Multiple odontogenic keratocysts are one of the major diagnostic criteria of Gorlin syndrome and may represent an early manifestation of the disorder in pediatric patients. This report describes the diagnostic process and management of an 11-year-old boy who presented with multiple mandibular cystic lesions associated with displacement of developing permanent teeth. Clinical and radiographic examination, including cone-beam computed tomography, revealed several well-defined radiolucent lesions suggestive of odontogenic keratocysts. A conservative treatment approach was adopted, consisting of decompression of the largest lesion and enucleation of smaller lesions, with the aim of preserving developing dentition and reducing treatment-related morbidity. Histopathological examination confirmed the diagnosis of odontogenic keratocysts. Genetic evaluation by Sanger sequencing identified a heterozygous de novo PTCH1 variant, NM_000264.5(PTCH1):c.1340T>A (p.Leu447∗), confirming the diagnosis of Gorlin syndrome. After 18 months of radiographic surveillance and 30 months of clinical monitoring, progressive bone regeneration, reduction in lesion size, favorable spontaneous repositioning of the affected teeth, and no evidence of recurrence were observed. This case highlights the diagnostic value of multiple odontogenic keratocysts as an early manifestation of Gorlin syndrome and supports conservative management and multidisciplinary follow-up in growing patients.

Objective There is a paucity of studies evaluating computed tomography (CT) scores in patients with Glasgow Coma Scale (GCS) scores of 3-8. This study assessed the associations between risk factors (including admission GCS score, head Abbreviated Injury Scale (AIS) score, brain mass effect score (MES), and age) and unfavorable outcomes (including in-hospital mortality, adverse outcomes, failure to follow commands at hospital discharge, and failure to follow commands at three months) in mechanically ventilated patients with intracranial hemorrhage (ICH) and GCS scores of 3-8. In relation to these outcomes, we also compared the MES with the Marshall (MAR) classification and Rotterdam (ROT) score. Methods The adult blunt trauma cohort had ICH, GCS 3-8, need for mechanical ventilation, and level I trauma center admission (2018-2024). The GCS, age, AIS, ventilator status, intensive care unit (ICU) stay, hospital stay, and hospital mortality were obtained from the trauma registry. Adverse outcomes included hospital death, ICU stay ≥18 days, or hospital stay >20 days. MES indicated the presence (1) or absence (0) for each of the following: basal cistern compression, midline shift, and lateral ventricle compression (0-3). Brain CT images were reviewed to compute MES, MAR, and ROT. Electronic medical records (EMRs) were reviewed to determine following command status at hospital discharge and at three months after injury. Results Among the 148 blunt trauma patients, univariate associations with mortality were MES (p < 0.01), GCS (p = 0.46), age ≥70 (p < 0.01), and AIS (p < 0.01); multivariate associations were MES (p < 0.01), age ≥70 (p < 0.01), and AIS (p > 0.10). For adverse outcomes, univariate associations were MES (p < 0.01), GCS (p = 0.46), age ≥70 (p = 0.04), and AIS (p < 0.01); multivariate associations were MES (p < 0.01), age ≥70 (p > 0.05), and AIS (p > 0.05). For failure to follow commands at discharge, univariate associations were MES (p < 0.01), GCS (p = 0.75), age (p = 0.01), and AIS (p < 0.01); multivariate associations were MES (p < 0.01), age (p = 0.01), and AIS (p > 0.10). For failure to follow commands at three months, univariate associations were MES (p < 0.01), GCS (p = 0.30), age (p < 0.01), and AIS (p < 0.01); multivariate associations were MES (p < 0.01), age (p < 0.01), and AIS (p > 0.10). MES correlated strongly with MAR (p < 0.01; r = 0.83) and ROT (p < 0.01; r = 0.82). In multivariate stepwise continuous score regression (MCR), mortality and adverse outcome were associated with MES (both p < 0.01), but not MAR or ROT (both p > 0.05). For failure to follow commands at discharge and three months, MCR showed an association with ROT (both p < 0.01), but not MES or MAR (both p > 0.05). In multivariate stepwise dichotomous score regression (MDR), mortality and adverse outcomes were associated with MES ≥2 (both p < 0.01), but not MAR ≥4 or ROT ≥4 (both p > 0.05). Failure to follow commands at discharge was associated with ROT ≥4 (p < 0.01), but not MES ≥2 or MAR ≥4 (p > 0.05). Failure to follow commands at three months was associated with MES ≥2 (p < 0.01), but not MAR ≥4 or ROT ≥4 (p > 0.05). Conclusions MES was a better predictor of adverse outcomes than AIS and GCS in comatose patients with ICH. MES was competitive with other established brain CT scores for predicting adverse outcomes. Further studies are needed to confirm these findings.

