Objective We explored the relationship between urinary incontinence (UI) and depression or anxiety. Methods We searched the Cochrane Library, Embase, and PubMed for articles on the association between depression, anxiety, and UI. We calculated pooled 95% confidence intervals (CIs) and odds ratios (ORs). Results Twelve articles (31,462 participants) were included. The UI group had significantly higher depression and anxiety levels than the non-UI group (OR = 1.73, 95%CI: 1.64–1.82, I2 = 75.5%). In subgroup analysis, depression and anxiety were significantly higher in participants with UI than in those without UI (OR = 1.95, 95%CI: 1.82–2.10, I2 = 64.3% and OR = 1.54, 95%CI: 1.43–1.65, I2 = 59.2%, respectively).  In subgroup analysis by age, participants with UI had significantly higher depression and anxiety, regardless of age, than the non-UI group (OR = 1.59, 95%CI: 1.29–1.95, I2 = 59.1% and OR = 1.98, 95%CI: 1.62–2.43, I2 = 75.5%, respectively). Conclusion Patients with UI had significantly higher depression and anxiety levels than those without UI. Depression and anxiety were higher in patients with UI than in those without UI, regardless of age. Larger sample sizes and more high-quality studies are needed to validate our findings.

BackgroundThe omentum is one of the initial sites for peritoneal metastasis because it possesses milky spots that provide a microenvironment for cancer cells to readily migrate and grow into micrometastases. This study investigated the role of the CCL22-CCR4 axis in gastric cancer cells selectively infiltrating into milky spots.MethodsGastric cancer MFC cells labelled with DiI were injected intraperitoneally into strain 615 mice. The mice were euthanised at specified intervals and the omentum was excised for immunohistochemistry. The effects of CCL22 on the proliferation and migration of MFCs were assessed by MTT and trans-well assays. RT-PCR and Western blot analysis detected CCR4 mRNA and protein expression levels in MFCs. Immunohistochemistry was used to analyse CCL22 and CCR4 expression in the milky spot micrometastases.ResultsTwo weeks after intraperitoneal injection, the milky spot areas were completely occupied by proliferating gastric cancer cells and cell cluster-type micrometastases were observed. In contrast, cancer cells formed single cell-type micrometastases in the non-milky spot areas. MFCs expressed CCR4, which was localised on the cell surface and or in the cytoplasm. Different concentrations of CCL22 significantly increased the proliferation ability of MFCs. Additionally, concentrations of CCL22 between 10–100 ng/ml significantly increased the migration of MFCs. Within omental milky spots, CCL22 was localised mainly on the cell surface and or in the cytoplasm. Within sections of omental milky spot micrometastases, CCR4 was recognised on or in gastric cancer cells, constituent cells milky spots, blood cells and blood endothelial cells.ConclusionsOmental milky spots are a congenial microenvironment for peritoneal free gastric cancer cells to migrate, survive, and establish cell cluster-type metastases. The CCL22-CCR4 axis contributes to this selective infiltration process.

GSC has a particular pattern in lymph node metastasis and organs invasion. Surgical resection is considered an effective therapeutic strategy for GSC.

The incidence of lymph node MM in patients with node negative early gastric cancer was 21.3%, and cancer cell cluster type of MM proved a primary independent prognostic factor for pN0 early gastric cancer patients.

As a novel multifaceted player in cancer, Pentraxin3(PTX3) was recognized to be a possible factor related with tumor development. Recent researches have indicated that PTX3 is involved in immune response, inflammation, as well as cancer, and is greatly controlled by numerous cytokines. Tumor necrosis factor (TNF-α) is an imperative cytokine that demonstrates an extensive array of biological consequences in gastric cancer advancement. Here, we inspected the expression of PTX3 in gastric carcinoma tissues along with gastric cell lines and established that PTX3 was suggestively inferior in gastric cancer tissue and cells. The treatment of the gastric cell lines BGC-823 as well as SGC-7901 with rhTNF-α caused substantial decrease in the expression of PTX3. Furthermore, PTX3 controlled the capability of cell migration, invasion as well as epithelial-mesenchymal transition (EMT) in gastric cancer cell lines mediated by TNF-α. Additionally, PTX3 upregulation inhibited tumorigenicity in vivo and could be reversed by exogenous TNF-α. Conversely, overexpression of PTX3 inhibited progress both in vitro as well as in vivo in gastric cancer mediated by TNF-α. Further studies are necessary to demonstrate the mechanism of interaction between PTX3 and cytokines.