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{"title":"Q&A with Carolyn S.P. Lam.","authors":"Carolyn S P Lam","doi":"10.1016/j.medj.2026.101191","DOIUrl":"https://doi.org/10.1016/j.medj.2026.101191","url":null,"abstract":"<p><p>Professor Carolyn S.P. Lam is a senior consultant cardiologist at the National Heart Centre Singapore, where she founded Singapore's first women's heart clinic, and a tenured full professor at Duke-NUS Medical School. She is co-founder of Us2.ai, an award-winning startup applying artificial intelligence to echocardiography, with regulatory clearance across more than 35 countries. Her research spans heart failure with preserved ejection fraction, sex differences in cardiovascular disease, and Asian heart failure phenotypes. She is principal investigator of the ASIAN-HF registry and chairs several large international trials, including SURMOUNT-MMO, LIBREXIA-AF, HF-POLARIS, and CASTLE-HFpEF. She is co-chair of the 2024 KDIGO Controversies Conference and a leading voice on women's heart health and AI-enabled cardiovascular care.</p>","PeriodicalId":29964,"journal":{"name":"Med","volume":"7 7","pages":"101191"},"PeriodicalIF":13.3,"publicationDate":"2026-07-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148424848","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The atlas of abdominal organ remodeling in hepatocellular carcinoma patients: An artificial intelligence-based multicenter imaging study.","authors":"Yusheng Guo, Xiaona Fu, Tianxiang Li, Ning Wang, Shanshan Jiang, Shanmei Li, Xiaofang Guo, Rundong Wang, Shichao Long, Mengsi Li, Qiuping Liu, Kai Zhao, Yangyang Xie, Xuejun Chen, Lixia Wang, Chuansheng Zheng, Lian Yang","doi":"10.1016/j.medj.2026.101176","DOIUrl":"10.1016/j.medj.2026.101176","url":null,"abstract":"<p><strong>Background: </strong>Morphological changes of abdominal organs in hepatocellular carcinoma (HCC) remain uncharacterized. This study aimed to automatically quantify these changes using deep learning, assess their treatment-related outcome associations, and evaluate prognostic value.</p><p><strong>Methods: </strong>Abdominal computed tomography (CT) images from 2,747 patients with HCC and 2,869 healthy controls across 15 cohorts from 10 centers (8 Chinese and 2 international) were analyzed. The patients included those receiving immune checkpoint inhibitors (ICIs), transarterial chemoembolization (TACE), or surgical resection. A deep learning algorithm automatically segmented the spleen, liver, kidneys, pancreas, and adrenal glands. Organ volumes and height-normalized indexes (volume/height²) were calculated. Propensity score matching balanced baseline differences. Cox regression assessed associations with overall survival (OS), progression-free survival (PFS), and disease-free survival (DFS), with subgroup and interaction analyses.</p><p><strong>Findings: </strong>Compared with healthy controls, patients with HCC showed significant organ remodeling, with enlarged spleen, liver, kidneys, and adrenal glands (all p < 0.001). Multivariable analysis showed that in the ICI cohort, left kidney volume/index, right kidney index, and left adrenal gland volume/index predicted longer OS and PFS; in the TACE cohort, spleen volume/index and left kidney volume predicted OS and PFS; and in the surgical cohort, spleen volume, left kidney volume, left adrenal gland volume/index, and liver index were independent predictors. Restricted cubic spline analysis suggested nonlinear relationships between adrenal and kidney volumes and survival.</p><p><strong>Conclusions: </strong>HCC is associated with systemic abdominal organ remodeling. Automated CT-based multi-organ quantification offers reproducible, non-invasive prognostic biomarkers, particularly in cases involving adrenal glands, spleen, and kidneys, supporting personalized treatment and prognosis assessment.</p><p><strong>Funding: </strong>This work was funded by the National Natural Science Foundation of China.