Search

Background: Low anterior resection syndrome (LARS) severely impairs patient postoperative quality of life, especially major LARS. However, there are few tools that can accurately predict major LARS in clinical practice., Aim: To develop a machine learning model using preoperative and intraoperative factors for predicting major LARS following laparoscopic surgery of rectal cancer in Chinese populations., Methods: Clinical data and follow-up information of patients who received laparoscopic anterior resection for rectal cancer from two medical centers (one discovery cohort and one external validation cohort) were included in this retrospective study. For the discovery cohort, the machine learning prediction algorithms were developed and internally validated. In the external validation cohort, we evaluated the trained model using various performance metrics. Further, the clinical utility of the model was tested by decision curve analysis., Results: Overall, 1651 patients were included in the present study. Anastomotic height, neoadjuvant therapy, diverting stoma, body mass index, clinical stage, specimen length, tumor size, and age were the risk factors associated with major LARS. They were used to construct the machine learning model to predict major LARS. The trained random forest (RF) model performed with an area under the curve of 0.852 and a sensitivity of 0.795 (95%CI: 0.681-0.877), a specificity of 0.758 (95%CI: 0.671-0.828), and Brier score of 0.166 in the external validation set. Compared to the previous preoperative LARS score model, the current model exhibited superior predictive performance in predicting major LARS in our cohort (accuracy of 0.772 for the RF model vs 0.355 for the preoperative LARS score model)., Conclusion: We developed and validated a robust tool for predicting major LARS. This model could potentially be used in the clinic to identify patients with a high risk of developing major LARS and then improve the quality of life., Competing Interests: Conflict-of-interest statement: All the authors report having no relevant conflicts of interest for this article., (©The Author(s) 2023. Published by Baishideng Publishing Group Inc. All rights reserved.)

Helicobacter pylori , a Gram-negative microaerobic bacteria belonging to the phylum Proteobacteria, can colonize in the stomach and duodenum, and cause a series of gastrointestinal diseases such as gastritis, gastric ulcer and even gastric cancer. At present, the high diversity of the microorganisms in the stomach has been confirmed with culture-independent methods; some researchers have also studied the stomach microbiota composition at different stages of H. pylori carcinogenesis. Here, we mainly review the possible role of H. pylori -mediated microbiota changes in the occurrence and development of gastric cancer to provide new ideas for preventing H. pylori infection and regulating microecological imbalance.

Background: Anastomotic leakage (AL) is a fatal complication in patients with rectal cancer after undergoing anterior resection. However, the role of abdominal composition in the development of AL has not been studied., Aim: To investigate the relationship between abdominal composition and AL in rectal cancer patients after undergoing anterior resection., Methods: A retrospective case-matched cohort study was conducted. Complete data for 78 patients with AL were acquired and this cohort was defined as the AL group. The controls were matched for the same sex and body mass index (± 1 kg/m 2 ). Parameters related to abdominal composition including visceral fat area (VFA), subcutaneous fat area (SFA), subcutaneous fat thickness (SFT), skeletal muscle area (SMA), skeletal muscle index (SMI), abdominal circumference (AC), anterior to posterior diameter of abdominal cavity (APD), and transverse diameter of abdominal cavity (TD) were evaluated based on computed tomography (CT) images using the following Hounsfield Unit (HU) thresholds: SFA: -190 to -30, SMA: -29 to 150, and VFA: -150 to -20. The significance of abdominal composition-related parameters was quantified using feature importance analysis; an artificial intelligence method was used to evaluate the contribution of each included variable., Results: Two thousand two hundred and thirty-eight rectal cancer patients who underwent anterior resection from 2010 to 2020 in a large academic hospital were investigated. Finally, 156 cases were enrolled in the study. Patients in the AL group showed longer operative time (225.03 ± 55.29 vs 207.17 ± 40.80, P = 0.023), lower levels of preoperative hemoglobin (123.32 ± 21.17 vs 132.60 ±1 6.31, P = 0.003) and albumin (38.34 ± 4.01 vs 40.52 ± 3.97, P = 0.001), larger tumor size (4.07 ± 1.36 vs 2.76 ± 1.28, P < 0.001), and later cancer stage ( P < 0.001) compared to the controls. Patients who developed AL exhibited a larger VFA (125.68 ± 73.59 vs 97.03 ± 57.66, P = 0.008) and a smaller APD (77.30 ± 23.23 vs 92.09 ± 26.40, P < 0.001) and TD (22.90 ± 2.23 vs 24.21 ± 2.90, P = 0.002) compared to their matched controls. Feature importance analysis revealed that TD, APD, and VFA were the three most important abdominal composition-related features., Conclusion: AL patients have a higher visceral fat content and a narrower abdominal structure compared to matched controls., Competing Interests: Conflict-of-interest statement: The authors declare no conflict of interest for this article., (©The Author(s) 2022. Published by Baishideng Publishing Group Inc. All rights reserved.)

