Katarzyna Barczak

Background: Intraoral explosions of pyrotechnic devices are exceptionally rare and combine blast overpressure, penetrating fragments, thermal injury, and extensive wound contamination. The immediate threats include airway obstruction, hemorrhage, loss of facial buttresses, and destruction of the occlusal unit. This report describes the acute multidisciplinary management of a self-inflicted intraoral pyrotechnic explosion in a male patient during an exacerbation of paranoid schizophrenia. Case presentation: The explosion caused bilateral comminution of the midface, fractures of the mandibular body/symphysis and right condylar process, a right orbital floor defect, extensive injury to the palate and tongue, bilateral wounds of the oral commissures and cheeks, and retention of metallic and pyrotechnic debris. Concomitant polytrauma included spinal, pelvic, rib, and pulmonary injuries. Massive edema and oral bleeding necessitated emergency tracheostomy. The otolaryngology team reconstructed the tongue and floor of the mouth, after which the maxillofacial team performed prolonged skeletal reconstruction through combined external and intraoral approaches. The midface was stabilized with 13 titanium miniplates, the mandibular body with a 2.0-mm fixation system, and the right orbital floor with a polydioxanone sheet. Nonviable teeth were removed. Because of severe edema and the high risk of iatrogenic facial nerve injury, the right condylar fracture was managed conservatively, and the patient’s habitual occlusion could not be fully restored during the acute operation. Approximately four months after the injury, computed tomography (CT) demonstrated partial osseous bridging and stable residual right zygomatic displacement without signs of an active inflammatory process. Conclusions: In devastating intraoral blast injury, airway security, preservation of viable soft tissue, control of contamination, and restoration of a stable skeletal framework take priority over complete acute correction of every fracture and occlusal discrepancy. Staged reconstruction and coordinated psychiatric and internal medicine care are essential components of definitive management.

The de novo biosynthesis of two major glycerophospholipids, phosphatidylethanolamine and phosphatidylcholine, occurs through the Kennedy pathway. In this process, ethanolamine or choline is initially phosphorylated to phosphoethanolamine or phosphocholine, respectively, and subsequently converted by cytidylyltransferases into CDP-ethanolamine and CDP-choline. Dysregulation of this pathway has been implicated in various diseases. This review provides a comprehensive overview of the enzymatic components of the Kennedy pathway and their physiological roles. Furthermore, it explores the involvement of these enzymes in diseases, with particular emphasis on cancer, while also considering other conditions such as type II diabetes, obesity, and liver disorders. To assess potential links between Kennedy pathway enzymes and cancer, a bioinformatics analysis was conducted using data from the GEPIA portal, covering 33 different cancer types.

Background/Objectives: Implant explantation is often considered the standard treatment for severe peri-implant inflammatory lesions, including cases with apical involvement. However, this approach is relatively invasive and aggressive, which can lead to significant loss of bone and soft tissues, potentially compromising future prosthetic rehabilitation, particularly in the esthetic zone. This study aimed to present implant apicoectomy as a conservative alternative that would allow preservation of implant stability while effectively treating localized inflammation. Methods: This case report presents a female patient who was diagnosed with retrograde peri-implant inflammation, and an implant apicoectomy was performed as a conservative approach to implant explantation. The procedure was carried out using a minimally invasive microsurgical technique. Results: The treatment resulted in complete clinical and radiographic healing, maintenance of implant osseointegration and stability, and resolution of clinical symptoms, including fistula closure. No recurrence of periapical infection was observed during the twelve-month clinical and radiological follow-up visit. Conclusions: Implant apicoectomy may be considered a minimally invasive and effective alternative to explantation in selected cases of retrograde peri-implantitis, preserving hard and soft-tissue architecture while maintaining implant functionality. This approach may be particularly beneficial in esthetic regions where preservation of tissue architecture is critical for optimal clinical outcomes.