</p>","PeriodicalId":29964,"journal":{"name":"Med","volume":" ","pages":"101176"},"PeriodicalIF":13.3,"publicationDate":"2026-07-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148206365","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Tirzepatide monotherapy in Chinese patients with early type 2 diabetes: A randomized, double-blind, placebo-controlled phase 3 trial (SURPASS-CN-MONO).","authors":"Yaqi Yin, Jianhua Ma, Dexue Liu, Wei Duan, Zhifeng Cheng, Hongwei Jiang, Yawei Zhang, Guangyu Wu, Haoxin Zhuang, Weijun Gu, Yiming Mu","doi":"10.1016/j.medj.2026.101183","DOIUrl":"10.1016/j.medj.2026.101183","url":null,"abstract":"<p><strong>Background: </strong>We report findings from the Chinese SURPASS-CN-MONO trial (ClinicalTrials.gov: NCT05963022) of tirzepatide monotherapy.</p><p><strong>Methods: </strong>A multicenter, randomized, double-blind, phase 3 trial conducted at 29 centers in China. Adults with type 2 diabetes who had not received antihyperglycemic medication in the previous 90 days were randomized 1:1:1:1 to receive once-weekly 5, 10, or 15 mg tirzepatide or placebo. The primary endpoint was the mean change from baseline in hemoglobin A1c (HbA1c) at week 40.</p><p><strong>Findings: </strong>In total, 206 patients received 5 (n = 52), 10 (n = 51), or 15 (n = 52) mg tirzepatide or placebo (n = 51). Under the efficacy estimand, the least-squares mean reductions in HbA1c from baseline to week 40 were significantly greater with 5, 10, and 15 mg tirzepatide than with placebo (-2.17%, -2.06%, and -2.15% vs. -0.13%, with treatment differences vs. placebo of -2.04% [95% confidence interval (CI): -2.46, -1.63], -1.93% [95% CI: -2.35, -1.51], and -2.02% [95% CI: -2.44, -1.60], respectively; p < 0.001 for all comparisons). The least-squares mean reductions in body weight from baseline to week 40 were significantly greater with 5, 10, and 15 mg tirzepatide vs. placebo (-6.0, -6.1, and -9.7 vs. -1.0 kg, respectively; p < 0.001 for all comparisons). In the tirzepatide groups, the most common treatment-emergent adverse events were gastrointestinal related; there was no clinically significant (<54 mg/dL) or severe hypoglycemia.</p><p><strong>Conclusion: </strong>Tirzepatide effectively reduced hyperglycemia and body weight with no increased risk of hypoglycemia in Chinese patients with early type 2 diabetes. The safety profile was consistent with previous trials of tirzepatide.</p><p><strong>Funding: </strong>This work was funded by Eli Lilly and Company.</p>","PeriodicalId":29964,"journal":{"name":"Med","volume":" ","pages":"101183"},"PeriodicalIF":13.3,"publicationDate":"2026-07-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148259817","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Power and sample-size estimation in human microbiome research.","authors":"Qianyi Zhou, Yingzhou Lu, Luman Wang, Wei Zhou, Haley Oba, Yanjiao Zhou, Minjie Shen, Xiaodong Qu, Cristabelle De Souza, Andre Rayner, Yanfei Chen, Tess Y Cheng, Zongxin Ling, Lanjuan Li, Chang Liu, Anita Y Voigt, Ruoyun Xiong, Julia Oh, Daniel Spakowicz, Caroline Dravillas, Amy Wen Tian, Mark R Nicolls, Amber-Thy Huynh, Xin Chen, Jiyuan Hu, Mingguang He, Fuchu He, Michael P Snyder, Jing Yang, Xin Zhou","doi":"10.1016/j.medj.2026.101174","DOIUrl":"10.1016/j.medj.2026.101174","url":null,"abstract":"<p><p>Human microbiome research has become pivotal in advancing our understanding of complex diseases such as diabetes, inflammatory bowel disease, and cancer. Much of this work relies on comparing microbial communities across health and disease states, or case-control cohorts, using high-throughput metagenomic sequencing. Yet the very nature of sequencing-derived microbiome data makes robust cohort design and power-based sample-size estimation unusually difficult. Unlike other omics, microbiome profiles are compositional, sparse, and often zero inflated, properties that complicate statistical modeling and inflate sample-size requirements. These challenges are further compounded by the diversity of analytical frameworks-ranging from diversity indices to causal inference-each built on different statistical assumptions and optimized for a distinct research hypothesis. This review synthesizes current approaches around the study design and sample-size estimation in microbiome research, aiming to provide clinicians and researchers with practical guidance for navigating the statistical complexities unique to this field.