BackgroundInvasive ductal carcinoma is a kind of very typical breast cancer. The goal of our research was to figure out the molecular mechanism of Invasive ductal carcinoma and to find out its potential therapy targets.ResultsThe total amount of 478 differentially expressed genes in Invasive ductal carcinoma which compared with normal breast epithelial cells were recognized. Functional enrichment analysis proved the most part of differentially expressed genes had connection with ECM-receptor interaction. The two genes lists were contrasted in PPI network, and miRNA regulation networks, The most two crucial genes were identified in our study, which may be helpful to improve Invasive ductal carcinoma treatment. Additionally, experimental results shows that the COL4A1 gene, one of identified genes, played important roles in both of proliferation and colony formation in Invasive ductal carcinoma.ConclusionsInvasive ductal carcinoma could have connection with ECM-receptor mutations. These 9 vital genes could be an important part in the progression of Invasive ductal carcinoma and be offered as therapy targets and prognosis indicator. and the experimental results showed that one of the most crucial genes, COL4A1, was the key gene that influence the proliferation and colony formation of the Invasive ductal carcinoma cell.

No abstract

The present study aimed to evaluate the effects of ulinastatin on the permeability and apoptosis of lipopolysaccharide (LPS)-induced cardiac microvascular endothelial cells (CMVECs), and investigate its molecular mechanisms in sepsis. The sepsis rat model was induced by cecal ligation and puncture (CLP), and rat CMVECs were isolated and treated with LPS or/and ulinastatin. Then, cell permeability was evaluated by transendothelial electrical resistance, reactive oxygen species (ROS) levels were assessed by 2,7-dichlorofluorescein diacetate, cell apoptosis was detected using Annexin V-FITC apoptosis detection kit, and the expression levels of Bcl-2, Bax, caspase-3, metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) and EZH2 were detected by RT-qPCR and/or western blotting. In addition, the relationship of MALAT1 and EZH2 was evaluated by RNA immunoprecipitation (RIP) assay and chromatin immunoprecipitation (ChIP) assay. Compared with LPS-induced CMVECs, treatment with ulinastatin significantly reduced CMVEC permeability and the percentage of apoptotic cells, as well as an increased level of Bcl-2 and inhibited the levels of ROS, caspase-3 and Bax (all p<0.05). In addition, long non-coding RNA (lncRNA) MALAT1 was confirmed to interact with EZH2 in CMVECs. Overexpression of lncRNA MALAT1 and EZH2 was found in the hearts of the sepsis rat and LPS-induced CMVECs, while ulinastatin inhibited the upregulation of lncRNA MALAT1 and EZH2 in the LPS-induced CMVECs (all p<0.05). Ulinastatin protected against LPS-induced CMVEC cell hyperpermeability and apoptosis via downregulation of lncRNA MALAT1 and EZH2 in sepsis.

Rationale: Pupil monitoring for neurologic examination has become a regular clinical practice during extracorporeal membrane oxygenation (ECMO) therapy. Sudden dilation of pupils always indicates a severe cerebrovascular event. However, bilateral dilated nonreactive pupils secondary to neuromuscular blockade are uncommon and widely ignored in adult acute respiratory distress syndrome (ARDS) patients. This is the first case report of bilateral dilated nonreactive pupils caused by rocuronium in an ARDS patient receiving ECMO treatment. Patient concerns: Bilateral dilated nonreactive pupils were found in an ARDS patient who received V-V ECMO therapy. However, CT angiography did not indicate the occurrence of a cerebrovascular event. Drugs that could potentially result in dilated nonreactive pupils were checked. Diagnosis: Bilateral dilated nonreactive pupils were caused by rocuronium infusion. Interventions: Rocuronium infusion was stopped. Outcomes: Bilateral dilated nonreactive pupils were resolved 20 h after rocuronium infusion was stopped. Lessons: Neuromuscular blockade should be taken into consideration when bilateral dilated nonreactive pupils are found in ARDS patients treated with ECMO therapy.

Aims The aim of this study was to investigate the effects of the aqueous extract of Nardostachys chinensis Batalin (NCBAE) on blood pressure and cardiac hypertrophy using two-kidney one-clip (2K1C) hypertensive rats. Methods 2K1C rat models were set up by clipping the left renal artery. Sham-operated rats underwent the same surgical procedure except for renal arterial clipping. 2K1C hypertensive rats were orally given NCBAE at doses of 210, 420, and 630 mg·kg−1·d−1 for 6 weeks. Twelve weeks after surgery, rat SBP and echocardiographic parameters were measured, cardiac histopathology was assessed, serum NO and LDH were detected, and the expression of Bcl-2 and caspase-3 of left ventricular tissue was assessed by western blot. Results Treatment with NCBAE resulted in a decrease of SBP, LVPWd, LVPWs, IVSd, IVSs, LVW/BW ratio, and cardiomyocyte CSA, an increase of LVEF, and inhibition of 2K1C-induced reduction in serum NO and elevation of LDH compared with 2K1C group. NCBAE intervention also showed a significant increase of Bcl-2 expression and reduction of cleaved caspase-3 level dose-dependently in left ventricular tissue. Conclusion Our data demonstrate that NCBAE has an antihypertensive property and protective effect on 2K1C-induced cardiac hypertrophy especially at the dose of 630 mg·kg−1·d−1.