Corrosion Characteristics of Rolling Oil on the Rolled Copper Foil.

Static corrosion experiments were carried out to investigate the corrosion of each kind of component in the rolling oil on the rolled copper foil. The surface morphology and chemical composition of corrosion products were detected by a digital camera, scanning electron microscope (SEM), energy dispersive spectrometer (EDS) and X-ray photoelectron spectroscopy (XPS). The results showed that the maximum corrosion rate of rolled copper foil in the base stock and friction modifiers (butyl stearate and dodecanol) was close to zero, while that of rolled copper foil in the N-containing borate, phosphate and the fully formulated rolling oil were 0.17, 1.12 and 0.78 mm/a, respectively. The color of rolled copper foil changing from pink into purple-black when corroded in the N-containing borate. The composition of it was mainly CuO and Cu2O with some N-containing borate adsorbed on it. However, the color and composition of the corroded copper foil in the phosphate were similar to that of the original copper foil. It was complicated for the corroded copper foil in the fully formulated rolling oil, which showed characteristics both in the N-containing borate and in the phosphate according to different positions. It indicated that there might be little corrosion for the base stock and friction modifiers on the rolled copper foil. It might mainly be extreme pressure additives (N-containing borate and phosphate) that caused the corrosion of rolled copper foil. There might be competition between N-containing borate and phosphate for the corrosion of rolled copper foil in the fully formulated rolling oil, resulting in a lower corrosion rate compared with that in the phosphate.

Reverting doxorubicin resistance in colon cancer by targeting a key signaling protein, steroid receptor coactivator.

Although there have been notable improvements in treatments against cancer, further research is required. In colon cancer, nearly all patients eventually experience drug resistance and stop responding to the approved drugs, making treatment difficult. Steroid receptor coactivator (SRC) is an oncogenic nuclear receptor coactivator that serves an important role in drug resistance. The present study generated a doxorubicin-resistant colon cancer cell line, in which the upregulation/activation of SRC was responsible for drug resistance, which in turn activated AKT. Overexpression of receptor tyrosine kinase-like epidermal growth factor receptor and insulin-like growth factor 1 receptor also induced SRC expression. It was observed that doxorubicin resistance in colon cancer also induced epithelial to mesenchymal transition, a decrease in expression of epithelial marker E-cadherin and an increase in the expression of mesenchymal markers, including N-cadherin and vimentin. Additionally, the present study indicated that SRC acts as a common signaling node, and inhibiting SRC in combination with doxorubicin treatment in doxorubicin-resistant cells aids in reversing the resistance. Thus, the present study suggests that activation of SRC is responsible for doxorubicin resistance in colon cancer. However, further research is required to understand the complete mechanism of how drug resistance occurs and how it may be tackled to treat patients.

Clinical efficacy of Yangxueqingnao granule improve cerebral small vessel disease cognitive impairment / 中国基层医药

Objective To explore the effect of Yangxueqingnao granule in treatment of cerebral small vessel disease (SVD)patients with mild cognitive dysfunction (MCI).Methods 52 patients with SVD related MCI were selected.They were treated with Yangxueqingnao granule,each 4.0 g,3 times a day,3 months for a course of treat-ment.Montreal cognitive scale (MoCA),simple mental state scale (MMSE)and event related potential (P300)were detected before and after treatment,and the clinical effect was observed.Results After a course of treatment by Yan-gxueqingnao granule,the cognitive function and memory of 52 patients were improved to some extent.In addition to the attention of an MoCA meter to a foreign project[Visual space:before taking the medicine (2.92 ±0.26)points,after taking the medicine (3.25 ±0.66)points;Named:before taking the medicine (2.26 ±0.70)points,after taking the medicine(2.92 ±0.49)points;Language:before taking the medicine (1.47 ±0.70)points,after taking the medicine (2.17 ±0.98)points;Abstraction:before taking the medicine (0.45 ±0.38)points,after taking the medicine (0.68 ±0.63)points;Delayed recall:before taking the medicine (1.67 ±0.74)points,after taking the medicine (2.52 ±1.50)points;Directional:before taking the medicine (4.73 ±0.35 )points,after taking the medicine (5.52 ±0.57)points ]and total score[Before taking the medicine (18.75 ±0.66)points,after taking the medicine (19.12 ±1.45)points],the differences were statistically significant (the total score:t =7.56,P =0.000;Visual space:t =5.86,P =0.002;Named:t =5.42,P =0.000;Be careful:t =1.23,P =0.121;Language:t =4.52,P =0.000;Abstraction:t =2.65,P =0.001;Delayed memory:t =7.96,P =0.000).While the total score of MMSE scale [before taking the medicine (25.36 ±1.89)points,after taking the medicine (28.53 ±2.91 )points],memory [before taking the medicine (2.64 ±0.42)points,after taking the medicine (2.75 ±0.53)points]and recall [before taking the medicine (1.52 ±0.48)points,after taking the medicine (1.98 ±0.78)points ],the differences were statistically significant(the total score:t =2.78,Memory:t =1.95,Recall:t =3.43,all P <0.05).P300 before and after treatment[before taking the medicine P300 latency of (389 ±21)ms,after taking the medicine P300 latency of (341 ±18)ms)],the difference was significant (t =12.514,P <0.001).Conclusion Yangxueqingnao granule had therapeutic effect in patients with SVD -MCI.

