Calcific myonecrosis: Report of 4 cases and review.

Calcific myonecrosis presents as a rare, late complication stemming from trauma or a neurovascular injury, predominantly affecting the lower limb. It manifests as a progressively enlarging, painful, dystrophic calcified mass, often following compartment syndrome and vascular or neurological compromise, leading to necrosis and fibrosis. While its radiological appearance is typically distinctive, biopsy is commonly pursued due to concerns of malignancy (as calcific myonecrosis may resemble soft tissue sarcoma), often resulting in superimposed infections.

Pathogenesis of non-infection related inflammatory root resorption in permanent teeth: A narrative review.

Background: The mechanism of action of root resorption in a permanent tooth can be classified as infection-related (e.g., microbial infection) or non-infection-related (e.

A Size-Based Criteria for Flap Reconstruction After Thigh-Adductor, Soft-Tissue Sarcoma Resection.

Background: Resection of soft-tissue sarcomas from the adductor compartment is associated with significant complications. Free/pedicled flaps often are used for wound closure, but their effect on healing is unclear. We compared wound complications, oncologic, and functional outcomes for patients undergoing flap reconstruction or primary closure following resection of adductor sarcomas.

RNF4~RGMb~BMP6 axis required for osteogenic differentiation and cancer cell survival.

Molecular understanding of osteogenic differentiation (OD) of human bone marrow-derived mesenchymal stem cells (hBMSCs) is important for regenerative medicine and has direct implications for cancer. We report that the RNF4 ubiquitin ligase is essential for OD of hBMSCs, and that RNF4-deficient hBMSCs remain as stalled progenitors. Remarkably, incubation of RNF4-deficient hBMSCs in conditioned media of differentiating hBMSCs restored OD.

How Do the Outcomes of Radiation-Associated Pelvic and Sacral Bone Sarcomas Compare to Primary Osteosarcomas following Surgical Resection?

Radiation-associated sarcoma of the pelvis and/or sacrum (RASB) is a rare but challenging disease process associated with a poor prognosis. We hypothesized that patients with RASB would have worse surgical and oncologic outcomes than patients diagnosed with primary pelvic or sacral bone sarcomas. This was a retrospective, multi-institution, comparative analysis.

Bone Involvement in Hyperphosphatemic Familial Tumoral Calcinosis: A New Phenotypic Presentation.

Mutations in FGF23, KL, and GALNT3 have been identified as the cause for the development of hyperphosphatemic familial tumoral calcinosis (HFTC). Patients with HFTC typically present in childhood or adolescence with periarticular soft tissue deposits that eventually progress to disrupt normal joint articulation. Mutations in the GALNT3 gene were shown to account for the hyperphosphatemic state in both HFTC and hyperostosis-hyperphosphatemia syndrome (HHS), the latter characterized by bone involvement.

RNF4-Dependent Oncogene Activation by Protein Stabilization.

Ubiquitylation regulates signaling pathways critical for cancer development and, in many cases, targets proteins for degradation. Here, we report that ubiquitylation by RNF4 stabilizes otherwise short-lived oncogenic transcription factors, including β-catenin, Myc, c-Jun, and the Notch intracellular-domain (N-ICD) protein. RNF4 enhances the transcriptional activity of these factors, as well as Wnt- and Notch-dependent gene expression.

A c-Myc/miR17-92/Pten Axis Controls PI3K-Mediated Positive and Negative Selection in B Cell Development and Reconstitutes CD19 Deficiency.

PI3K activity determines positive and negative selection of B cells, a key process for immune tolerance and B cell maturation. Activation of PI3K is balanced by phosphatase and tensin homolog (Pten), the PI3K's main antagonistic phosphatase. Yet, the extent of feedback regulation between PI3K activity and Pten expression during B cell development is unclear.

Canal-to-Diaphysis Ratio as an Osteoporosis-Related Risk Factor for Hip Fractures.

Prevention of osteoporosis is essential to health, quality of life, and independence in the elderly. The accepted diagnostic method for evaluation of fracture risk after osteopenia and osteoporosis is the measurement of bone mineral density with dual-energy x-ray absorptiometry (DEXA). This method is limited because of its low accessibility, high capital costs, and low sensitivity.

CXCL11-dependent induction of FOXP3-negative regulatory T cells suppresses autoimmune encephalomyelitis.

A single G protein-coupled receptor (GPCR) can activate multiple signaling cascades based on the binding of different ligands. The biological relevance of this feature in immune regulation has not been evaluated. The chemokine-binding GPCR CXCR3 is preferentially expressed on CD4+ T cells, and canonically binds 3 structurally related chemokines: CXCL9, CXCL10, and CXCL11.

The MAPK/ERK and PI3K pathways additively coordinate the transcription of recombination-activating genes in B lineage cells.

Rag-1 and Rag-2 are essential for the construction of the BCR repertoire. Regulation of Rag gene expression is tightly linked with BCR expression and signaling during B cell development. Earlier studies have shown a major role of the PI(3)K/Akt pathway in regulating the transcription of Rag genes.

Caspase-cleaved HPK1 induces CD95L-independent activation-induced cell death in T and B lymphocytes.

Life and death of peripheral lymphocytes is strictly controlled to maintain physiologic levels of T and B cells. Activation-induced cell death (AICD) is one mechanism to delete superfluous lymphocytes by restimulation of their immunoreceptors and it depends partially on the CD95/CD95L system. Recently, we have shown that hematopoietic progenitor kinase 1 (HPK1) determines T-cell fate.