Objective Watanabe Heritable Hyperlipidaemic (WHHL) rabbits with low density lipoprotein receptor (LDLr) gene mutation have provided unprecedented opportunities for the study of human atherosclerosis, in order to confirm LDL receptor gene status in rabbits, we developed a simple PCR technique to detect LDL mutations in rabbits. Methods Rabbits genomic DNA were extracted from ear biopsy, and amplified by PCR to detect 12 bp deletion mutation in WHHL rabbits. PCR products were directly digested with BglⅠ, and then applied to polyacrylamide gel electrophoresis. Results PCR products from homozygous LDLr +/+ rabbits generated 2 bands of 212 and 94 bp after BglⅠ digestion, LDLr +/- rabbits generated 3 bands (294, 212, and 94 bp), LDLr -/- animals, however, generated only 1 product (294 bp). Conclusion This modified PCR method is simple and reliable.

By summarizing and analizing the relevant literature of modern special acupuncture method in clinic treating posttraumatic stress disorder (PTSD), this paper aims to provide a reference for acupuncture and moxibustion in the era of post epidemic situation. At present, there are four major specific acupuncture treatments which include: Anshen- Xingnao- Tiaoshen Method, Tongdu- Tiaoshen Method, Shugan- Tiaoshen Method, Wentong Method. Although there are some differences in diagnosis, treatment ideas, meridian and acupoint selection and operation methods, the diagnosis and treatment ideas are mainly focusing on regulating the spirit and soothing the liver. The rules of selecting meridians and acupoints are Nao-acupoints, soothing Liver-qi, regulating mind and strengthening the spleen and kidney. Electric acupuncture is used more offen, but pure acupuncture treatment is used more less.

OBJECTIVETo investigate the signaling pathways involved in β-arrestin1-induced proliferation of K562 cells.

METHODSWe established stable cell lines K562-siβ1 and K562-β1 by lentivirus-mediated β-arrestin1 knock-down or overexpression in K562 cells, with cells transfected with non-specific siRNA as the control (K562-Ctrl). The proliferation of these cells were evaluated by cell counting and CCK-8 assays. Western blotting was used to detect the expression of JNK and p-JNK in the cells, and co-immunoprecipitation (Co-IP) assay was employed to investigate the interaction between β-arrestin1 and Src.

RESULTSK562-β1 cells showed significantly greater but K562-siβ1 cells had significantly lower proliferation ability and cell survival rate than K562-Ctrl cells. Western blotting showed that β-arrestin1 specifically enhanced the expression of p-JNK, and the JNK inhibitor SP600125 obviously suppressed p-JNK and cell proliferation of K562 cells. Co-IP assay revealed the binding of β-arrestin1 to Src.

CONCLUSIONSIn K562 cells, β-arrestin1 activates JNK signaling pathway by binding to Src to promote the cell proliferation.

Arrestins ; metabolism ; Cell Proliferation ; Cell Survival ; Humans ; K562 Cells ; Leukemia, Myelogenous, Chronic, BCR-ABL Positive ; metabolism ; MAP Kinase Signaling System ; RNA, Small Interfering ; beta-Arrestins