Objective The goal of this study was to explore the effect of exercise preconditioning on the expression of calcitonin gene-related peptide(CGRP)in the dorsal root ganglion of rats.Methods Fifty healthy male SD rats were randomly divided into control group (C) and exercise preconditioning group(EP).Group EP performed intervial treadmill exercise for 3 weeks for establishing exercise preconditioning animal model.The expression of CGRP mRNA in dorsal root ganglion was investigated by real-time fluorescence quantitative PCR.The immunoreaetion of CGRP in dorsal root ganglion was shown by immunohistochemistry.Results There was no significant difference in the expression of CGRP mR.NA in two groups(P>0.05).As compared with the group C,the immunoreaction of CGRP was increased in group EP,and the positive area and mean optical density of CGRP immunoreaction in group PE were significant higher than that in group C(P<0.05).Conclusion Exercise preconditioning does not change the expression of CGRP mRNA in dorsal root ganglion,but enhances the expression of CGRP in dorsal root ganglion to promote the reserve and release of CGRP in peripheral nerve endings and has the same endogenous protection as ischemie preconditioning.

Biochemical markers of bone metabolism are some of the final product which are released into the blood during the process of bone resorption or bone formation.Accumulative evidence shows that biochemical markers of bone metabolism through enzyme-linked immunoassay (ELISA) are more sensitive and specific than imaging examination.Moreover,biochemical markers of bone metabolism also display their superiorities on the early diagonosis,monitoring efficacy and prognosis evaluation in patients with bone metastases.Applications of biochemical markers of bone metabolism combined with imaging examination are more value for the early diagonosis,monitoring efficacy and prognosis evaluation in patients with bone metastases.

To study the effect of exercise on cardiac calcitonin gene-related peptide (CGRP) using immunnohistochemistry and the technique of computer image analysis, the expression and mechanism of cardiac CGRP on the animal model trained with different exercise intensities were investigated. The result showed that long-term low intensity of exercise was not able to induce obvious change in cardiac CGRP. After long-term moderate intensity of exercise, the expression of cardiac CGRP increased so as to improve blood supply and protect myocardium. Long-term high intensity of exercise decreased expression of cardiac CGRP and weakened the protection of myocardium which could be a chief cause of myocardial ischemia.

Hypoxia is an inherent feature of the majority of solid tumors,which can increase the resistance of tumor cells to radiotherapy and chemotherapy,promote tumor angiogenesis and lead to poor prognosis.Therefore,targeting the hypoxic tumor cells has become a spot in cancer therapy.Bioreduction drugs can be activated by a specific reduction to become cytotoxic metabolites,thus killing hypoxic tumor cells,while small molecular targeting inhibitors can selectively act on the key point of hypoxia pathway.They have paved a new way for hypoxia targeted therapy.

FGFR2 plays an important role in cell proliferation and differentiation and FGFR2 gene has its own genetic polymorphism. It has recently been demonstrated that this genetic polymorphism is associated with risk of development of breast cancer and clinically pathological factors

Bone-modifying agents (BMA) is a series drugs to alleviate the pain,pathological fractures,spinal cord compression,hypercalcemia,bone-related events which induced by bone metastases.Bisphosphonate drugs and denosumab are two dominant kinds of BMA at present.It has been proved that BMA is used in bone metastases patients with bone destruction,as adjuvant therapy for chemotherapy and radiotherapy,which can significantly improve the efficacy and prolong the survival of patients.In addition,some traditional Chinese medcine can effectively relieve a series of related symptoms caused by bone metastases and improve prognosis.Choosing right medication in clinical work can maximize the reduction of pain caused by bonerelated events and improve the quality of life of patients.

Hematoma growth is an independent risk factor for the prognosis of htracerebral hemorrhage.It is very common in the acute stage of intracerebral hemorrhage.There are many uncertainties about the definition,mechanisms,and influential factors of hematoma growth,and the effective therapy is lacking,therefore,early prevention and identification are critical.

The lymphatic metastasis affects prognosis and survival of colorectal cancer seriously,and lymphangiogenesis plays an important role in the lymphatic metastasis. Many factors such as COX-2 and MMP-7 which are found in many researches recently can promote the expression of VEGF-C which can promote the lym-phangiogenesis by connecting with its receptor and activating the relevant signal pathway. At present,as these related factors of lymphangiogenesis are found in colorectal cancer,the process of lymphangiogenesis in colorec-tal cancer becomes more clear,but the exact mechanism of these factors needs to be researched in future.

OBJECTIVE:To prepare nanostructured lipid carrier of adefovir dipivoxil(ADV-NLC),and optimize the formula-tion. METHODS:Using stearic acid and glycerin monostearate as solid lipid,oleic acid as liquid lipid,Gemini surfactant and poly-sorbate 80 as emulsifier,sodium dodecyl sulfate (SDS) as stabilizer,solvent dispersion ultrasonic method was used to prepare ADV-NLC. And using particle size,polydispersity index,Zeta potential,encapsulation efficiency as indexes,single factor test was conducted to screen Gemini surfactant-polysorbate 80 ratio,emulsifier dosage(ratio of emulsifier to water phase),drug-lipid ratio, solid-liquid lipid ratio. RESULTS:The formula was as follow as 3% emulsifier (Gemini surfactant-polysorbate 80 ratio of 1:2), 4.5% drug-lipid ratio,solid-liquid lipid ratio of 6:5. The average particle size of the prepared ADV-NLC was(48.83±2.65)nm, polydispersity index<0.3,Zeta potential was(-28.7±1.8)mV,encapsulation efficiency was(77.65±0.03)%(n=3). CONCLU-SIONS:ADV-NLC is successfully prepared,and the formulation is reasonable and feasible.

Objective To study the inhibitory effect of panax notoginseng saponins (PNS) on 3-nitrotyrosine (3-NT) formation in brain induced by heme/NO2 -/H2O2 or ONOO - pathways in vitro. Methods According to the two major pathways of 3-NT formation in vivo, the models of protein nitration induced by heme/NaNO2/H2O2 or ONOO-system were established, respectively, in vitro. Bovine serum albumin (BSA)/rat plasma protein or rat brain homogenate protein were utilized as reactive substrates in both systems. Samples were divided into blank-control group, 3-NT group and PNS group (including low-, medium-and high-concentration subgroups). In 3-NT group, samples were exposed to heme/NaNO2/H2O2 or ONOO-system, respectively, at 37℃for 30 min, whereas in PNS group, samples were pre-incubated with PNS (at final concentrations of 50 mg/L, 100 mg/L, and 200 mg/L) at 37℃for 5 min before the nitrating system exposure. The 3-NT level in each group was detected by Western blot assy. Results Compared with the blank-control group, both heme/NaNO2/H2O2 and ONOO-system can induce significant 3-NT generation in BSA/rat plasma protein or rat brain homogenate protein (P<0.05). Compared with model group, PNS pre-treatment markedly inhibited 3-NT expression in BSA/rat plasma protein in a dose-dependent manner (P<0.05), the inhibitory effect of low intervention on the level of 3-NT in rat brain homogenate protein was not significant (P>0.05). Medium- and high-concentrations of PNS pre-treatment markedly inhibited 3-NT accumulation, with maximum effect at the concentration of 200 mg/L (P<0.05). Conclusion Medium- and high-concentrations of PNS can inhibit 3-NT formation in brain tissue mediated by either heme/NO2-/H2O2 or ONOO-pathways, implying that potential neuroprotective action against 3-NT involves pathological conditions, like trauma, stroke, and neurodegenerative diseases.