Knee osteotomy remains a fundamental joint-preserving intervention for unicompartmental osteoarthritis and lower limb malalignment, yet traditional two-dimensional planning is often limited by inter-observer variability and geometric imprecision. Over the past five years, artificial intelligence (AI) has transitioned from basic landmark detection into comprehensive surgical platforms encompassing automated alignment assessment, biomechanical simulation, and intraoperative navigation. This structured review, conducted according to PRISMA guidelines across PubMed, Embase, and Web of Science, evaluates the clinical integration of AI-driven reconstruction, biomechanical modeling, and prognostic algorithms. The results indicate that AI-driven workflows significantly enhance surgical precision; convolutional neural networks demonstrated mean absolute errors of less than 1.2 mm in landmark detection, while three-dimensional reconstructions achieved high anatomical fidelity with mechanical axis deviations averaging 0.52°±0.31°. Furthermore, biomechanical simulations utilizing recurrent neural networks proved substantially faster than traditional finite element analysis, and AI-enhanced robotic platforms achieved corrections within 1° of planned targets in over 95% of cases. Prognostic models reported ROC-AUC values up to 0.81, showing strong correlation with long-term joint survival. While statistical validation confirms high reproducibility across multicenter cohorts, the current literature is limited by a scarcity of prospective randomized controlled trials. In conclusion, AI in knee osteotomy has evolved into an essential tool for precision medicine, offering improved accuracy in patient-specific planning. Future research should prioritize explainable AI and digital twin platforms, alongside large-scale clinical trials, to definitively establish the impact of these technologies on long-term patient-reported outcomes and surgical success rates.

Morphological variability remains one of the principal challenges in the taxonomy and species delimitation of gregarines (Apicomplexa: Gregarinomorphea). In the present study, we investigated morphometric variability in gametocysts and syzygies of Gregarina polymorpha infecting Tenebrio molitor larvae through quantitative morphometric and molecular analyses. A total of 100 gametocysts and 100 independent syzygies were examined using light microscopy and digital morphometry. Gametocyst size exhibited extensive variability, with estimated areas ranging from 4850 to 30,844 μm[2] and coefficients of variation exceeding 30%. Size distributions significantly departed from normality and displayed marked heterogeneity associated with the presence of unusually small gametocysts. However, Hartigan's dip test did not detect statistically significant deviation from unimodality. Within syzygies, primite and satellite areas were strongly positively correlated (Pearson's r = 0.726, p < 0.001), and standard major axis regression indicated growth patterns consistent with approximate isometry despite substantial dispersion among larger associations. Molecular characterization of small and large gametocyst pools recovered identical SSU rRNA sequences, indicating that the observed variability occurs within the same species. These results reveal substantial reproductive morphometric plasticity in G. polymorpha and highlight limitations of morphology alone for species delimitation in gregarines.

A 78-year-old man presented to the c ancer assessment bay with a history of progressive fatigue, generalised muscle pain, and bilateral ptosis after completing two cycles of nivolumab/ipilimumab for metastatic renal cancer. Physical examination revealed mild bilateral ptosis (right > left), worsening with upward gaze, binocular diplopia, and fatigable weakness in the right shoulder. Electrocardiogram (ECG) showed a new right-bundle branch block (RBBB), with left-axis deviation, and left ventricular hypertrophy. Blood analyses showed elevated troponin I, brain natriuretic peptide, and creatine kinase with values of 221 ng/L, 114 ng/L, and 1,109 U/L, respectively. He was managed as immune checkpoint inhibitor-related severe myocarditis, myositis, and myasthenia gravis overlap (triple M) syndrome with high-dose steroids and pyridostigmine, resulting in clinical and biochemical improvement. However, immunotherapy was permanently discontinued, and follow-up imaging after three months showed evidence of disease progression. This case explores the importance of a multi-disciplinary approach in the effective management of a rare and severe immune-related toxicity and the impact of toxicities on treatment options and cancer progression.

