease.

Subject of Research: Animals
Article Title: Creeping fat-derived mechanosensitive fibroblasts drive intestinal fibrosis in Crohn’s disease strictures
News Publication Date: 17-Sep-2025
Web References: https://profiles.stanford.edu/jeong-hyun, https://profiles.stanford.edu/michael-longaker, https://profiles.stanford.edu/khristian-bauer-rowe-ramos, https://med.stanford.edu/
References: Study published in Cell, September 17, 2025
Keywords: Crohn disease, inflammatory bowel diseases, intestinal fibrosis, creeping fat, fibroblasts, mechanosensitive signaling, YAP/TAZ pathway, intestinal strictures

A pioneering study conducted by researchers at Stanford Medicine delves deeply into how different timekeeping strategies—permanent standard time, permanent daylight saving time, and the current biannual clock changes—impact the body’s internal clock, or circadian rhythm, and consequently affect long-term health outcomes. The circadian rhythm, an intrinsic biological timer approximating a 24-hour cycle, orchestrates a host of physiological processes from hormone production to metabolism and immune function. Disruptions to this rhythm have been increasingly implicated in various chronic conditions, calling into question the ubiquity of seasonal time shifts.

According to the researchers’ findings, published in the prestigious Proceedings of the National Academy of Sciences, the current pattern of switching clocks twice per year is the least beneficial from the standpoint of circadian alignment and public health. Through detailed modeling that accounts for regional variations in light exposure, as well as demographic characteristics, the team concludes that adopting a permanent time standard—especially permanent standard time—would significantly reduce the burden on people’s biological clocks and yield measurable health benefits.

The crux of the research lies in translating light exposure patterns, shaped by the timing of sunrise and sunset under different time policies, into a metric the researchers call “circadian burden.” This measure quantifies how much an individual’s natural circadian cycle must adjust daily to stay synchronized with the 24-hour solar day. Since human circadian rhythms are naturally slightly longer than 24 hours—approximately 24 hours and 12 minutes on average—timely light exposure is essential to reset the clock each day. Morning light acts to advance the circadian phase, effectively speeding up the clock and helping it align, while evening light delays it.

Their sophisticated mathematical models demonstrated that permanent standard time, which maximizes morning light exposure, imposes the lowest circadian burden for the majority of the population. This finding lends empirical weight to longstanding propositions from sleep and medical organizations that advocate for year-round standard time, arguing that early morning light has uniquely restorative effects on circadian health. Conversely, permanent daylight saving time, which shifts daylight to later hours in the evening, ranks second in circadian benefits but carries less advantage overall.

Interestingly, the study reveals a nuanced picture regarding individual differences. Approximately 15% of people, known as morning larks, possess circadian cycles naturally shorter than 24 hours. For these individuals, increased evening light provided by permanent daylight saving time can synchronize their internal clocks more effectively, lowering their circadian burden. This complexity highlights the challenge of designing public policies that fit diverse biological rhythms within the population.

Beyond circadian modeling, the research team took an innovative step by integrating their circadian data with county-level health statistics from the Centers for Disease Control and Prevention. They specifically examined conditions linked to circadian disruption, including obesity, stroke, diabetes, coronary heart disease, depression, cancer, arthritis, and chronic obstructive pulmonary disease. Their results reveal that permanent standard time could prevent an estimated 300,000 strokes and reduce the prevalence of obesity by 2.6 million cases annually across the U.S. Permanent daylight saving time would achieve roughly two-thirds of these benefits.

Of note, the models showed no significant change in diseases like arthritis, which lack established connections to circadian misalignment, reinforcing the specificity of circadian-mediated health impacts. These findings make a compelling case for reevaluating seasonal clock changes not just as an inconvenience, but as a significant public health concern with tangible long-term effects.

Despite the robustness of their modeling, the authors caution that their work is not the definitive conclusion on the subject. Their simulations made simplifying assumptions about human behavior and light exposure—such as regular sleep-wake schedules from 10 p.m. to 7 a.m. and consistent outdoor light exposure—but real-world scenarios often diverge due to indoor lifestyles, irregular schedules, and various environmental factors like weather and geography. For example, although regions like California offer abundant sunshine, people reportedly spend less than 5% of their day outdoors, limiting natural light’s capacity to entrain circadian rhythms.