In recent years, with the acceleration of life rhythm and the increase of social competition, the incidence of obesity and depression has been increasing, which has seriously affected the quality of life and health of people. Obesity and depression, two seemingly unrelated physical and psychological diseases, in fact, are closely related: obese people are more likely to have depression than nonobese ones. We have reviewed and analyzed the relevant research literature and found that the inflammatory response plays a key role in obesity-induced depression. This article will discuss in detail the inflammatory mechanisms by which obesity induces depression., Competing Interests: No potential conflict of interest was reported by the authors., (Copyright © 2020 Shu-Lin Shao et al.)

4-Coumaric acid: coenzyme A ligase (4CL) is a key enzyme in the phenylpropanoid metabolic pathway that regulates the biosynthesis of lignin and flavonoids. Therefore, the study of 4CL is important to explore the accumulation and regulation of metabolites. This study investigated the role that the 4CL2 gene from Dryopteris fragrans (Df4CL2) plays in the metabolite synthesis. Changes in gene expression, enzyme activity, and the content of lignin and flavonoids were measured in different tissues of tobacco as model plant that was successfully transferred with Df4CL2. Tobacco plants with Df4CL2 (transgenic tobacco, TT) were successfully obtained via the Agrobacterium-transformation method. This TT tended to be thicker and had an earlier flowering period than wild type tobacco (WT). The expression levels of Df4CL2 were higher in the stem, leaf, and root in TT compared to WT. In addition, compared to WT, TT had higher 4CL enzyme activity and higher lignin and flavonoids contents. This suggests that Df4CL2 is involved in the synthesis of lignin and flavonoids in D. fragrans. This research provides important evidence toward understanding the phenylpropanoid metabolic pathway in ferns.

Autophagy is a catabolic biological process in the body. By targeting exogenous microorganisms and aged intracellular proteins and organelles and sending them to the lysosome for phagocytosis and degradation, autophagy contributes to energy recycling. When cells are stimulated by exogenous pathogenic microorganisms such as viruses, activation or inhibition of autophagy is often triggered. As autophagy has antiviral effects, many viruses may escape and resist the process by encoding viral proteins. At the same time, viruses can also use autophagy to enhance their replication or increase the persistence of latent infections. Here, we give a brief overview of autophagy and DNA viruses and comprehensively review the known interactions between human and animal DNA viruses and autophagy and the role and mechanisms of autophagy in viral DNA replication and DNA virus-induced innate and acquired immunity.

Prostate cancer (PCa) is the most frequently diagnosed malignancy in men and its incidence has increased rapidly worldwide. Notably, the molecular mechanisms underlying prostate tumorigenesis have not been fully identified. The levels of microRNA (miR)-381 have been explored in numerous types of malignancy; however, the expression levels and biological function of miR-381 in PCa remain largely unknown. In the present study, reverse-transcription polymerase chain reaction was used to detect the expression levels of miR-381 in PCa cells and normal prostate epithelial cells. Subsequently, miR-381 antisense oligonucleotides and mimics were transfected into LNCaP PCa cells. Bioinformatics analysis was performed to identify the potential target genes of miR-381. Protein expression analysis, dual-luciferase reporter assay and a rescue assay were used to confirm the target of miR-381. The data suggested that the expression levels of miR-381 were significantly decreased in PCa cells compared with in normal prostatic epithelial cells. Furthermore, transfection of LNCaP cells with miR-381 mimics suppressed their proliferation, migration and invasion. In addition, bioinformatics analysis suggested that the androgen receptor (AR) was a target gene of miR-381. miR-381 suppressed the expression levels of AR by directly binding to its 3'-untranslated region. Furthermore, transfection with an AR plasmid partially attenuated miR-381-induced inhibition of cell proliferation, migration and invasion. The results of the present study suggested that miR-381 may act as a tumor suppressor in PCa by directly targeting the AR.

Background: Prostate cancer is the most common cancer in men in the United States. Fucoidan is a bioactive polysaccharide extracted mainly from algae. The aim of this study was to investigate anti-tumor and anti-angiogenic effects of fucoidan in both cell-based assays and mouse xenograft model, as well as to clarify possible role of JAK-STAT3 pathway in the protection., Methods: DU-145 human prostate cancer cells were treated with 100-1000 μg/mL of fucoidan. Cell viability, proliferation, migration and tube formation were studied using MTT, EdU, Transwell and Matrigel assays, respectively. Athymic nude mice were subcutaneously injected with DU-145 cells to induce xenograft model, and treated by oral gavage with 20 mg/kg of fucoidan for 28 days. Tumor volume and weight were recorded. Vascular density in tumor tissue was determined by hemoglobin assay and endothelium biomarker analysis. Protein expression and phosphorylation of JAK and STAT3 were determined by Western blot. Activation of gene promoters was investigated by chromatin Immunoprecipitation., Results: Fucoidan could dose-dependently inhibit cell viability and proliferation of DU-145 cells. Besides, fucoidan also inhibited cell migration in Transwell and tube formation in Matrigel. In animal study, 28-day treatment of fucoidan significantly hindered the tumor growth and inhibited angiogenesis, with decreased hemoglobin content and reduced mRNA expression of CD31 and CD105 in tumor tissue. Furthermore, phosphorylated JAK and STAT3 in tumor tissue were both reduced after fucoidan treatment, and promoter activation of STAT3-regulated genes, such as VEGF, Bcl-xL and Cyclin D1, was also significantly reduced after treatment., Conclusions: All these findings provided novel complementary and alternative strategies to treat prostate cancer.

