Bennedsenmcknight0910

We aimed to investigate the effects of epidermal growth factor-like domain 7 (EGFL7) on breast cancer cell proliferation and angiogenesis and its association with the p38 mitogen-activated protein kinase (p38MAPK) signaling pathway.

The vectors for stable overexpression of EGFL7 and the vectors for EGFL7 knockout were constructed. The breast cancer cell line MDA-MB-231 was selected for this study and the cells were divided into four groups the control group, the empty vector group (transfected with an empty vector), the EGFL7 overexpression group (transfected with the EGFL7 overexpression vector), and the EGFL7 knockout group (transfected with the EGFL7 knockout vector). After 72 h of transfection, the mRNA and protein levels of EGFL7 in the cells were detected by RT-PCR and Western blot, respectively. The cell proliferation rates at 12 h, 24 h, 48 h and 72 h of culture in each group were detected using the MTT method. An

tumor angiogenesis model of tumor-endothelial cells co-culture system was establiGF, p38MAPK, and p-p38MAPK were lower in the EGFL7 knockout group and higher in the EGFL7 overexpression group, respectively (all P<0.05). After the cells overexpressing EGFL7 were treated with SB203580, the level of p-p38MAPK was deceased, and the protein expression level of VEGF was inversely related with the SB203580 concentration (F=44.24, P<0.01).

EGFL7 can promote the proliferation of breast cancer cells and angiogenesis, and the mechanism may be associated with the activation of p38MAPK signaling pathway and promotion of VEGF expression.

EGFL7 can promote the proliferation of breast cancer cells and angiogenesis, and the mechanism may be associated with the activation of p38MAPK signaling pathway and promotion of VEGF expression.

To investigate the effect of C1orf63 on breast cancer cell (BCC) proliferation, apoptosis, and cycle distribution and related mechanisms.

The expression of C1orf63 was interfered with in BCC line MCF and cells were divided into a C1orf63 overexpression group, C1orf63 silence group, blank group, and empty group. The mRNA expression of C1orf63 and the proliferation, apoptosis, and cycle distribution of BCCs were detected. The mRNA expression levels of NF-κB signaling pathway factors (p-IκBα, CyclinD1, CDK4, Bcl-2, and Bax) in each group were also detected.

There was no significant difference between the blank group and empty group in the expression level of C1orf63 mRNA, cell proliferation rate, apoptosis rate, cell distribution rate, or mRNA expression levels of the NF-κB signaling pathway factors (all P>0.05). The expression levels of C1orf63 mRNA in the C1orf63 silenced group were lower than those in the other two groups (P<0.05). The cell proliferation rate, cell distribution in S phase and G2/M phase, and the mRNA expression levels of NF-κB signaling pathway factors (p-IκBα, CyclinD1, CDK4, and Bcl-2) in the C1orf63 silenced group at each time point were lower than those in the other two groups (all P<0.05). The apoptosis rate, cells in G1 phase, and the Bax mRNA expression level in C1orf63 silenced group at each time point were higher than those in the other two groups (all P<0.05).

Down-regulation of C1orf63 acts on the NF-κB signaling pathway to regulate the expression of p-IκBα, CyclinD1, and CDK4, so as to inhibit BCC proliferation, promote cell apoptosis, and block the cell cycle.

Down-regulation of C1orf63 acts on the NF-κB signaling pathway to regulate the expression of p-IκBα, CyclinD1, and CDK4, so as to inhibit BCC proliferation, promote cell apoptosis, and block the cell cycle.

This study was designed to analyze the clinical efficacy of ceftazidime combined with levofloxacin on heart failure complicated with pulmonary infection and its influence on cardiopulmonary function.

A total of 124 patients with heart failure and pulmonary infection admitted to our hospital from June 2018 to October 2019 were divided into groups according to different treatment schemes. Thereinto, 60 patients who were given ceftazidime intravenous drip on the basis of routine treatment were included in group A, and 64 who were given levofloxacin hydrochloride injection based on intravenous drip in group A were included in group B. The clinical efficacy, cardiac and lung function, pathogenic bacteria, infection, immune indexes and adverse reactions before and after treatment were compared.

After treatment, the adjusted levels of LVEF, LVEDD and LA in group B after treatment were greater than those in group A (P<0.05); the levels of MMV, TLC and FEV1 in group B were increased more than those in group A (P<0.05). After treatment, the levels of BNP, PCT and CRP in groups A and B decreased compared with those before treatment (P<0.05). Furthermore, the down-regulated levels of BNP, PCT and CRP in group B were higher than those in group A after treatment (P<0.05). After treatment, the levels of serum CD3

, CD4

, CD4

/CD8

in group B increased more and CD8

decreased more. The clinical efficacy of group B after 7 days was higher than that of group A (P<0.01). Patients were followed up for one month, and there was no marked difference in their adverse drug reaction rates (P>0.05).

To sum up, ceftazidime combined with levofloxacin on patients with heart failure and pulmonary infection can improve the immune function while optimizing the clinical efficacy and cardiopulmonary function.

To sum up, ceftazidime combined with levofloxacin on patients with heart failure and pulmonary infection can improve the immune function while optimizing the clinical efficacy and cardiopulmonary function.

To investigate the value of the combined detection of lactate dehydrogenase (LDH), β2-transferrin (β-2Tf), and interleukin-10 (IL-10) for identification of acute intracranial infections such as meningitis.

A total of 103 patients were placed in the suppurative meningitis group (SMG), 124 patients in the viral meningitis group (VMG). Another 86 patients without any infectious diseases of the central nervous system constituted the control group (CG). see more The levels of LDH and β-2Tf in the cerebrospinal fluid were determined by enzymatic methods; IL-10 expression was measured by ELISA. The correlation between infection and the LDH, β-2Tf, and IL-10 levels was analyzed by linear correlation analysis, and ROC curve analysis was applied to determine the diagnostic value of combined detection of LDH, β-2Tf, and IL-10 levels for intracranial infections.

LDH, β-2Tf, and IL-10 levels negatively correlated with the treatment time in both the SMG (r = -0.52, -0.97, and -0.24, respectively, P < 0.01) and VMG (r = -0.