Uniquely practical education, producing specialist clinical leaders and transforming local healthcare.
AI has emerged as a pivotal tool in redefining TBI rehabilitation, bridging gaps in traditional care with innovative, data-driven approaches. While its potential to enhance diagnostic accuracy, outcome prediction, and individualized therapy is evident, challenges such as bias in datasets and ethical implications must be addressed. Continued research and multidisciplinary collaboration will be key to harnessing AI’s full potential, ensuring equitable access and optimizing recovery outcomes for TBI patients.
Overall, the integration of AI in TBI rehabilitation presents numerous opportunities to advance patient care and enhance the effectiveness of therapeutic interventions.
Scientists at EPFL have developed an innovative, non-invasive brain stimulation therapy to significantly improve visual function in stroke patients who have suffered vision loss following a stroke. The approach could offer a more efficient and faster way to regain visual function in such cases.
Each year, thousands of stroke survivors are left with hemianopia, a condition that causes loss of half of their visual field (the “vertical midline”). Hemianopia severely affects daily activities such as reading, driving, or just walking through a crowded space.
There are currently no treatments that can restore lost visual function in hemianopia satisfactorily. Most available options focus on teaching patients how to adapt to loss of vision rather than recovering it. To achieve some degree of recovery, months of intensive neurorehabilitative training are required for only moderate restoration at best.
This issue’s cover features companion papers that exemplify how understanding a rare disease can inform treatment strategies in other conditions.
Fassihi et al. and Nakazawa et al. report on the C-terminal deletion of transcription factor TFIIH-p52 subunit as a cause of xeroderma pigmentosum.
The cover art was created using PyMOL; TFIIH-p52 subunit (blue; C-terminus in white). Image credit: Keiko Itano.
https://www.jci.org/articles/view/195731 https://www.jci.org/articles/view/195732
1National Xeroderma Pigmentosum Service, Rare Disease Centre, Guy’s and St Thomas’ NHS Trust, London, United Kingdom.
2Department of Molecular Genetics, Nagoya University Graduate School of Medicine, Nagoya, Japan.
A San Diego biotech has set out to solve the formula for best-in-class antibody-drug conjugates, raising $120 million with support from Big Pharma Merck & Co. to fuel its efforts.
Solve Therapeutics’ new fundraise was led by oncology-focused VC Yosemite, with participation from new investors Abingworth and Merck, plus existing investors Alexandria Venture Investments and Citadel’s Surveyor Capital, among others.
A research team in South Korea has successfully developed a novel technology that combines nanoparticles with stem cells to significantly improve 3D bone tissue regeneration. This advancement marks a step forward in the treatment of bone fractures and injuries, as well as in next-generation regenerative medicine.
The research is published in the journal ACS Biomaterials Science & Engineering.
Dr. Ki Young Kim and her team at the Korea Research Institute of Chemical Technology (KRICT), in collaboration with Professor Laura Ha at Sunmoon University, have engineered a nanoparticle-stem cell hybrid, termed a nanobiohybrid by integrating mesoporous silica nanoparticles (mSiO₂ NPs) with human adipose-derived mesenchymal stem cells (hADMSCs). The resulting hybrid cells demonstrated markedly enhanced osteogenic (bone-forming) capability.
Aging is accompanied by complex cellular and molecular changes that compromise CNS function. Among these, glial cells (astrocytes, microglia, and oligodendrocytes) play a central role in maintaining neural homeostasis, modulating synaptic activity, and supporting metabolic demands. Emerging evidence indicates that aging disrupts glial cell physiology through processes including mitochondrial dysfunction, impaired proteostasis, chronic low-grade inflammation, and altered intercellular signaling. These alterations contribute to synaptic decline, myelin degeneration, and persistent, low-grade inflammation of the CNS. This review synthesizes current knowledge on the bidirectional relationship between aging and glial cell dysfunction, highlighting how age-related systemic and CNS-specific factors exacerbate glial impairments and, in turn, accelerate neural deterioration.
Non-small cell lung cancer (NSCLC) is the most prevalent form of lung cancer, accounting for approximately 85% of all cases, and is associated with a poor prognosis. Despite significant advancements in treatment modalities, therapeutic efficacy remains suboptimal, underscoring the urgent need for novel strategies. In recent years, increasing attention has been directed toward the pivotal role of gut microbiota-host interactions in the treatment of NSCLC. This review systematically examines the influence of current NSCLC therapies on gut microbiota and metabolism, explores the relationship between the microbiome and therapeutic response, and highlights the critical functions of probiotics, microbial metabolites, fecal microbiota transplantation (FMT), and dietary interventions in NSCLC management. By elucidating the mechanisms through which gut microbiota and their metabolites modulate treatment efficacy, we investigate the potential of exogenous interventions targeting the gut ecosystem to enhance therapeutic outcomes and mitigate adverse effects. Modulating the intestinal microbiota represents a promising clinical avenue and offers a new frontier for the development of future NSCLC treatment strategies.
The human microbiome comprises a diverse and dynamic community of microorganisms—including bacteria, fungi, viruses—their genetic material, and metabolic byproducts. The resident microbiota is an essential component of host health and homeostasis (1). Most microbiome research to date has focused on bacterial populations, which constitute a major proportion of these resident microbes (2). In the gut, Bacteroidetes, Firmicutes, Proteobacteria, and Actinobacteria dominate the bacterial composition (3– 5). The gut microbiota plays a pivotal role in regulating host immunity and metabolism through the production of numerous metabolites that function as signaling molecules and metabolic substrates, linking dysbiosis with inflammation and tumorigenesis (6– 8).
The cross-link between gut microbiota and lung cancer is a complex multifactorial relationship. Studies have shown that in patients with lung cancer, the abundance of Bacteroidetes, Fusobacteria, Cyanobacteria, and Spirochaetes increases in both pulmonary and intestinal microbiomes, while Firmicutes are significantly reduced (4, 9). Research on both gut and respiratory tract microbiota has revealed notable dysregulation in NSCLC, which is further associated with distant metastasis (DM) (10). The pathogenic contribution of the gut microbiome and its specific metabolites to NSCLC lies in their modulation of chronic inflammation and immune dysregulation (11). A study combining serum metabolomics and fecal microbiome profiling identified potential biomarkers in patients with early-stage NSCLC. The metabolomic analysis revealed elevated levels of sphingolipids (e.g. D-erythrosphingosine 1-phosphate, palmitoylsphingomyelin), fatty acyls (e.g.