T-2 toxin is a trichothecene mycotoxin produced by Fusarium species and can cause disease after contaminated food or feed ingestion. This study aimed to investigate the impact of lycopene (Ly) on systemic inflammation, oxidative stress, and dysbiosis in mice exposed to T-2 toxin. A total of 20 male BALB/c mice (6 weeks old, weighing 23.5 ± 0.32 g) randomly divided into four groups (n = 5): Control (Cont), Ly, T-2, and T-2 + Ly groups. Findings revealed that Ly enhanced the body weight, feedd, and water intake that have been reduced by T-2. Ly increased the villus height (VH) and VH: crypt depth (CD) and decreased CD and villus width (VW) in ileum compared to the T-2 group. In alpha diversity, Staphylococcus and Corynebacterium were the most prevalent in Cont group; Staphylococcus, and Lactobacillus, were the most prevalent in T-2 group; Candidatus-Arthromitus and Staphylococcus were the most prevalent in T-2 + Ly group. Moreover, T-2 mice had significantly (p < 0.05) greater levels of interleukin-1 beta (IL-1β), interferon gamma (IFN-γ), Interleukin-17 (IL-17), and tumor necrosis factor-alpha (TNF-α) than Cont, while the Ly significantly (p < 0.05) lowered their concentration. The T-2 mice had significantly (p < 0.05) higher levels of reactive oxygen species (ROS) and malondialdehyde (MDA), while their catalase (CAT),, glutathione (GSH), adenosine triphosphate (ATP), and superoxide dismutase 1(SOD1) activities were significantly (p < 0.05) lower than Cont. Ly significantly (p < 0.05) restored their concentration. Moreover, there was a significant reduction (p < 0.05) of hexanoic, butyric, acetic, pentanoic, and Heptanoic acids in the T-2 mice compared to Cont. In contrast, treatment with Ly was found to significantly restore their levels compared to T-2 group. We conclude that Ly administration in the context of T-2-induced toxicity may help attenuate systemic oxidative stress and inflammation, possibly through modulation of gut microbiota and fecal short-chain fatty acids (SCFAs).

Vascular anomalies, including hemangiomas, which have slow blood flow, can develop anywhere on the body. They are mostly isolated lesions and are more common in women. The deformity does not regress on its own. A rare variety, known as subcutaneous hemangioma, grows aggressively and occasionally recurs after excision. In this report, we present a case of a 44-year-old female who experienced a slowly growing, painful nasal hump as a result of nasal trauma she sustained 7 years ago. She denied any associated symptoms apart from pain. Physical examination revealed a palpable, soft, nonmobile mass measuring ∼1 cm by 0.5 cm over the nasal dorsum. There was mild tenderness, and the skin appeared normal. Imaging workup with a CT scan showed a destructive process in the cortex of the left nasal bone, with soft-tissue density noted in the anterior left nasal cavity abutting the anterior nasal septum. Furthermore, an MRI study showed a well-defined, rounded, isointense lesion on T1 FSE images under the nasal bridge and hyperintense on T2 FSE images. Ultimately, the patient underwent open rhinoplasty. According to the histopathology results, there was reactive bone with skeletal muscle fibers, fibrosis, and dilated vascular channels. Atypia, mitosis, and necrosis were not present. The patient was doing well postoperatively with no complications and was scheduled for routine clinic follow-ups.

Dysferlinopathy is a rare muscular dystrophy characterized by chronic muscle damage and ineffective regeneration. While late-stage morphological changes, such as fibroadipose replacement, are well described, the early molecular mechanisms driving muscle fiber loss and regenerative failure at the onset of the disease remain largely uncharacterized. To address this gap, we investigated the skeletal muscles of dysferlin-deficient Bla/J mice during the early manifestation stage (3 months of age). This exploratory study aimed to identify primary pathomorphogenetic events by correlating the transcriptomic profile of the tissue with its specific histopathological and ultrastructural alterations. We performed a comparative analysis of the m. gastrocnemius in 3-month-old Bla/J mice versus wild-type controls using RNA sequencing, RT-qPCR, histomorphometry and transmission electron microscopy. The results revealed atrophy and muscle fiber necrosis without the expected induction of Fbxo32 and Trim63 ubiquitin ligases, suggesting ubiquitin-proteasome system-independent muscle mass loss. Furthermore, the absence of Casp3, Bak1, and Bad induction, confirmed by the lack of active caspase-3, excluded apoptosis as the primary death mechanism. A differentiation block in satellite cells was confirmed by the lack of Myf5, Myod1, and Myog induction and a trend toward Tead4 suppression, pointing to an early failure of the reparative program. Exploratory RNA sequencing also identified a suppression of Prkn expression accompanied by LC3B-II-positive autophagosome accumulation. Immunohistochemical and immunofluorescent evaluation of the mitochondrial network (TOMM20) revealed abnormal accumulations and dense clumping, indicating impaired organelle clearance. Furthermore, ultrastructural analysis demonstrated internal organelle damage and the presence of myelin-like structures, consistent with a state of stalled mitophagy. Collectively, this exploratory study demonstrates that early muscle atrophy and myofiber necrosis in dysferlinopathy occur independently of canonical ubiquitin-proteasome and apoptotic pathways. Instead, the disease manifestation stage is structurally characterized by stalled mitochondrial clearance and a delayed regenerative response.