Selective serotonin reuptake inhibitor (SSRI)-associated bruxism is an increasingly recognized medication-associated phenomenon, although its incidence, neuropharmacologic mechanisms, and optimal management remain incompletely understood. This focused narrative review examines the clinical evidence, proposed mechanisms, and therapeutic implications of SSRI-associated bruxism. Available literature demonstrates recurring temporal associations between SSRI initiation or dose escalation and the emergence of jaw clenching, tooth grinding, pain, and related orofacial symptoms across multiple agents. Proposed mechanisms are multifactorial and may involve altered monoaminergic regulation within central motor networks, including serotonergic-dopaminergic interactions, 5-hydroxytryptamine (serotonin) receptor 1A (5-HT1A) signaling, and possible noradrenergic contributions; however, these mechanisms remain unconfirmed in affected patients. Adjunctive buspirone is the most consistently described pharmacologic strategy and may permit the continuation of an otherwise effective SSRI, although evidence for benefit remains primarily case-based. The literature is limited by heterogeneous bruxism definitions, inconsistent differentiation between awake and sleep manifestations, variable antidepressant exposures, and sparse objective physiologic assessment. Prospective studies using standardized assessment methods and controlled treatment designs are needed to clarify incidence, susceptibility, pathophysiology, and treatment response.

Wilson disease (WD) is a rare autosomal recessive disorder of copper metabolism that usually presents with a wide spectrum of seemingly unrelated symptoms, such as dysarthria, tremors, dystonia, features of advanced liver disease, and psychiatric manifestations. Atypical presentation may lead to delayed diagnosis. We present the case of a 25-year-old man who presented with slurred speech and abdominal distension. Workup revealed the presence of Kayser-Fleischer rings, reduced serum ceruloplasmin levels, elevated 24-hour urinary excretion of copper, and decompensated liver disease. Magnetic resonance imaging (MRI) of the brain was significant for altered signals in the basal ganglia, thalami, and periventricular white matter. He was diagnosed with WD and commenced on D-penicillamine and zinc therapy, with clinical improvement on follow-up. This case signifies that WD must be considered in any adult presenting with unexplained neurological symptoms. Early diagnosis is essential to prevent disease progression and complications.

Mitophagy is a form of selective autophagy in which an isolation membrane (IM or phagophore) sequesters damaged or superfluous mitochondria for lysosomal degradation. Recent advances in receptor-mediated mitophagy, particularly the BNIP3/NIX-mediated mitophagy, have highlighted the importance of this pathway in mitochondrial regulation across various biological settings, along with the well-established Parkin-mediated pathway. Parkin-mediated mitophagy senses mitochondrial damage through loss of membrane potential, whereas BNIP3/NIX-mediated mitophagy plays an important role in basal or physiologically induced mitochondrial turnover, thereby contributing to mitochondrial quality control and remodeling. These two pathways employ distinct sets of molecules to recruit the autophagy machinery to the mitochondria and exhibit different IM dynamics that are closely linked to mitochondrial fission and segregation. In this review, we first provide an updated overview of the autophagy process and then compare these two major forms of mitophagy, with particular emphasis on the molecular mechanisms of mitophagy initiation and IM dynamics. We also discuss the functional implications of these mechanistic differences in physiological and pathological context.

The plant cell harbours three genomes, nuclear, plastid and mitochondrial ones, the former being responsible for most plant functions and features. Earlier we sequenced complete plastid and mitochondrial genomes of 91 accessions of pea (Pisum L.), mostly genuine wild and traditional landraces from all over the region of pea traditional cultivation, and reconstructed their phylogenies which turned to be quite discordant. In this work, we undertook a phylogenetic and cluster analysis based on genotyping-by-sequencing (GBS) data on the same set of accessions and compared the result with those based on the plastid and mitochondrial genomes. The GBS phylogenetic tree, overwhelmingly based on the nuclear genome data, well corresponded to the current taxonomy. The plastid and mitochondrial trees showed some discordance, especially the mitochondrial one. The latter suggests cases of exchange of mitochondria between wild and cultivated peas, not accompanied by exchange of plastids or nuclear genes thus posing questions of the underlying mechanisms. The cluster analysis of GBS data is interpreted in terms of clusters evolving from each other and retaining a share of ancestral diversity, rather than through profound hybridisation and admixture. In accordance with the Core Area Hypothesis, the cultivated peas (except for the Abyssinian pea) were monophyletic in the GBS tree and diverged to two main branches immediately after domestication. Attention is drawn to a so far neglected peculiar basally diverged branch of Pisum sativum.

