BACKGROUND:Adjuvant chemotherapy following D2 gastrectomy constitutes the standard-of-care for resectable gastric or gastroesophageal junction (GEJ) carcinoma. The CAPITAL trial is a multicenter, randomized, phase 3 study, aiming to assess the efficacy and safety of adjuvant oxaliplatin plus S-1 (SOX) versus S-1 alone. METHODS:Patients with histologically confirmed pathological stage II-III gastric or GEJ adenocarcinoma after gastrectomy with D2 lymphadenectomy were randomly assigned (1:1) to receive either the SOX regimen (n = 362) or the S-1 regimen (n = 362). The primary endpoint was overall survival. This study is registered with ClinicalTrials.gov (NCT01795027). FINDINGS:The median follow-up was 74.0 months (interquartile range [IQR], 35.5-89.3). The 5-year overall survival rates were 70.9% (95% confidence interval [CI], 66.0-76.1) in the SOX group and 62.9% (95% CI, 57.8-68.5) in the S-1 group (hazard ratio [HR], 0.74; 95% CI, 0.58-0.95; p = 0.018). The 3- and 5-year disease-free survival rates were 71.2% (95% CI, 66.5-76.3) and 66.2% (95% CI, 61.2-71.6) in the SOX group, as compared with 65.1% (95% CI, 60.2-70.5) and 55.6% (95% CI, 50.4-61.3) in the S-1 group (HR, 0.76; 95% CI, 0.61-0.96). Treatment-related adverse events of grade 3-4 occurred in 87 (25%) of 349 patients in the SOX group and 45 (13%) of 347 patients in the S-1 group. The most common grade 3-4 adverse event was neutropenia, occurring in 44 (13%) of 349 patients in the SOX group and 23 (7%) of 347 patients in the S-1 group. CONCLUSIONS:The addition of adjuvant oxaliplatin to S-1 chemotherapy significantly improved overall survival and disease-free survival in patients with gastric cancer. FUNDING:This research was supported by the National Natural Science Foundation of China (82573092 and 82573387).

Colorectal micropapillary adenocarcinoma (CMPA) is a rare and highly aggressive subtype of colorectal cancer with high metastatic potential and the proportion of CMPA to the entire tumor ranged from 5 to 80

BACKGROUND: Colorectal cancer (CRC) is one of the most common malignancies, but the molecular mechanisms underlying CRC progression are not well-understood. Accumulating evidence suggests that circular RNAs (circRNAs) play important roles in genesis and development of cancer. However, the roles and molecular mechanisms of circRNAs in CRC remain largely unelucidated. METHODS: The differential expression patterns of circRNAs between primary CRC tumor tissues and corresponding liver metastases were profiled by RNA sequencing. Associations between circPTGR1 expression and clinicopathological features as well as prognosis were analyzed among CRC patients. The effect of circPTGR1 on CRC growth and metastasis was explored through in vitro, in vivo—comprising subcutaneous xenograft, tail-vein lung metastasis, and intrasplenic liver metastasis models—and notably, patient-derived organoid (PDO) assays. The reciprocal regulation among circPTGR1, miR-4725-5p, and EIF4A3, together with the interaction between miR-4725-5p and FAK (Focal Adhesion Kinase), was predicted by bioinformatic analyses and subsequently validated using qRT-PCR, western blotting, RNA immunoprecipitation (RIP), and dual-luciferase reporter assays. Further confirmation of these regulatory interactions was performed in clinical CRC tissues, PDOs, and xenograft models by qRT-PCR, western blotting, and immunohistochemistry (IHC). RESULTS: Expression of circPTGR1 was significantly upregulated in CRC and elevated circPTGR1 was associated with poor prognosis in CRC patients. In vitro and in vivo experiments demonstrated that circPTGR1 promoted the growth, migration, invasion, and metastasis of CRC. The role of circPTGR1 in enhancing CRC cell proliferation and invasiveness was confirmed utilizing PDO models. Mechanistically, circPTGR1 acted as a molecular sponge for miR-4725-5p, leading to upregulation of its target FAK and consequently activating the FAK/AKT signaling pathway. Importantly, EIF4A3 was identified as a promoter which facilitated the biogenesis of circPTGR1 and a direct downstream target of miR-4725-5p. These findings were validated through clinical CRC tissues, PDO models, and xenograft assays, supporting a novel positive feedback loop involving EIF4A3, circPTGR1, and miR-4725-5p in CRC progression via activating the FAK/AKT signaling pathway. CONCLUSIONS: EIF4A3/circPTGR1/miR-4725-5p positive feedback loop accelerates CRC proliferation and metastasis by activating the FAK/AKT signaling pathway. Therefore, circPTGR1 could serve as a potential prognostic indicator and therapeutic target for CRC.

