Search Results (2,154)

Retinal diseases such as age-related macular degeneration (AMD) and diabetic retinopathy (DR) are major causes of visual impairment and are closely associated with oxidative stress, inflammation, vascular dysfunction, and metabolic imbalance. Increasing evidence suggests that gut microbiota also contributes to retinal homeostasis, supporting the emerging concept of the gut–eye axis. In this context, dietary anthocyanins—with blueberry anthocyanins serving as a primary representative model—have attracted attention as potential adjunctive nutritional modulators of ocular health. However, their biological effects are strongly influenced by their limited bioavailability and extensive gastrointestinal metabolism. The objective of this review is to analyze the gastrointestinal fate of dietary anthocyanins and to discuss how their absorption, enzymatic transformation, and microbial biotransformation may influence ocular protection through the gut–eye axis. The review summarizes current knowledge regarding anthocyanin stability in the oral cavity, stomach, small intestine, and colon, as well as the formation of circulating phenolic metabolites generated by the host and through microbial metabolism. In addition, the molecular mechanisms through which anthocyanins and their metabolites may support retinal health are examined, including antioxidant, anti-inflammatory, vasoprotective, and neuroprotective actions. Overall, dietary anthocyanins, illustrated through the rich profile of blueberries, represent promising adjunctive compounds for supporting ocular health, although further clinical and mechanistic studies are still required. Full article

Endothelial dysfunction (ED) is an early event in cardiovascular and metabolic diseases, including atherosclerosis, diabetes, and hypertension. Emerging evidence highlights the interplay between chronic inflammation and oxidative stress, collectively termed OxInflammation, as a major driver of vascular injury and impaired tissue repair. Among the key mediators of this response is the Nod like receptor family pyrin domain containing 3 (NLRP3) inflammasome, a multiprotein complex that promotes the release of inflammatory cytokines, including Interleukin 1β (IL-1β) and Interleukin-18 (IL-18), and induces gasdermin D-mediated pyroptotic cell death. Activation of NLRP3 disrupts endothelial function, reduces nitric oxide availability, and accelerates vascular inflammation and injury. This review discusses current evidence on pharmacological strategies targeting NLRP3 inflammasome signaling using both natural and synthetic inhibitors. Studies have shown that inhibiting NLRP3 can reduce inflammation and oxidative stress, preserve endothelial integrity, improve vascular function, and support tissue repair. Several NLRP3-targeting compounds have advanced into early-phase clinical trials, showing encouraging safety profiles and efficacy in individuals with cardiovascular risk factors. By integrating the emerging concept of OxInflammation with endothelial dysfunction, this review critically evaluates the therapeutic and translational potential of NLRP3 inflammasome inhibition in cardiovascular and metabolic disorders. Collectively, the available evidence supports NLRP3 as a promising therapeutic target for restoring endothelial homeostasis and promoting vascular repair. However, further clinical studies are needed to establish long-term efficacy, optimal dosing strategies, and appropriate patient selection criteria. Full article

Background: The oral microbiome has emerged as a potential contributor to cardiovascular physiology through its role in the enterosalivary nitrate–nitrite–nitric oxide pathway. Oral nitrate-reducing bacteria convert dietary nitrate into nitrite, which can subsequently be reduced to nitric oxide, a signaling molecule associated with vascular tone, endothelial function, platelet activity, and blood pressure regulation. Disruption of this pathway has been associated with reduced nitric oxide bioavailability and impaired vascular responses. Methods: This narrative review summarizes current evidence regarding the relationship between the oral microbiome, nitrate metabolism, and cardiovascular function. Relevant literature was identified through searches of PubMed/MEDLINE and Google Scholar up to May 2026. Evidence from mechanistic, observational, and interventional human studies was reviewed and synthesized thematically. Results: Available evidence suggests that oral nitrate-reducing bacteria may influence nitric oxide bioavailability and vascular function. Studies have reported associations between oral microbiome disruption and changes in blood pressure, endothelial responsiveness, plasma nitrite concentrations, and other surrogate cardiovascular markers. However, findings remain heterogeneous and are influenced by factors such as diet, oral hygiene practices, smoking status, medication use, oral health, and underlying cardiometabolic conditions. Most studies are limited by small sample sizes, short intervention durations, and reliance on surrogate outcomes rather than major cardiovascular events. Conclusions: The oral microbiome may influence cardiovascular health through its role in nitrate metabolism and nitric oxide bioavailability. However, current evidence is largely limited to surrogate vascular outcomes, while data on major cardiovascular events remain scarce. Further longitudinal and interventional studies are needed to clarify causality and evaluate microbiome-targeted interventions. Full article

