The investigation began with an integrated bioinformatics screen of colorectal cancer datasets, from which SUCLG2 emerged as a candidate gene whose expression tracks with disease severity. Multi-omics validation in clinical specimens confirmed the pattern: SUCLG2 levels were significantly downregulated in colorectal cancer tissue compared with healthy tissue, and the degree of loss correlated tightly with advanced TNM staging and poor patient prognosis. Patients whose tumors expressed the least SUCLG2 fared worst, positioning the enzyme not only as a mechanistic player but also as a potential prognostic biomarker that could help clinicians stratify risk at the time of diagnosis.

To probe function, the team manipulated SUCLG2 in colorectal cancer cell lines and in animal models. Functional assays showed that SUCLG2 restrains the proliferation of colorectal cancer cells in culture and suppresses xenograft tumor growth in vivo. When the enzyme was depleted, cells grew more aggressively; when it was restored, growth slowed appreciably. These results established SUCLG2 as a bona fide tumor suppressor rather than a metabolic bystander, raising the central question of how a tricarboxylic acid cycle enzyme exerts such direct control over cancer cell behavior.

The answer, uncovered through transcriptomic, metabolomic, and epigenetic analyses, lies in an unexpected biochemical pathway involving S-adenosylmethionine, or SAM, the universal methyl donor of the cell. SUCLG2 activity reduces intracellular SAM levels. Because SAM is the substrate required by DNA methyltransferases, or DNMTs, to attach methyl groups to DNA, lower SAM availability dampens DNMT activity genome-wide. The consequence for colorectal cancer cells is profound: hypermethylation of tumor suppressor gene promoters is alleviated, and genes silenced by this epigenetic brake can be switched back on.

Among the genes reactivated by this mechanism, one stood out. GADD45G, a growth arrest and DNA damage-inducible gene with well-documented anti-proliferative functions, regained transcriptional activity when SUCLG2 was present. The researchers showed that SUCLG2 demethylates the GADD45G promoter through this SAM-dependent epigenetic remodeling, relieving promoter hypermethylation and restoring GADD45G expression. Gene set enrichment analysis reinforced the picture, revealing that SUCLG2 overexpression activates p53 and apoptosis signaling while inhibiting cell cycle pathways, consistent with GADD45G acting as a conduit between the mitochondrial enzyme and the cell’s central tumor-suppressive machinery.

Causality was tested directly. When the researchers knocked down GADD45G in cells engineered to overexpress SUCLG2, the tumor-suppressive effects of the enzyme were largely abolished. This loss-of-function experiment established GADD45G as a critical downstream mediator of the SUCLG2/p53 signaling axis. In other words, SUCLG2 does not simply slow cancer cells through metabolic exhaustion; it reactivates a specific genetic program, via demethylation of GADD45G, that engages p53-mediated growth inhibition and programmed cell death.

Clinical validation strengthened the mechanistic model considerably. Across patient cohorts, the team confirmed a robust positive correlation between SUCLG2 and GADD45G expression, and, in keeping with the proposed epigenetic mechanism, a negative correlation between SUCLG2 levels and methylation of the GADD45G promoter. Tumors with abundant SUCLG2 tended to carry unmethylated, transcriptionally active GADD45G, whereas SUCLG2-poor tumors showed the silenced, hypermethylated state. These correlative findings in human tissue mirror the experimental results and suggest that the SAM-DNMT-GADD45G axis operates in actual disease, not merely in laboratory models.

The study carries notable therapeutic implications. Epigenetic silencing of tumor suppressor genes is a hallmark of colorectal cancer, and demethylating agents exist but act globally, with limited specificity and considerable toxicity. If SUCLG2 activity, or downstream nodes of its pathway, could be pharmacologically enhanced, it might offer a more targeted way to lift methylation repression specifically at tumor suppressor promoters. Alternatively, the SUCLG2-GADD45G-p53 axis could be exploited indirectly, for example by screening for compounds that mimic the enzyme’s effect on SAM metabolism or DNMT activity. The authors position SUCLG2 as both a promising prognostic biomarker and a candidate therapeutic target, though translating these findings into clinical interventions will require further preclinical development and validation in larger patient populations.