Cancer survivors newly diagnosed with second primary colorectal cancer (SPCRC) is rapidly growing. However, the impact of different prior cancers on survival of patients who underwent surgery for SPCRC remains unclear; therefore, we conducted an analysis to investigate the influence of prior cancer history. In this study, the data of patients diagnosed with CRC between 2004 and 2013 were extracted from the Surveillance, Epidemiology, and End Results database. The bias was minimized by Propensity Score Matching, and the Kaplan-Meier method as well as Cox proportional hazards models were used to analyze the impact of different prior cancer histories on overall survival (OS) and colorectal cancer-specific survival (CCSS) in patients undergoing surgery for SPCRC. Subgroup analyses were further conducted based on the time since first cancer diagnosis, age at SPCRC diagnosis, and SPCRC stage.Here, we included 68,410 patients who underwent surgery for FPCRC and 12,010 patients for SPCRC. KM curves showed that the OS and CCSS of patients with a history of prior thyroid cancer undergoing surgery for SPCRC were similar to those undergoing surgery for FPCRC (P ≥ 0.05). Patients with a history of prior colorectal cancer, prostate cancer, breast cancer, uterine cancer, bladder cancer, skin cancer, lung cancer, kidney cancer, or stomach cancer undergoing surgery for SPCRC had inferior OS compared to those undergoing surgery for FPCRC (P < 0.05). Taken together, our findings demonstrate that the history of prior cancers, except for prior thyroid cancer, might adversely influence the OS of patients who underwent surgery for SPCRC.

OBJECTIVE:To investigate the prognostic potential of preoperative blood neutrophil to lymphocyte ratio (NLR), hematocrit (HCT) and Fibrinogen (FIB) level in patients with colorectal cancer (CRC). METHODS:The data of 268 patients with CRC who underwent radical surgery from March 2013 to August 2017 in the First Affiliated Hospital of Guangzhou Medical University (Guangzhou, China) were retrospectively collected. The correlations between preoperative blood NLR, HCT and FIB level and the clinicopathologic features and prognosis were explored by Cox regression in the patients with CRC. RESULTS:Univariate and multivariate analyses identified preoperative blood with high NLR (HR = 2.265, 95% CI: 1.437-3.570), low HCT (HR = 1.575, 95% CI: 1.010-2.454), and high FIB (HR = 1.667, 95% CI: 1.067-2.605) as independent predictors of reduced 5-year overall survival (OS). Furthermore, the patients were stratified into high (with 3 predictors), middle (with 2 predictors) and low (with 0 or 1 predictors) risk groups according to the number of the 3 independent prognostic predictors. The more independent predictors a patient has, the poorer their prognosis tends to be. CONCLUSIONS:Preoperative NLR, HCT, and FIB serve as cost-effective prognostic biomarkers in CRC. Their combination enables precise risk stratification, guiding personalized postoperative management.