The researchers also emphasize that choosing a particular time policy simply defines which clock hours correspond with daylight; it does not alter the fundamental solar cycle or increase total daylight hours during winter months. The immutable celestial mechanics that govern sunrise and sunset remain unchanged regardless of human timekeeping decisions, imposing bound limits on what can be achieved through clock adjustments alone.

This study represents a major advance toward data-driven policymaking about time standards, providing empirical backing where previously only theory and speculation prevailed. However, the authors acknowledge the multidimensional nature of time policy decisions, which intersect with economic, social, and cultural factors not addressed in their circadian-centered analysis. They advocate for interdisciplinary studies to weigh these competing considerations holistically.

In sum, this compelling research highlights the hidden health costs of biannual clock changes while providing a scientifically grounded path forward: embracing permanent standard time to foster healthier circadian rhythms and reduce the burden of diseases tied to circadian misalignment. As society grapples with proposals to eliminate clock switching, these findings offer a crucial piece of evidence that could steer future legislative and public health debates toward more circadian-friendly timekeeping.

Subject of Research: People
Article Title: Circadian-Informed Modeling Predicts Regional Variation in Obesity and Stroke Outcomes Under Different Permanent U.S. Time Policies
News Publication Date: 15-Sep-2025
Web References: https://profiles.stanford.edu/jamie-zeitzer, https://profiles.stanford.edu/lara-weed, https://med.stanford.edu/
References: Proceedings of the National Academy of Sciences
Keywords: Sleep, Circadian Rhythms, Obesity, Stroke, Time Policy, Daylight Saving Time, Public Health

The research, soon to be published in Nature Medicine, was co-led by Michael Snyder, PhD, and Tracey McLaughlin, MD, with significant contributions from a multidisciplinary team blending genetics, endocrinology, and biomedical data science. Their observational study involved 55 adult participants, carefully selected without prior Type 2 diabetes diagnosis. These individuals underwent comprehensive metabolic phenotyping, including insulin resistance evaluation and beta cell function testing, paired with advanced multi-omics analyses incorporating lipidomics, metabolomics, liver function assessments, and gut microbiome profiling.

Central to the investigation was the deployment of continuous glucose monitoring systems, which captured dynamic blood sugar fluctuations in response to a controlled and repeated intake of seven carbohydrate-rich foods. The tested foods—ranging from jasmine rice and buttermilk bread to shredded potatoes, pasta, canned black beans, grapes, and a berry mixture—were consumed in standardized portions by participants in a fasted state to ensure baseline comparability. Each food item was ingested twice by every subject, enabling robust within-individual and between-group comparisons over three-hour postprandial windows.

The findings disrupt the simplistic categorization of carbohydrates based on glycemic index or load. Notably, certain starchy foods provoked heterogeneous glucose responses contingent upon the individual’s underlying metabolic derangements. For example, individuals with insulin resistance displayed pronounced glycemic spikes following pasta consumption, whereas those with both insulin resistance and beta cell dysfunction exhibited highest glucose excursions after potato ingestion. Conversely, glucose responses to rice or grapes were elevated across participants, independent of metabolic health status, suggesting some carbohydrate sources exert universal impacts on glycemia.

Delving deeper, multi-omics profiling illuminated metabolic signatures correlating with these response patterns. Participants exhibiting potato-induced glucose spikes harbored elevated levels of circulating triglycerides, fatty acids, and other metabolites characteristic of insulin resistance phenotypes. Intriguingly, glycemic elevations after black bean consumption aligned with alterations in histidine and ketogenic metabolism pathways, indicating shifts toward increased fat utilization as an energy substrate. Moreover, those who experienced blood sugar surges post-bread consumption were more frequently diagnosed with hypertension, underscoring the metabolic interconnectivity between carbohydrate intolerance and cardiovascular risk factors.