</p>","PeriodicalId":29964,"journal":{"name":"Med","volume":" ","pages":"101174"},"PeriodicalIF":13.3,"publicationDate":"2026-07-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148266381","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Inhibiting glycan degradation prevents HIV-induced inflammaging and cognitive impairment.","authors":"Leila B Giron, Alejandra Borjabad, Eran Hadas, Janeway Granche, Erika G Marques de Menezes, Thomas A Premeaux, Hongxia He, Stephen T Yeung, Shalini Singh, Courtney Friday, Joshua Glover, Eric Balboa, Derrick Dopkin, Michelle Burrows, Anthony Secreto, Nicolas Skuli, Hiroaki Tateno, Paul W Denton, Frank Palella, Michael J Corley, Lishomwa C Ndhlovu, Philip J Norris, Katherine Tassiopoulos, David J Volsky, Mohamed Abdel-Mohsen","doi":"10.1016/j.medj.2026.101175","DOIUrl":"10.1016/j.medj.2026.101175","url":null,"abstract":"<p><strong>Background: </strong>Cognitive impairment is a frequent outcome of chronic viral infections linked to premature aging, including HIV. The mechanisms underlying this decline remain poorly understood. Here, we identify pro-inflammatory glycan degradation, characterized by loss of sialic acid and galactose, both hallmarks of premature aging, as a key contributor to HIV-associated cognitive impairment (HIV-CI).</p><p><strong>Methods: </strong>We analyzed two cohorts of people with HIV, with and without HIV-CI, and tested causality through intervention studies in two complemetary mouse models of virally mediated inflammation and cognitive deceline.</p><p><strong>Findings: </strong>Degradative glycomic changes were enriched in people with HIV with cognitive impairment, particularly females, and correlated with worse cognitive performance. In both a humanized mouse model of HIV and EcoHIV model, a complementary model that enables cognitive testing, pharmacological inhibition of glycan degradation with sialidase inhibitors prevented virally induced inflammation, immune activation, accelerated aging, and memory deficits.</p><p><strong>Conclusions: </strong>These findings implicate glycan degradation as a contributor to inflammation and cognitive impairment in HIV and highlight glycan preservation as a promising strategy to mitigate inflammation, premature aging, and cognitive decline during viral infections.</p><p><strong>Funding: </strong>This study was funded by the National Institutes of Health (NIH).</p>","PeriodicalId":29964,"journal":{"name":"Med","volume":" ","pages":"101175"},"PeriodicalIF":13.3,"publicationDate":"2026-07-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13618882/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148176895","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Single-cell profiling unveils an exhaustion trajectory of ZNF683^hi tissue-resident alveolar CD8⁺ T cells in checkpoint inhibitor pneumonitis.","authors":"Xiaoxiang Zhou, Ziming Jiang, Yanhong Ren, Yunzhi Zhou, Lei Deng, Zhenting Liu, Sijin Sun, Jieli Zhang, Wenyang Liu, Yin Yang, Wenting Ren, Yanfeng Wang, Hongxia Li, Yiqun Li, Fei Ma, Nan Bi, Luhua Wang, Yibo Gao, Jie He","doi":"10.1016/j.medj.2026.101180","DOIUrl":"10.1016/j.medj.2026.101180","url":null,"abstract":"<p><strong>Background: </strong>Checkpoint inhibitor pneumonitis (CIP) is the leading cause of treatment-related deaths for immune checkpoint inhibitor (ICI) combination therapies. CIP is problematic to diagnose and differentiate, particularly from radiation pneumonitis (RP), due to the lack of mechanistic distinctions between them.