Cuproptosis is a copper-dependent form of regulated cell death that begins when ferredoxin 1 (FDX1) reduces Cu²⁺ to Cu¹⁺, allowing the ion to bind lipoylated enzymes of the tricarboxylic-acid (TCA) cycle, drive protein aggregation, dismantle iron–sulphur clusters and trigger fatal proteotoxic stress. Most tumours, despite accumulating copper, evade this fate through glucose-metabolic rewiring. First, oncogenic stabilisation of hypoxia-inducible factor-1 alpha (HIF-1α) and MYC increases pyruvate dehydrogenase kinase (PDK) activity, which phosphorylates and inactivates the pyruvate dehydrogenase complex (PDC), shrinking the lipoylated target pool in mitochondria and cutting the feed into the TCA cycle. Second, glycolytic signalling suppresses cuproptosis-promoting genes such as FDX1 and dihydrolipoamide S-acetyltransferase while inducing the negative regulator glutaminase (GLS), further lowering copper sensitivity. Third, diversion of glycolytic intermediates into the pentose-phosphate pathway (PPP) supplies abundant nicotinamide adenine dinucleotide phosphate (NADPH), whereas enhanced glutamine catabolism furnishes glutamate; together these fuels expand reduced glutathione (GSH) and metallothionein (MT) pools that chelate Cu¹⁺ and quench reactive oxygen species exactly where cuproptosis is executed. Consequently, glycolysis-dependent cancer cells are far less sensitive to copper-ionophore drugs such as elesclomol or disulfiram than respiration-dependent counterparts, and clinical datasets consistently link high PDK and low PDC-subunit expression with poor prognosis. These insights highlight rational combination strategies: re-activating the TCA cycle with PDK inhibitors, draining PPP- or GLS-driven NADPH/GSH supply, and concurrently delivering copper ionophores could reopen the cuproptotic trap in tumours. Validating such approaches in vivo, charting upstream regulators of FDX1 and mapping crosstalk between cuproptosis and other lethal programmes remain key steps toward exploiting this copper-centred vulnerability in cancer therapy.

BACKGROUND:Phosphatidylinositol 3-kinase catalytic subunit Alpha (PIK3CA) is closely correlated with colorectal cancer (CRC). However, the role of PIK3CA in colorectal cancer, particularly in non-metastatic disease, remains inconsistent. In this study, the clinicopathological significance of PIK3CA and its common exon mutations in non-mCRC was explored. METHODS:Data from 448 non‑mCRC patients were obtained from The Cancer Genome Atlas (TCGA), and from 655 non‑mCRC patients at our center. Associations of PIK3CA and its common exon mutations with clinicopathological features and overall survival (OS) were analyzed in non‑mCRC. RESULTS:In the TCGA cohort, the PIK3CA mutation rate was 26.3%, and mutations were associated with tumor site, TNM stage, and regional lymph node metastasis. Exon 9 mutations correlated with tumor site, while exon 20 mutations were linked to tumor site and lymph node metastasis. In our institutional cohort, the mutation rate was 7.8%, with PIK3CA and exon 20 mutations showing correlations with age, tumor site, TNM stage, and lymph node metastasis. However, neither in TCGA nor in our cohort were PIK3CA mutations or common exon mutations associated with overall survival (OS). CONCLUSION:PIK3CA mutation is correlated with age, tumor site, TNM stage, and regional lymph node metastasis in non-mCRC. However, PIK3CA and common exon mutations are not associated with OS in patients with non-mCRC.

Colorectal cancer (CRC) is the most common malignancy of the digestive system. Although research into the causes of CRC's origin and progression has advanced over the past few decades, many details are still not fully understood. Circular RNAs (circRNAs), as a novel regulatory molecule, have been found to be closely involved in various key biological processes in CRC. CircRNAs also have been shown to encode proteins, which could offer new possibilities for therapeutic applications. This ability to produce tumor-specific proteins makes circRNA-based vaccines a potentially valuable approach for targeted cancer treatment. In this review, we summarize recent findings on the various roles of circRNAs in CRC and explore their potential in the development of protein-encoding circRNA vaccines for CRC therapy.

