RESUMEN
INTRODUCTION: Severe ischemia is a rare complication of radial artery catheterization (RAC). This study aims to summarize risk factors of RAC-elicited severe hand ischemia, preventive, and therapeutic management. METHODS: Literature search was conducted in eight electronic English and Chinese databases to identify relevant published cases. Data of interest was extracted and analyzed. RESULTS: Database search identified 28 articles reporting cases of 57 patients developing hand ischemia following RAC. Patients aged between 1 day and 88 years. The indications for RAC included surgery, shock, cardiac arrest, and Neonatal Intensive Care Unit (NICU) admission. Identified risk factors included pre-existing vascular diseases, hypotension, arterial anatomical abnormality or small diameter, vasoconstrictors, and catheter-related problems. Totally, 18 patients complained pain; 32 developed discoloration; 19 pulselessness; 3 paresthesia; 13 swolleness and 19 coldness. Eventually, 30 patients recovered well, but 20 patients unfortunately underwent digital amputation and three patients deceased due to non-RAC-related causes. CONCLUSION: Severe hand ischemia following RAC is a rare complication, with the reported incidence of approximately 0.09%. There is no definite predictor for RAC-related hand ischemia, but patients with risk factors are prone to the occurrence of hand ischemia. It's vital to initiate early recognition and proactive strategies for a best practice RAC insertion.
RESUMEN
BACKGROUND: Gastric cancer (GC) is the most prevalent gastrointestinal tumor with an unfavorable clinical prognosis. GC patients are largely threatened owing to metastasis and drug resistance. Tumor angiogenesis plays an important role in the development of gastric cancer and is a challenge in the treatment of gastric cancer. METHODS: Mouse xenograft models were used for screening of therapeutic peptides on GC growth and metastasis. Routine laboratory experimental methods including conditional cell culture, tube formation assay, qRT-PCR, Western blotting, immunohistochemistry (IHC), ubiquitination assay, and immunofluorescence (IF) were used in mechanism investigation; protein docking analysis and coimmunoprecipitation (Co-IP) were used for prediction and confirmation of interactions between JP3/SP1 and TRIM25/MEK1/2. RESULTS: We identified an MMP2-targeted peptide JP3 that plays inhibiting roles in modulating growth and metastasis of GC in vivo and has no observable toxic side effects. JP3 reduced tumor microvessel density (MVD) in vivo and human umbilical vein endothelial cells (HUVECs) tube formation in vitro. Mechanistic studies revealed that JP3 reduces polyubiquitination-mediated degradation of TRIM25 by increasing the stability of TRIM25 through phosphorylating it at Ser12. TRIM25, as an E3 ubiquitin ligase, promoted the ubiquitin of SP1 at K610, further suppressed expression of MMP2 and inhibited angiogenesis in GC. Importantly, the inversely association between TRIM25 and SP1 protein level was further verified in human GC tissues. Decreased TRIM25 expression and increased SP1 expression in tumor tissues were positively correlated with poor prognosis of GC patients. CONCLUSIONS: MMP2-targeted peptide JP3 plays a therapeutic role in GC through anti-angiogenesis by modulating TRIM25/SP1/MMP2.