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Objective To evaluate the effect of different doses of thoracic radiotherapy (TRT) upon the clinical prognosis of patients with extensive-stage (stage Ⅳ) small cell lung cancer (ES-SCLC) and establish a Nomogram prediction model.Methods Clinical data of 144 patients pathologically diagnosed with ES-SCLC undergoing TRT in Tianjin Medical University Cancer Hospital from month,2010 to month,2016 were retrospectively analyzed.Clinical characteristics,treatment data and responses were evaluated.A Nomogram was established by using Cox's proportional hazard regression model to predict the overall survival (OS).The prediction capability and accuracy were assessed by the concordance index (C-index) and a calibration curve between the model and verification groups.Results The median follow-up time was 31.9 months.The 2-year OS rate was 20.3％.The Nomogram model demonstrated that TRT dose,liver metastases,oligometastases/polymetastases,number of chemotherapy cycle and response to chemotherapy were significantly correlated with clinical prognosis.The calibration curve revealed that the predicted and actual OS were highly consistent.The C-index was calculated as 0.701.In the subgroup analyses,patients with high-dose TRT obtained significantly better OS than their counterparts with low-dose TRT.Conclusion The Nomogram prediction model based on different TRT doses can accurately predict the OS rate of ES-SCLC patients,which is an individualized model for predicting the survival probability.
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Objective To investigate the protective effect of PolyphyllinⅠ(PPI) on myocardial ischemia/reperfusion (I/R) injury in rats and its mechanism. Methods The 6-month-old Sprague-Dawley (SD) rats were divided into sham operation group (Sham group), I/R model group, and low, medium, high dose PPI groups according to the random number table method, with 10 in each group. The rat myocardial I/R model was prepared by ligating the left anterior descending branch of the coronary artery by 30 minutes and reperfusion by 120 minutes. Sham group was exposure to open chest without ligation. Low, medium, high dose PPI groups were injected with PPI 75, 150, 300 mg·kg-1·d-1 in front of the film for 4 weeks; dimethyl sulfoxide (DMSO) was gastric infused in the I/R model group. After the end of reperfusion, the myocardial infarction area (IA) was determined by triphenyltetrazole (TTC) and Evans blue (EB) staining;the apoptosis of myocardial cells was detected by TdT-mediated dUTP nick end labeling stain (TUNEL); the expressions of apoptosis related protein (Bax, Bcl-2), and cytoplasmic and nucleus expressions of P65 in nuclear factor-κB (NF-κB) signal pathway were detected by Western Blot. Results Compared with the Sham group, the myocardial IA was significantly increased in the I/R model group, the apoptosis rate of myocardial cells was significantly increased, the expression of Bcl-2 was significantly decreased, and the expression of Bax was significantly increased, and the intranuclear transfer of P65 was significantly increased. Compared with the I/R model group, low, medium and high dose PPI pretreatment could significantly reduce the myocardial IA [(21.6±0.9)%, (14.3±1.6)%, (15.0±0.8)% vs. (29.6±1.4)%], the apoptosis rate of myocardial cells was significantly decreased [(38.6±1.9)%, (24.3±2.6)%, (26.3±2.8)% vs. (56.8±2.4)%], the protein expression of Bcl-2 was significantly increased, while the protein expression of Bax was significantly decreased (Bcl-2/GAPDH: 0.24±0.07, 0.36±0.02, 0.34±0.09 vs. 0.13±0.04; Bax/GAPDH: 0.39±0.10, 0.21±0.08, 0.23±0.06 vs. 0.53±0.12); and P65 nuclear transfer was significantly decreased after middle and high dose PPI pretreatment [nuclear P65/Histone 3: 0.49±0.09, 0.51±0.06 vs. 0.83±0.11; cytoplasmic P65/GAPDH: 0.31±0.03, 0.30±0.05 vs. 0.22±0.07], with statistically significant differences (all P < 0.05). However, there was no significant difference in each index between the medium and high dose PPI groups (all P > 0.05). Conclusion PPI alleviates myocardial I/R injury in rats via NF-κB signal pathway, and the PPI effect of 150 mg·kg-1·d-1 is most especially significant.
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Cancer is a serious disease threatening human life and social development,and has become one of the most important medical and health problems in the world.As the changing of disease patterns change and the trending of aging population,the burden of cancer patients is increasing in China.In clinical practice,various anesthesia methods are indispensable to complete surgery,invasive examinations and other operations.Therefore,safe and effective narcotic analgesic for cancer patients is the key factor for successful completion of examination and treatment.Dexmedetomidine (Dex) is a novel α2-adrenergic receptor agonist.Comparing with traditional opioids,Dex is more effective and safer,and can provide sedation,anxiolytic and analgesia after administration.In this paper,the progress of the usage of Dex in cancer patients was summarized to guide clinical treatment programs.