Beyond its immediate clinical relevance, the research adds to a growing appreciation that metabolic enzymes can double as epigenetic regulators. Because metabolites such as SAM, alpha-ketoglutarate, acetyl-CoA, and NAD+ serve as substrates and cofactors for chromatin-modifying enzymes, shifts in cellular metabolism can directly reshape the epigenetic landscape. The SUCLG2 story is a vivid example: a change in the activity of a TCA cycle enzyme propagates through the methyl donor economy of the cell to determine whether a key anti-cancer gene is audible or silenced. As colorectal cancer remains a major clinical challenge, uncovering such regulatory mechanisms may open entirely new avenues for early detection, risk stratification, and treatment.

Subject of Research: SUCLG2-mediated epigenetic activation of the GADD45G-p53 axis in colorectal cancer progression

Article Title: SUCLG2 demethylates GADD45G to activate the p53 pathway and inhibit malignant progression in colorectal cancer

Article References: Guo, T., Lai, S., Yang, K., Tong, J., Liao, G., Lu, L., Jiang, C., Liu, H., Wu, Z., Yang, M., & Guo, J. (2026). SUCLG2 demethylates GADD45G to activate the p53 pathway and inhibit malignant progression in colorectal cancer. Cancer Cell International. https://doi.org/10.1186/s12935-026-04454-5

Image Credits: AI Generated

DOI: 10.1186/s12935-026-04454-5

Keywords: colorectal cancer, SUCLG2, GADD45G, p53 pathway, DNA methylation, demethylation, S-adenosylmethionine, DNA methyltransferase, tumor suppressor, cancer metabolism, epigenetics, prognostic biomarker

Bariatric surgery is among the most effective treatments for severe obesity, reducing body weight and often improving type 2 diabetes, high blood pressure, sleep apnoea and other obesity-related conditions. But the operations can alter the body’s handling of nutrients, hormones and mechanical forces in ways that affect bone. Sleeve gastrectomy removes much of the stomach, creating a narrow tube and reducing food intake, while Roux-en-Y gastric bypass both restricts intake and reroutes food around the stomach and the first part of the small intestine. That rerouting can reduce the absorption of calcium and vitamin D, nutrients essential for maintaining mineralised bone. Rapid weight loss also decreases the loading forces transmitted through the skeleton, potentially reducing the stimulus that normally helps preserve bone mass. Changes in gut hormones and bone-remodelling signals may add to the effect.

The new study focused on 120 postmenopausal women treated at a single centre: 97 had undergone primary Roux-en-Y gastric bypass, and 23 had received the operation as a revision after sleeve gastrectomy. Revisional surgery is performed for several reasons, including inadequate weight loss, weight regain, reflux or other complications after the original operation. It is not simply a repeat of the first procedure. The patient has already experienced one period of weight loss and anatomical alteration, and the second operation may produce an additional shift in nutrient absorption and gastrointestinal physiology. Postmenopausal women are a particularly important group for studying bone because declining oestrogen levels accelerate bone turnover and increase the risk of osteoporosis. The researchers compared demographic characteristics, medical conditions and recognised osteoporosis risk factors before examining the women’s skeletal and body-composition measurements.

Bone mineral density was measured using dual-energy X-ray absorptiometry, or DXA, the standard clinical technique for estimating bone mass. DXA uses two low-dose X-ray beams to distinguish bone mineral from soft tissue, producing measurements in grams per square centimetre. It also generates T-scores, which compare a patient’s bone density with the average density of a healthy young adult. A T-score between −1.0 and −2.5 is generally classified as low bone mass, or osteopenia, while a score of −2.5 or below is consistent with osteoporosis, although diagnosis also depends on clinical context and fracture history. In this study, scans assessed the lumbar spine, femoral neck and total hip. The same examinations also estimated fat mass and lean mass, allowing the investigators to determine whether differences in bone density simply reflected differences in body size or muscle and fat composition.

Before statistical adjustment, the revisional-surgery group had a mean femoral-neck bone mineral density of 0.693 grams per square centimetre, compared with 0.761 grams per square centimetre among women who had primary bypass surgery. This difference was statistically significant, with a P value of 0.011. The corresponding average T-scores were −1.4 and −0.9, respectively, a difference that was also significant. In practical terms, the revisional group’s average femoral-neck measurement fell further into the low-bone-mass range, although the study does not report that every individual patient had osteopenia or osteoporosis. Initial comparisons found no meaningful differences in body-mass index, major comorbidities or recorded osteoporosis risk factors. Bone density at the lumbar spine and total hip appeared similar before adjustment, showing that the signal was most pronounced at the femoral neck.