Immune checkpoint blockade has led to breakthroughs in the treatment of advanced gastric cancer. However, the prominent heterogeneity in gastric cancer, notably the heterogeneity of the tumor microenvironment, highlights the idea that the antitumor response is a reflection of multifactorial interactions. Through transcriptomic analysis and dynamic plasma sample analysis, we identified a metabolic "face-off" mechanism within the tumor microenvironment, as shown by the dual prognostic significance of nicotinamide metabolism. Specifically, macrophages and fibroblasts expressing the rate-limiting enzymes nicotinamide phosphoribosyltransferase and nicotinamide N-methyltransferase, respectively, regulate the nicotinamide/1-methylnicotinamide ratio and CD8+ T cell function. Mechanistically, nicotinamide N-methyltransferase is transcriptionally activated by the NOTCH pathway transcription factor RBP-J and is further inhibited by macrophage-derived extracellular vesicles containing nicotinamide phosphoribosyltransferase via the SIRT1/NICD axis. Manipulating nicotinamide metabolism through autologous injection of extracellular vesicles restored CD8+ T cell cytotoxicity and the anti-PD-1 response in gastric cancer.

Abstract Aims HNF1B syndrome is caused by defects in the hepatocyte nuclear factor 1B (HNF1B) gene, which leads to maturity‐onset diabetes of the young type 5 and congenital organ malformations. This study aimed to identify a gene defect in a patient presenting with diabetes and severe diarrhea, while also analyzing the prevalence of hypomagnesemia and its correlation with the HNF1B genotype. Materials and Methods Whole exome sequencing was used to identify responsible point mutations and small indels in the proband and their family members. Multiplex ligation‐dependent probe amplification was carried out to identify HNF1B deletions. Furthermore, an analysis of published data on 539 cumulative HNF1B cases, from 29 literature sources, was carried out to determine the correlation between the HNF1B genotype and the phenotype of serum magnesium status. Results Using multiplex ligation‐dependent probe amplification, we identified a de novo heterozygous HNF1B deletion in the patient, who showed dorsal pancreas agenesis and multiple kidney cysts, as detected by magnetic resonance imaging. Magnesium supplementation effectively alleviated the symptoms of diarrhea. Hypomagnesemia was highly prevalent in 192 out of 354 (54.2%) patients with HNF1B syndrome. Compared with patients with intragenic mutations, those with HNF1B deletions were more likely to suffer from hypomagnesemia, with an odds ratio of 3.1 (95% confidence interval 1.8–5.4). Conclusions Hypomagnesemia is highly prevalent in individuals with HNF1B syndrome, and those with HNF1B deletion are more susceptible to developing hypomagnesemia compared with those with intragenic mutations. The genotype–phenotype associations in HNF1B syndrome have significant implications for endocrinologists in terms of genotype detection, treatment decisions and prognosis assessment.

Abstract Purpose Worldwide, colon cancer (CC) is one of the most commonly occurring malignancies. However, the molecular basis of the pathogenesis of CRC needs to be further explored. Studies have demonstrated that the chaperonin-containing TCP1 (CCT) complex contributes to the development and progression of various tumors. However, the functional significance of CCT in CC is unclear. Methods This study explored the potential functions of CCT family genes in CC by bioinformatics analysis. In addition, we established a risk score model based on the CCT family genes, which was validated to effectively predict the prognosis of CC patients. Results We found that CCTA6, one of the CCT family genes, was significantly more highly expressed in CC tissues than in normal tissues, and that increased expression of CCT6A was associated with a lower survival rate in CC patients. These findings were validated by real-world data. Conclusion Through the preliminary exploration of the role of CCT family genes in CC in this study, we found that CCT6A may contribute significantly in CC, and thus this gene may be an attractive therapeutic target for CC patients.

