2.The regulatory role of autophagy in tumor process.
Acta Pharmaceutica Sinica 2016;51(1):23-28
Autophagy is a classical regulatory mechanism of energy metabolism and self-update system in the maintenance of the intracellular homeostasis and cell development. Autophagy has been recently found to play a role in tumor development. Autophagy regulates tumor formation, proliferation, metastasis, and metabolism. At the same time, the anticancer drugs formed with autophagic mediators have been used in the treatment, which suggested that improving autophagy activity to inhibit tumor has become a new way for cancer treatment of cancer patients. This article gives an overview of the regulatory mechanism of autophagy, the relationship between autophagy and tumor, and tumor therapy by targeting autophagy.
Antineoplastic Agents
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Autophagy
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Humans
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Neoplasms
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physiopathology
3.New strategies to overcome imatinib resistance in treatment for chronic myelocytic leukemia.
Chinese Journal of Oncology 2006;28(8):561-563
Animals
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Antineoplastic Agents
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therapeutic use
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Benzamides
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Dasatinib
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Drug Resistance, Neoplasm
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drug effects
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Fusion Proteins, bcr-abl
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genetics
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metabolism
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Humans
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Imatinib Mesylate
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Leukemia, Myelogenous, Chronic, BCR-ABL Positive
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drug therapy
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genetics
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metabolism
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Piperazines
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therapeutic use
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Protein-Tyrosine Kinases
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antagonists & inhibitors
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Pyrimidines
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pharmacology
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therapeutic use
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Thiazoles
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pharmacology
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therapeutic use
4. Efficacy and safety of prophylactic use of nimodipine in patients with aneurysmal subarachnoid hemorrhage: A meta-analysis
Chinese Journal of Cerebrovascular Diseases 2011;8(2):70-76
Objective: To evaluate the efficacy and safety of nimodipine for cerebral vasospasm (CVS) in patients with aneurysmal subarachnoid hemorrhage. Methods: The database of searched Pubmed, OVID, EMBase, Cochrane library, Stroke Trials Register (U. S. Clinical Trials Registry) , and the National Science and Technology Library up to November 2010 were reviewed. The prospective, randomized, controlled clinical trials about preventive application of nimodipine in patients with aneurysmal subarachnoid hemorrhage controlled clinical trials was collected. Meta-analysis was performed for the studies met the inclusion criteria. Results: Circled digit oneEight studies met the inclusion criteria. A total of 1499 patients completed the trials and observations of the different indicators respectively. In all the patients, the complete recovery rate increased 64% in the nimodipine group compared to the placebo group (P = 0.0002, OR = 1.64, 95% CI 1.26-2.13; the number of patients needed to treat [NNT] = -1.048). The patients with complete recovery or moderate disability increased 79% (P = 0.0007, OR = 1.79, 95% CI 1.28-2.51; NNT = -5.889); the rates of death, severe disability or vegetative survival decreased 38% (P = 0.0003, OR = 0.62, 95% CI 0.48-0.80; NNT = 1.529); the mortality of the patients with CVS decreased 74% (P = 0.008, OR = 0.26, 95% CI 0.09-0.71; NNT = 2.29%); the incidence of symptomatic CVS decreased 46% (P < 0.00001, OR = 0.54, 95% CI 0.42-0.69; NNT = 1.952); the incidence of delayed neurological deficits in all patients decreased 38% (P < 0.0001, OR = 0.62, 95% CI 0.50-0.78; NNT = 1.078); the incidence of symptomatic cerebral infarction decreased 46% (P < 0.00001, OR = 0.54, 95% CI 0.42-0.69; NNT = 1.079); the incidence of cerebral infarction confirmed by CT was 58% of the placebo group (P < 0.001, OR = 0.58, 95% CI 0.42-0.81; NNT = 3.314); the incidence of cerebral infarction in patients with CVS was 35% of the placebo group (P = 0.003, OR = 0.35, 95% CI 0.17-0.69; NNT = 3.688), and the incidence of cerebral infarction in all the patients was only 52% of the placebo group (P < 0.00001, OR = 0.52, 95% CI 0.41-0.66; NNT = 1.196); and there were no significant differences for the incidences of rehemorrhage and adverse reaction between the nimodipine group and the placebo group (rehemorrhage: P = 0.15, OR = 0.75, 95% CI 0.50-1.11; adverse reaction; P = 0.59, OR = 1.13, 95% CI 0.71 -1.81). Conclusion: Nimodipine may significantly improve the clinical outcome in patients with aneurysmal subarachnoid hemorrhage, and decrease the incidence of symptomatic CVS, delayed neurological deficits and cerebral infarction, while the incidence of rehemorrhage and adverse reaction were almost the same with the placebo group.
5.Comparison of the clinical safety and efficacies of percutaneous pedicle screw fixation and open pedicle screw fixation for thoracolumbar fracture: a meta-analysis.
Lei LIU ; Guang-wang LIU ; Chao MA
China Journal of Orthopaedics and Traumatology 2016;29(3):220-227
OBJECTIVETo evaluate the efficacy and safety of percutaneous pedicle screw fixation (PPSF) and open pedicle screw fixation (OPSF) in the treatment of single level of thoracolumbar fracture.
METHODSDatabases including Pubmed, Embasem, CNKI were searched to collect clinical trials of the clinical safety and efficiency of PPSF and OPSF for single level of thoracolumbar unstable fracture, relevant proceedings and references were also retrieved manually. Studies from 1990 to 2014 that met the inclusion and exclusion standards were researched. The data were extracted and the methods from the studies were also evaluated. Data analysis was conducted with the Review Manager 5.3 software. Observation targets included operation time, intraoperative bleeding, postoperative bleeding, hospitalization time, the bed time, postoperative vertebral Cobb angle, vertebral body height, pain score and the length of incision operation.
