Single-incision plus one-port laparoscopy surgery versus conventional multi-port laparoscopy surgery for colorectal cancer: a systematic review and meta-analysis.

OBJECTIVE: The efficacy of single-incision plus one-port laparoscopic surgery (SILS + 1) versus conventional laparoscopic surgery (CLS) for colorectal cancer treatment remains unclear. This study compares the short-term and long-term outcomes of SILS + 1 and CLS using a high-quality systematic review and meta-analysis. METHOD: Literature search followed the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines, drawing from PubMed, Embase, Web of Science, and the Cochrane Library until December 10, 2023. Statistical analysis was conducted using RevMan and Stata. RESULT: The review and meta-analysis included seven studies with 1740 colorectal cancer patients. Compared to CLS, SILS + 1 showed significant improvements in operation time (WMD = - 18.33, P < 0.00001), blood loss (WMD = - 21.31, P < 0.00001), incision length (WMD = - 2.07, P < 0.00001), time to first defecation (WMD = - 14.91, P = 0.009), time to oral intake (WMD = - 11.46, P = 0.04), and time to ambulation (WMD = - 11.52, P = 0.01). There were no significant differences in lymph node harvest, resection margins, complications, anastomotic leakage, hospital stay, disease-free survival, overall survival, and postoperative recurrence. CONCLUSIONS: Compared to CLS, SILS + 1 demonstrates superiority in shortening the surgical incision and promoting postoperative recovery. SILS + 1 can provide a safe and feasible alternative to CLS.

Boosted Mg-CO2 Batteries by Amine-Mediated CO2 Capture Chemistry and Mg2+ -Conducting Solid-electrolyte Interphases.

Mg-CO2 battery has been considered as an ideal system for energy conversion and CO2 fixation. However, its practical application is significantly limited by the poor reversibility and sluggish kinetics of CO2 cathode and Mg anode. Here, a new amine mediated chemistry strategy is proposed to realize a highly reversible and high-rate Mg-CO2 battery in conventional electrolyte. Judiciously combined experimental characterization and theoretical computation unveiled that the introduced amine could simultaneously modify the reactant state of CO2 and Mg2+ to accelerate CO2 cathodic reactions on the thermodynamic-kinetic levels and facilitate the formation of Mg2+ -conductive solid-electrolyte interphase (SEI) to enable highly reversible Mg anode. As a result, the Mg-CO2 battery exhibits boosted stable cyclability (70 cycles, more than 400 h at 200 mA g-1 ) and high-rate capability (from 100 to 2000 mA g-1 with 1.5 V overpotential) even at -15 °C. This work opens a newly promising avenue for advanced metal-CO2 batteries.

Strong Solvent and Dual Lithium Salts Enable Fast-Charging Lithium-Ion Batteries Operating from -78 to 60 °C.

Current lithium-ion batteries degrade under high rates and low temperatures due to the use of carbonate electrolytes with restricted Li+ conduction and sluggish Li+ desolvation. Herein, a strong solvent with dual lithium salts surmounts the thermodynamic limitations by regulating interactions among Li+ ions, anions, and solvents at the molecular level. Highly dissociated lithium bis(fluorosulfonyl)imide (LiFSI) in dimethyl sulfite (DMS) solvent with a favorable dielectric constant and melting point ensures rapid Li+ conduction while the high affinity between difluoro(oxalato)borate anions (DFOB-) and Li+ ions guarantees smooth Li+ desolvation within a wide temperature range. In the meantime, the ultrathin self-limited electrode/electrolyte interface and the electric double layer induced by DFOB- result in enhanced electrode compatibility. The as-formulated electrolyte enables stable cycles at high currents (41.3 mA cm-2) and a wide temperature range from -78 to 60 °C. The 1 Ah graphite||LiCoO2 (2 mAh cm-2) pouch cell achieves 80% reversible capacity at 2 C rate under -20 °C and 86% reversible capacity at 0.1 C rate under -50 °C. This work sheds new light on the electrolyte design with strong solvent and dual lithium salts and further facilitates the development of high-performance lithium-ion batteries operating under extreme conditions.