The more revealing result emerged when the team adjusted the analysis for age, body-mass index and time since surgery. After this correction, total-hip bone mineral density remained lower in the revisional group, with an adjusted mean of 0.834 grams per square centimetre, compared with 0.899 grams per square centimetre in the primary-surgery group. The P value was 0.017, and the 95 per cent confidence intervals were 0.786 to 0.882 and 0.877 to 0.921, respectively. At the femoral neck, adjusted density averaged 0.682 grams per square centimetre after revision and 0.763 grams per square centimetre after primary bypass, with a P value of 0.003. Because the confidence intervals and statistical tests indicate a persistent group difference, the findings are unlikely to be explained solely by the women being older, having different body sizes or simply having undergone surgery at different times.

The absence of a body-composition difference is scientifically important. The researchers found similar proportions of fat and lean tissue in the two groups, so the lower hip density after revisional surgery could not be readily attributed to a greater loss of muscle or a markedly different physical build. Nevertheless, the study cannot establish that revisional surgery directly caused the bone loss. Its cross-sectional design means that participants were assessed after their operations rather than followed from before surgery through successive years. The women may have differed in unmeasured ways, such as the amount of weight they lost after each procedure, dietary intake, calcium and vitamin-D supplementation, physical activity, smoking, alcohol use, medication exposure or pre-existing bone density. The small revisional group, comprising only 23 women, also limits the precision with which the results can be generalised.

The biological explanation is plausible, however. Bone is living tissue that is continuously remodelled: osteoclasts remove old or damaged bone, while osteoblasts form new tissue. When resorption outpaces formation, mineral density declines. After Roux-en-Y bypass, reduced exposure of nutrients to the duodenum and proximal jejunum can impair calcium absorption. A fall in absorbed calcium may stimulate parathyroid hormone, which helps maintain blood calcium partly by increasing calcium release from bone. Vitamin-D deficiency can compound the problem by reducing intestinal calcium uptake. At the same time, weight loss reduces skeletal loading, and altered concentrations of gut hormones such as glucagon-like peptide-1 and peptide YY may influence bone turnover. A revisional bypass could expose patients to overlapping or repeated metabolic stresses, although the present study did not measure all these pathways or prove that any one mechanism accounted for the hip findings.

The location of the difference may also matter. The femoral neck and total hip are weight-bearing regions that respond strongly to changes in body mass, muscle forces and physical activity. The lumbar spine, by contrast, can be affected by degenerative changes that sometimes make DXA readings appear higher than the amount of healthy bone would suggest, particularly in older adults. Lower density at the hip is clinically concerning because hip fractures can lead to prolonged loss of independence, complications and increased mortality in older people. Yet a low DXA value is not itself a fracture forecast, and the study did not report fracture outcomes. It therefore signals a risk that merits attention rather than demonstrating that revisional bypass inevitably leads to fractures. The researchers’ conclusion is more measured: women undergoing revisional procedures may need targeted, long-term skeletal monitoring.

That monitoring could include assessment of fracture history and risk factors, periodic DXA scans when clinically appropriate, and laboratory evaluation of calcium, vitamin D and related markers. Nutritional follow-up is already a central part of bariatric care, but the findings suggest that skeletal surveillance should be especially deliberate after a sleeve-to-bypass conversion. Clinicians may need to review whether patients are taking prescribed supplements, absorbing them adequately and maintaining sufficient protein and calcium intake, while also encouraging safe resistance and weight-bearing exercise tailored to individual ability. Decisions about osteoporosis medication require specialist judgement because altered gastrointestinal anatomy and nutritional status can affect treatment choices. The study does not argue against revisional bariatric surgery, which can provide substantial health benefits, nor does it show that primary bypass is harmless to bone. Instead, it adds a warning to the rapidly expanding medical conversation around obesity treatment: success measured on the bathroom scale may conceal changes in tissues that are harder to see.

