We further investigated the effects of N-HDL and H-HDL on the cell migration and invasion of MDA-MB-231 and MCF7 cell lines. It was shown that H-HDL promotes MDA-MB-231 and MCF7 cell migration and invasion while N-HDL was inhibitory. For MDA-MB-231 cells, the migration induced by H-HDL increased by 111.9% and 82.0% in the transwell migration assay and by 110.1% and 91.7% in the wound healing assay compared with N-HDL and control respectively (both at P P P P P
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Integrins are involved in hypochlorite-modified HDL-induced invasion and adhesion of breast cancer cells. We previously found integrin β1, integrin β2, integrin β3 and integrin αν play an important role in the in the adhesion of MDA-MB-231 and MCF7 cells to HUVEC and ECM by using blocking antibodies to intergrins [23]. In the present study, it was found that H-HDL induced elevated expression levels of integrin β1 (Figure 3A), integrin β2 (Figure 3B), integrin β3 (Figure 3C) and integrin αv (Figure 3D) compared with N-HDL on both the MDA-MB-231 and MCF7 cell surface. Specifically, for MDA-MB-231 cells, integrin β1 was increased by 26.4% and 16.6% respectively (both at P P P P P P P P P P P
The above data indicates that N-HDL has an elevated ability to promote breast cancer cells proliferation, migration, invasion and adhesion to both HUVEC and ECM compared with N-HDL in vitro. In order to determine if these effects also occur in vivo, we utilized a tail vein metastasis model and a mammary fat pad spontaneous metastasis model to check the metastasis ability of HDL-treated MCF7 cells in nude mice (Figure 6A). For the tail vein metastasis model, H-HDL significantly promoted both pulmonary and hepatic metastasis of MCF7 cells as was observed by an increase in the nodules on the lungs of H-HDL group by 164.3% and 117.6% as compared with that of N-HDL and control (both at P P P P P P
In our present study, we have utilized both an in vitro model system, using both hormone-independent (MDA-MB-231) and hormone-dependent (MCF7) cell lines, and an in vivo model utilizing both a metastasis model and a spontaneous metastasis model. The in vitro experiments demonstrate that hypochlorite-oxidized HDL can promote cell migration, invasion and adhesion to HUVEC and ECM. These studies also indicate that hypochlorite-oxidized HDL can induce higher cell surface expression of integrins and increased activity of PKC. Moreover, we observed that antibodies against integrins, PKC inhibitor (staurosporine), and siRNA targeted at PKC can inhibit hypochlorite-oxidized HDL induced breast cancer cell invasion and adhesion to HUVEC and ECM. In addition, integrins expression was regulated by PKC. The present data demonstrates that the increased capabilities of hypochlorite-oxidized HDL in promoting breast cancer cell invasion and adhesion to HUVEC and ECM is mainly due to the elevated PKC activity.
On the other hand, many factors such as age, gender, smoking, and sedentary lifestyle have correlated closely with CRP and systemic cytokine concentrations [54, 87, 88]. Furthermore, elevated CRP level may be associated with some pathological conditions and used as a marker for more severe conditions; e.g. high levels of CRP among patients with myocardial infarction may lead to left ventricular systolic dysfunction [89]. Sleep restriction was also correlated with cardiovascular diseases (CVD), because it was hypothesized to elevate CRP [90]. Likewise, obstructive sleep apnea was linked directly with the progression of CVDs, which has been associated significantly with high CRP levels and BMI [27].
When running winget without administrator privileges, some applications may require elevation to install. When the installer runs, Windows will prompt you to elevate. If you choose not to elevate, the application will fail to install.
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We identified 13 patients (male: 8, female: 5) during the time period of May 2003 to December 2007 with acute liver failure caused by cardiac failure (Figure 1). The mean age of the patients was 48.4 17.4 years. All patients suffered from cardiogenic shock at admission.
Fulminant hepatic failure caused by congestive heart failure has rarely been documented; furthermore the exact pathophysiology remains unclear. Seeto et al. [13] stated that systemic hypotension or shock alone did not lead to liver failure in any patient. The majority of patients in their study with liver failure had severe underlying cardiac disease that had often led to passive congestion of the liver. They conclude that right-sided heart failure resulting in hepatic venous congestion, may predispose the liver to hepatic injury induced by a hypotensive event. The most presumed causes of car diac induced ALF are hepatic congestion from venous hypertension and decreased oxygen delivery (DO) from a decreased CI [17]. Once DO underwent a critical threshold, hepatic hypoxia initiates a process that results in hemorrhage centrilobular necrosis [2]. Venous hypertension results in periventricular sinusoidal congestion, endothelial injury, replacement of hepatocytes with erythrocytes, and ultimatively, centrilobular necrosis [2, 6]. In our study patients fulfilled all criteria for cardiogenic shock with elevated CVP. Patients who survived and recovered from cardiogenic shock remained a high CVP, but showed an improvement in liver function. This led us to the conclusion that a low CI has more impact on the liver congestion than a high CVP. Indeed, a low CI induces a high CVP which ultimately may cause liver congestion. However, an association of liver failure with high CVP (> 10 mmHg) as a sign of volume overload but regular CI has never been reported.
The Doppler ultrasound pattern of reversed pulsatile flow (RPF) of the PV is strongly associated with high right atrial pressure (> 20 mmHg) [1, 12]. Tricuspid regurgitation is considered to be the main cause of RPF in patients with congestive heart failure, but the precise pathophysiological mechanism of the portal veins RPF remains unsolved. In our study the PV flow was only partially reversed, but with very severe impaired hepatopedal flow. After improvement of cardiac function the hepatopedal flow improved but remained pulsatile. A very similar RPV was reported in patients with a Budd-Chiari syndrome [16]. This syndrome leads to occlusion of the hepatic vein and/or inferior vena cava and therefore resembles the situation of elevated right atrial pressure. The venous outflow obstruction of the liver leads to increased portal vein and hepatic sinusoid pressures as the blood flow stagnates with total or partial RPV flow [3].
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