Background/Objectives: Ultra-processed foods (UPFs) are increasingly recognized as dietary exposures associated with cardiometabolic, hepatic, and neurocognitive outcomes. However, UPFs are often treated mainly as nutrient-poor foods, whereas their processing-related features may perturb gut–liver–brain communication. This review examines whether metabolic dysfunction-associated steatotic liver disease (MASLD) can be conceptualized as a hepatic metabolic amplifier linking UPF exposure to cognitive aging. Methods: We conducted a structured narrative search of PubMed/MEDLINE, Web of Science Core Collection, and Scopus from January 2010 to 11 May 2026 across four evidence modules: UPFs and MASLD/NAFLD; UPFs and cognitive aging or dementia; UPFs and gut–liver–brain mechanisms; and MASLD/NAFLD and cognitive aging. Representative studies were prioritized according to direct relevance to the proposed axis, study design, exposure and outcome validity, mechanistic specificity, and contribution to major evidence gaps. Results: Observational and mechanistic evidence links higher UPF consumption with liver steatosis, MASLD/NAFLD-related outcomes, cognitive decline, cognitive impairment, stroke, and dementia-related outcomes, although causality remains incompletely established and residual confounding is important. Candidate pathways include food-matrix disruption, rapid eating, displacement of microbial substrates, selected additives and processing-derived compounds, intestinal barrier dysfunction, metabolic endotoxemia, bile acid signaling, hepatic lipotoxicity, systemic inflammation, vascular dysfunction, and neuroimmune activation. Many pathways overlap with general cardiometabolic dysfunction; the processing-centered contribution lies in positioning industrial formulation as an upstream exposure and MASLD as a hepatic node that may amplify gut-derived and metabolic signals relevant to brain aging. Conclusions: A processing-centered gut–liver–brain framework integrates UPFs, MASLD, and cognitive aging as linked metabolic-aging phenomena. Future studies should test UPF substitution using liver imaging, microbiome profiling, metabolomics, bile acid and inflammatory biomarkers, neuroimaging, and cognitive assessment. Full article

Obesity is a major global health challenge strongly associated with increased cardiometabolic morbidity and mortality. In men, obesity is characterized by a predominance of visceral adiposity, which is metabolically active and closely linked to systemic inflammation, hormonal dysregulation, and adverse cardiovascular outcomes. Despite its clinical relevance, male obesity remains underrecognized as a distinct pathophysiological condition. This study aimed to analyze the inflammatory mechanisms underlying male obesity and their relationship with cardiometabolic risk. A structured narrative review was conducted based on a PICo-guided research question, with literature searches performed in PubMed/MEDLINE, Scopus, Web of Science, Embase, and ScienceDirect, covering publications from 2015 to 2026. Studies focusing on male obesity, inflammatory pathways, and cardiometabolic outcomes were included. Evidence indicates that visceral adipose tissue acts as an active endocrine organ, releasing pro-inflammatory cytokines such as TNF-α and IL-6, contributing to chronic low-grade inflammation. This inflammatory state is associated with insulin resistance (IR), endothelial dysfunction, and oxidative stress, mediated by intracellular pathways including NF-κB and JNK. Additionally, adipokine imbalance, characterized by reduced adiponectin and increased leptin levels, further exacerbates metabolic and vascular impairment. Hormonal alterations, particularly reduced testosterone levels, play a key role in amplifying visceral fat accumulation and inflammation, creating a bidirectional relationship between hypogonadism and metabolic dysfunction. Clinically, these mechanisms highlight the importance of integrating inflammatory biomarkers, body composition assessment, and hormonal evaluation into the management of male obesity. Emerging therapies, including GLP-1 receptor agonists and immunometabolic interventions, offer promising strategies for reducing cardiometabolic risk. In conclusion, male obesity represents a complex, inflammation-driven condition requiring a comprehensive and mechanism-based approach to improve clinical outcomes and guide future therapeutic developments. Full article