Extensive lumbosacral defects remain a major reconstructive challenge because of limited regional tissue mobility, contamination risk, proximity to neural structures, and frequent association with prior surgery or spinal instrumentation. Although lumbar artery perforator (LAP) flaps are recognized as muscle-sparing options for posterior trunk reconstruction, their capacity to safely reconstruct very large midline lumbosacral defects and their applicability in rare adult presentations of lumbosacral myelomeningocele remain insufficiently defined. We report two adult female patients who underwent reconstruction of extensive midline lumbosacral defects using bilateral pedicled LAP flaps to illustrate the applicability of this approach in exceptionally large post-instrumentation and adult dysraphic defects. The first patient, a 19-year-old woman, presented with a 36 × 28 cm post-instrumentation defect with exposed L4-S1 hardware following multi-trauma and repeated soft-tissue necrosis. After serial debridements and prolonged culture-directed intravenous antibiotic therapy, bilateral LAP flaps measuring 22 × 12 cm were elevated based on bilateral L4 perforators identified by computed tomography angiography and Doppler ultrasonography. The second patient, a 28-year-old paraplegic woman with spina bifida, presented with recurrent cerebrospinal fluid leakage associated with a 22 × 16 cm lumbosacral myelomeningocele defect. Following neurosurgical dural repair, bilateral LAP flaps measuring 18 × 10 cm were harvested based on medially displaced L4 perforators. In both cases, the flaps were designed according to defect geometry and perforator location, then rotated approximately 90° medially to achieve tension-reduced midline closure while facilitating primary donor-site closure. Complete flap survival was achieved in both patients without venous congestion or total flap loss. In the first case, limited wound dehiscence related to hardware prominence was successfully revised with a local V-Y advancement flap, and a small donor-site tension area was managed with split-thickness skin grafting. In the second case, a limited lateral donor defect also required split-thickness skin graft coverage. At 13 months, spinal instrumentation was electively removed in the first patient after adequate osseous stabilization, while flap stability was preserved. At 15 and 9 months of follow-up, respectively, both patients demonstrated durable soft-tissue coverage without recurrent breakdown or cerebrospinal fluid leakage. These cases suggest that bilateral pedicled LAP flaps may facilitate stable, muscle-sparing reconstruction in selected extensive lumbosacral defects, including exceptionally large post-instrumentation wounds and rare adult presentations of lumbosacral myelomeningocele.

The thumb contributes nearly half of overall hand function, and its loss is profoundly disabling. Bilateral thumb amputation is rare and catastrophic, often necessitating complex reconstruction. Toe-to-thumb transfer is considered the gold standard, whereas index pollicization is a powerful alternative when microsurgical transfer fails. This report describes a rare case of bilateral thumb amputation managed with both techniques, highlighting their complementary roles. A 32-year-old right-handed soldier sustained bilateral thumb amputations from a high-velocity gunshot injury while holding a sniper rifle. On arrival, both thumbs were amputated at the proximal metacarpals with exposed bone, though the remaining fingers and systemic evaluation were intact. He underwent bilateral second toe-to-thumb transfers. The left reconstruction remained viable and fully functional, but the right developed ischemic necrosis. Salvage included repeated debridements, vacuum-assisted closure therapy, free anterolateral thigh flap coverage, and a groin flap with scar revision. Functional restoration was later achieved with index pollicization, followed by flap debulking and liposuction. At the final follow-up, both reconstructions demonstrated a full range of motion and opposition. The patient reported the pollicized right thumb to be subjectively stronger and more reliable than the contralateral toe transfer, enabling independence in daily living with satisfactory functional and aesthetic outcomes. This case illustrates that even when microsurgical toe transfer fails, staged salvage with flap coverage and index pollicization can restore bilateral function. The coexistence of both reconstructions in one patient provided a unique comparison, highlighting their complementary strengths.

Infection-associated inflammatory diseases such as periodontitis are driven not only by persistent bacterial biofilms but also by dysregulated host immune responses amplified by excessive reactive oxygen species (ROS). Although antimicrobial photodynamic therapy (PDT) efficiently eradicates pathogens, uncontrolled ROS accumulation often aggravates inflammation and impairs tissue repair, limiting its clinical translation. Here, we report a self-regulated ROS nanoplatform based on a one-dimensional porphyrin-diketopyrrolopyrrole covalent organic framework (COF) loaded with the natural flavonoid naringin (COF-Por-DPP@Naringin), which enables temporally programmed ROS generation and scavenging. Under 660 nm irradiation, the COF scaffold induces a transient ROS surge sufficient to eradicate Porphyromonas gingivalis and Fusobacterium nucleatum biofilms with 99.43 ± 0.56% and 99.87 ± 0.22% killing efficiency, respectively. Subsequently, the controlled release of naringin selectively scavenges residual ROS, suppresses pro-inflammatory cytokine expression, and alleviates PDT-induced oxidative stress. Transcriptomic analysis of inflammatory macrophages revealed coordinated downregulation of tumor necrosis factor (TNF), interleukin-17 (IL-17), and p53 signaling pathways, indicating ROS-mediated immune-inflammatory reprogramming rather than empirical anti-inflammatory effects alone. In a ligature-induced murine periodontitis model, this sequential ROS regulation effectively reduced bacterial burden, attenuated inflammatory infiltration, preserved alveolar bone architecture, and promoted periodontal tissue repair. Collectively, this work demonstrates that precise temporal regulation of ROS can transform PDT from a purely antimicrobial strategy into an immunomodulatory therapeutic approach, providing a generalizable framework for nanotherapeutic design targeting infection-driven inflammatory diseases.