Objective: Solute carrier family 39, member 14 (SLC39A14), has been identified as a potential biomarker for various cancers. However, its roles in prostate cancer (PCa) are still unclear. The aim of this study was to investigate the clinical significance of SLC39A14 in patients with PCa and its functions in malignant phenotypes of PCa cells., Patients and Methods: Subcellular localization and expression pattern of SLC39A14 protein were examined by immunohistochemistry. Then, the associations of SLC39A14 expression with various clinicopathological features and clinical outcome of patients with PCa were statistically evaluated. Subsequently, the effects of SLC39A14 overexpression and knockdown on PCa cell proliferation and motility were, respectively, examined by Cell Counting Kit-8, transwell, and wound-healing assays., Results: The immunoreactive scores of SLC39A14 protein in human PCa tissues were significantly lower than those in normal prostate tissues. Based on the Taylor dataset, SLC39A14 downregulation occurred more frequently in patients with PCa with a higher Gleason score (P<0.001), advanced clinical stage (P=0.008), presence of metastasis (P=0.009), and prostate-specific antigen failure (P=0.006). More interestingly, the survival analysis identified SLC39A14 as an independent factor for predicting the biochemical recurrence-free survival of patients with PCa (P=0.017). Functionally, the enforced expression of SLC39A14 could suppress cell proliferation, invasion, and migration of PCa cell lines in vitro, which could be reversed by the knockdown of SLC39A14., Conclusion: Decreased expression of SLC39A14 may lead to malignant phenotypes of PCa cells and aggressive tumor progression in patients with PCa. Importantly, SLC39A14 may function as a tumor suppressor and a biomarker for screening patients with biochemical recurrence following radical prostatectomy.

Up-regulation of multidrug resistance-associated protein 1 (MRP1) is regarded as one of the main causes for multidrug resistance (MDR) of tumor cells, leading to failure of chemotherapy-based treatment for a multitude of cancers. However, whether silencing the overexpressed MRP1 is sufficient to reverse MDR has yet to be validated. This study demonstrated that RNAi-based knockdown of MRP1 reversed the increased efflux ability and MDR efficiently. Two different short haipin RNAs (shRNAs) targeting MRP1 were designed and inserted into pSilence- 2.1-neo. The shRNA recombinant plasmids were transfected into cis-dichlorodiamineplatinum-resistant A549 lung (A549/DDP) cells, and then shRNA expressing cell clones were collected and maintained. Real time PCR and immunofluorescence staining for MRP1 revealed a high silent efficiency of these two shRNAs. Functionally, shRNA-expressing cells showed increased rhodamine 123 retention in A549/DDP cells, indicating reduced efflux ability of tumor cells in the absence of MRP1. Consistently, MRP1-silent cells exhibited decreased resistance to 3- (4, 5-dimethylthiazol-2-yl)-2, 5-diphenyltetrazolium bromide (MTT) and DDP, suggesting reversal of MDR in these tumor cells. Specifically, MRP1 knockdown increased the DDP-induced apoptosis of A549/DDP cells by increased trapping of their cell cycling in the G2 stage. Taken together, this study demonstrated that RNAi- based silencing of MRP1 is sufficient to reverse MDR in tumor cells, shedding light on possible novel clinical treatment of cancers.

Objective: To investigate the impact of gender on outcomes in patients with non-ST segment elevation acute coronary syndrome undergoing intervention treatment., Methods: In a multi-center randomized trial, the patients diagnosed as non-ST segment elevation acute coronary syndrome were randomly assigned to undergo early intervention (coronary angiography ≤ 24 h after randomization) or delayed intervention (coronary angiography ≥ 36 h after randomization). The primary outcome was a composite of death, myocardial infarction or stroke at 180 days. The secondary outcomes were death, myocardial infarction, refractory ischemia, stroke or revascularization at 180 days., Results: Among 815 patients (545 males, 270 females), the incidences of primary and secondary outcome were equivalent for both genders (P > 0.05). Males of the early intervention group had a greater incidence of the primary outcome (7.1% vs 14.8%, P = 0.00). The secondary outcome was a composite of death, myocardial infarction or refractory ischemia occurring in 12.5% of males in early intervention group and 21.2% in delayed intervention group. Significant difference existed (P = 0.00). The incidence of another secondary outcome as a composite of death, myocardial infarction, refractory ischemia, stroke or revascularization was equivalent for males in early intervention group and delayed intervention group (26.8% vs 32.4%, P > 0.05). The incidences of primary outcome (12.6% vs 14.3%, P > 0.05) and secondary outcome (18.5% vs 23.5% P > 0.05; 28.5% vs 27.7% P > 0.05) were equivalent for females in early intervention group and delayed intervention group (P > 0.05)., Conclusion: Patients with non-ST segment elevation acute coronary syndrome undergoing intervention demonstrate no significant gender differences in efficacy and safety. Early intervention reduces the rate of myocardial infarction for males, but it is not superior to delayed intervention for females.