Objective: To report a rare case of bilateral iris metastasis from small cell lung carcinoma (SCLC) and systematically review the literature on SCLC-associated iris metastases, with emphasis on clinical presentation, management, and outcomes. Materials and Methods: A systematic literature review was conducted in accordance with the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines. PubMed, ScienceDirect, Scopus, and Web of Science were comprehensively searched on 10 July 2025. Eligible studies included English-language reports of iris metastasis originating from SCLC in human subjects. Case report: A 58-year-old woman with previously treated SCLC developed bilateral iris metastases one year after complete remission of the primary tumor. Ophthalmic examination revealed whitish-gray, vascularized iris masses with iridocorneal angle involvement, associated with secondary angle-closure glaucoma and markedly elevated intraocular pressure (48 mm Hg) in the left eye. Cyclocryotherapy, preceded by systemic and topical antiglaucoma therapy, resulted in pain relief and a reduction in intraocular pressure; the patient died four months later due to pneumonia. Results (Systematic Review): Seventeen studies comprising 17 patients were included; the median age was 60 years, and 64.7% were male. The median interval from SCLC diagnosis to ocular presentation was 4 months, although iris metastasis was occasionally the initial or concurrent manifestation of disease. The most common presenting features were visual impairment (58.8%), ocular pain (41.2%), and elevated intraocular pressure (41.2%), while iris neovascularization (35.3%) and synechiae (29.4%) were also frequent. Bilateral involvement was reported in only one previous case. Treatment approaches were heterogeneous and included antiglaucoma therapy, systemic chemotherapy, local radiotherapy, anti-VEGF therapy, and enucleation. Among patients with available follow-up (n = 12), 58.3% died within a median follow-up of 7.5 months. Conclusions: Bilateral iris metastasis from SCLC is rare and may occur as a manifestation of recurrent disease after remission. It is an aggressive condition characterized by nonspecific ocular symptoms, variable management, and poor survival, underscoring the importance of early recognition and the need for evidence-based diagnostic and therapeutic strategies. Full article

Chronic coronary syndromes (CCSs) are increasingly recognized as complex immunometabolic vascular disorders in which coronary microvascular dysfunction (CMD), persistent low-grade inflammation, oxidative stress, and maladaptive cellular remodeling contribute to ischemic symptoms and adverse outcomes beyond epicardial stenosis. CMD represents a heterogeneous condition comprising both functional and structural endotypes and constitutes a major determinant of myocardial ischemia, heart failure progression, and adverse cardiovascular outcomes, even in the absence of obstructive coronary artery disease. Emerging evidence indicates that immunometabolic reprogramming of endothelial cells, vascular smooth muscle cells, and immune cells sustains microvascular dysfunction in CCSs. Metabolic shifts toward glycolysis, mitochondrial dysfunction, redox imbalance, and dysregulated lipid metabolism promote chronic inflammatory activation within the coronary microenvironment. Convergent mitochondrial stress (including NAD⁺ decline) and redox injury promote endothelial senescence and increase susceptibility to regulated cell death, progressively limiting vasodilatory reserve and predisposing to microvascular rarefaction. Pyroptosis and ferroptosis-like lipid peroxidation further exacerbate endothelial barrier disruption and inflammatory amplification. In parallel, inflammasome activation, iron-dependent lipid peroxidation, impaired autophagy, and endoplasmic reticulum stress form interconnected molecular networks that amplify vascular injury through self-reinforcing mechanisms. This narrative review integrates mechanistic and translational evidence linking immunometabolic dysregulation, mitochondrial stress, thromboinflammatory signaling, endothelial senescence, and regulated cell death to distinct CMD endotypes. We propose a systems-level framework in which coronary microvascular dysfunction is conceptualized as an immunometabolic vascular network disorder, with reduced coronary flow reserve (CFR)—often termed myocardial flow reserve (MFR) in PET studies—emerging as the integrative functional endpoint of these interacting molecular perturbations and a robust predictor of major cardiovascular events. Full article