结直肠癌(colorectal cancer,CRC)是人类常见的恶性肿瘤之一,其发病率和死亡率呈逐年上升的趋势.在全球范围内,CRC发病率居恶性肿瘤第三位,死亡率居恶性肿瘤第二位[1];在我国,其发病率居恶性肿瘤第二位,是肿瘤相关死亡的第四个最常见原因[2].

Gastric cancer is the fifth most common cancer worldwide. With the development of immunotherapy, especially the application of immune checkpoint inhibitors (ICIs), the prognosis of advanced gastric cancer has improved. At present, ICIs combined with other therapies or dual ICI strategies in the treatment of advanced gastric cancer have shown clinical effectiveness and controllable safety. In addition, predictive biomarkers facilitate the precise selection of patients. Therefore, it is crucial to explore rational combinations and reliable predictive biomarkers for ICI therapy. This article reviews the recent advances in ICIs and relevant predictive biomarkers in the treatment of gastric cancer.

Background and objectives In patients with colorectal cancer and clinically suspected para-aortic lymph node metastasis, the survival benefit of para-aortic lymphadenectomy is unknown. We conducted a meta-analysis and systematic review to investigate it. Methods PubMed, Web of Science, and EMBASE were searched until January 2000 to April 2022 to identify studies reporting overall survivals, complication rates, and hazard ratios of prognostic factors in patients with colorectal cancer undergoing para-aortic lymphadenectomy, and those data were pooled. Results Twenty retrospective studies (1021 patients undergoing para-aortic lymphadenectomy) met the inclusion criteria. Meta-analysis indicates that participants undergoing para-aortic lymphadenectomy were associated with 5-year survival benefit, compared to those not receiving para-aortic lymphadenectomy (odds ratio = 3.73, 95% confidence interval: 2.05–6.78), but there was no significant difference in complication rate (odds ratio = 0.97, 95% confidence interval: 0.46–2.08). Further analysis of para-aortic lymphadenectomy group showed that 5-year survival of the positive group with pathologically para-aortic lymph node metastasis was lower than that of the negative group (odds ratio = 0.19, 95% confidence interval: 0.11–0.31). Moreover, complete resection (odds ratio = 5.26, 95% confidence interval: 2.02–13.69), para-aortic lymph node metastasis (≤4) (hazard ratio = 1.88, 95% confidence interval: 0.97–3.62), and medium-high differentiation (hazard ratio = 2.98, 95% confidence interval: 1.48–5.99) were protective factors for survival. Preoperative extra-retroperitoneal metastasis was associated with poorer relapse-free survival (hazard ratio = 1.85, 95% confidence interval: 1.10–3.10). Conclusion Para-aortic lymphadenectomy had promising clinical efficacy in prolonging survival rather than complication rate in patients with colorectal cancer and clinically diagnostic para-aortic lymph node metastasis. Further prospective studies should be performed. Trial registration PROSPERO: CRD42022379276.

Background: The incidence of early-onset colorectal cancer (EOCRC) has increased globally since the early 1990s. Comprehensively examining the risk factors would be helpful for risk stratification and the development of personalized colorectal cancer screening strategies. Methods: We performed a prospective study of the Chinese population aged 30-50 years to identify potential risk factors during a median follow-up of 9.1 years. We compared the distribution of demographic characteristics, lifestyle factors, dietary habits, and medical history among 222 EOCRC cases and 87,833 normal controls. Multivariate adjusted Cox hazard models were used for estimating EOCRC risks of each risk factor. Results: Our final analyses indicated that participants with a higher body mass index (HR, 1.04; 95% CI:1.00,1.08), regular alcohol consumption (HR, 1.69; 95% CI: 1.12, 2.91), higher intake of fish (HR, 1.64; 95% CI: 1.01, 2.67), hypertension (HR, 1.99; 95% CI: 1.04, 3.81), diabetes (HR, 2.20; 95% CI: 1.08, 4.49), and first-degree relatives with cancer (HR, 1.70; 95% CI: 1.23, 2.36) were at higher risk of EOCRC. Conclusion: We identified several modifiable as well as nonmodifiable risk factors, such as higher BMI, alcohol and fish consumption, hypertension, and diabetes, were associated with EOCRC.

