The first case report of an intraosseous epidermoid cyst in the distal phalanx of the index finger with infection resulting in single clubbing finger: A case report and review of the literature

An intraosseous epidermoid cyst at the distal phalanx of the index finger is extremely rare. These cysts are asymptomatic unless ruptured, severely infected, or transformed into malignant squamous cell carcinoma. We present a case of a single clubbing finger in an adult diagnosed with an intraosseous epidermoid cyst in the distal phalanx of the left index finger with no history of pulmonary or cardiovascular diseases. Preoperative MRI showed an expansile lytic lesion with a sclerotic margin. Histopathological examination indicates that there is keratinous cell debris in the cyst with a wall of stratified squamous epithelium, which was the key to the correct diagnosis of an intraosseous epidermoid cyst. Written informed consent was obtained from the patient for publication of this case report and any accompanying images

Techniques and graft materials for repairing peripheral nerve defects

Peripheral nerve defects refer to damage or destruction occurring in the peripheral nervous system, typically affecting the limbs and face. The current primary approaches to address peripheral nerve defects involve the utilization of autologous nerve transplants or the transplantation of artificial material. Nevertheless, these methods possess certain limitations, such as inadequate availability of donor nerve or unsatisfactory regenerative outcomes post-transplantation. Biomaterials have been extensively studied as an alternative approach to promote the repair of peripheral neve defects. These biomaterials include both natural and synthetic materials. Natural materials consist of collagen, chitosan, and silk, while synthetic materials consist of polyurethane, polylactic acid, and polycaprolactone. Recently, several new neural repair technologies have also been developed, such as nerve regeneration bridging technology, electrical stimulation technology, and stem cell therapy technology. Overall, biomaterials and new neural repair technologies provide new methods and opportunities for repairing peripheral nerve defects. However, these methods still require further research and development to enhance their effectiveness and feasibility

Mechanisms and recent advances in the diagnosis and treatment of nitrous oxide-induced peripheral neuropathy: a narrative review

Under standard conditions, nitrous oxide (N2O) manifests as a colorless, odorless gas with a mildly sweet taste. The compound finds applications in various fields, including its use as an aerosol propellants, an accelerant in motor racing, and an anesthetic in surgical procedures and dentistry. Unfortunately, the recreational misuse of N2O has become prevalent among young individuals due to its euphoric and hallucinogenic effects. Compounding this issue is the fact that nitrous oxide can be easily obtained from over-the-counter household items, facilitating its non-medical use. The global community has witnessed a surge in the recreational utilization of nitrous oxide gas in recent years. Despite the widespread non-medical abuse of N2O, there remains inadequate understanding of the potential adverse effects resulting from exposure to it. This paper provides an overview of management findings, laboratory and electrodiagnostic characteristics, as well as clinical presentations associated with neurological disorders induced by nitrous oxide usage

Imaging diagnosis in peripheral nerve injury

Peripheral nerve injuries (PNIs) can be caused by various factors, ranging from penetrating injury to compression, stretch and ischemia, and can result in a range of clinical manifestations. Therapeutic interventions can vary depending on the severity, site, and cause of the injury. Imaging plays a crucial role in the precise orientation and planning of surgical interventions, as well as in monitoring the progression of the injury and evaluating treatment outcomes. PNIs can be categorized based on severity into neurapraxia, axonotmesis, and neurotmesis. While PNIs are more common in upper limbs, the localization of the injured site can be challenging. Currently, a variety of imaging modalities including ultrasound (US), computed tomography (CT) and magnetic resonance imaging (MRI) and positron emission tomography (PET) have been applied in detection and diagnosis of PNIs, and the imaging efficiency and accuracy many vary based on the nature of injuries and severity. This article provides an overview of the causes, severity, and clinical manifestations of PNIs and highlights the role of imaging in their management

A working model that ICR-Mo stops colistin-induced hydroxyl radical killing in <i>E</i>. <i>coli</i>.

<p><b>A.</b> Scheme for ROS production triggered by colistin in <i>E</i>. <i>coli</i>. <b>B.</b> Impairment of colistin-induced ROS formation in <i>icr-Mo</i>-bearing <i>E</i>. <i>coli</i>. <b>C.</b> Chemical rescue experiments reveal that a Fenton reaction is involved in the colistin-activated hydroxyl radical killing pathway in <i>E</i>. <i>coli</i>. The LPS-lipid A moiety refers to an initial target for colistin treatment. Bipyridine is a well-studied ferric chelator, and L-cysteine is the ROS scavenger.</p

Relative ratio of colistin-induced ROS levels in <i>E</i>. <i>coli</i> carrying <i>icr-Mo</i> (<i>mcr-1</i> and/or <i>eptA</i>).

