A Performance-enhanced Electroosmotic Pump with Track-etched Polycarbonate Membrane by Allylhydridopolycarbosilane Coating.

Nanochannel plastic membranes are excellent materials for electroosmotic pump (EOP) elements owing to their surface charge properties, flexibility and cost-effectiveness. However, the surface charge properties of plastics are inferior to those of silicate-based materials. This paper reports a performance-enhanced EOP equipped with a glassified track-etch polycarbonate membrane (PC), which has a nanochannel surface covered by allylhydridopolycarbosilane (AHPCS). The effects of applied voltage, pH and membrane pore size on the electroosmotic flow velocity, along with a comparative study of the EOP with coated and pure membranes were investigated. It was found that when low DC voltage (10 - 40 V) was applied to both ends of the pump, the magnitude of the electroosmotic flow was linearly proportional to the voltage when the pore size of the membrane was less than 600 nm. A higher flow rate was obtained with larger pore size membranes. Compared with the uncoated film, the coated one showed faster electroosmosis velocity, with higher stability under the same conditions. For pH 10.0 buffer solution, a flow rate of 89.13 µL/min was obtained in the modified membrane-based EOP with excellent repeatability and durability, while the flow rate was only 37.89 µL/min in the bare PC membrane under 20 V. In order to demonstrate the performance of the developed EOP, the EOP was used for microcomplexometric titration to determine actual tap water hardness. The measured results were highly consistent with the results of a conventional complexometric titration methed. The EOP with an AHPCS-coated plastic membrane expanded the application range to harsh condition solutions, such as high-concentration acids or bases.

Apatinib with EGFR-TKIs in advanced wild gene-type NSCLC: A case report.

RATIONALE: For advanced non-small-cell lung cancer (NSCLC), targeted therapy and chemoradiotherapy are recommended as the first-line treatment. For patients with a performance status (PS) score over 2 and without gene mutation, however, only supportive treatment is provided and survival time is extremely short. We believe that more can be done to improve the patient's survival time and their quality of life. PATIENT CONCERNS AND DIAGNOSES: A 65-year-old female came to our hospital due to "cough and pain and lack of movement in the left leg". The diagnosis was advanced wild gene-type lung adenocarcinoma and PS score over 2. INTERVENTIONS AND OUTCOMES: She was treated in our clinic with apatinib and erlotinib and has had no progression of the disease for 15.4 months. Except for the presence of hand-foot syndrome and diarrhea, no other serious adverse reactions were seen. LESSONS: For patients in poor physical condition and unacceptable of chemo-radiotherapy, apatinib combined with an epidermal growth factor receptor tyrosine kinase inhibitor (EGFR-TKI) is a safe and effective therapeutic method for advanced wild gene-type NCSCL.

miR302a inhibits the proliferation of esophageal cancer cells through the MAPK and PI3K/Akt signaling pathways.

MicroRNAs (miRNAs/miRs) are involved in the regulation of various types of cancer, either as oncogenes or tumor suppressors. miR302a has been reported that it could suppress tumor cell proliferation by inhibiting Akt in prostate cancer. The present study examined the effect of miR302a on proliferation and invasion in esophageal cancer cell lines. The expression levels of miR302a in esophageal cancer cell lines was determined by reverse transcription-polymerase chain reaction. Subsequently, miR302a mimics were transfected into esophageal cancer cells, and cell viability and invasion were assessed by MTT and Transwell assays. In addition, the effects of miR302a on the mitogen-activated protein kinase (MAPK) and phosphoinositide 3-kinase (PI3K)/protein kinase B (Akt) signaling pathways were investigated by western blot analysis. The results revealed that miR302a expression was significantly decreased in the esophageal cancer cell lines compared with a healthy esophagus epithelium cell line. Upregulation of miR302a inhibited the proliferation and invasion of esophageal cancer cells, and decreased the phosphorylation of extracellular signal-regulated kinase 1/2 and Akt. Taken together, the results of the present study indicated that miR302a overexpression inhibited the proliferation and invasion of esophageal cancer cells through suppression of the MAPK and PI3K/Akt signaling pathways, indicating the potential value of miR302a as a treatment target for human esophageal cancer.