Skeletal muscle functions not only as a mechanical apparatus for locomotion but also serves as a pivotal metabolic hub and endocrine organ essential for systemic homeostasis. While traditional perspectives focused on macro-volumetric measurements, contemporary biology posits that muscle quality is fundamentally an integration of mechanotransduction, biochemical metabolism, and ultrastructural coupling. Under comorbidity conditions, the progressive decline of skeletal muscle is intricately linked to multi-systemic dysfunction. In chronic inflammatory environments, mechanical imbalance and metabolic derangements are not merely additive; instead, they construct a sophisticated "mechano-metabolic-immune" network by co-regulating immune cell phenotypes and inflammatory thresholds. Pathological remodeling represents the destabilization of this homeostatic axis: lipotoxic metabolic stress induces the phenotypic deviation of fibro-adipogenic progenitors (FAPs) and M1 polarization of macrophages, establishing a pro-inflammatory priming state. Furthermore, the leakage of mitochondrial DNA (mtDNA) resulting from impaired mitochondrial quality control amplifies local metabolic disturbances into cGAS-STING pathway activation that secondary drives macrophage M1 polarization, serving as a critical driver of muscle atrophy. Within this pathological context, mechanical signals act not only as physical stimuli but as active variables that remodel microenvironmental stability. Through molecular transducers such as Piezo1, FAK, and TRPV4, kinetic loading facilitates mechano-chemical transduction and activates the energy sensor AMPK, thereby maintaining mitochondrial dynamic equilibrium and suppressing inflammatory cascades. This metabolic remodeling promotes the transition of macrophages toward a pro-regenerative/anti-inflammatory phenotype, supporting functional maintenance by resolving chronic inflammation and restoring tissue homeostasis. This review proposes the "mechano-metabolic-immune" axis as a pivotal regulatory framework governing skeletal muscle quality. Given that the biological benefits of mechanical intervention are constrained by physiological thresholds, precisely defining exercise load parameters across diverse pathological backgrounds is a rational foundation for transitioning from macro-rehabilitation to mechanism-driven precision interventions targeting FAPs adipogenic differentiation, intramuscular fat accumulation, and AMPK-mediated mitochondrial quality control, providing essential criteria for developing safe and effective clinical exercise prescriptions.

When precursor germ cells enter meiosis, chromosomes condense into an array of chromatin loops. Using Hi-C and Micro-C, we explored the trajectory of chromatin reorganization from mouse spermatogonia to spermatocytes at the highest temporal and spatial resolution to date. We show that meiotic chromatin reorganization, characterized by a shift from mitotic-to-meiotic cohesins, precedes the traditionally defined meiotic entry point (meiotic G1/S-phase). We find that large-scale A/B compartments are lost during prophase I, while local sub-compartments and interactions between regulatory elements of gene expression remain. For the first time, we detect distinct looping positions in mammalian meiosis I prophase. These loops are anchored by a subset of CTCF sites at the base of chromatin loops but formed without enriched interactions within the intervening regions, deviating from the typical pattern observed in somatic interphase cells. Our findings allow us to reconcile the current discrepancy in the length of meiotic chromatin loops and support a model where meiotic loops are formed by association of existing loops modulated by CTCF rather than by loop extrusion.

Iatrogenic arteriovenous (AV) fistula is a rare but treatable cause of high-output heart failure that can mimic restrictive cardiomyopathy and may lead to inappropriate listing for heart transplantation.

The classic presentation of Guillain-Barré syndrome (GBS), as described in older medical textbooks, is that of a patient with a preceding history of diarrhoea who develops rapidly progressive, symmetrical quadriparesis with areflexia. These clinical features have often been deeply entrenched in the minds of physicians, such that deviation from this pattern frequently casts doubt on the diagnosis of GBS. In contrast, it is widely recognised that GBS presents across a diverse spectrum of variants sharing a similar pathophysiology. The heterogeneity of GBS is driven by the different neural targets in different parts of the neural axis. This explains the diverse manifestations of GBS and alerts clinicians to focus on the hard and invariable signs of GBS rather than the other soft and variable features of GBS chameleon to ensure early diagnosis and prompt initiation of immunomodulatory treatment. GBS presentation can range from the classic acute inflammatory demyelinating polyradiculoneuropathy (AIDP) to rarer variants such as Miller Fisher syndrome (MFS), acute pan-dysautonomia, Bickerstaff encephalitis, and even triple overlap syndromes involving Miller Fisher syndrome, GBS, and Bickerstaff encephalitis, among others, documented in the literature. This case report and narrative review follows a 69-year-old Caucasian man who presented atypically and was diagnosed with Miller Fisher-GBS overlap syndrome. This article highlights an atypical presentation of a Miller Fisher-GBS overlap syndrome with right-sided weakness and severe back pain, ophthalmoparesis, and proximal limb weakness, before progressing to classical GBS with quadriparesis. Despite initial misdiagnoses of vasculitis and myasthenic crisis, a definitive diagnosis of GBS was eventually made, and the patient received prompt immunomodulatory treatment with a favourable outcome. It underscores the importance of thorough neurological localisation, emphasising the need to build diagnostic frameworks on hard neurological signs rather than variable and inconsistent soft signs. Most importantly, it highlights the varied presentations of GBS and reviews the underlying immunopathogenesis and management of GBS variants.