To date, many studies have been conducted to find out the underlying mechanisms of hyperglycemia-induced complications in diabetes mellitus, attributed to the cellular pathologies of different cells-especially endothelial cells. However, there are still many ambiguities and unresolved issues to be clarified. Here, we investigated the alteration in biophysical and biochemical properties in human umbilical vein endothelial cells exposed to a high-glucose concentration (30mM), comparable to glucose content in type 2 diabetes mellitus, over a course of 120 hours. In addition to a reduction in the rate of cell viability and induction of oxidative stress orchestrated by the high-glucose condition, the dynamic of the fatty acid profile-including polyunsaturated, monounsaturated, and saturated fatty acids-was also altered in favor of saturated fatty acids. Genetic imbalances were also detected at chromosomal level in the cells exposed to the abnormal concentration of glucose after 120 hours. Moreover, the number of tip cells (CD31 /CD34 ) and in vitro tubulogenesis capability negatively diminished in comparison to parallel control groups. We found that diabetic hyperglycemia was associated with a decrease in the cell-cell tight junction and upregulation in vascular endothelial cadherin and zonula occludens (ZO)-1 molecules after 72 and 120 hours of exposure to the abnormal glucose concentration, which resulted in a profound reduction in transendothelial electrical resistance. The surface plasmon resonance analysis of the human umbilical vein endothelial cells immobilized on gold-coated sensor chips confirmed the loosening of the cell to cell intercellular junction as well as stable attachment of each cell to the basal surface. Our findings highlighted the disturbing effects of a diabetic hyperglycemia on either biochemical or biophysical properties of endothelial cells.
Background: In brain metastatic lesions, peritumoral edema assessed by advanced imaging modalities is reported to have infiltration by neoplastic cells; however, determining the tumor border is still inaccurately depicted even by applying such modalities. More importantly, the apparent diffusion coefficient (ADC) values of this area for predicting tumor-related characteristics such as diametric and morphologic characteristics of lesions, as well as their primary source, remain uncertain. Objectives: In the current study, we aimed at assessing the value of ADCs in both intratumoral and peritumoral areas to determine the metastatic brain tumor source and to predict the morphological characteristics of the tumor. Methods: This study was conducted on 80 biopsy-proven patients with brain metastasis and underwent magnetic resonance imaging (MRI) and diffusion-weighted imaging (DWI) examination. All tumor characteristics including the number and size of lesions, the origin of metastasis, the zone of metastasis, and the presence of necrosis or edema in the lesions were collected based on imaging. The origins of the metastasis were also determined. Results: The ADCmin and ADCmean values of the peritumoral area were strongly associated with the grade of edema in this area; however, none of the values could accurately predict the origin of metastasis. Determining the ADCmin and ADCmean in the intratumoral area could not be indicators for lesion characteristics such as size and location of the lesion, the presence of necrosis or edema, as well as the source of the metastatic tumor such as breast or lung. Similarly, the ADCmin and ADCmean in the peritumoral area could not be an effective predictor for determining the source of metastasis and also diameter, location, or necrotic nature of the tumor and only can predict the edematous pattern of the lesion. Conclusions: The ADC values in both intratumoral and peritumoral areas of the brain tumor metastatic lesion may not be predictive for the assessment of tumor morphology or its origin.
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