ABSTRACT
Objective:To explore the application of sound thinking combined with Sandwich teaching in oncology nursing practice teaching.Methods:A total of 68 nursing students who were interns in the Department of Oncology, The First Affiliated Hospital of Air Force Medical University from 2020 to 2021 were included in the study, and they were divided into a control group ( n=34) and an observation group ( n=34). The control group took routine teaching for interns, while the observation group took sound thinking combined with Sandwich teaching. The examination results, critical thinking abilities, and the evaluation of nursing teaching effectiveness of the two groups of nursing interns were evaluated. SPSS 22.0 was used for Chi-square test and t-test. Results:The examination scores of nursing students in the observation group were higher than those in the control group ( t=3.44, 2.87, 3.45, P<0.05). Compared with those before training, the scores of critical thinking ability of nursing interns in both groups increased after the training, and the observation group was better than the control group ( t=0.180, 3.64, 0.61, 2.92, 0.31, 2.74, 0.45, 2.65, 0.25, 3.58, 1.16, 2.85, 0.36, 3.20, 0.33, 2.38, P<0.05). The scores of autonomous learning ability, communication and collaboration ability, independent thinking ability, clinical reasoning ability, and problem-analyzing and -solving ability in the observation group were higher than those in the control group ( t=2.82, 3.46, 2.68, 3.29, 2.44, P<0.05). Conclusion:Combining sound thinking with Sandwich teaching in nursing clinical practice teaching in department of oncology can improve the examination scores of nursing students, improve their critical thinking abilities, and enable them to give a high evaluation of nursing teaching effectiveness.
ABSTRACT
Traumatic brain injury (TBI) triggers the activation of the endogenous coagulation mechanism, and a large amount of thrombin is released to curb uncontrollable bleeding through thrombin receptors, also known as protease-activated receptors (PARs). However, thrombin is one of the most critical factors in secondary brain injury. Thus, the PARs may be effective targets against hemorrhagic brain injury. Since the PAR1 antagonist has an increased bleeding risk in clinical practice, PAR4 blockade has been suggested as a more promising treatment. Here, we explored the expression pattern of PAR4 in the brain of mice after TBI, and explored the effect and possible mechanism of BMS-986120 (BMS), a novel selective and reversible PAR4 antagonist on secondary brain injury. Treatment with BMS protected against TBI in mice. mRNA-seq analysis, Western blot, and qRT-PCR verification in vitro showed that BMS significantly inhibited thrombin-induced inflammation in astrocytes, and suggested that the Tab2/ERK/NF-κB signaling pathway plays a key role in this process. Our findings provide reliable evidence that blocking PAR4 is a safe and effective intervention for TBI, and suggest that BMS has a potential clinical application in the management of TBI.
ABSTRACT
Traumatic brain injury (TBI)-induced coagulopathy has increasingly been recognized as a significant risk factor for poor outcomes, but the pathogenesis remains poorly understood. In this study, we aimed to investigate the causal role of acrolein, a typical lipid peroxidation product, in TBI-induced coagulopathy, and further explore the underlying molecular mechanisms. We found that the level of plasma acrolein in TBI patients suffering from coagulopathy was higher than that in those without coagulopathy. Using a controlled cortical impact mouse model, we demonstrated that the acrolein scavenger phenelzine prevented TBI-induced coagulopathy and recombinant ADAMTS-13 prevented acrolein-induced coagulopathy by cleaving von Willebrand factor (VWF). Our results showed that acrolein may contribute to an early hypercoagulable state after TBI by regulating VWF secretion. mRNA sequencing (mRNA-seq) and transcriptome analysis indicated that acrolein over-activated autophagy, and subsequent experiments revealed that acrolein activated autophagy partly by regulating the Akt/mTOR pathway. In addition, we demonstrated that acrolein was produced in the perilesional cortex, affected endothelial cell integrity, and disrupted the blood-brain barrier. In conclusion, in this study we uncovered a novel pro-coagulant effect of acrolein that may contribute to TBI-induced coagulopathy and vascular leakage, providing an alternative therapeutic target.
ABSTRACT
Clinical advances in the treatment of intracranial hemorrhage (ICH) are restricted by the incomplete understanding of the molecular mechanisms contributing to secondary brain injury. Acrolein is a highly active unsaturated aldehyde which has been implicated in many nervous system diseases. Our results indicated a significant increase in the level of acrolein after ICH in mouse brain. In primary neurons, acrolein induced an increase in mitochondrial fragmentation, loss of mitochondrial membrane potential, generation of reactive oxidative species, and release of mitochondrial cytochrome c. Mechanistically, acrolein facilitated the translocation of dynamin-related protein1 (Drp1) from the cytoplasm onto the mitochondrial membrane and led to excessive mitochondrial fission. Further studies found that treatment with hydralazine (an acrolein scavenger) significantly reversed Drp1 translocation and the morphological damage of mitochondria after ICH. In parallel, the neural apoptosis, brain edema, and neurological functional deficits induced by ICH were also remarkably alleviated. In conclusion, our results identify acrolein as an important contributor to the secondary brain injury following ICH. Meanwhile, we uncovered a novel mechanism by which Drp1-mediated mitochondrial oxidative damage is involved in acrolein-induced brain injury.