Further research will need to follow larger groups of patients before and after both operations, measure bone-turnover markers and nutrient levels, and track fractures over time. Direct comparisons should also examine whether the interval between sleeve gastrectomy and revision, the length of the bypassed intestine, the magnitude of weight loss or the use of anti-obesity medicines changes skeletal outcomes. Randomised trials of supplementation, exercise programmes or bone-protective therapies could reveal how much of the decline is preventable. For now, the French study offers one of the clearest indications that revisional Roux-en-Y gastric bypass may affect postmenopausal bone differently from the same operation performed as a first procedure. As bariatric surgery becomes more common and more patients undergo sequential operations, the hip—not just the waistline—may become an essential part of measuring long-term success.

Subject of Research: Bone mineral density, body composition and skeletal health after primary or revisional Roux-en-Y gastric bypass in postmenopausal women

Article Title: Revisional Roux-en-Y gastric bypass after sleeve gastrectomy impacts bone health in postmenopausal women

Article References: Karam, L., Philippoteaux, C., Ramdane, N. et al. “Revisional Roux-en-Y gastric bypass after sleeve gastrectomy impacts bone health in postmenopausal women.” Archives of Osteoporosis 21, 130 (2026). Original research article

Image Credits: AI Generated

DOI: 10.1007/s11657-026-01772-z

Keywords: bariatric surgery, Roux-en-Y gastric bypass, sleeve gastrectomy, bone mineral density, osteoporosis, postmenopausal women, hip health, obesity

In a new study, a physics team led by Baoli Liu at the Institute of Physics, Chinese Academy of Sciences, investigates how cryogenic biaxial compression modulates excitons in multilayer ZrSe₃. The work focuses on a key challenge for practical optics and sensing: obtaining a large, controllable optical response from manageable strain engineering strategies, especially under environmentally constrained conditions.

The researchers implemented a temperature-driven approach to generate biaxial compressive strain. ZrSe₃ flakes were carefully transferred onto a flexible polycarbonate substrate, and then the system was cooled to cryogenic temperatures. As the polycarbonate contracted, it imposed compressive strain on the attached ZrSe₃, enabling strain transfer without mechanical fixtures that could complicate device integration.

To read out the optical consequences of this strain, they employed differential reflectance spectroscopy across various temperatures. The spectra revealed a striking redshift of excitonic resonances, demonstrating that exciton energies in ZrSe₃ can be strongly shifted by the applied biaxial compression.

Quantitatively, the exciton energy shift corresponds to a gauge factor of approximately 136 meV/%—a magnitude described as comparable to the highest strain responses reported for two-dimensional materials. Such a large response implies unusually strong strain sensitivity of both excitonic transitions and the underlying band structure.

The study places ZrSe₃ within the broader context of group IV–V transition metal trichalcogenides, materials that have gained attention for their orientation-resolved strain response arising from reduced in-plane symmetry. Earlier results showed substantial gauge factors under uniaxial tension; here, the team extends the concept by demonstrating that biaxial strain can be even more effective for exciton modulation.

Beyond reporting a strong effect, the findings emphasize the practicality of temperature-assisted strain control for flexible optoelectronics. With excitons acting as a direct bridge between strain and optical signals, the approach offers a route toward strain-tunable photodetectors and other wearable or stretchable sensing technologies.

The publication appears in Nano Research on May 12, 2026. The authors expect the results to advance band structure engineering in anisotropic 2D semiconductors and to accelerate research toward viral “strain-to-light” device concepts.

The team acknowledges contributions from researchers including Hao Li, Yu Hua, Jiaru Zhou, Geng Li, Changzhi Gu, Gang Wang, and Xiaofeng Fan. Financial support was provided by multiple Chinese national and institutional programs, including key national research funding and foundational science initiatives.

Subject of Research: Straintronics; exciton modulation in multilayer ZrSe₃ via cryogenic biaxial compression
Article Title: Large strain tunability of excitons in ZrSe₃ via cryogenic environment
News Publication Date: 12-May-2026
Web References: http://dx.doi.org/10.26599/NR.2026.94908438
References: Nano Research (May 12, 2026); DOI: 10.26599/NR.2026.94908438
Image Credits: Nano Research, Tsinghua University Press

Keywords

Straintronics; ZrSe₃; excitons; biaxial compression; cryogenic environment; differential reflectance spectroscopy; gauge factor; flexible optoelectronics; 2D anisotropic semiconductors; photodetectors

Radiation therapy is a cornerstone in oncologic treatment, utilized in more than half of all cancer cases. The therapy typically requires patients to attend multiple sessions over an extended period, making geographic accessibility a critical factor in treatment adherence and outcomes. The study’s findings underscore the severe disparity in care access: while urban areas that lost facilities often maintained multiple alternatives, rural counties frequently faced the complete loss of local radiation treatment options.