High-intensity mechanical bowel preparation before curative colorectal surgery is associated with poor long-term prognosis.

PURPOSE: Mechanical bowel preparation (MBP) has been widely used to reduce intestinal feces and bacteria and is considered necessary to prevent surgical infections. However, it is still controversial which intensity level of MBP is the most beneficial for patients before colorectal surgery. Our study aimed to determine the impact of different intensity levels of MBP on the progression-free survival (PFS) and overall survival (OS) for colorectal cancer (CRC) patients. METHODS: We evaluated 694 patients pathologically diagnosed with CRC and underwent MBP before surgery at 4 general hospitals from January 2011 to December 2015. The survival status of patients, the disease progression, and the time of death or progression were obtained through telephone follow-up at the deadline October 10, 2018. Hazard ratios were estimated by Cox proportional hazard models. Survival was assessed using the Kaplan-Meier method followed by the log-rank test. RESULTS: Of 694 patients included, 462 received low-intensity MBP and 232 received high-intensity MBP. A significantly higher PFS in low-intensity MBP was observed (p = 0.009). PFS at 2000 days was 69.331% in the low-intensity arm and 58.717% in the high-intensity arm. Patients who underwent low-intensity MBP also showed higher OS (p = 0.009). Nine patients in the low-intensity MBP group received secondary surgery, and two patients in the high-intensity MBP group received secondary surgery. CONCLUSIONS: In this retrospective cohort, low-intensity MBP was associated with better PFS and OS, which could provide a reference for doctors when choosing the intensity of MBP.

SNAI2/FTH1P3/miR-218-5p Positive Feedback Loop Promotes Colorectal Cancer Metastasis.

Colorectal cancer (CRC) is a type of intestinal cancer that causes more than 600,000 deaths every year. Overcoming the problems of metastasis requires detailed studies to reveal the potential molecular mechanisms. This study aims to reveal the molecular mechanism of CRC metastasis involving non-coding RNA regulation. The expression profile of FTH1P3 was analyzed based on the data of TCGA-COAD patient cohorts. Q-PCR analysis was performed to validate the expression of FTH1P3 in colorectal cancer cells. JASPR was used to screen transcription factors of FTH1P3. q-ChIP analysis was used to validate the target between FTH1P3 and transcription factor. Scratch assay and transwell assay were used to evaluate the migration and invasion ability of colorectal cancer cells. FTH1P3 is highly expressed in CRC patient cohort. FTH1P3 induced migration and invasion of SW480 cell through regulating epithelial-mesenchymal transition (EMT). In addition, FTH1P3 is a direct target of SNAI2. SNAI2 promotes the expression of FTH1P3. Both FTH1P3 and SNAI2 were directly targeted and repressed by miR-218-5p. Interestingly, ectopic FTH1P3 caused a decreased miR-218-5p level and an elevated nucleic SNAI2 protein expression level. Of note, only ectopic SNAI2 protein resulted in a repressed miR-218-5p and an increased FTH1P3, whereas SNAI2 3'UTR failed to affect the expression of miR-218-5p and FTH1P3. SNAI2 transcriptionally activates FTH1P3 expression. Both SNAI2 and FTH1P3 are targets of miR-218-5p. SNAI2/FTH1P3/miR-218-5p form a positive feedback loop in the regulation of CRC metastasis.

The prognostic importance of red blood cell distribution width for gastric cancer: a systematic review and meta-analysis.