Chemokine CXCL1, also known as Gro-α and MGSA, a ligand of CXCR2, is the best-known CXC chemokine in cancer processes, after CXCL8/IL-8 and CXCL12/SDF-1. This paper is the first review on the role of CXCL1 in general molecular processes associated with cancer. It provides a comprehensive overview that allows for an in-depth understanding of the importance of CXCL1 in tumor-related processes. In this review, however, we did not address the clinical aspects of CXCL1, as these were discussed in our previous review articles. The present paper focuses on the involvement of CXCL1 in cancer processes such as proliferation, cancer stem cell (CSC) function, senescence, angiogenesis, lymphangiogenesis, migration and metastasis, and effects on tumor-associated cells such as neutrophils, tumor-associated macrophages (TAMs), myeloid-derived suppressor cells (MDSCs), mesenchymal stem cells (MSCs), and cancer-associated fibroblasts (CAFs). It also describes the significance of CXCL1 in cancer-associated diseases such as cancer cachexia, cancer-associated immunodeficiency, neuroinflammatory-mediated affective-like behaviors, bone cancer pain, and acute kidney injury. We also present the effects of obesity on CXCL1-related cancer processes.

Multiple myeloma (MM) is a plasma cell neoplasm. Studies of chemokines in MM pathogenesis have primarily focused on CCR1 ligands such as CCL3 (MIP-1α), CXCL12 and its receptor CXCR4, as well as CXCR2 and CXCR3 ligands. However, the roles of the remaining 30 chemokines have been investigated much less frequently. This review compiles current knowledge on the significance of lesser-known chemokines in MM tumor processes, including CXCL13, CCR2 ligands (CCL2 [MCP-1], CCL7 [MCP-3]), CCL4, CCL5 (RANTES), CCL17, CCL20, CCL27, CCL28, and CX₃CL1 (fractalkine). It describes their impact on bone destruction, bone marrow angiogenesis, chemoresistance, and the recruitment of cells into the MM niche, such as macrophages, myeloid-derived suppressor cells, and cytotoxic lymphocytes, along with their effects on mesenchymal stromal cells. A bioinformatic analysis highlights the significance of these chemokines in MM, and the possibility of targeting them in MM therapy is also considered.

Lead (Pb) disrupts mitochondrial function, but its impact on the mitochondrial dynamics and biogenesis during early brain development remains insufficiently understood. This study aimed to investigate the effects of pre- and neonatal Pb exposure on the processes involved in mitochondrial network formation in the brains of rat offspring, simulating environmental exposure. We quantified mRNA expression (qRT-PCR) and protein levels (ELISA) of key mitochondrial fusion (Mfn1, Mfn2, Opa1), fission (Drp1, Fis1) regulators, as well as biogenesis markers (PGC-1α, TFAM, NRF1) in the hippocampus, forebrain cortex, and cerebellum of rats exposed to Pb. Mitochondrial ultrastructure was evaluated using transmission electron microscopy (TEM), and the expression of mitochondrial electron transport chain (ETC) genes was analysed (qRT-PCR). Furthermore, to examine the involvement of the cGAS–STING pathway in Pb-induced neuroinflammation, we measured the expression of ISGs (qRT-PCR), TBK1 phosphorylation (Western blot), and 2′,3′-cGAMP synthesis (ELISA). Our results showed that Pb exposure markedly reduced PGC-1α and region-specific NRF1 levels, broadly supressed fusion proteins (Mfn1, Mfn2, Opa1), increased Fis1, and depleted Drp1. ETC gene expression (mtNd1, mtCyb and mtCo1) were upregulated in a brain-structure-dependent manner. These molecular changes were accompanied by pronounced mitochondrial morphological abnormalities. Despite upregulation of Mx1, Ifi44, and Sting1, along with synthesis of 2′3′-cGAMP, TBK1 activation was not detected. All these findings demonstrate that early-life Pb exposure, even low-dose, disrupts mitochondrial biogenesis and the fusion–fission machinery, thus impairs brain energy homeostasis, and implicates mitochondria as central mediators of Pb-induced neuroinflammation and neurodevelopmental toxicity.

Multiple myeloma (MM) is a neoplasm of plasma cells. Despite the development of increasingly advanced treatments, multiple myeloma remains challenging to cure completely. Consequently, the underlying mechanisms of this neoplasm are being investigated to identify new therapeutic targets and understand chemoresistance. A particular focus has been placed on the MM bone marrow microenvironment, with chemokines being one of its key components. This review examines the role of chemokines that activate the CXCR2 and CXCR3 receptors in both monoclonal gammopathy of undetermined significance (MGUS) and MM, highlighting all CXC chemokines and their receptors, including CXCL1, CXCL8/IL-8, CXCL9, CXCL10, and platelet factor 4. We focus on the direct effects of selected CXC chemokines on MM cells, specifically their roles in proliferation, migration, interaction with bone marrow cells, the formation of extramedullary disease, and chemoresistance. Additionally, we explore the impact of these chemokines on the MM bone marrow microenvironment, particularly in relation to mesenchymal stromal cells, myeloid-derived suppressor cells, osteoclasts, M2 macrophages, and natural killer cells, as well as processes such as bone destruction and angiogenesis. Finally, we discuss the potential use of drugs targeting the two chemokine axes described, with a focus on inhibitors and adoptive cell therapy.