The analysis quantified that 68.5% of U.S. counties lacked a radiation oncology site by 2025, affecting approximately 50.8 million people. Furthermore, 427 counties experienced a net site loss during the study period. Statistical modeling revealed rural practice sites had a 44% higher likelihood of closure than their urban counterparts, and freestanding, community-based centers were 56% more likely to shutter compared to hospital-affiliated facilities. These vulnerabilities manifest against a backdrop of socioeconomic challenges; counties without radiation oncology access typically report lower median incomes, higher uninsured rates, and fewer primary care physicians per capita.

Exacerbating the crisis are the steep Medicare reimbursement cuts implemented in 2026, which were not reflected in the current data but threaten to deepen the financial instability of community-based practices. The payment reductions jeopardize the sustainability of freestanding oncology centers, force closures, and further restrict cancer treatment access in already underserved areas. This financial pressure underscores the urgent necessity for targeted policy intervention to stabilize and safeguard oncology infrastructure.

Experts emphasize that these closures carry profound consequences beyond mere inconvenience. Previous research correlates increased distance to radiation therapy facilities with elevated cancer mortality, signifying that diminished local access translates directly into poorer patient survival rates. “When a rural community loses a radiation oncology clinic, patients may lose local access entirely, compounding hardship during an already difficult diagnosis,” said Dr. Sindhu.

ASTRO, the American Society for Radiation Oncology, is advocating for reform through legislative proposals such as the Radiation Oncology Case Rate (ROCR) Act, which aims to shift Medicare reimbursement toward a patient-centered, episode-based payment system. Such reforms seek to mitigate financial strain on clinics, particularly in vulnerable rural and community settings, aiming to preserve critical access for patients nationwide.

The study not only documents the ongoing erosion of the United States’ radiation oncology delivery system but also serves as a clarion call for systemic change. Without urgent policy solutions, cancer patients in rural and economically disadvantaged areas risk losing life-saving therapy, underscoring the intersection of healthcare access, socioeconomic inequity, and health outcomes in modern oncology.

Subject of Research: Structural Vulnerability in Radiation Oncology Access in the U.S.
Article Title: Structural Vulnerability in the United States Radiation Oncology Delivery System: Predictors and Consequences of Practice Site Disappearance
News Publication Date: July 9, 2026
Web References: https://www.redjournal.org/article/S0360-3016(26)03986-6/fulltext
Image Credits: International Journal of Radiation Oncology • Biology • Physics (Red Journal)
Keywords: Radiation therapy, cancer treatment access, healthcare disparities, rural health, oncology practice closures, Medicare reimbursement, healthcare policy

Pregnancy, as a unique immunological state, presents a complex environment where maternal and fetal immune systems coexist and interact through various biological mechanisms. SARS-CoV-2 infection during gestation triggers a maternal immune response characterized by the production of specific antibodies. However, the efficiency and extent to which these antibodies cross the placental barrier to confer immunity to the fetus have been largely debated, with significant implications for neonatal vulnerability.

The study employs a prospective cohort design, enrolling pregnant women with confirmed SARS-CoV-2 infection at different stages of gestation. By systematically collecting maternal blood, placental tissue, and neonatal samples at birth, researchers meticulously quantified IgG and IgM antibody levels and assessed viral RNA presence. This methodological rigor provides unparalleled clarity in mapping the serologic landscape associated with maternal COVID-19.

One of the pivotal findings underscores that the timing of maternal infection critically influences placental antibody transfer. Infections occurring in the late second trimester and third trimester correlate with higher neonatal IgG titers, indicating more efficient transplacental passage. Conversely, infections earlier in pregnancy exhibit diminished antibody transfer, possibly due to the maturation state of the placenta and evolving maternal immune responses.

The placental microenvironment itself plays a formidable role in mediating antibody transfer. The study reveals that placental expression of Fc receptors, which facilitate immunoglobulin G transport, varies significantly among individuals and is altered in SARS-CoV-2 affected pregnancies. These alterations may either potentiate or impede the trafficking of protective antibodies to the fetus, suggesting a delicate balance dictated by placental health and viral impact.