Background: For cancer patients, red blood cell distribution width (RDW) is a readily accessible and cost-effective preoperative prognostic predictor. This study aimed to determine whether RDW is a predictive factor for individuals undergoing radical surgery for gastric cancer (GC). Methods: A literature search was performed to select relevant studies for inclusion in the subsequent meta-analysis. Relevant data were pooled to assess the association between RDW and GC results, including overall survival (OS), disease-free survival (DFS), and cancer-specific survival (CSS), as well as clinicopathological features. Results: The meta-analysis and systemic review included data from 8 studies comprising 1,587 individuals diagnosed with GC. In this context, RDW refers to the coefficient of variation of RDW (RDW-CV). A high level of RDW-CV was significantly associated with older age [odds ratio (OR) =2.25; 95% confidence interval (CI): 1.72-2.94; P<0.00001], larger tumor diameter (OR =1.90; 95% CI: 1.42-2.56; P<0.0001), and vascular invasion (OR =2.22; 95% CI: 1.10-4.49; P=0.03). After hazard ratios (HRs) and 95% CIs were pooled, RDW-CV was found to be an independent prognostic factor of OS (HR =1.79; 95% CI: 1.21-2.66; I2=85%; P=0.004), DFS (HR =1.81; 95% CI: 1.37-2.39; I2=0%; P<0.0001), and CSS (HR =2.73; 95% CI: 1.36-5.49; I2=0%; P=0.005) in patients with GC. Conclusions: The association between high levels of RDW-CV and poor survival in GC suggests that RDW-CV may be a viable prognostic indicator for patients with GC.

MBNL1­AS1 attenuates tumor cell proliferation by regulating the miR­29c­3p/BVES signal in colorectal cancer.

Dysregulation of long non­coding RNAs (lncRNAs) is involved in the development of colorectal cancer (CRC). In the present study, the identification of muscle blind like splicing regulator 1 antisense RNA 1 (MBNL1­AS1) lncRNA was reported. Firstly, Cell Counting Kit­8, EdU and colony formation assays were uesed to explore the role of MBNL1­AS1 in regulating the proliferation of CRC cells. According to TCGA database, it was found that MBNL1­AS1 was correlated with microRNA (miR)­29c­3p and blood vessel epicardial substance (BVES) expression in CRC cells. Then, the regulation among MBNL1­AS1, miR­29C­3P and BVES was detected by dual luciferase reporter assay and the function of MBNL1­AS1/miR­29C­3P/BVES axis was explored by rescue assay. The results demonstrated that MBNL1­AS1 expression was decreased in CRC and was associated with the size of tumors derived from patients with CRC. Functionally, the upregulation of MBNL1­AS1 suppressed CRC cell proliferation in vitro and inhibited tumor growth in vivo, while knockdown of MBNL1­AS1 expression caused the opposite effects. MBNL1­AS1 expression correlated with BVES expression in CRC tissues and MBNL1­AS1 enhanced the stability of BVES mRNA by functioning as a competing endogenous RNA to sponge miR­29c­3p; the latter directly targeted MBNL1­AS1 and BVES mRNA 3'UTR. Collectively, the results indicated that MBNL1­AS1 suppressed CRC cell proliferation by regulating miR­29c­3p/BVES signaling, suggesting that the MBNL1­AS1/miR­29c­3p/BVES axis may be a potential therapeutic target for CRC.

SDPR Inhibits TGF-ß Induced Cancer Metastasis Through Fatty Acid Oxidation Regulation in Gastric Cancer.

Our previous studies have confirmed that transforming growth factor-ß (TGF-ß) plays an important role in tumor metastasis, and the serum deprivation protein response (SDPR) is a potential downstream target of TGF-ß. However, the role and mechanism of SDPR in gastric cancer are still unclear. We performed gene microarray, bioinformation analysis, combined with in vivo and in vitro experimental verification, we identified that SDPR is significantly downregulated in gastric cancer, and participates in TGF-ß-mediated tumour metastasis. Mechanically, SDPR interacts with extracellular signal-regulated kinase (ERK) and inhibits fatty acid metabolism key gene Carnitine palmitoyl transferase 1A (CPT1A) at transcriptional level by supressing ERK/PPAR pathway. Our findings suggest that the TGF-ß/SDPR/CPT1A axis play an important role in the fatty acid oxidation of gastric cancer, and provides a new insight into the crosstalk of tumour microenvironments and metabolism reprogramming and suggest that strategies to intervene the fatty acid metabolism may therapy gastric cancer metastasis.

