Cigarette smoking is a well-known risk factor in the development and progression of malignant diseases. Nicotine, the major constituent in cigarette smoke, has also shown negative effects on stem cells. Mesenchymal stem cells (MSCs) have been widely demonstrated to migrate into tumors and play key roles in cancer progression. However, the mechanisms by which nicotine impacts MSCs and tumorigenesis of lung cancer are still undetermined. In this study we investigated the effects of nicotine on human umbilical cord mesenchymal stem cells (hUC-MSCs) and the impacts of nicotine-treated hUC-MSCs on tumor formation and progression. We found that nicotine has a toxic effect on hUC-MSCs and changes the morphology, inhibits proliferation and promotes apoptosis of hUC-MSCs in a dose-dependent manner. Nicotine-treated hUC-MSCs produce higher level of IL-6. Moreover, nicotine promotes migration, stemness and epithelial-mesenchymal transition (EMT) of hUC-MSCs by inhibiting E-cadherin expression and upregulating mesenchymal markers such as N-cadherin and Vimentin, leading to the induction of stem cell markers Sox2, Nanog, Sall4, Oct4 and CD44. Migration and proliferation of non-small cell lung cancer A549 cells and breast cancer MCF-7 cells are promoted after their coculture with nicotine-treated hUC-MSCs in a cell-cell contact-independent manner. Furthermore, nicotine-treated hUC-MSCs promote tumor formation and growth of A549 cells in nude mice. These studies demonstrated that the enhanced stemness and EMT of hUC-MSCs induced by nicotine are critical for the development of tobacco-related cancers.
Mechanical ventilation support is commonly required in abdominal compartment syndrome (ACS). In the present study, pressure-regulated volume control ventilation (PRVCV) was compared to pressure control ventilation (PCV) in patients with ACS. The prospective study included 40 patients with ACS who were randomized into the PCV or PRVCV groups and subjected to the different modes of ventilation. After 6 h of ventilation, arterial blood gas, respiratory mechanics and hemodynamics parameters, as well as the intra-abdominal pressure (IAP) and Sequential Organ Failure Assessment (SOFA) scores were calculated. Compared to the PCV mode, mechanical ventilation with PRVCV lead to a significant decrease in the partial pressure of carbon dioxide, the peak inspiratory pressure, the mean inspiratory pressure, the central venous pressure, the heart rate and the extravascular lung water index. In addition, a marked improvement in pH, partial pressure of oxygen, oxygenation index and pulmonary static compliance was noted. However, no significant differences in airway resistance, mean arterial pressure, or IAP and SOFA scores were obtained. In conclusion, the PRVCV mode is better than the PCV mode in ventilation patients with ACS, and should therefore be used as a lung protective strategy. The present study was registered at Chictr.org (no. ChiCTR1800016869).
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