Comparison of postoperative complication rates between a novel endoluminal balloon-assisted drainage and diverting stoma after low rectal cancer.

AIM: To introduce a novel endo-luminal balloon-assisted drainage (EBAD) and compare postoperative complication rates between EBAD and diverting stoma (DS) groups. METHODS: The single center prospective non-random cohort study included a total of 163 patients in convenience patients with rectal cancer between January 2019 and January 2021. Out of 163 patients, 83 underwent DS and 80 EBAD. Primary endpoints were postoperative complication rate. RESULTS: The total number of complications was 28 in the DS group vs. 22 in the EBAD group (P = 0.388). 18 patients (21.7%) in the DS group and 14 patients (17.5%) in the EBAD group developed postoperative complication (P = 0.501). There were no differences identified for anastomotic leak rates between the two groups (P = 0.677). The rate of the pelvic abscess was lower in the EBAD group (1/80, 1.3%) than in the DS group (4/83, 4.8%) but with no statistical significance (P = 0.386). Compared with the DS group, the median operative time was shorter in the EBAD group (225 vs. 173.5 min, P < 0.001). Regarding incomplete small bowel obstruction, a higher prevalence was observed in the DS group compared to the EBAD group (7.2% vs 2.5%, P = 0.301). 7 patients (11.3%) in the DS group developed a para-stomal hernia, while no patient suffered a catheter-related complication. The median postoperative hospital stay was shorter in the DS groups than in the EBAD group (7 vs 8 days, P = 0.009). The median residence time of endo-luminal balloon-assisted drainage was 5.41 days. The median average and total volume of drainage were 51.57 ml/day and 255 ml, respectively. CONCLUSION: EBAD is feasible and safe with similar postoperative complications when compared with a DS. EBAD may replace DS after rectum resection.

Gene expression profiling of epithelial ovarian cancer reveals key genes and pathways associated with chemotherapy resistance.

The aim of this study is to analyze gene expression data to identify key genes and pathways associated with resistance to platinum-based chemotherapy in epithelial ovarian cancer (EOC) and to improve clinical treatment strategies. The gene expression data set was downloaded from Gene Expression Omnibus and included 12 chemotherapy-resistant EOC samples and 16 chemotherapy-sensitive EOC samples. A differential analysis was performed to screen out differentially expressed genes (DEGs). A functional enrichment analysis was conducted for the DEGs using the database for annotation, visualization, and integration discovery. A protein-protein interaction (PPI) network was constructed with information from the human protein reference database. Pathway-pathway interactions were determined with a test based on the hypergeometric distribution. A total of 1564 DEGs were identified in chemotherapy-sensitive EOC, including 654 upregulated genes and 910 downregulated genes. The top three upregulated genes were HIST1H3G, AKT3, and RTN3, while the top three downregulated genes were NBLA00301, TRIM62, and EPHA5. A Gene Ontology enrichment analysis showed that cell adhesion, biological adhesion, and intracellular signaling cascades were significantly enriched in the DEGs. A KEGG pathway enrichment analysis revealed that the calcium, mitogen-activated protein kinase, and B cell receptor signaling pathways were significantly over-represented in the DEGs. A PPI network containing 101 interactions was acquired. The top three hub genes were RAC1, CAV1, and BCL2. Five modules were identified from the PPI network. Taken together, these findings could advance the understanding of the molecular mechanisms underlying intrinsic chemotherapy resistance in EOC.

miR-125a-5p expression is associated with the age of breast cancer patients.

Dysregulated miR-125 observed in multiple cancer types has suggested that it is involved in malignant proliferation and invasion. However, the clinical significance of miR-125 in human breast cancer (BC) has not yet been fully elucidated. In the present study, the expression of miR-125a-5p/3p and miR-125b in 143 pairs of BC and normal adjacent tissues (NATs) was measured by real-time quantitative PCR, and the correlation between expression and clinicopathological features was explored. miR-125a-5p and miR-125b were significantly down-regulated in BC tissue samples compared with their matched NAT samples, while the difference in miR-125a-3p expression between BC tissues and NATs was not statistically significant. The expression level of miR-125a-5p was found to be significantly higher in younger patients (<35 years) than in older patients (≥35, P = 0.005). When the patients were divided into three groups according to age (<35, 36-48, and ≥48 years), a gradual reduction in miR-125a-5p expression was observed in BC tissue samples that correlated to increases in age (P = 0.009). There were no significant correlations between miR-125 expression and other clinicopathological features including tumor size, histological grade, hormone receptor status, Her-2 status, and lymph node metastasis. Taken together, these findings suggest that miR-125a-5p may play an important role in BC progression in an age-dependent manner, and that the down-regulation of miR-125a-5p and miR-125b may serve as independent predictors for breast cancer.