目的 比较冷冻前和复苏后脐带血样本的造血功能,探讨冷冻袋附属小管是否可用于脐带血质量控制及移植供体发放前复核.方法 选取2009年3月—2021年2月在广州脐血库冻存的53份脐带血为研究对象,常规复温后,从冷冻袋和附属小管抽取样本,分为冷冻前、小管复苏和大袋复苏组.评价各组的总有核细胞(to-tal nucleated cells,TNCs)数、细胞活率、CD34阳性细胞数量、粒-巨噬细胞集落(colony-forming units-granulocyte/macrophages,CFU-GMs)数量、祖细胞集落(colony-forming units,CFUs)数量等质量参数.结果 小管复苏后TNCs数量、细胞活率、CFU-GMs数量及CFUs数量较冷冻前均显著减少,差异有统计学意义(P<0.05),而二者的CD34阳性细胞数量差异无统计学意义(P>0.05);大袋复苏后TNCs数量、细胞活率及CFUs数量较冷冻前各相应值比较,差异有统计学意义(P<0.05),而二者的CD34阳性细胞数量及CFU-GMs数量差异无统计学意义(P>0.05);小管复苏后的TNCs数量、细胞活率、CD34阳性细胞活率、CFU-GMs数量及CFUs数量较大袋复苏后的相应值均减少,差异有统计学意义(P<0.05),而二者的CD34阳性细胞数量差异无统计学意义(P>0.05).小管复苏与大袋复苏后的各项参数存在高度相关性.结论 附属小管在一定程度上可作为脐血库质量控制和产品发放前复核的取材.

The postoperative survival time and quality of life of patients with colon adenocarcinoma (COAD) varies widely. In order to make accurate decisions after surgery, clinicians need to distinguish patients with different prognostic trends. However, we still lack effective methods to predict the prognosis of COAD patients. Accumulated evidences indicated that the inhibition of peroxisome proliferator-activated receptors (PPARs) and a portion of their target genes were associated with the development of COAD. Our study found that the expression of several PPAR pathway-related genes were linked to the prognosis of COAD patients. Therefore, we developed a scoring system (named PPAR-Riskscore) that can predict patients' outcomes. PPAR-Riskscore was constructed by univariate Cox regression based on the expression of 4 genes (NR1D1, ILK, TNFRSF1A, and REN) in tumor tissues. Compared to typical TNM grading systems, PPAR-Riskscore has better predictive accuracy and sensitivity. The reliability of the system was tested on six external validation datasets. Furthermore, PPAR-Riskscore was able to evaluate the immune cell infiltration and chemotherapy sensitivity of each tumor sample. We also combined PPAR-Riskscore and clinical features to create a nomogram with greater clinical utility. The nomogram can help clinicians make precise treatment decisions regarding the possible long-term survival of patients after surgery.