</p><p><strong>Methods: </strong>Using single-cell RNA sequencing (scRNA-seq) and single-cell T cell receptor sequencing (scTCR-seq), we characterize the cellular landscape of bronchoalveolar lavage fluid (BALF) and peripheral blood from a discovery cohort (seven CIP, six RP, and six treatment-naive controls) and a validation cohort (five patients receiving combined ICI and radiotherapy who were diagnosed with RP).</p><p><strong>Findings: </strong>We report a striking accumulation of alveolar CD8⁺ exhausted T cells (Texs) in CIP. The alveolar CD8⁺ Texs of CIP primarily differentiate from tissue-resident ZNF683^hi CD8⁺ T cells, whereas those of RP predominantly originate from peripherally related GZMK^hi CD8⁺ T cells. These findings were further validated in a prospectively enrolled validation cohort and ultimately guided successful clinical decisions regarding ICI rechallenge.</p><p><strong>Conclusions: </strong>These results highlight distinct cellular and molecular features in CIP and RP, thereby providing insights into clinical decision-making regarding ICI rechallenge in lung cancer patients.</p><p><strong>Funding: </strong>This study was supported by the National Natural Science Foundation of China.</p>","PeriodicalId":29964,"journal":{"name":"Med","volume":" ","pages":"101180"},"PeriodicalIF":13.3,"publicationDate":"2026-07-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148212902","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Withdrawal effects following treatment discontinuation: A blind spot in evidence-based medicine.","authors":"Alexander G Mathioudakis","doi":"10.1016/j.medj.2026.101181","DOIUrl":"10.1016/j.medj.2026.101181","url":null,"abstract":"<p><p>Treatment withdrawal effects are transient increases in clinical risk following treatment discontinuation that exceed the loss of treatment effect alone. They have been described across multiple therapeutic classes spanning diverse disease areas yet remain under-recognized and insufficiently addressed in both research and clinical practice. Because treatment interruption and non-adherence are common in routine care, failure to account for these effects can distort clinical decision-making and the generation and interpretation of research evidence. Withdrawal effects arise from treatment-induced biological adaptations that persist after cessation, creating a transient period of heightened vulnerability. Despite their clinical relevance, they are not consistently anticipated or explicitly incorporated into research design, analysis, or guideline development. This perspective argues that treatment discontinuation represents a distinct and clinically meaningful phase of exposure and outlines implications across the evidence continuum and clinical practice, alongside approaches to better identify and interpret withdrawal-related risks.</p>","PeriodicalId":29964,"journal":{"name":"Med","volume":" ","pages":"101181"},"PeriodicalIF":13.3,"publicationDate":"2026-07-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148273186","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Impact of lead-in ADT on grade ≥3 neutropenia in patients with metastatic hormone-sensitive prostate cancer treated with triplet therapy.","authors":"Xudong Ni, Yufan Zhao, Shanshan Wang, Lei Zhong, Xuedong Shi, Xiaomeng Li, Qi Ma, Yi Wu, Dingwei Ye, Yao Zhu","doi":"10.1016/j.medj.2026.101140","DOIUrl":"10.1016/j.medj.2026.101140","url":null,"abstract":"<p><strong>Background: </strong>Severe neutropenia (grade ≥3) is a major adverse event in patients with metastatic hormone-sensitive prostate cancer (mHSPC) receiving triplet therapy. The purpose of this study was to investigate the influence of lead-in androgen-deprivation therapy (ADT) on the incidence of grade ≥3 neutropenia.