A child with intravascular fasciitis mimicking deep vein thrombosis: a case report.

BACKGROUND: Intravascular fasciitis (IF) is a benign, reactive, myofibroblastic proliferation that originates from the superficial or deep fascia of small / medium-sized arteries and veins. CASE REPORT: An 8-year-old male patient was admitted to a health center with the complaint of swelling in the inguinal region. Lower extremity venous Doppler ultrasonography showed deep vein thrombosis (DVT) of the femoral vein and anticoagulation with low-molecular weight heparin (LMWH) was initiated. The patient was referred to our center for follow-up. The D-dimer level was detected within normal limits. Doppler ultrasonography was repeated and showed an intraluminal expanding mass lesion with increasing vascularity, without distinct borders and LMWH was discontinued. This lesion at the sapheno-femoral junction was excised surgically and the histopathological examination revealed intravascular fasciitis. CONCLUSION: Clinicians should be aware that the clinical findings of IF may mimic sarcoma and thrombosis.

Transcriptomics and Proteomics Analyses Reveal JAK Signaling and Inflammatory Phenotypes during Cellular Senescence in Blind Mole Rats: The Reflections of Superior Biology.

The blind mole rat (BMR), a long-living subterranean rodent, is an exceptional model for both aging and cancer research since they do not display age-related phenotypes or tumor formation. The Janus kinase-signal transducer and activator of transcription (JAK-STAT) signaling is a cytokine-stimulated pathway that has a crucial role in immune regulation, proliferation, and cytokine production. Therefore, the pathway has recently attracted interest in cellular senescence studies. Here, by using publicly available data, we report that JAK-STAT signaling was suppressed in the BMR in comparison to the mouse. Interestingly, our experimental results showed upregulated Jak1/2 expressions in BMR fibroblasts during the replicative senescence process. The transcriptomic analysis using publicly available data also demonstrated that various cytokines related to JAK-STAT signaling were upregulated in the late passage cells, while some other cytokines such as MMPs and SERPINs were downregulated, representing a possible balance of senescence-associated secretory phenotypes (SASPs) in the BMR. Finally, our proteomics data also confirmed cytokine-mediated signaling activation in senescent BMR fibroblasts. Together, our findings suggest the critical role of JAK-STAT and cytokine-mediated signaling pathways during cellular senescence, pointing to the possible contribution of divergent inflammatory factors to the superior resistance of aging and cancer in BMRs.

Translation of Cellular Senescence to Novel Therapeutics: Insights From Alternative Tools and Models.

Increasing chronological age is the greatest risk factor for human diseases. Cellular senescence (CS), which is characterized by permanent cell-cycle arrest, has recently emerged as a fundamental mechanism in developing aging-related pathologies. During the aging process, senescent cell accumulation results in senescence-associated secretory phenotype (SASP) which plays an essential role in tissue dysfunction. Although discovered very recently, senotherapeutic drugs have been already involved in clinical studies. This review gives a summary of the molecular mechanisms of CS and its role particularly in the development of cardiovascular diseases (CVD) as the leading cause of death. In addition, it addresses alternative research tools including the nonhuman and human models as well as computational techniques for the discovery of novel therapies. Finally, senotherapeutic approaches that are mainly classified as senolytics and senomorphics are discussed.