Vasoactive intestinal polypeptide suppresses proliferation of human cord blood-derived hematopoietic progenitor cells by increasing TNF-α and TGF-ß production in the liver.

The physiology of hepatic hematopoiesis is largely unknown, although studies have indicated that vasoactive intestinal polypeptide (VIP) is involved in this disease. To validate this hypothesis, we assessed the effects of VIP on human cord blood CD34+ cells. We also measured VIP levels and the capacity of vasoactive intestinal polypeptide receptor (VIPR) to bind to VIP in the rat liver during different developmental phases. VIP inhibited the proliferation of cord blood-derived CD34(+) cells from concentrations of 10-7-10-12 M. The highest suppression was achieved with 10-8 M VIP at day 10. Intracellular levels of tumor necrosis factor (TNF)-α and transforming growth factor (TGF)-ß1 in CD34(+) cells treated with VIP were increased by 50.70 and 43.46%, respectively. Variations in VIP levels in the rat fetal liver generally increased rapidly with the stage of fetal development. In addition, the affinity of VIPR for VIP increased from relatively low levels in the rat fetal liver and peaked at birth, after which it gradually decreased. VIP had a suppressive effect on the proliferation of human cord blood-derived CD34(+) cells, partially by increasing the production of TNF-α and TGF-ß. Low VIP levels in the fetal liver and gradually increasing levels after birth may in part be responsible for suppressing hematopoietic stem cell and progenitor proliferation in the liver.

Keloid microRNA expression analysis and the influence of miR-199a-5p on the proliferation of keloid fibroblasts.

The purpose of this study was to identify microRNAs (miRNAs) involved in keloid formation and determine their influence on the proliferation of keloid fibroblasts (KFs). Eight specimens each of resected keloid tissue and normal skin tissue were collected. miRNAs that are differentially expressed in keloid tissue and normal skin were detected using an miRNA microarray and verified by quantitative real-time polymerase chain reaction (RT-PCR). Seventeen differentially expressed miRNAs, including miR-199a-5p, were identified by microarray hybridization. qRT-PCR analysis confirmed the decrease in miR-199a-5p expression in keloid vs normal tissue that was detected by the microarray analysis. Mimics of differentially expressed miRNAs were then transfected into a KF cell line, and the effect of miRNA overexpression on the proliferation of KFs was assayed using the EdU assay. Compared with mock-transfected cells, KFs transfected with a miR-199a-5p mimic showed significantly lower cell proliferation and an altered cell cycle, with cells having significantly longer S and G2/M phases. The significantly lower expression of miRNA-199a-5p in keloids likely influences the cell cycle of KFs and restrains their proliferation, suggesting that miR-199a-5p probably plays a role in the regulation of KF proliferation.

Genetic and phylogenetic analyses of capsid protein gene in feline calicivirus isolates from Rio Grande do Sul in southern Brazil.

Feline calicivirus (FCV) is an important pathogen that affects domestic cats, inducing acute oral and upper respiratory tract clinical signs. The aim of this study was to analyze the variability of the capsid protein in different FCV isolates from southern Brazil. The sequencing analyses of thirteen Brazilian FCV samples, phylogenetic analyses and assessments of ten previously published sequences were conducted by examining the open reading frame 2 (ORF2, regions B-F). Comparisons of the predicted amino acid sequences of the ORF2 in Brazilian FCV isolates with those of the FCV-F9 strain indicated that the main differences are located within the regions C and hypervariable E (HVR_E). Epitopes that were mapped to the regions D, 5'HVR_E and conserved E also presented with some variability when compared to the strain F9. This is the first study describing sequence analyses and the phylogenetic relationships among FCV isolates from Brazil. The results presented here may expand upon current knowledge regarding aspects of FCV biology, epidemiology and genetic diversity and provide insights into improving the efficacies of current FCV vaccines.