</p><p><strong>Methods: </strong>This post hoc analysis of the ARASENS phase 3 trial compared patients with and without lead-in ADT. Inverse probability of treatment weighting (IPTW) balanced baseline characteristics. The primary endpoint was grade ≥3 neutropenia incidence. External validation utilized multicenter real-world data.</p><p><strong>Findings: </strong>The ARASENS cohort included 847 patients (lead-in ADT, n = 748; no lead-in, n = 99). The lead-in-ADT group showed a lower incidence of grade ≥3 neutropenia during the first docetaxel cycle than the no-lead-in-ADT group (11.36% vs. 17.17%, p = 0.0328; adjusted odds ratio [OR]: 0.50, 95% confidence interval [CI]: 0.26-0.95). Overall survival showed no significant difference. Real-world validation (N = 202; lead-in ADT, n = 136; no lead-in ADT, n = 66) confirmed this lower incidence with lead-in ADT (11.03% vs. 37.88%, p < 0.0001; adjusted OR: 0.19, 95% CI: 0.09-0.42).</p><p><strong>Conclusions: </strong>Patients receiving lead-in ADT experienced a lower incidence of grade ≥3 neutropenia during the first docetaxel cycle than those not receiving lead-in ADT. This finding may contribute to improved prevention strategies for grade ≥3 neutropenia.</p><p><strong>Funding: </strong>This study was funded by the National Natural Science Foundation of China.</p>","PeriodicalId":29964,"journal":{"name":"Med","volume":" ","pages":"101140"},"PeriodicalIF":13.3,"publicationDate":"2026-07-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147933975","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Inhaled treprostinil and the vascular turn in pulmonary fibrosis.","authors":"Toyoshi Yanagihara, Martin Kolb","doi":"10.1016/j.medj.2026.101190","DOIUrl":"https://doi.org/10.1016/j.medj.2026.101190","url":null,"abstract":"<p><p>TETON trials recently evaluated inhaled treprostinil in idiopathic pulmonary fibrosis (IPF) using two parallel phase 3 studies in different world regions. Both met the primary endpoint, demonstrating significantly less one-year forced vital capacity decline versus placebo. This viewpoint critically appraises the findings and contextualizes them within the evolving IPF treatment landscape.</p>","PeriodicalId":29964,"journal":{"name":"Med","volume":"7 7","pages":"101190"},"PeriodicalIF":13.3,"publicationDate":"2026-07-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148424860","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Rethinking parenteral nutrition as supportive therapy for neonatal sepsis.","authors":"Ole Bæk, Christoph Härtel, Claus Klingenberg, Charles C Roehr, Eleanor J Molloy, Per T Sangild, Duc Ninh Nguyen","doi":"10.1016/j.medj.2026.101182","DOIUrl":"10.1016/j.medj.2026.101182","url":null,"abstract":"<p><p>It is paramount to optimize prevention and therapy for severe neonatal infections, particularly in high-risk infants. This perspective highlights the lack of guidelines for parenteral nutrition (PN) during suspected or confirmed infections in vulnerable newborns, especially those born preterm. Drawing on insights from immunometabolism and translational preclinical models, we argue that nutritional support during infection should not only meet energy demands but also actively shape immunity by modulating inflammation, organ injury, and clinical outcome. Conventional glucose-rich PN may fuel excessive glycolysis-driven immune activation and harmful hyperinflammation. In contrast, alternative macronutrient strategies, including partial replacement of glucose with galactose, glucogenic amino acids, or ketone bodies, may redirect host metabolism toward balanced immune responses, reduced tissue damage, and improved survival. We propose that neonatal nutrition during infection should be viewed as a modifiable therapeutic intervention and call for clinical trials to develop targeted PN protocols for vulnerable newborns at risk of infection.</p>","PeriodicalId":29964,"journal":{"name":"Med","volume":" ","pages":"101182"},"PeriodicalIF":13.3,"publicationDate":"2026-07-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148266366","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}