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Primary mediastinal large B-cell lymphoma (PMBCL) is morphologically similar to diffuse large B-cell lymphoma (DLBCL) and nodular sclerosis Hodgkin lymphoma.For most PMBCL patients, chemotherapy plus consolidation radiotherapy showed that the latter could improve PMBCL responsiveness and progression-free survival (PFS), and its combined use with chemotherapy demonstrated higher therapeutic efficacy.Recent clinical studies suggested that rituximab and anthracycline chemotherapy regimens could increase PMBCL treatment efficacy, reduce early treatment failure, enhance PFS and overall survival, and improve prognosis.Although rituximab combined with some high-intensity chemotherapy without radiotherapy have achieved good results, many studies still support the use of post-immunochemotherapy consolidation mediastinal radiotherapy.Based on the results of a few studies with a small sample size, patients who were assessed as complete metabolic remission by PET following high-intensity immunochemotherapy may omit consolidation radiotherapy.However, these results will need to be further confirmed by large-sample multicenter clinical trials.Consolidation radiotherapy is recommended for patients with poor prognostic factors or PET score>3.
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Radiation?induced heart disease ( RIHD) is a common type of radiation?induced damages in chest radiotherapy. There are no obvious short?term symptoms in patients with RIHD. However, RIHD causes irreversible permanent damages to the heart over time, which undermines the quality of life. Patients with severe RIHD even have a risk of death from myocardial infarction caused by coronary atherosclerosis. This paper summarizes the research advances in epidemiology, diagnosis, mechanisms of radiation?induced injury in various parts of the heart, radiotherapy techniques, and treatment. Reduction in radiation range and dose, early diagnosis, and early treatment are recommended for patients to reduce heart injury and improve the quality of life.
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Objective To evaluate the ischemic postconditioning on endoplasmic reticulum stress during cerebral ischemia/reperfusion (I/R) in rats.Methods Ninety adult male Sprague-Dawley rats,aged 350-450 g,were randomly divided into 3 groups (n =30 each) using a random number table:sham operation group (S group),I/R group,and ischemic postconditioning group (group P).Focal cerebral I/R was induced by electrocoagulation of left middle cerebral artery and 30 min occlusion of bilateral common carotid arteries followed by reperfusion.In group P,bilateral common carotid arteries were subjected to 3 cycles of 30 s reperfusion and 10 s ischemia at the beginning of reperfusion.At 24 h of reperfusion,neurological deficit was scored,and cerebral infarct size was detected by TTC staining.At 6,12 and 24 h of reperfusion,the expression of glucose-regulated protein 78 (GRP78),C/EBP homologous protein (CHOP) and caspase-12 in the ischemic area were measured (using immunohistochemistry).The neuronal apoptosis in the ischemic area was detected by TUNEL.Results Compared with S group,the neurological deficit score was significantly increased,cerebral infarct size was enlarged,the neuronal apoptosis was increased,and the expression of GRP78,CHOP and caspase-12 was up-regulated in I/R and P groups.The neurological deficit score was significantly lower,cerebral infarct size was smaller,the expression of GRP78 was higher at 12 and 24 h of reperfusion,the neuronal apoptosis was lower at 24 h of reperfusion,and the expression of CHOP and caspase-12 was lower in group P than in group I/R.Concluion Ischemic postconditioning can inhibit neuronal apoptosis mediated by endoplasmic reticulum stress during cerebral I/R,which dose not play a leading role in cerebral protection in rats.
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Objective To investigate the effects of remote ischemic postconditioning (RIPoC) on global cerebral ischemia-reperfusion (I/R) injury in rats.Methods One hundred and twenty-eight male adult SD rats weighing 200-250 g were randomly divided into 4 groups ( n =32 each):sham operation group (group S),group I/R,group I/R + RIPoC and remote I/R group (group RI/R ).Global cerebral I/R was induced by four-vessel occlusion.Group I/R + RIPoC received 3 cycles of 15 min reperfusion followed by 15 min ischemia in bilateral femoral arteries at the beginning of cerebral reperfusion.The rats were sacrificed at 24 and 48 h of cerebral reperfusion,and brains were removed for determination of neuronal apoptosis (by TUNEL method) in hippocampal CA1 region and the parietal cortex,Bcl-2 and Bax expression (by Western blot) in hippocampal CA1 region.The superoxide dismutase (SOD) and catalase (CAT) activity and malondialdehyde (MDA) content in hippocampal CA1 region and the parietal cortex were also measured at 48 h of cerebral reperfusion.Morris water maze task was used to test the learning and memory function at 4 d of cerebral reperfusion,and the rats were sacrificed at 7 d of cerebral reperfusion,and brains were removed for determination of neuronal density in hippocampal CAl region and the parietal cortex.Results Cerebral I/R significantly increased the number of apoptotic neurons and MDA content,upregulated Bcl-2 and Bax expression,decreased neuronal density,SOD and CAT activity and learning and memory function in group I/R as compared with group S.RIPoC significantly attenuated these cerebral I/R-induced changes.Conclusion RIPoC could protect brain against global cerebral I/R-induced injury,and the mechanism may be related to inhibiting lipid peroxidation,regulating the balance between Bcl-2 and Bax and inhibiting apoptosis.