Oxidation resistance protein 1 (OXR1) protects cells from oxidative injury in several vertebrate systems, but its role during viral infection in teleosts is unknown. We cloned and characterized grass carp OXR1 (Ctenopharyngodon idella; CiOXR1) and examined its response to grass carp reovirus (GCRV). The 959-bp CiOXR1 cDNA contains a 774-bp open reading frame encoding a 257-amino-acid TLDc-domain protein. CiOXR1 transcripts were detected in all tissues examined in healthy grass carp, with the highest basal abundance in brain, followed by heart. Following genotype II GCRV-HZ08 challenge in grass carp, CiOXR1 transcript abundance increased in brain and heart. In vitro, treatment with LPS, poly(I:C), or H2O2 increased CiOXR1 transcript abundance in grass carp ovary (GCO) cells. GFP-CiOXR1 localized mainly to the cytoplasm of GCRV-infected GCO cells. Cell-based localization and functional assays used genotype I GCRV-873, which increased DCFH-probe fluorescence. Infected cells transfected with 3HA-CiOXR1 showed lower DCFH fluorescence, lower SOD1 and SOD2 transcript abundance, and reduced accumulation of viral RNA and total-protein markers. TCID50 assays further supported inhibition of infectious-virus production by CiOXR1. Total caspase-3 and caspase-9 protein abundance, their transcript levels, and selected innate immune-response markers were also reduced, whereas no significant difference in STING transcript abundance was detected. Cas13d-mediated knockdown of CiOXR1 yielded reciprocal transcript-level changes. Together, the complementary expression and knockdown results show that CiOXR1 expression is inversely related to GCRV molecular-marker accumulation and accompanies coordinated changes in intracellular oxidation, total caspase abundance, and selected innate immune-response markers. These findings further support an antiviral role for CiOXR1 and provide a foundation for research on the prevention and control of grass carp hemorrhagic disease.

Central post-stroke pain (CPSP) is a chronic form of pain that develops after ventral posterolateral thalamus (VPL) lesions and may involve maladaptive plasticity within central somatosensory pathways. Although abnormalities in the primary somatosensory cortex (S1) are observed in patients and animal models, the mechanism by which thalamic lesions alter cortical processing of sensory stimuli remains unclear. Here, we investigated stimulus intensity encoding and dendritic remodeling in S1 using a VPL-lesion CPSP rat model. Behavioral assessments were conducted, and mechanical allodynia was observed 3 weeks after lesion induction. Accordingly, the animals were examined during the early (1 week) and late (4-5 weeks) phases after VPL lesions. A distorted stimulus-response relationship was observed in S1 during the late phase, as indicated from voltage-sensitive dye imaging. The responses to low-intensity stimuli were enhanced, and response scaling at higher stimulus intensities was reduced. Increased cortical sensitivity to weak stimuli was associated with the severity of mechanical allodynia. Additionally, morphological analyses were conducted on layer II/III pyramidal neurons. Distinct patterns of dendritic remodeling were observed. Apical dendritic length and branching diminished during the early phase, while basal dendritic arborization increased during the late phase. These findings suggest that time-dependent structural and functional reorganization occurs in S1 following thalamic injury. This reorganization may contribute to abnormal sensory processing in patients with CPSP and offer new insights into the underlying pathophysiological mechanisms.

Bioluminescence resonance energy transfer (BRET) biosensors allow direct quantification of heterotrimeric G protein activation downstream of G protein-coupled receptors (GPCRs), although restricted dynamic range can limit the detection of subtle, subunit-specific, or constitutively active signalling. We engineered NuPath, a TRUPATH-based biosensor in which Renilla luciferase 8 (RLuc8) within Gα was substituted with NanoLuc luciferase (nLuc) and enhanced yellow fluorescent protein (eYFP) replaced green fluorescent protein 2 (GFP2) fused to Gγ, while preserving the original sensor insertion architecture. NuPath is adapted for use in conventional 96-well plate format and supports direct, no-transfer readouts after receptor expression, whether receptors are introduced transiently or via stable cell lines, thereby simplifying experimental procedures. Side-by-side comparisons of matched NuPath and TRUPATH systems were performed across six GPCRs, Gαi2, GαOA, GαsL, and Gα11, and a range of Gβγ dimers. NuPath produced approximately 3- to 14-fold greater maximal agonist responses with Gαi2, GαsL, and Gα11, whereas GαOA sensors produced responses of broadly comparable magnitude with lower variability. The broadened dynamic range uncovered receptor-dependent variations in Gβγ pairing that were largely undetectable in TRUPATH measurements. NuPath further enabled detection of inverse agonist-mediated suppression of constitutive signalling at the growth hormone secretagogue receptor (GHSR) by liver-expressed antimicrobial peptide 2 (LEAP2), an effect not discernible using TRUPATH. AlphaFold 3 structural models suggested reduced donor-acceptor separation and diminished displacement of the Gα α-helical domain in NuPath compared with equivalent TRUPATH complexes. Collectively, these results position NuPath as a robust, modular enhancement of TRUPATH for resolving agonist-driven, Gβγ-specific, and constitutive GPCR signalling.