Inosine monophosphate dehydrogenase type 2 polymorphism IMPDH2 3757T>C (rs11706052) and 12-month evolution of the graft function in renal transplant recipients on mycophenolate-based immunosuppression
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Functional assessment of autologous tissue expansion grafts for vaginal reconstruction in a rabbit model
This study explores a novel approach to vaginal reconstructive surgery using autologous tissue grafts, which may provide new therapeutic options for women with congenital or acquired vaginal anomalies. Using a small autologous vaginal tissue segment, we engineered a six-fold expanded graft perioperatively, leveraging the body as a bioreactor and avoiding preoperative tissue culture. In adolescent White New Zealand rabbits, a vaginal defect was created and repaired using a PLATE graft (perioperative, layered, autologous, tissue-expansion graft) containing mucosa, smooth muscle, collagen, and surgical mesh. After seven months, PLATE grafts were well integrated with native tissues, exhibited reduced fibrosis, and enhanced muscle regeneration compared to acellular grafts. Gene analysis revealed upregulation of smooth muscle and ECM organisation markers. Functional validation included successful breeding and vaginal delivery of live pups. PLATE grafts proved safe for vaginal reconstruction in rabbits, presenting a new direction in tissue engineering and expanding surgical options for women.
A first-in-human study of quantitative ultrasound to assess transplant kidney fibrosis
Kidney transplantation is the optimal treatment for renal failure. In the United States, a biopsy at the time of organ procurement is often used to assess kidney quality to decide whether it should be used for transplant. This assessment is focused on renal fibrotic burden, because fibrosis is an important measure of irreversible kidney injury. Unfortunately, biopsy at the time of transplant is plagued by problems, including bleeding risk, inaccuracies introduced by sampling bias and rapid sample preparation, and the need for round-the-clock pathology expertise. We developed a quantitative algorithm, called renal H-scan, that can be added to standard ultrasound workflows to quickly and noninvasively measure renal fibrotic burden in preclinical animal models and human transplant kidneys. Furthermore, we provide evidence that biopsy-based fibrosis estimates, because of their highly localized nature, are inaccurate measures of whole-kidney fibrotic burden and do not associate with kidney function post-transplant. In contrast, we show that whole-kidney H-scan fibrosis estimates associate closely with post-transplant renal function. Taken together, our data suggest that the addition of H-scan to standard ultrasound workflows could provide a safe, rapid and easy-to-perform method for accurate quantification of transplant kidney fibrotic burden, and thus better prediction of post-transplant renal outcomes.
Advancements in bioengineering for descemet membrane endothelial keratoplasty (DMEK)
Corneal diseases are the third leading cause of blindness worldwide. Descemet’s Membrane Endothelial Keratoplasty (DMEK) is the preferred surgical technique for treating corneal endothelial disorders, relying heavily on high-quality donor tissue. However, the scarcity of suitable donor tissue and the sensitivity of endothelial cells remain significant challenges. This review explores the current state of DMEK, focusing on advancements in tissue engineering as a promising solution to improve outcomes and address donor limitations.
Energy metabolism in health and diseases
Energy metabolism is indispensable for sustaining physiological functions in living organisms and assumes a pivotal role across physiological and pathological conditions. This review provides an extensive overview of advancements in energy metabolism research, elucidating critical pathways such as glycolysis, oxidative phosphorylation, fatty acid metabolism, and amino acid metabolism, along with their intricate regulatory mechanisms. The homeostatic balance of these processes is crucial; however, in pathological states such as neurodegenerative diseases, autoimmune disorders, and cancer, extensive metabolic reprogramming occurs, resulting in impaired glucose metabolism and mitochondrial dysfunction, which accelerate disease progression. Recent investigations into key regulatory pathways, including mechanistic target of rapamycin, sirtuins, and adenosine monophosphate-activated protein kinase, have considerably deepened our understanding of metabolic dysregulation and opened new avenues for therapeutic innovation. Emerging technologies, such as fluorescent probes, nano-biomaterials, and metabolomic analyses, promise substantial improvements in diagnostic precision. This review critically examines recent advancements and ongoing challenges in metabolism research, emphasizing its potential for precision diagnostics and personalized therapeutic interventions. Future studies should prioritize unraveling the regulatory mechanisms of energy metabolism and the dynamics of intercellular energy interactions. Integrating cutting-edge gene-editing technologies and multi-omics approaches, the development of multi-target pharmaceuticals in synergy with existing therapies such as immunotherapy and dietary interventions could enhance therapeutic efficacy. Personalized metabolic analysis is indispensable for crafting tailored treatment protocols, ultimately providing more accurate medical solutions for patients. This review aims to deepen the understanding and improve the application of energy metabolism to drive innovative diagnostic and therapeutic strategies.
The role of Neuregulin-1 in steatotic and non-steatotic liver transplantation from donors after cardiocirculatory death
Liver grafts from donors after cardiocirculatory death (DCDs) are sometimes not considered for liver transplantation (LT). Plasma Neuregulin-1 (NRG1) is altered in cardiac abnormalities and the liver is one of the most important targets of NRG1. We study the role of NRG1 in DCD LT. Under these conditions, NRG1 was pharmacologically modulated and their pathways were characterized. NRG1 levels were increased in steatotic and non-steatotic grafts from DCDs; NRG1 was derived from adipose tissue. When NRG1 was inhibited, injury and inflammation were exacerbated. The benefits of endogenous NRG1 in DCD grafts were associated with increased hepatic accumulation of adipocyte-derived vascular endothelial growth factor-A (VEGFA). The Id1-Wnt2 signaling pathway was involved in the action mechanisms of endogenous VEGFA. Exogenous NRG1 exacerbated damage and inflammation. Here differential role of NRG1 (endogenous versus exogenous) was demonstrated and VEGFA treatment was proposed as a highly protective strategy in steatotic and non-steatotic DCD LT.
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