ABSTRACT
Clinical advances in the treatment of intracranial hemorrhage (ICH) are restricted by the incomplete understanding of the molecular mechanisms contributing to secondary brain injury. Acrolein is a highly active unsaturated aldehyde which has been implicated in many nervous system diseases. Our results indicated a significant increase in the level of acrolein after ICH in mouse brain. In primary neurons, acrolein induced an increase in mitochondrial fragmentation, loss of mitochondrial membrane potential, generation of reactive oxidative species, and release of mitochondrial cytochrome c. Mechanistically, acrolein facilitated the translocation of dynamin-related protein1 (Drp1) from the cytoplasm onto the mitochondrial membrane and led to excessive mitochondrial fission. Further studies found that treatment with hydralazine (an acrolein scavenger) significantly reversed Drp1 translocation and the morphological damage of mitochondria after ICH. In parallel, the neural apoptosis, brain edema, and neurological functional deficits induced by ICH were also remarkably alleviated. In conclusion, our results identify acrolein as an important contributor to the secondary brain injury following ICH. Meanwhile, we uncovered a novel mechanism by which Drp1-mediated mitochondrial oxidative damage is involved in acrolein-induced brain injury.
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Objective The aim of this study was to evaluate the effect of postoperative radiotherapy on local recurrence-free survival(LRFS)and overall survival(OS)in patients with triple-negative breast cancer (TNBC).Methods The clinical data of 186 cases for TNBC were collected from the Affiliated Tumor Hospital of Harbin Medical University from January 2003 to December 2006.These cases were confirmed by pathology.The patients were divided into radiotherapy and non-radiotherapy groups.The survival curves were plotted by Kaplan-Meier method.Log-rank test method was used to detect the difference between the radiotherapy and non-ra-diotherapy groups for 10 years.Univariate and multivariate analyses were used to determine the prognostic factors for TNBC patients.Results The 10-year LRFS of radiotherapy group and non-radiotherapy group were 80.2%and 76.0%,respectively.The 10-year OS was 86.0%and 74.0%in radiotherapy group and non-ra-diotherapy group,respectively.Both of them showed a statistically difference(P <0.05).Subgroup analysis showed that LRFS and OS were 81.8%and 81.8%in 10 years for radiotherapy in patients with T 1-2N1(1-3 lymph node metastases)M0,respectively,76.4% and 79.4% for non-radiotherapy group,respectively.No differences were observed in both of LRFS and OS in radiotherapy and non-radiotherapy groups(P>0.05). Multivariate analysis showed that radiotherapy and clinical staging were independent factors influencing the sur-vival of TNBC patients.Conclusion Radiotherapy can improve the LRFS and OS in TNBC patients,but radio-therapy does not improve LRFS and OS for TNBC patients with T 1-2N1(1~3 lymph node metastases)M0.Radio-therapy and clinical staging are independent factors that affect the prognosis of TNBC patients.
ABSTRACT
Objective The aim of this study was to evaluate the effect of postoperative radiotherapy on local recurrence-free survival(LRFS)and overall survival(OS)in patients with triple-negative breast cancer (TNBC).Methods The clinical data of 186 cases for TNBC were collected from the Affiliated Tumor Hospital of Harbin Medical University from January 2003 to December 2006.These cases were confirmed by pathology.The patients were divided into radiotherapy and non-radiotherapy groups.The survival curves were plotted by Kaplan-Meier method.Log-rank test method was used to detect the difference between the radiotherapy and non-ra-diotherapy groups for 10 years.Univariate and multivariate analyses were used to determine the prognostic factors for TNBC patients.Results The 10-year LRFS of radiotherapy group and non-radiotherapy group were 80.2%and 76.0%,respectively.The 10-year OS was 86.0%and 74.0%in radiotherapy group and non-ra-diotherapy group,respectively.Both of them showed a statistically difference(P <0.05).Subgroup analysis showed that LRFS and OS were 81.8%and 81.8%in 10 years for radiotherapy in patients with T 1-2N1(1-3 lymph node metastases)M0,respectively,76.4% and 79.4% for non-radiotherapy group,respectively.No differences were observed in both of LRFS and OS in radiotherapy and non-radiotherapy groups(P>0.05). Multivariate analysis showed that radiotherapy and clinical staging were independent factors influencing the sur-vival of TNBC patients.Conclusion Radiotherapy can improve the LRFS and OS in TNBC patients,but radio-therapy does not improve LRFS and OS for TNBC patients with T 1-2N1(1~3 lymph node metastases)M0.Radio-therapy and clinical staging are independent factors that affect the prognosis of TNBC patients.
ABSTRACT
Triple negative breast cancer ( TNBC) is defined by the lack of expressions of the estrogen re-ceptor(ER)、progesterone receptor(PR)and human epidermal growth factor receptor 2(HER-2).Although it is sensitive to radiation and chemotherapy ,it lacks of appropriate targeted therapy and endocrine therapy .It performs characteristics of the strong invasion ,high risk of recurrence and poor prognosis .So in recent years ,triple negative breast cancer gets more and more attention from international oncology community .In-depth study of triple nega-tive breast cancer will help the prevention ,early diagnosis ,judge the progress of the disease and improve progno-sis.TNBC drug treatment and relevant research progress are reviewed in the present article .