Moreover, the study explores the role of viral presence within placental tissues. While SARS-CoV-2 RNA was detected in a subset of placentas, active viral replication and significant histopathological changes were rare. This dissociation between viral presence and tissue damage hints at complex mechanisms by which the placenta attempts to shield the fetus from infection while potentially modulating immune signaling pathways.

In terms of neonatal outcomes, the investigation carefully evaluates evidence for vertical transmission. Despite maternal infection and occasionally detectable viral RNA in placental samples, neonatal swabs at birth were predominantly negative, and serologic evidence indicated passive immunity rather than active neonatal infection. This finding is crucial as it supports the concept that maternal antibodies provide a protective shield, reducing the likelihood of neonatal infection immediately postpartum.

The kinetics of maternal antibody decay also emerge as a vital consideration. The study observes that while maternal IgG levels remain elevated several weeks post-infection, they gradually wane, impacting the durability of neonatal immunity. This temporal aspect may inform vaccination strategies and timing in pregnant populations to optimize antibody levels at delivery.

Crucially, the interplay between maternal vaccination status and natural infection was examined. Women vaccinated prior to or during pregnancy demonstrated higher and more consistent antibody titers that translated into enhanced placental transfer compared to those relying solely on natural infection. This supports the ongoing public health emphasis on vaccinating pregnant individuals to confer both maternal and neonatal protection.

Furthermore, the researchers undertook a comprehensive literature review to contextualize their findings. They synthesized previous reports documenting inconsistent neonatal seropositivity and variable detection of viral RNA in placental studies. Their prospective data add a solid quantitative framework that may reconcile these discrepancies and underscore critical biological variables influencing these outcomes.

An additional layer of complexity arises from the heterogeneity of SARS-CoV-2 variants circulating during the study period. Variants with distinct spike protein mutations may alter antigenicity and antibody binding affinity, potentially impacting transplacental transfer efficiency. The study suggests ongoing surveillance is necessary to monitor how evolving viral lineages affect maternal-fetal immunity.

The inflammatory milieu during SARS-CoV-2 infection also warrants attention. Elevated pro-inflammatory cytokines within the placental tissue may disrupt barrier integrity or receptor expression patterns, further influencing antibody transfer and susceptibility. The study’s analysis of placental inflammatory markers suggests a multifactorial process where immune activation may ironically impair efficient fetal protection.

From a clinical perspective, these findings offer nuanced guidance. While natural infection induces some degree of fetal antibody acquisition, vaccination remains the most reliable method to ensure robust and sustained protective immunity in both mother and child. Obstetric care protocols may need to integrate serologic monitoring and tailored immunization schedules to mitigate neonatal risks.

The broader implications extend beyond SARS-CoV-2, opening avenues for understanding maternal-fetal immunology in viral infections. These insights could enhance preparedness for future pandemics and inform vaccine technologies targeting gestational immunity. It exemplifies the confluence of virology, immunology, and perinatology in confronting contemporary health challenges.

As scientific knowledge advances, this study stands as a testament to meticulous investigation combining clinical observation with molecular and immunological analysis. By illuminating the variables governing SARS-CoV-2 antibody transfer and neonatal infection risk, it empowers healthcare providers, researchers, and policymakers with actionable data to protect the most vulnerable: the newborns entering a world still grappling with viral threats.

In conclusion, the landscape of maternal SARS-CoV-2 infection and its impact on neonatal serologic status is complex yet increasingly decipherable through rigorous, prospective research. The interplay of infection timing, placental biology, maternal immunity, and vaccination status creates a multifaceted matrix that determines neonatal outcomes. This study marks a significant leap toward safeguarding neonatal health amid ongoing viral pandemics and underscores the vital importance of integrated maternal-fetal healthcare strategies.

Subject of Research:
SARS-CoV-2 serologic status in pregnant women, factors influencing placental antibody transfer, and neonatal transmission dynamics following gestational COVID-19.

Article Title:
Factors influencing SARS-CoV-2 placental antibody transfer and neonatal transmission. A prospective, cohort study and review of available literature.

Article References:
Candel-Pau, J., Maya-Enero, S., García-García, J. et al. Factors influencing SARS-CoV-2 placental antibody transfer and neonatal transmission. A prospective, cohort study and review of available literature. J Perinatol (2026). https://doi.org/10.1038/s41372-026-02640-x

Image Credits:
AI Generated

DOI:
30 March 2026