Dimethyl Sulfoxide Suppresses Mouse 4T1 Breast Cancer Growth by Modulating Tumor-Associated Macrophage Differentiation / 한국유방암학회지

PURPOSE: The universal organic solvent dimethyl sulfoxide (DMSO) can be used as a differentiation inducer of many cancer cells and has been widely used as a solvent in laboratories. However, its effects on breast cancer cells are not well understood. The aim of this study is to investigate the effect and associated mechanisms of DMSO on mouse breast cancer. METHODS: We applied DMSO to observe the effect on tumors in a mouse breast cancer model. Tumor-associated macrophages (TAMs) were tested by flow cytometry. Ex vivo tumor microenvironment was imitated by 4T1 cultured cell conditioned medium. Enzyme-linked immunosorbent assays were performed to detect interleukin (IL)-10 and IL-12 expression in medium. To investigate the cytotoxicity of DMSO on TAMs, 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assays were performed. RESULTS: We found that DMSO produced tumor retardation when injected into mouse peritoneal cavities in a certain concentration range (0.5-1.0 mg/g). Furthermore, as detected by flow cytometry, TAM subtypes were found to be transformed. We further imitated a tumor microenvironment in vitro by using 4T1 cultured cell conditioned medium. Similarly, by using low concentration DMSO (1.0%-2.0% v/v), TAMs were induced to polarize to the classically activated macrophage (M1-type) and inhibited from polarizing into the alternatively activated macrophage (M2-type) in the conditioned medium. IL-10 expression in tumors was reduced, while IL-12 was increased compared with the control. Furthermore, we reported that 2.0% (v/v) DMSO could lead to cytotoxicity in peritoneal macrophages after 48 hours in MTT assays. CONCLUSION: Our findings suggest that DMSO could exert antitumor effects in 4T1 cancer-bearing mice by reversing TAM orientation and polarization from M2- to M1-type TAMs. These data may provide novel insight into studying breast cancer immunotherapy.

Pirarubicin inhibits multidrug-resistant osteosarcoma cell proliferation through induction of G2/M phase cell cycle arrest.

AIM: Pirarubicin (THP) is recently found to be effective in treating patients with advanced, relapsed or recurrent high-grade osteosarcoma. In this study, the effects of THP on the multidrug-resistant (MDR) osteosarcoma cells were assessed, and the underlying mechanisms for the disruption of cell cycle kinetics by THP were explored. METHODS: Human osteosarcoma cell line MG63 and human MDR osteosarcoma cell line MG63/DOX were tested. The cytotoxicity of drugs was examined using a cell proliferation assay with the Cell Counting Kit-8 (CCK-8). The distribution of cells across the cell cycle was determined with flow cytometry. The expression of cell cycle-regulated genes cyclin B1 and Cdc2 (CDK1), and the phosphorylated Cdc2 and Cdc25C was examined using Western blot analyses. RESULTS: MG63/DOX cells were highly resistant to doxorubicin (ADM) and gemcitabine (GEM), but were sensitive or lowly resistant to THP, methotrexate (MTX) and cisplatin (DDP). Treatment of MG63/DOX cells with THP (200-1000 ng/mL) inhibited the cell proliferation in time- and concentration-dependent manners. THP (50-500 ng/mL) induced MG63/DOX cell cycle arrest at the G(2)/M phase in time- and concentration-dependent manners. Furthermore, the treatment of MG63/DOX cells with THP (200-1000 ng/mL) downregulated cyclin B1 expression, and decreased the phosphorylated Cdc2 at Thr(161). Conversely, the treatment increased the phosphorylated Cdc2 at Thr(14)/Tyr(15) and Cdc25C at Ser(216), which led to a decrease in Cdc2-cyclin B1 activity. CONCLUSION: The cytotoxicity of THP to MG63/DOX cells may be in part due to its ability to arrest cell cycle progression at the G(2)/M phase, which supports the use of THP for managing patients with MDR osteosarcoma.