Background: Long COVID (LC) has been associated with persistent endothelial dysfunction and vascular impairment. Although nutrition is a key modifiable determinant of cardiovascular health, the relationship between dietary macronutrient intake and vascular alterations in LC remains poorly understood. Objective: To evaluate the association between dietary macronutrient intake and markers of vascular structure, arterial stiffness, and vascular aging in patients with LC, including potential sex differences. Methods: We conducted a cross-sectional study including 304 patients with LC. Dietary intake was assessed using a validated 7-day dietary record (EVIDENT study). Vascular evaluation included carotid intima–media thickness (cIMT), carotid–femoral pulse wave velocity (cfPWV), brachial–ankle pulse wave velocity (baPWV), cardio-ankle vascular index (CAVI), augmentation index adjusted to a heart rate of 75 beats per minute (AIx@75), and vascular aging index (VAI), measured using carotid ultrasound and validated devices (SphygmoCor^® and VaSera^®). Results: The mean age was 53 ± 12, higher in men (p = 0.001). The study included 207 women (68%) and 97 men (32%). Energy intake and carbohydrate intake in g/day showed a negative association with cfPWV in Model 2 (energy intake: β = −0.06; 95% CI: −0.11 to −0.01; p = 0.02; carbohydrate intake: β = −0.47; 95% CI: −0.87 to −0.07; p = 0.02). The percentage of carbohydrate/total energy intake was positively associated with AIx@75 in Model 2 (β = 0.8; 95% CI 0.12 to 1.49; p = 0.02), and percentage of fat/total energy intake showed a consistent inverse association (β = −0.30; 95% CI: −0.49 to −0.11; p = 0.002). No significant associations were observed for cIMT, baPWV, CAVI or VAI. Conclusions: In patients with LC, total energy intake and absolute carbohydrate intake were negatively associated with cfPWV, whereas the relative contribution of carbohydrates and fats to total energy intake showed divergent associations with AIx@75. These findings suggest that both absolute macronutrient intake and relative macronutrient distribution may be related to central arterial stiffness and wave reflection parameters LC. However, given the cross-sectional design of the study, these results should be interpreted as exploratory and do not allow causal inference. Further longitudinal and interventional studies are needed to confirm these findings and to assess whether nutritional strategies may contribute to modulating vascular risk in this population. Full article

Maternal psychoactive substance use during pregnancy represents a major threat to placental integrity and fetal development. As the central interface for maternal–fetal exchange, the placenta is highly susceptible to psychoactive substances, including alcohol, tobacco, cannabis, cocaine, opioids, and synthetic drugs, which can cross the placental barrier and induce structural and functional alterations. This review synthesizes current evidence on the biological mechanisms, diagnostic approaches, and forensic relevance of psychoactive substances-induced placental pathology. We summarize how different substances disrupt placental vascularization, oxidative balance, epigenetic regulation, and cellular viability, leading to impaired nutrient and oxygen transfer and increasing the risk of adverse outcomes such as intrauterine growth restriction, preterm birth, congenital anomalies, and long-term neurodevelopmental impairment. We further discuss the role of placental tissue in identifying prenatal drug exposure and reconstructing exposure timelines. Beyond its clinical relevance, placental examination provides objective evidence with potential forensic value in cases of suspected maternal substance use, while also informing non-punitive, evidence-based interventions. Overall, integrating placental pathology into reproductive health research and prenatal care offers a multidisciplinary framework to improve maternal–fetal outcomes and guide public health strategies addressing substance use during pregnancy. Full article

The potential health hazards caused by microwave exposure have attracted increasing attention. Microwave radiation has been reported to induce oxidative stress in neural tissues, which is considered one of the primary mechanisms underlying its adverse effects on central nervous system function. The hippocampus is sensitive to microwave radiation, whereas underlying cellular and molecular mechanisms remain incompletely understood. In this study, microwave-exposed mice exhibited significantly impaired performance in the Go/No-go, Y-maze, and novel object recognition tests at 6 h and 7 days post-exposure, indicating deficits in hippocampus-dependent working memory. Single-cell RNA sequencing of hippocampal tissues from control and microwave-exposed mice yielded 94,088 high-quality cells across eight major cell types. Astrocyte sub-clustering identified five transcriptionally distinct subpopulations, with Astrocyte_S100a6 and Astrocyte_Son proportions increased and Astrocyte_Serpinf1 decreased in the radiation group. Analysis of astrocyte transcriptional state transitions showed microwave-exposed astrocytes were preferentially distributed toward terminal reactive states with depletion at early homeostatic nodes. Cell–cell communication analysis revealed increased total interactions and interaction strength following radiation. Astrocyte outgoing signaling was increased for pathways associated with vascular remodeling, phagocytic regulation, and neuroinflammation, while pathways related to trophic support were decreased. Incoming signaling showed increased activity in pathways linked to phagocytic recruitment and inflammatory mediation. Taken together, these findings indicate that microwave exposure is associated with hippocampus-dependent working memory deficits accompanied by transcriptional remodeling of astrocyte subpopulation composition, directional astrocyte state transitions toward reactive phenotypes, and broad alterations in astrocyte-centered intercellular communication, providing a cellular and molecular framework for understanding astrocyte involvement in microwave radiation-associated hippocampal dysfunction. Full article

