Objective To explore the potential mechanisms of carcinogenesis for human eukaryotic translation elongation factor 1 alpha 2(EEF1A2).Methods Specific inhibition of EEF1A2 with siRNA was achieved in human pancreatic cancer cell line,BxPC-3,which usually expresses high level of EEF1A2.The changes of EEF1A2 expression were determined by Western blot.The effect of siRNA in suppressing the proliferation of BxPC-3 cells was determined by MTT assay,and its role in inducing BxPC-3 cell apoptosis evaluated by flow cytometry,TUNEL and transmission electron micro- scope.Results The sequence-specific siRNA effectively suppressed the expression of both EEF1A2 mRNA and protein.Specific inhibition of EEF1A2 with siRNA in pancreatic cancer cell line BxPC-3 could suppress proliferation and induce apoptosis.Conclusion The oncogenicity of EEF1A2 may be related to its role in suppressing the apoptosis and promoting the growth of pancreatic cancer cells.

In countries and regions with high vaccination coverage, several vaccine-preventable diseases have been resurged in recent years, such as measles, varicella, pertussis and mumps. Some studies have found that the clinical manifestation and epidemiological characteristics of these diseases were different from those in pre-vaccine era. This article reviewed the clinical and epidemiological features of vaccine-preventable diseases before and after wide immunization implementation, focusing on the situation in China, in order to attract the attention of clinicians, raise awareness, strengthen prevention and control, and promote in-depth research for these diseases.
Chickenpox ; China ; Humans ; Measles ; Mumps ; Vaccination ; Vaccines

Porous calcium polyphosphate (CPP) has shown promise of tissue engineered implant application because of the biocompatibility and biodegradation. CPP with different polymerization degree were prepared by controlling the calcining time, and its polymerization degree could be calculated by developed method in this paper. Different crystal types CPP were prepared by quenching from the melt and crystallization of amorphous CPP. From the in vitro degradation, carried out in Tris-HCl buffer, the degradation velocity of CPP was controllable. The weight loss of CPP with different polymerization degrees and crystal types were different. With the increasing of polymerization degree, the weight loss during the degradation was decreasing, contrarily the strength of CPP was increasing. The amorphous CPP could degrade completely in 17 days while gamma-CPP do completely in 25 days. The degradation velocity beta-CPP and alpha-CPP was slower than gamma-CPP and the weight loss was about 12% and 5% respectively. The results of this study indicate that CPP have potential applications for bone tissue engineering as inorganic polymeric biomaterials.
Absorbable Implants ; Biocompatible Materials ; chemistry ; Bone Substitutes ; chemistry ; Calcium Phosphates ; chemistry ; Humans ; Tissue Engineering

OBJECTIVETo investigate the protective effects of terpenes from fructus corni (TFC) on diabetic cardiomyopathy (DCM).

METHODSDiabetes was produced by a single injection of alloxan (220 mg/kg, i.p.) in mice. The fasting blood glucose of mice were tested 15 days later and that greater than 13.9 mmol/L were regarded as the diabetic mice which were divided randomly into the model and TFC groups. TFC dissolved by physiological saline (P.O, 80 mg/kg) was administrated to the TFC group for successive 8 weeks since the 15th day.

RESULTSCompared to the control group, the weight index increased significantly. The level of superoxide dismutase (SOD) was markedly decreased and malondialdehyde(MDA), the inflammatory factors (TNF-alpha, IL-6) were obviously increased in myocardium. The histopathological examination suggested that myocardial cells disarranged, swelling and the intercellular space increased in model group. It also showed the infiltration of inflammatory cells and fibroblasts in TFC group. The above change was improved significantly.

CONCLUSIONTFC ameliorated the alterations of cardiomyopathy in diabetic mice induced by alloxan. the mechanism might be related to decrease blood glucose, antioxidative stress and inflammatory factors.

Alloxan ; adverse effects ; Animals ; Cornus ; chemistry ; Diabetic Cardiomyopathies ; chemically induced ; metabolism ; prevention & control ; Interleukin-6 ; metabolism ; Male ; Malondialdehyde ; metabolism ; Mice ; Mice, Inbred Strains ; Oxidative Stress ; drug effects ; Superoxide Dismutase ; metabolism ; Terpenes ; pharmacology ; therapeutic use ; Tumor Necrosis Factor-alpha ; metabolism

Skeletal muscle is the largest tissue in the human body, and it plays a major role in exerting force and maintaining metabolism homeostasis. The role of muscle transcription factors in the regulation of metabolism is not fully understood. MondoA is a glucose-sensing transcription factor that is highly expressed in skeletal muscle. Previous studies suggest that MondoA can influence systemic metabolism homeostasis. However, the function of MondoA in the skeletal muscle remains unclear.

We generated muscle-specific MondoA knockout (MAKO) mice and analyzed the skeletal muscle morphology and glycogen content. Along with skeletal muscle from MAKO mice, C2C12 myocytes transfected with small interfering RNA against MondoA were also used to investigate the role and potential mechanism of MondoA in the development and glycogen metabolism of skeletal muscle.

MAKO caused muscle fiber atrophy, reduced the proportion of type II fibers compared to type I fibers, and increased the muscle glycogen level. MondoA knockdown inhibited myoblast proliferation, migration, and differentiation by inhibiting the phosphatase and tensin homolog (PTEN)/phosphoinositide 3-kinase (PI3K)/Akt pathway. Further mechanistic experiments revealed that the increased muscle glycogen in MAKO mice was caused by thioredoxin-interacting protein (TXNIP) downregulation, which led to upregulation of glucose transporter 4 (GLUT4), potentially increasing glucose uptake.

MondoA appears to mediate mouse myofiber development, and MondoA decreases the muscle glycogen level. The findings indicate the potential function of MondoA in skeletal muscle, linking the glucose-related transcription factor to myogenesis and skeletal myofiber glycogen metabolism.

Skeletal muscle is the largest tissue in the human body, and it plays a major role in exerting force and maintaining metabolism homeostasis. The role of muscle transcription factors in the regulation of metabolism is not fully understood. MondoA is a glucose-sensing transcription factor that is highly expressed in skeletal muscle. Previous studies suggest that MondoA can influence systemic metabolism homeostasis. However, the function of MondoA in the skeletal muscle remains unclear.

We generated muscle-specific MondoA knockout (MAKO) mice and analyzed the skeletal muscle morphology and glycogen content. Along with skeletal muscle from MAKO mice, C2C12 myocytes transfected with small interfering RNA against MondoA were also used to investigate the role and potential mechanism of MondoA in the development and glycogen metabolism of skeletal muscle.

MAKO caused muscle fiber atrophy, reduced the proportion of type II fibers compared to type I fibers, and increased the muscle glycogen level. MondoA knockdown inhibited myoblast proliferation, migration, and differentiation by inhibiting the phosphatase and tensin homolog (PTEN)/phosphoinositide 3-kinase (PI3K)/Akt pathway. Further mechanistic experiments revealed that the increased muscle glycogen in MAKO mice was caused by thioredoxin-interacting protein (TXNIP) downregulation, which led to upregulation of glucose transporter 4 (GLUT4), potentially increasing glucose uptake.

MondoA appears to mediate mouse myofiber development, and MondoA decreases the muscle glycogen level. The findings indicate the potential function of MondoA in skeletal muscle, linking the glucose-related transcription factor to myogenesis and skeletal myofiber glycogen metabolism.