A compelling revelation emerged in the form of the potato-to-grape glucose spike ratio as a potential biomarker for insulin resistance. Since grapes induced glucose elevations uniformly, contrasting their response with the variable potato response enabled differentiation of metabolic impairments. This ratio—if validated in larger populations—could furnish clinicians with a practical and non-invasive proxy to detect insulin resistance, a condition currently difficult to diagnose without specialized testing yet critically amenable to lifestyle and pharmacological interventions aimed at diabetes risk reduction.

Further exploring dietary modulation, the researchers tested whether pre-loading meals with macronutrients such as fiber, protein, or fat could mitigate carbohydrate-induced glucose spikes. In metabolically healthy participants, ingestion of pea fiber or egg white protein prior to rice consumption effectively blunted postprandial glycemic excursions, while consuming fat (in the form of crème fraîche) delayed the peak glucose concentration. However, these mitigating effects were absent in participants exhibiting insulin resistance or beta cell dysfunction, indicating that the pathophysiology of metabolic disease attenuates the efficacy of such nutritional strategies—a finding with significant clinical implications for therapeutic meal planning.

This study challenges prevailing paradigms by demonstrating that metabolic dysfunctions not only influence the magnitude but also the temporal dynamics of postprandial glucose metabolism, highlighting personalized nutrition as a critical frontier in metabolic disease management. Michael Snyder advocates for pragmatic dietary ordering, suggesting that consuming protein- or fat-rich foods prior to carbohydrates (like eating a salad or hamburger before fries) may prove beneficial, even as the optimal macronutrient sequence remains to be conclusively identified.

The research integrates collaborations across institutions including Johns Hopkins University, Ultima Genomics, Amrita Vishwa Vidyapeetham University, the University of Bergen, and Cairo University, reflecting the global urgency in tackling diabetes through precision medicine. Financial support from a consortium of prestigious funding bodies such as the National Institutes of Health, the American Diabetes Association, and the Stanford Diabetes Center underscores both the significance and anticipated impact of these findings.

Beyond implications for diabetes care, this study also enriches the broader understanding of human metabolic diversity, offering insights into how genetic, environmental, and microbial factors intertwine to shape individual responses to dietary carbohydrates. The meticulous multi-omics approach champions a holistic perspective necessary for decoding complex metabolic networks and tailoring interventions that transcend simplistic dietary prescriptions.

In summary, this pioneering research elucidates the critical heterogeneity in glycemic responses based on individual metabolic health, heralding a new era where carbohydrate recommendations may be customized rather than generalized. The study not only underscores the physiological underpinnings of carbohydrate metabolism in health and disease but also identifies actionable biomarkers and interventions that bring personalized nutrition within reach for millions at risk of diabetes and metabolic disorders.

Subject of Research: People

Article Title: Individual variations in glycemic responses to carbohydrates and underlying metabolic physiology

News Publication Date: June 4, 2025

Web References:

• Nature Medicine article

References:

• Snyder, M., McLaughlin, T., et al. (2025). Individual variations in glycemic responses to carbohydrates and underlying metabolic physiology. Nature Medicine. DOI: 10.1038/s41591-025-03719-2

Image Credits: Emily Moskal/Stanford Medicine

Keywords: Type 2 diabetes, Metabolic disorders, Blood glucose variability, Insulin resistance, Beta cell dysfunction, Personalized nutrition, Continuous glucose monitoring, Multi-omics profiling, Glycemic response, Starchy foods, Biomarkers, Dietary interventions

Traditionally recognized for its role in energy metabolism, glucose has now been found to perform a dual function that includes modulating the pathways through which stem cells mature into various cell types in the body. The compelling evidence presented in this research suggests that glucose interacts with a plethora of proteins, thereby affecting the activity and functionality of these proteins. This interaction occurs at critical junctures in cellular differentiation, marking a transformative shift in how glucose is perceived in cell biology.

The researchers, led by Dr. Paul Khavari, conducted extensive experiments with human skin stem cells differentiating into keratinocytes, the predominant cells in the outer layer of skin. Utilizing advanced techniques such as mass spectrometry and high-throughput screening, they measured the fluctuations in biomolecule concentrations throughout the differentiation process. Surprisingly, instead of observing a decrease in glucose levels—as one might expect during a phase where cells begin to slow down division—researchers observed a significant increase in glucose uptake as the differentiation process progressed.

