Fracture Fixation, Internal ; methods ; Humans ; Joint Dislocations ; surgery ; Spinal Fractures ; surgery

Animals ; Antineoplastic Agents ; therapeutic use ; Benzamides ; Dasatinib ; Drug Resistance, Neoplasm ; drug effects ; Fusion Proteins, bcr-abl ; genetics ; metabolism ; Humans ; Imatinib Mesylate ; Leukemia, Myelogenous, Chronic, BCR-ABL Positive ; drug therapy ; genetics ; metabolism ; Piperazines ; therapeutic use ; Protein-Tyrosine Kinases ; antagonists & inhibitors ; Pyrimidines ; pharmacology ; therapeutic use ; Thiazoles ; pharmacology ; therapeutic use

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 ; Autophagy ; Humans ; Neoplasms ; physiopathology

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.

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

Aged ; Humans ; Male ; Palatal Neoplasms ; pathology ; Uvula ; pathology

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.

Asthma was considered to be a kind of chronic airway inflammatory diseases mediated by eosinophils(EOS),mast cells,T lymphocytes for a long time,and the typical pathologic features of asthma was airway EOS inflammation.The current study had found out that elevated neutrophils in airway were seen in severe asthma,and this kind of asthma had a poor response to corticosteroids.Impaired neutrophil chemotaxis and apoptosis of airway neutrophilia may be associated with persistent neutrophilic inflammation in the airways of severe asthma.A deep research into the mechanisms of neutrophilic phenotypes asthma would contribute to the new strategy of therapy.This article discusses a range of topics related to the role of neutrophilic inflammation in severe asthma in children,which were organizedas follows.

Obesity has been a world-wide growing health problem in children and adolescents,insulin resistance plays a pivotal role in the pathogenesis of obesity-associated complications,the mechanism is still unknown.There is growing evidence that obesity is associated with low-grade inflammation in youth.The onset of low-grade inflammation in obesity may be associated with the inflammatory cytokine secreted by adipose tissue,local Monocyte/Macrophage system and role of oxidative stress.The study of inflammatory cytokines in pathogenesis of obesity and insulin resistance will help to develop new treatment strategies to prevent obesity and obesity-associated complications.