HES5 Activates Long Noncoding RNA UCA1 to Induce Colorectal Cancer Progression by Modulating miR-185/NOTCH3 Signaling.

Colorectal cancer (CRC) is one of the most common diagnosed cancers around the world. The poor prognosis and high fatality caused by metastasis are still the challenges for clinical treatment. Therefore, it is promising to clarify the detailed molecular mechanism of CRC metastasis. Accumulating evidences indicate that long noncoding RNAs (lncRNAs) play important roles in cancer progression including CRC. In this study, the function of lncRNA UCA1 was investigated. UCA1 was confirmed to be highly expressed in colorectal cancer. Moreover, the UCA1 expression level was positively related to tumor stages. Silencing UCA1 showed inhibitory effect on cell proliferation and metastasis. Both UCA1 and NOTCH3 were validated as direct targets of miR-185. Silencing UCA1 repressed NOTCH3 expression through the miR-185 sponge. NOTCH3 was found to be highly expressed in CRC patients and positively related to UCA1 expression. Furthermore, HES5 was verified as a transcription factor of UCA1, which induced UCA1 expression. In conclusion, UCA1 is a direct target of HES5. UCA1 promotes CRC metastasis through regulating the miR-185/NOTCH3 axis.

IL-34 Inhibits Acute Rejection of Rat Liver Transplantation by Inducing Kupffer Cell M2 Polarization.

BACKGROUND: Recent studies have demonstrated that IL-34 is implicated in the regulation of macrophage functions. However, the effect of IL-34 on Kupffer cells (KCs) in acute rejection (AR) of liver transplantation remains unclear. METHODS: IL-34 expression was detected in graft and serum from allotransplantation and syngeneic transplantation groups. The adeno-associated virus-expressing IL-34 was used to assess the effect of IL-34 on AR of rat liver transplantation. The effect of IL-34 on KC polarization was evaluated by in vitro and in vivo assays. Kupffer cells in donors were depleted by clodronate treatment before transplantation, and the nontreated KCs or lipopolysaccharide-treated KCs were transferred into recipients during liver transplantation. RESULTS: IL-34 expression levels in grafts and serum were decreased in the allotransplantation group compared with the syngeneic transplantation group. Adeno-associated virus-expressing IL-34 treatment induced KC M2 polarization in vivo and inhibited the AR of rat liver transplantation. Moreover, we found that IL-34 switched the phenotype of KCs from M1 to M2 by activating the PI3K/Akt pathway in vitro. In addition, the results of KC deletion and adaptive transfer experiments showed that the AR inhibition induced by IL-34 was M2 KC-dependent. CONCLUSIONS: IL-34 plays an important role in KC M2 polarization-dependent AR inhibition of rat liver transplantation.

Soluble fibrinogen-like protein 2 ameliorates acute rejection of liver transplantation in rat via inducing Kupffer cells M2 polarization.

Soluble fibrinogen-like protein 2 (sFGL2) could ameliorate acute rejection (AR) in rat cardiac transplantation. However, the role of sFGL2 in AR of liver transplantation has not been addressed. In this study, we found that FGL2 was upregulated in rat orthotropic liver transplantation (OLT) models of tolerance and positive correlation with the frequency of M2 Kupffer cells (KCs). Gain-of-function experiments in vitro showed that sFGL2 promoted the secretion of anti-inflammatory cytokines (IL-10, TGF-ß) and the expression of CD206, and inhibited the activities of STAT1 and NF-κB signaling pathway. Consistently, in vivo assays showed that adeno-associated virus-mediated FGL2 (AAV-FGL2) transfer to recipients could ameliorate AR of rat OLT and induce KCs M2 polarization in allografts. Notably, we found that the recipients receiving transferred KCs from AAV-FGL2-treated allograft showed alleviated AR. Taken together, we revealed that sFGL2 ameliorated AR by inducing KCs M2 polarization.