This increase in glucose concentration prompted a reevaluation of its significance. By employing fluorescent and radioactive glucose analogs, the team was able to visualize glucose dynamics within the cells during differentiation. Notably, as the cells advanced in their differentiation journey, an increase in fluorescence indicated heightened glucose activity, suggesting that glucose levels serve as crucial signals that promote differentiation.

Further investigations revealed that the increased glucose levels were attributed to both heightened import mechanisms and diminished export processes within the cells. Notably, this accumulation did not correlate with elevated glucose metabolism, suggesting that glucose’s role as a signaling molecule is distinct from its function as a mere energy substrate. These revelations echoed throughout diverse human cell types, hinting at glucose’s potentially universal role in tissue differentiation across various biological contexts.

Intrigued by these findings, the researchers turned their attention to skin organoids—engineered tissue models intended to mimic the characteristics of native skin. In a striking experiment, organoids were unable to undergo proper differentiation when glucose levels were artificially lowered. This setback was resolved simply by reintroducing a glucose analog that could not be metabolized, reinforcing the notion that glucose’s functionality in differentiation transcends its energetic properties.

The implications of this discovery extend beyond basic biology and delve into realms such as diabetes and cancer. For individuals with elevated blood sugar levels due to diabetes, impaired healing and regeneration may be attributed to disrupted glucose signaling pathways. The findings also propose a reevaluation of therapeutic strategies targeting glucose metabolism in cancer treatment, where forcing undifferentiated cancer cells into a more mature state via glucose signaling could open avenues for innovative treatments.

Scholarly literature has hinted at glucose’s potential signaling capabilities in the past, with studies showing that embryonic stem cells lose their pluripotency when subjected to high glucose concentrations. This underscores the idea that glucose levels play a pivotal role in maintaining cellular states, particularly in stem cells whose differentiation demands precise regulatory mechanisms.

Crucially, the research team discovered that the increase in intracellular glucose levels corresponds with the enhanced production of a specific protein that facilitates glucose transport into the cell. Once inside, glucose can bind to proteins such as IRF6, a transcription factor involved in gene expression linked to differentiation. This binding triggers conformational changes that modulate IRF6’s ability to influence which genes are transcribed into proteins, effectively steering the cell’s differentiation toward a specialized fate.

In essence, this research provides a fresh perspective on how glucose functions within cellular contexts. Unlike the targeted pathways activated by other signaling molecules, glucose operates more like a broad-spectrum signaling agent, sending out signals that activate multiple cellular functions simultaneously. As levels rise in the cell, they create a systemic response that echoes throughout the cellular landscape—much like a fire alarm prompting immediate action across a community.

As the research team pushes forward, they aim to decipher the complexities surrounding glucose’s role in both healthy and diseased states. This newfound understanding could help address the complications caused by glucose dysregulation in diabetes and its association with cancer development—a condition characterized by failed differentiation and uncontrolled cellular growth.

This groundbreaking study paves the way for future research, illuminating the multifaceted roles that simple biomolecules like glucose may play in cellular processes. As the scientific community reconsiders glucose’s place in cellular biology, it becomes increasingly clear that deeper investigations into other small molecules may uncover similarly unexpected functions, broadening our comprehension of cellular physiology and its intricacies.

By revealing glucose’s critical roles beyond energy provision, we stand at the precipice of a transformative understanding that could manipulate cellular behavior with far-reaching consequences. Such insight could not only offer novel therapeutic strategies but might also redefine our conceptual frameworks for cell biology, metabolism, and health.

Subject of Research:
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Keywords: Stem cell research, Glucose, Tissue differentiation, Cellular biology, Cancer therapies, Diabetes

The report, which will be published in the prestigious journal JAMA Pediatrics, highlights that a staggering 59% of children who die in mass shootings are killed by family members. This statistic emphasizes the critical role of domestic violence in contributing to gun-related fatalities among minors, underscoring the urgent need to address the realities of firearm access in homes. Co-author Dr. Stephanie Chao, a prominent figure in pediatric surgery, expressed her surprise at the high prevalence of domestic violence reflected in the data, indicating a broader public health issue that demands immediate attention.