<p>Ratio of fluorescent cells was obtained by counting the number of cells with/without fluorescence (illustrated in <b><a href="http://www.plosgenetics.org/article/info:doi/10.1371/journal.pgen.1007389#pgen.1007389.g008" target="_blank">Fig 8</a></b>). In every group, over 500 cells counted from 4 individual photographs. The data was assessed using one-way analysis of variance (ANOVA) followed by Tukey–Kramer multiple comparisons post hoc test.</p

Malignant Peripheral Nerve Sheath Tumors: Latest Concepts in Disease Pathogenesis and Clinical Management

Malignant peripheral nerve sheath tumor (MPNST) is an aggressive soft tissue sarcoma with limited therapeutic options and a poor prognosis. Although neurofibromatosis type 1 (NF1) and radiation exposure have been identified as risk factors for MPNST, the genetic and molecular mechanisms underlying MPNST pathogenesis have only lately been roughly elucidated. Plexiform neurofibroma (PN) and atypical neurofibromatous neoplasm of unknown biological potential (ANNUBP) are novel concepts of MPNST precancerous lesions, which revealed sequential mutations in MPNST development. This review summarized the current understanding of MPNST and the latest consensus from its diagnosis to treatment, with highlights on molecular biomarkers and targeted therapies. Additionally, we discussed the current challenges and prospects for MPNST management

Paralleled PE-recognizing cavities amongst ICR-Mo, EptA and MCR-1.

<p><b>A.</b> Chemical structure of the PE lipid substrate molecule. <b>B.</b> EptA has a cavity for the entry of the PE lipid substrate. <b>C.</b> A PE-recognizable cavity is present in MCR-1 enzyme. <b>D.</b> A conservative PE-binding cavity is also shared by ICR-Mo (AXE82_07515). A Zn²⁺-bound five-residues forming motif is conserved in PE lipid substrate-interactive cavities of three enzymes EptA (<b>E</b>), MCR-1 (<b>F</b>) and ICR-Mo (<b>G</b>). Comparative analyses of the seven conserved PE-recognizable residues from EptA (<b>H</b>), MCR-1 (<b>I</b>) and ICR-Mo (<b>J</b>). The enlarged surface structures of PE-bound cavities are consistently generated through molecular docking together with structural modelling. PE molecules are illustrated with red sticks, and cavity is highlighted with an arrow. The photographs are generated using PyMol. The conserved residues are labelled, and also listed in <b><a href="http://www.plosgenetics.org/article/info:doi/10.1371/journal.pgen.1007389#pgen.1007389.s005" target="_blank">S2 Fig</a></b>. Designations: PE: phosphatidylethanolamine.</p

Chemical mechanism for PEA modification of lipid A by EptA/MCR-1/ICR-Mo.

<p><b>A.</b> Scheme for cleavage reaction of an alternative substrate NBD-glycerol-3-PEA by ICR-Mo (AXE82_07515) into NBD-glycerol and an adduct of ICR-Mo-bound PEA. PEA refers to <u>p</u>hospho<u>e</u>thanol<u>a</u>mine. NBD was highlighted in magenta, whereas PEA was indicated in red. LC/MS identification of the mixture of the ICR-Mo-mediated hydrolysis reaction (<b>B</b>) and the NBD-glycerol-3-PEA substrate (<b>C</b>). The inside gels denote the TLC-based visualization of the NBD-glycerol-3-PEA substrate (in <b>Panel B</b>) and the ICR-Mo-mediated hydrolytic product, NBD-glycerol (in <b>Panel C</b>). NBD-glycerol-3-PEA appears at m/z of 814.1, whereas the resultant product NBD-glycerol occurs at m/z of 691.5. <b>C.</b> Thin layer chromatography (TLC) detection for the conversion of NBD-glycerol-PEA lipid substrate by the ICR-Mo (AXE82_07515) into NBD-glycerol. <b>D.</b> Transfer of PEA from ICR-Mo-bound PEA to lipid A, generating the PPEA-lipid A product. Position of PPEA depicted is only suggestive. MALDI-TOF-MS evidence for the structural alteration of the lipid A moieties of lipopolysaccharide (LPS) in <i>E</i>. <i>coli</i> expressing EptA (<b>E</b>), MCR-1 (<b>F</b>) and ICR-Mo (AXE82_07515) (<b>G</b>). The peak of the bis-phosphorylated hexa-acylated lipid A varies at m/z of 1796.063 ~ 1797.426, whereas resultant derivative with PEA modification (PPEA-1(or 4’)-lipid A) exhibits at m/z varying from 1919.409 to 1920.087.</p

Domain-swapping analyses of ICR-Mo.

<p><b>A.</b> Schematic illustration for domain-swapping designing amongst the three transmembrane enzymes EptA, MCR-1 and ICR-Mo (AXE82_07515). <b>B.</b> Use of Western blotting to detect the expression of <i>icr-Mo</i> and its mosaic versions. <b>C.</b> Functional evaluation of ICR-Mo derivatives in ability of conferring appreciable growth of <i>E</i>. <i>coli</i> on LBA plates with varied levels of colistin. <b>D.</b> Measurement of colistin MIC of <i>E</i>. <i>coli</i> strains expressing ICR-Mo and its hybrid derivatives.</p