Postoperative inflammation influences recovery after abdominal and liver surgery. This narrative review critically synthesizes clinical and translational evidence on inflammation-modulating strategies using a structured search of PubMed, Scopus, Web of Science, and Cochrane Library for publications from 2015 to 2025. Case reports, pediatric studies, and publications lacking clinical or translational relevance were excluded. Immunonutrition and early enteral nutrition are the most established approaches, with benefits for postoperative recovery and infectious complications. Perioperative corticosteroids in liver resection and short-course antibiotics following adequate source control offer procedure- and indication-specific benefits. Emerging interventions, including microbiota modulation, N-acetylcysteine, activation of nuclear factor erythroid 2-related factor 2/heme oxygenase-1 signaling, and cell-based therapies, show biological promise but lack sufficient high-quality clinical evidence for routine implementation. Established strategies should be integrated into Enhanced Recovery After Surgery pathways according to patient risk and surgical context. Personalized management requires prospective validation of emerging therapies and candidate biomarkers, including interleukin-6, C-reactive protein, and heme oxygenase-1, with standardized assays and sampling schedules.
Proprotein convertase subtilisin/kexin type 9 (PCSK9) inhibition reduces cardiovascular events in type 2 diabetes, while experimental studies implicate PCSK9 in immune activation, platelet function and organ-specific metabolism. Whether these mechanisms contribute clinically beyond atherogenic lipoprotein lowering remains uncertain. This critical narrative review integrates an original corpus of 108 appraised publications, with targeted additions during revision. It evaluates whether findings from different compartments and experimental perturbations can be transferred to particular treatments and clinical outcomes. Mechanistic evidence implicates receptor trafficking, intracellular cholesterol, mitochondrial stress and inflammatory signalling. Effects vary by cell type and compartment: local PCSK9 promotes injury in some models but preserves pancreatic, glomerular or cardiac function in others. Global knockout, tissue-specific deletion, extracellular antibodies and hepatic silencing are therefore distinct exposures. Human biomarker and imaging studies provide translational signals but generally cannot isolate direct effects from concomitant lipoprotein changes. Randomised antibody trials establish cardiovascular efficacy and an overall reassuring glycaemic profile, without demonstrating clinically meaningful glucose lowering. PCSK9 has broader immunometabolic functions, but the available evidence does not quantify an additional clinical benefit independent of atherogenic lipoprotein lowering. Tissue-specific mechanisms and causal mediation require further investigation.
Good syndrome is commonly diagnosed when thymoma and hypogammaglobulinemia coexist, although universally accepted diagnostic criteria are lacking. Profound B-cell lymphopenia is one of its most consistent immunological features. We describe a woman followed for 30 years in our unit whose severe antibody deficiency preceded thymoma detection by 14 years. Circulating B cells were preserved before thymectomy and throughout 16 years of subsequent follow-up, with maintained class-switched memory B cells despite persistent antibody deficiency. Her clinical course was favorable under immunoglobulin replacement, without documented major opportunistic infections. T-cell differentiation abnormalities were present despite preserved absolute counts. These findings suggest that patients currently classified as Good syndrome may represent a more heterogeneous group than traditionally assumed. Although preserved B cells do not exclude Good syndrome under existing definitions, the present observation should be considered hypothesis-generating and supports further studies evaluating potential biological heterogeneity among patients diagnosed with Good syndrome. This case highlights the need for consensus diagnostic criteria that consider the temporal relationship between both conditions, B-cell numbers, and the accompanying immune abnormalities, rather than relying on the coexistence of thymoma and hypogammaglobulinemia alone.
Biodiesel is projected to reduce greenhouse gas and particulate matter emissions relative to petrodiesel, but biodiesel engine emissions (DEEs) contain higher levels of nitrogen oxides, nano-sized particles, and specific oxygenated volatile organic compounds and aromatics that may increase health risks. Most research on DEE health effects has focused on respiratory, cardiovascular, neurodegenerative, and reproductive outcomes, leaving a considerable knowledge gap regarding gastrointestinal effects. We therefore examined and compared the colon effects of DEE produced by combustion of first-generation B7 biofuel (7% v/v fatty acid methyl esters, FAMEs) or second-generation SHB20 biofuel (7% v/v FAME plus 13% v/v hydrotreated vegetable oils, HVOs), with or without a diesel particle filter (DPF). Male Fischer 344 rats were exposed to DEE for 7 consecutive days (6 h/day; seven exposure sessions, 42 h in total) in whole-body inhalation chambers, at measured particulate matter concentrations of 2.19 and 2.13 mg/m3 without DPF and 0.17 and 0.19 mg/m3 with DPF for B7 and SHB20, respectively. Whole-body DEE exposure induced lipid peroxidation, oxidative-stress-associated and redox-related changes, mobilisation of the antioxidant defence system, and an inflammatory-associated response in colon tissue. These colon effects were blend-specific and only partly and endpoint-dependently mitigated by DPF use, with SHB20 DEE without DPF producing the most pronounced responses.
Peripheral artery disease (PAD) is most commonly caused by atherosclerotic arterial stenosis or occlusion, which reduces downstream tissue perfusion and causes tissue ischemia. In response to ischemia, reparative angiogenesis is activated and may support tissue perfusion recovery and skeletal muscle protection. In contrast, neovascularization within atherosclerotic plaques may promote intraplaque hemorrhage and plaque destabilization. Thus, angiogenesis has dual roles in PAD-related ischemia and atherosclerotic plaques. Extracellular vesicles (EVs) are membrane-bound particles that carry various cargo, including proteins, lipids, nucleic acids, and metabolites. Through the transfer of bioactive cargo and surface-mediated signaling, EVs can modify recipient-cell functions and thereby influence angiogenic signaling. Investigation of EV-mediated communication may therefore help elucidate the mechanisms underlying angiogenic regulation in vascular disease. In addition, disease-promoting EVs may be therapeutically targeted, whereas engineered EVs may be developed as therapeutic agents or delivery platforms. Recent studies have shown that EVs regulate angiogenic responses in preclinical murine hindlimb ischemia models. However, these effects in ischemic limbs and the potential involvement of EVs in atherosclerotic plaque neovascularization have rarely been reviewed in an integrated manner. This narrative review discusses these contrasting angiogenic processes from a context-dependent perspective. Understanding this context dependency may help develop EV-based strategies that promote functional vascular repair in ischemic tissues while suppressing or normalizing pathological neovascularization in atherosclerotic plaques.