Xenogenic collagen matrices are used in clinical practice for soft tissue augmentation around teeth and implants, either alone or biofunctionalized with injectable platelet-rich fibrin (iPRF). Their direct interaction with inflammatory cells may influence both healing and destructive inflammation processes. Therefore, expression of cyclooxygenases (COX-1 and COX-2) and prostanoids (PGE2 and TXB2) was studied in THP-1 monocyte/macrophage cultures exposed to porcine collagen matrices (a non-cross-linked monolayer scaffold composed of collagen type I, collagen type III, and elastin (MLCM), a bilayer scaffold made of collagen types I and III (BLCM), and a volume-stable cross-linked monolayer scaffold (VSCM)). The study showed that VSCM and MLCM significantly reduced PGE2 concentrations in THP-1 monocyte cultures. iPRF further reduced PGE2 concentrations when exposed to MLCM. In contrast, incubation of THP-1 monocytes with VSCM and BLCM resulted in a significant increase in TXB2 concentrations compared with control conditions. Incubation of macrophages with MLCM, VSCM, and BLCM increased PGE2 concentrations, with VSCM and BLCM additionally increasing TXB2 concentrations. iPRF in macrophage cultures with VSCM and BLCM also resulted in increased PGE2 and TXB2 concentrations compared with control conditions. Confocal microscopy revealed no visible differences in COX-1 immunoexpression in monocytes and macrophages cultured with collagen matrices, either with or without iPFR. Weak positive COX-2 immunofluorescence was observed in monocytes, while moderate positive immunofluorescence was detected in macrophages. In conclusion, it can be suggested that the studied collagen matrices interact with monocytes/macrophages, with MLCM exhibiting the highest compatibility.

Phospholipids are crucial structural components of cells. Phosphatidylcholine and phosphatidylethanolamine (both synthesized via the Kennedy pathway) and phosphatidylserine undergo interconversion. The dysregulation of this process is implicated in various diseases. This paper discusses the role of enzymes involved in the interconversion of phosphatidylcholine, phosphatidylethanolamine, and phosphatidylserine, specifically phosphatidylethanolamine N-methyltransferase (PEMT), phosphatidylserine synthases (PTDSS1 and PTDSS2), and phosphatidylserine decarboxylase (PISD), with a focus on their biochemical properties. Additionally, we describe the effects of the deregulation of these enzymes and their roles in both oncological and non-oncological diseases, including nonalcoholic fatty liver disease (NAFLD), Alzheimer’s disease, obesity, insulin resistance, and type II diabetes. Current knowledge on inhibitors of these enzymes as potential therapeutic agents is also reviewed, although in most cases, inhibitors are yet to be developed. The final section of this article presents a bioinformatic analysis using the GEPIA portal to explore the significance of these enzymes in cancer processes.

Infectious disease pandemics pose a psychological challenge to the general population, particularly to healthcare professionals. This study aimed to evaluate the level of work stress and coping strategies used by healthcare professionals during the COVID-19 pandemic, considering sociodemographic and work-related variables. A cross-sectional study included 141 Polish healthcare professionals working with COVID-19 patients. The research was conducted using a diagnostic survey method, employing the Coping Inventory for Stressful Situations (CISS), the Perceived Stress Scale (PSS-10), and a self-written questionnaire. Among the respondents, 46.8% reported severe stress. The study found that older age was associated with less frequent use of avoidance-oriented coping styles, such as engaging in alternative activities (p = 0.031) and seeking social contacts (p = 0.005). Additionally, avoidance-oriented coping was more commonly used by individuals from large cities compared to those from villages, and more frequently by those from small cities than by those from villages and medium-sized cities (p = 0.004). Engaging in alternative activities was significantly more common among individuals from medium-sized cities (p = 0.01), while seeking social contacts was more frequent among those from large cities compared to villagers (p = 0.03). The study revealed that the majority of Polish medical staff working in hospital emergency departments experienced high levels of stress. Education, age, place of residence, and work experience significantly influenced the choice of coping styles among medical staff.