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Background and objective: Cancer is a life-threatening disease worldwide and current standard therapy cannot fulfill all clinical needs. Chinese herbal injections have been widely used for cancer in Chinese and Western hospitals in China. This study aimed to apply evidence mapping in order to provide an overview of the clinical application of Chinese herbal injections in cancer care based on randomized controlled trials, systematic reviews, and meta-analyses. Methods and results: Seven databases were systematically searched for eligible randomized controlled trials, systematic reviews, and meta-analyses for ten Chinese herbal injections used in cancer treatment and covered in the Chinese national essential health insurance program. Excel 2016 and RStudio were used to integrate and process the data. In total 366 randomized controlled trials and 48 systematic reviews and meta-analyses were included in the evidence mapping of herbal medicines including; Compound Kushen, Shenqi Fuzheng, Aidi, Kangai, Kanglaite, Xiaoaiping, Cinobufacin, Brucea javanica oil emulsion, Polyporus polysaccharide injection, and Astragalus polysaccharide for injection. Health insurance restricts the scope of clinical application for these herbal injections. The numbers of studies published increased, especially around 2013–2015. The most studied cancer types were lung cancer (118, 32.2%), colorectal cancer (39, 10.7%), and gastric cancer (39, 10.7%), and the most used injections were Compound Kushen (78, 21.3%), Shenqi Fuzheng (76, 20.8%), and Aidi (63, 17.2%). The most consistently reported benefits were observed for Compound Kushen, Shenqi Fuzheng, Aidi, and Kangai for tumor response, quality of life, myelosuppression, and enhancing immunity. Conclusion: The current evidence mapping provides an overview of the outcomes and effects of Chinese herbal injections used in cancer care, and offers information on their clinical application which warrants further evidence-based research in order to inform clinical and policy decision-making.

ObjectivesTo analyse the relationship between serum uric acid (SUA), all-cause and cardiovascular (CV) mortality in peritoneal dialysis (PD) patients to inform clinical practice and future research.DesignA systematic review of observational studies.Data sourcesPubMed, Embase, Web of Science, the Cochrane Library, China National Knowledge Infrastructure (CNKI), SinoMed, Chinese Science and Technology Journal Database (VIP) and Wan Fang databases were searched from their inception to January 2021 for cohort and case–control studies reporting SUA and mortality in patients with PD.MethodsThe Newcastle-Ottawa Quality Assessment Scale was used to appraise quality of cohort and case–control studies. Effect estimates were presented as HRs with 95% CIs in a meta-analysis using STATA V.16.0. Data not suitable for pooling were synthesised qualitatively.ResultsFourteen cohort studies with 24 022 patients were included. No case–control studies were identified. For prospective cohort studies, pooled results for the highest SUA category were significantly greater than the lowest for all-cause (one study; 1278participants; HR 1.79; 95% CI 1.17 to 2.75) and CV mortality (one study; 1278 participants; HR 2.63; 1.62–4.27). An increase of 1 mg/dL in SUA level was associated with a 16% increased risk of all-cause mortality (one study; 1278 participants; HR 1.16; 1.03–1.32) and 34% increased CV mortality risk (one study; 1278 participants; HR 1.34; 1.16–1.55). For retrospective cohort studies, the highest SUA category did not demonstrate an elevated all-cause (five studies; 4570 participants; HR 1.09; 0.70–1.70) or CV mortality (three studies; 3748 participants; HR 1.00; 0.44–2.31) compared with the lowest SUA category. Additionally, there was no increase in all-cause (eight studies; 11 541 participants; HR 0.94; 0.88–1.02) or CV mortality (three studies; 7427 participants; HR 0.90; 0.76–1.06) for every 1 mg/dL increase in SUA level.ConclusionsResults of prospective and retrospective cohort studies were inconsistent. Consequently, prospective, multicentre, long-term follow-up studies are required to confirm the relationship between SUA and mortality in patients with PD.

Background. Herpes zoster (HZ) is a common infection in individuals with acquired immunodeficiency syndrome (AIDS) patients. Traditional Chinese medicine (TCM) has been used widely in clinical practice for HZ, which remains not supportive of evidence. This review aimed to evaluate the effectiveness and safety of TCM in treating HIV-associated HZ. Methods. Nine electronic databases were searched for randomized controlled trials (RCTs) testing TCM in treating HIV-associated HZ. Data were extracted on citations, interventions, and outcomes, by two authors independently. For the quality evaluation, Cochrane risk-of-bias tool 2.0 was used. Meta-analyses were performed by Revman5.3 software. Effect estimation presented as risk ratio (RR) for dichotomous data and mean difference (MD) for continuous data with their 95% confidence interval (CI). Results. Twelve RCTs (n = 644) were included; the majority of them had a high or unclear risk of bias. Meta-analysis showed that pain intensity (VAS 0–5) in the Chinese herbal medicine (CHM) group was lower than it in the drugs group (MD = −0.87, 95% CI [−1.69, −0.04], two trials, n = 93). Duration of herpes-related pain (days) of patients in the combination group was shorter than those in the drugs group (MD = −9.19, 95% CI [−16.73, −1.65], n = 144). The incidence of postherpetic neuralgia (PHN) in the combination group was lower than in the drugs group (RR = 0.49, 95% CI [0.25, 0.99], n = 202). As for cure rate (complete absence of pain and herpes), two trials showed that CHM was better than drugs (RR = 1.58, 95% CI [1.13, 2.22], n = 93), five trials showed combination treatment was better than drugs (RR = 1.40, 95% CI [1.08, 1.82], n = 224). The cure rate in the acupuncture group was more than that in the drugs group (RR = 1.99, 95% CI [1.18, 3.36], n = 120). Four trials reported adverse effects and found no serious adverse events occurred. Conclusion. CHM and acupuncture demonstrate more benefits than drugs in pain relief, cure rate improvement, and incidence reduction of PHN. However, given the data limitation and TCM therapies’ diversity, the conclusions need to be verified in future trials.

