Objective: To evaluate the effects on reduction of peripherally inserted central catheter-related venous thrombosis by hand grip exercise. Methods: A detailed search was performed to identify literature about the impact of handgrip exercise on peripherally inserted central catheter-related venous thrombosis, using the Cochrane Library and the databases of PubMed, CINAHL, Embase, CNKI, WanFang and CBM. The meta-analysis or descriptive review were performed after two authors in-dependently searching databases,extracting data and assessing quality of included studies. Results: Seven RCTs were included in a total of 789 patients. Meta-analysis showed the effectiveness of handgrip exercise on reduction of peripherally inserted central catheter-related venous thrombosis (RR=0.27, 95% CI 0.17-0.42, P<0.01); and improving vein maximum velocity (WMD=6.53, 95%CI 3.34-9.73, P<0.01) and time-mean flow velocity (WMD=6.05, 95%CI 3.24-8.87, P<0.01). Conclusions Handgrip exercise can improve axillary vein blood flow parameters and reduce peripherally inserted central catheter-related venous thrombosis. Due to a small number of included studies and heterogeneity of indicators, multi-centered, high-quality RCTs with large sample size are needed in the future to assess the effect of handgrip exercise in PICC patients.

Uveal melanoma(UM)is the most frequent and life-threatening ocular malignancy in adults.Aberrant histone methylation contributes to the abnormal transcriptome during oncogenesis.However,a comprehensive understanding of histone methylation patterns and their therapeutic potential in UM remains enigmatic.Herein,using a systematic epi-drug screening and a high-throughput transcriptome profiling of histone methylation modifiers,we observed that disruptor of telomeric silencing-1-like(DOT1L),a methyltransferase of histone H3 lysine 79(H3K79),was activated in UM,especially in the high-risk group.Concordantly,a systematic epi-drug library screening revealed that DOT1 L inhibitors exhibited salient tumor-selective inhibitory effects on UM cells,both in vitro and in vivo.Combining Cleavage Under Targets and Tagmentation(CUT&Tag),RNA sequencing(RNA-seq),and bioinformatics analysis,we identified that DOT1 L facilitated H3K79 methylation of nicotinate phosphoribosyltransferase(NAPRT)and epigenetically activated its expression.Importantly,NAPRT served as an oncogenic accel-erator by enhancing nicotinamide adenine dinucleotide(NAD+)synthesis.Therapeutically,DOT1L inhi-bition epigenetically silenced NAPRT expression through the diminishment of dimethylation of H3K79(H3K79me2)in the NAPRT promoter,thereby inhibiting the malignant behaviors of UM.Conclusively,our findings delineated an integrated picture of the histone methylation landscape in UM and unveiled a novel DOT1L/NAPRT oncogenic mechanism that bridges transcriptional addiction and metabolic reprogramming.