Background: Sarcopenia and frailty are highly prevalent extrapulmonary manifestations of chronic obstructive pulmonary disease (COPD) and are strongly associated with reduced exercise tolerance, exacerbation risk, hospitalizations, and mortality. Beyond inflammation, oxidative stress, and physical inactivity, emerging evidence highlights nutrition as a major modifiable driver of muscle deterioration in COPD. Nutritional deficits impair anabolic signaling, exacerbate proteolysis, worsen mitochondrial dysfunction, and contribute to frailty progression. Methods: This narrative review synthesizes evidence from PubMed, Embase, Scopus, and Web of Science up to 2025, integrating mechanistic, metabolic, nutritional, and biomarker-related pathways underlying muscle dysfunction in COPD. Studies examining inflammation, hypoxemia, oxidative stress, hormonal imbalance, nutrition, and emerging biomarkers were included. Results: COPD-related sarcopenia results from converging inflammatory (TNF-α, IL-6), catabolic (FOXO, UPS), metabolic, and vascular mechanisms, compounded by energy deficiency, protein insufficiency, and micronutrient deficits. Inadequate intake of protein, vitamin D, antioxidants, and omega-3 fatty acids increase anabolic resistance, enhance muscle catabolism, and worsen frailty. Nutritional interventions, particularly high-protein supplementation, leucine-enriched formulas, vitamin D repletion, omega-3 fatty acids, and multimodal nutrition–exercise programs, demonstrate benefits in muscle mass, strength, and physical performance. Biomarkers such as GDF-15, CAF22, and specific microRNAs reflect nutritional status and correlate with muscle health in COPD. Conclusions: Sarcopenia and frailty in COPD arise from a complex interplay of inflammatory, metabolic, nutritional, and lifestyle-related factors. Integrating nutritional assessment and targeted dietary interventions with exercise and pulmonary rehabilitation is essential to counteract anabolic resistance and improve functional outcomes. Advances in biomarker research may support earlier diagnosis and personalized nutrition-based therapeutic strategies. Full article

Background/Objectives: Although vascular mechanisms are increasingly implicated in the etiology of sudden sensorineural hearing loss (SSNHL), the inability to directly visualize the labyrinthine artery remains a diagnostic obstacle. Sharing embryological and physiological parallels with the inner ear, the eye represents an accessible surrogate organ capable of reflecting systemic microvascular status. This study aimed to evaluate the diagnostic value of ocular hemodynamic and structural parameters in patients with acute unilateral idiopathic SSNHL. Methods: This prospective, comparative, cross-sectional study enrolled 30 patients with acute unilateral idiopathic SSNHL and 25 age and sex matched healthy controls. Three groups were defined: the affected eye, the contralateral eye, and the control eye. Retrobulbar hemodynamics (PSV, EDV, RI, PI) were assessed by color Doppler imaging; peripapillary choroidal thickness, RNFL, GCC+, and macular thickness by swept-source OCT; and macular microvascular perfusion by OCT angiography. Results: End diastolic velocity in the posterior ciliary arteries was significantly reduced in both patient eye groups relative to controls (p < 0.001), while RI and PI were significantly elevated (p = 0.001 and p = 0.004, respectively). Comparable hemodynamic impairment was observed in the ophthalmic artery. Peripapillary choroidal thickness was bilaterally reduced in the inferior and temporal quadrants in both patient groups (p = 0.003 and p = 0.010). No significant difference was detected between affected and contralateral eyes in any parameter. RNFL, GC+, and macular thickness remained comparable across all groups. Conclusions: The bilateral symmetry of hemodynamic impairment and choroidal thinning suggests that SSNHL arises against a background of systemic microvascular disease. The combined use of OCT and color Doppler ultrasonography holds clinical potential as a non-invasive biomarker panel for defining the vascular phenotype of the condition. Full article