RESULTSFifteen papers were finally studied, including 2 randomized controlled trials (RCT) and 13 case-control studies, involving 789 patients. Compared with OPSF, the PPSF in treating thoracolumbar fracture had shorter operation time, smaller operation incision, less intraoperative and postoperation bleeding, shorter hospitalization days, fewer pain (P<0.00001), the less improvement in the change of Cobb angle (P=0.0006). There was no significant difference in the improvement of vertebral body height (P=0.36), the bed time from operation to exercise (P=0.38) between OPSF and PPSF.
CONCLUSIONCompared with OPSF, PPSF is better, safer, and has fewer pain. But there is no evidence that the PPSF is better in the recovery of the spinal height, and they have the same effect in the long-term follow-up for thoracolumbar fractures. PPSF brines minimally invasive to patients with better effect. It is worth further study and clinical research.
Adult ; Aged ; Female ; Fracture Fixation, Internal ; methods ; Humans ; Male ; Middle Aged ; Minimally Invasive Surgical Procedures ; methods ; Pedicle Screws ; Spinal Fractures ; surgery ; Thoracic Vertebrae ; surgery ; Treatment Outcome
6.Exploration of influencing factors of price of herbal based on VAR model.
Nuo WANG ; Shu-Zhen LIU ; Guang YANG
China Journal of Chinese Materia Medica 2014;39(20):4070-4073
Based on vector auto-regression (VAR) model, this paper takes advantage of Granger causality test, variance decomposition and impulse response analysis techniques to carry out a comprehensive study of the factors influencing the price of Chinese herbal, including herbal cultivation costs, acreage, natural disasters, the residents' needs and inflation. The study found that there is Granger causality relationship between inflation and herbal prices, cultivation costs and herbal prices. And in the total variance analysis of Chinese herbal and medicine price index, the largest contribution to it is from its own fluctuations, followed by the cultivation costs and inflation.
Agriculture
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economics
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Commerce
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Costs and Cost Analysis
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Drugs, Chinese Herbal
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economics
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Humans
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Models, Statistical
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Plants, Medicinal
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growth & development
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Regression Analysis
8.Fenestrated endovascular repair in the treatment of aortic aneurysms
Guang LIU ; Ying HUANG ; Mier JIANG
International Journal of Surgery 2008;35(12):850-853
Aortic aneurysms involving major visceral arteries or those with short necks are always contraindications to traditional endovascular aortic repair(EVAR).The advent of the fenestrated endovascular aortic repair(F-EVAR)which could exclude aortic aneurysms while presenving blood flow to major organsthrough visceral branches using fenestrated stent-grafts raises the possibility for the treatment of these aorticaneurysms.To update our knowledge,we reviewed the publications on F-EVAR in recent years.
9.The therapeutic effects of fluoxetine on experimental autoimmune encephalomylitis
Xiqiu YUAN ; Guang QIU ; Xiaojia LIU
Chinese Journal of Behavioral Medicine and Brain Science 2011;20(3):211-213
Objective To investigate whether fluoxetine has therapeutic effect of clinical score and brain derived neurotrophic factor (BDNF) expression in serum of experimental autoimmune encephalomyelitis (EAE)model. Methods Rats were randomly divided into solvent control group (n=6) ,model control group ( n= 10)and fluoxetine group ( n= 10). The EAE model was prepared by injecting guinea pig spinal cord homogenate subcutaneously. The clinical score was daily measured according to the sign and symptoms of rats in the behavior examination. The serum BDNF level was measured by EL1SA. Results 1. Except for the solvent control group,the first sign of EAE(Piloerection) was detected on 4th day after immunization of rats from both model control group and fluoxetine group,then EAE rats had distal tail weakness on 8th day, and gradually developed into completely tail paralysis and limb paralysis. EAE rats' clinical score reached the peak on 16th day after immunization. 2. The clinical score of fluoxetine group became scientifically lower than model group since 18th day after immunization ( Fluoxetine group :3.27 ± 0. 33; Model control group :4.66 ± 0. 55, P < 0. 05 ). 3. Compared with the model control group,fluoxetine did not significantly increase the expression of serum BDNF in EAE model ( Fluoxetine group:62.27 ± 0.43; Model control group :61.67 ± 0.85, P > 0.05 ). Conclusion Fluoxetine reduced the clinical score of EAE since 18th day after immunization,which indicates fluoxetine could promote the recovery of neurological function in EAE rats. BDNF may not contribute to protective effect of fluoxetine in EAE animal.
10.Treatment of non-alcoholic fatty liver disease based on traditional Chinese medicine therapies for warming yang to activate qi.
Tao LIU ; Zhipeng TANG ; Guang JI
Journal of Integrative Medicine 2011;9(2):135-7
Fatty liver disease is caused by abnormal accumulation of lipids within hepatocytes. According to traditional Chinese medicine (TCM) theory, lipids belong to the category of essence obtained from cereals and the normal distribution of essence relies on the function of spleen yang. When spleen yang is injured, the normal distribution of essence (lipids) will be affected, leading to formation of phlegm retention in the liver. That is the TCM pathogenesis of fatty liver disease. Hence the treatment of fatty liver disease should be concentrated on warming yang to activate qi. With such a treatment, the normal distribution of essence will be restored, essence will be distributed, and phlegm will be dissipated.