Sarcopenia is an age-related accelerated loss of muscle strength and mass. Bone and muscle are closely related as they are physically adjacent, and bone can influence muscle. However, the temporal association between bone mineral density (BMD) and muscle mass in different regions of the body after adjustment for potential indicators and the mechanisms by which bone influences muscle in sarcopenia remain unclear. Therefore, this study aimed to explore the temporal association between muscle mass and BMD in different regions of the body and mechanisms by which bone regulates muscle in sarcopenia. Here, cross-lagged models were utilized to analyze the temporal association between BMD and muscle mass. We found that low-density lipoprotein (LDL-C) positively predicted appendicular lean mass. Mean whole-body BMD (WBTOT BMD), lumbar spine BMD (LS BMD), and pelvic BMD (PELV BMD) temporally and positively predicted appendicular lean mass, and appendicular lean mass temporally and positively predicted WBTOT BMD, LS BMD, and PELV BMD. Moreover, this study revealed that primary mice femur osteoblasts, but not primary mice skull osteoblasts, induced differentiation of C2C12 myoblasts through exosomes. Furthermore, the level of long noncoding RNA (lncRNA) taurine upregulated 1 (TUG1) was decreased, and the level of lncRNA differentiation antagonizing nonprotein coding RNA (DANCR) was increased in skull osteoblast–derived exosomes, the opposite of femur osteoblast–secreted exosomes. In addition, lncRNA TUG1 enhanced and lncRNA DANCR suppressed the differentiation of myoblasts through regulating the transcription of oxidative stress–related myogenin (Myog) gene by modifying the binding of myogenic factor 5 (Myf5) to the Myog gene promoter via affecting the nuclear translocation of Myf5. The results of the present study may provide novel diagnostic biomarkers and therapeutic targets for sarcopenia.

Objective:To investigate the clinical effect of dexmedetomidine combined with ultrasound-guided sacral canal block in the high ligation of laparoscopic hernia sac in children.Methods:90 cases of children undergoing laparoscopic high ligation of hernia sac in Lu’an People’s Hospital from January 2018 to December 2019 were prospectively included. All the children were divided into two groups by random number method. The conventional group received sacral block anesthesia with ropivacaine, and the combination group received sacral block anesthesia with dexmedetomidine plus ropivacaine. The operative time, recovery time、observation time in the resuscitation room and maintenance time of analgesia were compared between the two groups. Hemodynamics, including heart rate and mean arterial pressure, were compared between the two groups at pre-anesthesia (T1), post-sacral block (T2), dermectomy (T3), surgical completion (T4), tracheal catheter removal (T5), and 10 minutes after resuscitation (T6). The agitation of the two groups during the waking period was compared, including the incidence of agitation and the agitation score.Results:There were no significant differences in operation time, recovery time and observation time in recovery room between the two groups. The analgesia maintenance time in the conventional group was significantly shorter than that of the combination group (P<0.05). There were no significant differences in HR and MAP between the two groups at T1. HR of the combination group was significantly lower than that of the conventional group from T3 to T5 (P<0.05). MAP level in the combination group was lower than that of the conventional group at T5-T6 (P<0.05). The incidence of restlessness in the conventional group was 22.2%, which was significantly higher than that of the combination group (6.7%) (P<0.05). The agitation score of the combination group was significantly lower than that of the conventional group (P<0.05).Conclusion:The application of dexmedetomidine combined with ultrasound guided anesthesia in the high ligation of laparoscopic hernia sac in children can reduce the stress response of the body during the operation, maintain a more stable hemodynamic state, effectively reduce the occurrence of postoperative agitation during the recovery period, and improve the quality of the recovery period.

BACKGROUND:The purpose of the study was to evaluate whether KRAS mutation could be an independent prognostic biomarker in patients undergoing pulmonary metastasectomy (PM) for colorectal cancer (CRC).METHODS:A systemic review was performed by searching online databases to identify studies reporting overall survival (OS) and recurrence free survival (RFS) of CRC patients undergoing PM. Pooled HRs were calculated for OS and RFS.RESULTS:A total of 15233 patients from 60 studies were included. Pooled analysis showed that KRAS mutation was associated with worse OS (HR: 1.86, 95 % Cl: 1.35-2.57) and RFS (HR: 1.68, 95 % Cl: 1.38-2.04). A significant effect on OS and/or RFS was also shown by other 18 factors.CONCLUSIONS:This meta-analysis found that KRAS mutation is an important prognostic predictor for OS and RFS in CRC patients undergoing PM, supporting a comprehensive model including clinicopathological and biological factors for optimal patients selection and prognosis for surgical treatment.