Diabetes mellitus represents a major global health challenge with rapidly increasing prevalence and substantial morbidity driven by metabolic and vascular complications. Extracellular vesicles (EVs) have emerged as critical mediators of intercellular communication and are increasingly implicated in the pathogenesis and progression of diabetes. This review summarizes current knowledge on EV biology, including their classification, cellular sources, biogenesis, uptake mechanisms, and molecular cargo. We discuss the contribution of EV-associated microRNAs to immune dysregulation and β-cell damage in type 1 diabetes mellitus (T1DM), as well as the role of EVs in insulin resistance, metabolic signaling, and vascular dysfunction in type 2 diabetes mellitus (T2DM). Particular emphasis is placed on EV-mediated modulation of endothelial function, angiogenesis, and tissue repair, alongside their involvement in the impairment of insulin receptor integrity. We further explore how lifestyle factors may influence EV composition and function, highlighting their potential integration into preventive strategies. Finally, we evaluate the emerging therapeutic potential of EVs as biomarkers and delivery systems, while addressing current limitations and future directions. Collectively, EVs represent a promising frontier in understanding diabetes pathophysiology and developing innovative diagnostic and therapeutic approaches. Unlike previous reviews that examine EVs separately as biomarkers or therapeutic vehicles, this review integrates emerging evidence supporting EVs as mediators of systemic communication linking pancreatic islets, adipose tissue, immune cells, vascular endothelium, kidney, heart, and retina throughout diabetes progression. We further critically evaluate translational barriers that currently limit clinical implementation of EV-based diagnostics and therapeutics. Full article

Background: Type 2 Diabetes Mellitus (T2DM) is associated with a vascular-executive cognitive decline profile that early impacts complex daily tasks. Despite the increased risk of Mild Cognitive Impairment (MCI) in this population, there is a critical shortage of instruments specifically validated for this group. This scoping review aims to identify the instruments used to assess functionality in individuals with T2DM and MCI and to map their psychometric properties. Methods: We conducted a scoping review based on the JBI methodology and PRISMA-ScR guidelines. The search was performed across several electronic databases (PubMed, Cochrane Library, Web of Science, Scopus and SciELO), up to March 2026, focusing on the intersection of T2DM, mild cognitive impairment, and the psychometric properties of functional scales. Results: Our search identified only three studies meeting the eligibility criteria. The functional instruments evaluated across these publications were the ADCS-ADL scale, the A-FAQ, and a predictive nomogram including the Lawton-Brody scale. Methodological approaches, sample configurations and reported outcomes varied substantially within the included literature, with no comparative validation studies conducted among homogeneous T2DM cohorts. Conclusions: The notable scarcity and marked heterogeneity of the available literature prevent any definitive conclusions regarding the comparative diagnostic superiority of current functional scales. While gradated instruments show conceptual compatibility with the executive-vascular cognitive decline profile of T2DM, their psychometric properties remain unvalidated in this specific population. Future research should prioritize longitudinal validation designs in homogeneous diabetic cohorts to standardize screening protocols calibrated to metabolic and vascular variations. Full article

Background: Forearm nonunions represent a challenging clinical condition that significantly impairs upper limb function. Various surgical techniques have been proposed, including vascularized bone grafts. Although these procedures are not considered first-line treatment, they play a crucial role in complex or recalcitrant cases, particularly after failure of conventional methods, where their superior biological potential can significantly enhance bone healing. Despite the widespread use of the medial femoral condyle corticoperiosteal flap, simultaneous bilateral harvest has not been previously described in the literature. Case Presentation: We report the case of a 50-year-old male presenting with persistent nonunions of both the radius and ulna following previous osteosynthesis and revision surgery with iliac crest bone graft. The patient was successfully treated using bilateral vascularized corticoperiosteal free flaps harvested from both medial femoral condyles. Conclusions: Double vascularized corticoperiosteal free flaps may represent an effective and reliable option for the treatment of complex forearm nonunions, especially in cases with multiple previous surgical failures. To the best of our knowledge, this case represents the first report of simultaneous bilateral medial femoral condyle corticoperiosteal flap harvest. Full article