Aim： Human CXCR3, a seven-transmembrane segment （7TMS）, is predominantly expressed in Th1-mediated responses. Interferon-y-inducible protein 10 （IP-10） is an important ligand for CXCR3. Their interaction is pivotal for leukocyte migration and activation. Tyrosine sulfation in 7TMS is a posttranslational modification that contributes substantially to ligand binding. We aimed to study the role of tyrosine sulfation of CXCR3 in the protein＇s binding to IP-10. Methods： Plasmids encoding CXCR3 and its mutants were prepared by PCR and site-directed mutagenesis. HEK 293T cells were transfected with plasmids encoding CXCR3 or its variants using calcium phosphate. Transfected cells were labeled with [^35S]-cysteine and methionine or [35S]-Na2SO3 and then analyzed by immunoprecipitation to measure sulfation. Experiments with ^125 I-labeled IP-10 were carried out to evaluate the affinity of CXCR3 for its ligand. Calcium influx assays were used to measure intercellular signal transduction. Results： Our data show that sulfate moieties are added to tyrosines 27 and 29 of CXCR3. Mutation of these two tyrosines to phenylalanines substantially decreases binding of CXCR3 to IP-10 and appears to eliminate the associated signal transduction. Tyrosine sulfation of CXCR3 is enhanced by tyrosyl protein sulfotransferases （TPSTs）, and it is weakened by shRNA constructs. The binding ability of CXCR3 to IP-10 is increased by TPSTs and decreased by shRNAs. Conclusion： This study identifies two sulfated tyrosines in the N-terminus of CXCR3 as part of the binding site for IP-10, and it underscores the fact that tyrosine sulfation in the N-termini of 7TMS receptors is functionally important for ligand interactions. Our study suggests a molecular target for inhibiting this ligand-receptor interaction.

The clinical progression of small-cell lung cancer (SCLC) remains pessimistic. The aim of the present study was to promote the understanding of the clinical significance and mechanism of O-linked N-acetylglucosamine (GlcNAc) transferase (OGT) in SCLC. Wilcoxon tests, standardized mean difference (SMD), and Kruskal–Wallis tests were utilized to compare OGT level differences among the experimental and control groups. The univariate Cox regression analysis, Kaplan–Meier curves, and receiver operating characteristic curves were applied to determine OGT’s clinical relevance in cancers. The Spearman correlation analysis and enrichment analysis were utilized to explore the underlying mechanisms of OGT in cancers. For the first time in the field, we provide an overview of OGT in 32 cancers using a large number of samples (n = 21,196), determining distinct OGT expression in 25 cancers and its prognosis effects in 12 cancers. Furthermore, using 950 samples from multiple sources, upregulated OGT was found in both mRNA and protein levels in SCLC (SMD = 0.93, 95% CI [0.24, 1.63]). Higher OGT levels represented a more unfavorable disease-free interval for SCLC patients (p<0.001). The research also identified OGT expression as a potential marker for SCLC prediction (sensitivity = 0.79, specificity = 0.86, and AUC = 0.88). The high expression of OGT in SCLC may result from the positive regulation of two transcription factors—DEK and XRN2. We primarily investigated the underlying mechanisms of OGT in SCLC. Herein, based on the analyses from pan-cancer to SCLC, OGT demonstrated conspicuous clinical significance. OGT may be an underlying biomarker for the treatment and identification of some cancers, including SCLC.

Objective： To evaluate the association between p53 codon 72 polymorphism （R72P） and the risk ofcolorectal liver metastases. Methods： The p53 R72P genotype was identified by polymerase chain reaction-restriction fragment length polymorphism （PCR-RFLP） method in 78 consecutive colorectal cancer patients with liver metastases and 214 age- and sex-matched cases with nonmetastatic colorectal cancer. Results： The R allele of the p53 R72P polymorphism was more frequently found in metastatic cases than in nonmetastatic cases （P=0.075）. Carriers of the 72R allele had a 2.25-fold （95% CI （confidence interval）=1.05-4.83） increased risk of liver metastases. On the stratification analysis, 72R-carrying genotype conferred a 3.46-fold （95% CI=1.02-11.72） and a 1.05-fold （95% CI=0.36-3.08） increased risk of liver metastases for p53 overexpression-positive and negative colorectal cancers, respectively. Conclusion： These results demonstrate for the first time that the 72R allele of the p53 polymorphism has an increased risk for liver metastases in colorectal cancers positive for p53 overexpression.