In the context of gun violence, the data is particularly striking. By 2020, gun-related fatalities surpassed car accidents as the leading cause of death among children in the United States. The study serves as a poignant reminder of the shifting landscape of childhood safety, where firearms, instead of traditional hazards, pose a more immediate threat. According to Chao, this shift in mortality patterns should compel parents and policymakers to reconsider the focus of prevention efforts, particularly regarding gun safety within domestic environments.

The study meticulously analyzed incidents defined as mass shootings—events resulting in at least four fatalities that exclude the perpetrator. Spanning from January 2009 to December 2020, the researchers investigated 121 separate mass shootings, accounting for a total of 308 pediatric fatalities. The results revealed that more than 40% of child victims were killed by a parent, while relatives were responsible for 59%, indicating a familial tragedy occurring behind closed doors that is often overlooked.

Moreover, the remaining relationships between shooters and child victims included acquaintances, strangers, classmates, and neighbors. However, the predominant presence of family members as perpetrators challenges prevailing narratives that often emphasize external threats to children. The stark reality is that children are often most at risk from those who are supposed to protect them rather than from unpredictable, random acts of violence.

The public’s perception of gun violence has been primarily shaped by sensationalized media coverage, which tends to focus on high-profile incidents such as school shootings and mass gatherings that attract national attention. This has created a skewed understanding of gun violence dynamics, where domestic situations involving firearms remain under-reported. The frequency of domestic shootings, particularly those involving children, highlights a pressing need for a paradigm shift in how society conceptualizes the sources of gun violence.

Chao’s research points to a more effective approach for reducing pediatric gun deaths through the consideration of relationships in domestic contexts. In homes where violence or instability may arise, proactive measures to reduce firearm access could significantly lower children’s risk of injury or death. Recommendations could include firearm removal from households experiencing domestic disturbances, highlighting a clear pathway for preventative strategies.

In recognizing that over 22 million children currently reside in homes with guns, the findings bring a new dimension to the responsibilities of gun ownership. Preparing families for the potential risks involved with having a firearm at home is crucial in mitigating instances of domestic violence that escalate to fatal outcomes. Chao emphasizes the importance of educating families about the implications of gun ownership within their domestic lives, aiming to foster conversations about safety and responsibility that extend beyond mere ownership.

Despite the grim implications of the data, there is hope for a more comprehensive approach to addressing gun violence as a public health issue. With newfound awareness stemming from the findings, legislative efforts could be informed by these realities, leading to policies that support gun safety measures targeting homes with children. This could reshape educational programs and community resources to prioritize firearm injury prevention, aiming not just to react to incidents but to proactively address them.

In addition to the research, Chao and her team are working to develop educational initiatives aimed at children in K-12 schools. This program, called PLEDGE, seeks to equip young people with the knowledge and skills necessary to navigate the dangers of gun injuries and promote safety awareness. By engaging youth directly, these efforts may foster a generation more cognizant of the risks associated with firearms and better prepared to advocate for safer home environments.

This extensive investigation into the correlation between familial relationships and pediatric fatalities due to mass shootings positions the ongoing discourse around gun violence in a critical space. As national conversations continue to ripple through communities, educators, parents, and policymakers can leverage these insights to foster environments that prioritize the safety and well-being of children. Simple yet effective changes in perception and behavior regarding gun ownership and domestic violence can reshape a narrative around gun violence that has long needed reevaluation.

Ultimately, the critical nature of this research underscores the necessity for continued investigation into the relationships that facilitate gun violence in America. As patterns of violence evolve, so too must our understanding and prevention strategies. Embracing a holistic view of gun violence, particularly in relation to domestic environments, can pave the way for significant advancements in public health and safety for children across the nation.

Subject of Research: People
Article Title: Victim-Shooter Relationships in Mass Shootings Involving Child Victims
News Publication Date: 10-Feb-2025
Web References: JAMA Pediatrics
References: N/A
Image Credits: N/A
Keywords: Gun violence, Domestic violence, Mass shootings, Pediatric safety, Public health.