ABSTRACT
To investigate the correlation between the coefficient of variation of blood pressure and cognitive dysfunction in patients with hypertension complicated by cerebral small vessel disease. 415 patients with hypertension complicated by cerebral small vessel disease who received treatment in our hospital from January 2019 to June 2022 were retrospectively included in this study. These patients were divided into a cognitive dysfunction group (n = 74) and a non-cognitive dysfunction group (n = 341) according to whether they had cognitive dysfunction. Blood pressure and general data were recorded for each patient. The logistic regression coefficient was used to analyze the correlation between coefficient of variation of blood pressure and cognitive dysfunction in patients with hypertension complicated by cerebral small vessel disease. Multivariate logistic regression analysis showed that age, the weighted standard deviation of 24-hour systolic blood pressure (24hSBP-wSD), cholesterol level, and triglyceride level were risk factors for cognitive dysfunction in patients with hypertension complicated by cerebral small vessel disease (P < 0.05). The risk for cognitive dysfunction was increased by 3.532-fold in patients aged>65 years, increased by 1.203-fold in patients with a 24hSBP-wSD of 14.9-15.9%, and increased by 3.033-fold in patients with a 24hSBP-wSD>16.0% (P < 0.05). The coefficient of variation of blood pressure is markedly correlated with the risk for cognitive dysfunction; and a higher coefficient of variation of blood pressure leads to a higher risk for cognitive dysfunction in patients with hypertension complicated by cerebral small vessel disease.
ABSTRACT
The epithelialtomesenchymal transition (EMT) has been noted as a critical event in the early step of cancer metastasis. Recent studies showed that nuclear transcription factor caudal type homeobox transcription factor 2 (CDX2) is a prognostic factor, which acts as a marker of good outcome in gastric cancer (GC) patients. However, the association between CDX2 expression and EMT has remained to be fully elucidated. The present study reported that forced overexpression of CDX2 in MKN45/CDX2 cells inhibited GCcell growth and proliferation, and attenuated migration and invasion in vitro. Furthermore, MKN45/CDX2 cells exhibited a significant upregulation of Ecadherin protein and a significant downregulation of vimentin protein expression. These results were further supported by in vivo tumorigenicity assays, which showed that CDX2 suppressed gastric tumor xenograft growth and inhibited EMT in nude mice. These results indicated that CDX2 is capable of inhibiting GCcell growth and invasion. CDX2 may participate in the process of EMT of GC cells by regulating the expression of the epithelial and mesenchymal proteins Ecadherin and vimentin.