Objective: To investigate the role of integrin beta-1 (Itgb1) in radiation-induced tissue injury and elucidate its underlying molecular mechanisms. Methods: Differentially expressed genes associated with radiation injury were identified from the Gene Expression Omnibus (GEO) microarray database through bioinformatics analysis, followed by enrichment analysis to determine core hub genes. In vitro, Itgb1 was silenced using siRNA transfection in human chronic myeloid leukemia K562 and mouse alveolar epithelial MLE-12 cells. Protein expression was assessed by Western blot, while cell proliferation, apoptosis, and reactive oxygen species (ROS) levels were quantified by flow cytometry following Itgb1 inhibition. In vivo, C57BL/6 mice were divided into 4 experimental groups (n = 5 per group): Control (intraperitoneal injection of PBS without irradiation), RGD (intraperitoneal injection of RGD 10 mg/kg without irradiation), IR + PBS (8 Gy 60Co γ-ray total body irradiation with PBS), and IR + RGD (intraperitoneal injection of RGD 10 mg/kg, 2 h prior to 8 Gy 60Co γ-ray total body irradiation). Bronchoalveolar lavage fluid (BALF) was collected for macrophage analysis. Lung and intestine tissues were subjected to hematoxylin-eosin (H&E) staining and immunofluorescence (IF) examination. Peripheral blood samples were analyzed to evaluate hematopoietic function. Results: Bioinformatics analysis identified Itgb1 as a hub gene in radiation-induced injury. Western blot analysis demonstrated significant upregulation of Itgb1 protein following irradiation. In K562 cells, Itgb1 expression peaked at 12 h post-irradiation (t = 3.07, P < 0.01) and declined by 24 h, whereas MLE-12 cells exhibited sustained elevation at both time points (t = 10.44, P < 0.0001). Itgb1 silencing significantly exacerbated radiation-induced cellular damage. In K562 cells, knockdown reduced S-phase proliferation from 52.49% to 36.41% (t = 9.64, P < 0.01), increased apoptosis (t = 11.36, P < 0.001), and elevated ROS levels (t = 3.62, P < 0.05). Comparable effects were observed in MLE-12 cells: reduced proliferation (46.82% to 37.98%, t = 12.78, P < 0.0001), enhanced apoptosis (t = 10.16, P < 0.0001), and increased ROS (t = 5.58, P < 0.0001). In vivo, Itgb1 inhibition aggravated radiation-induced pulmonary, intestinal and hematopoietic injuries, characterized by increased inflammatory infiltration, alveolar septal thickening, and decreased peripheral blood cell counts (t = 2.34, P < 0.01). These findings indicate that Itgb1 functions as a protective factor against radiation injury. Conclusions: This study elucidates Itgb1 critical radioprotective role, where compensatory upregulation constitutes an endogenous defense mechanism, while its deficiency exacerbates injury through amplified apoptosis and inflammation, highlighting its clinical utility as a therapeutic target.

Objective To investigate the role of integrin beta-1 (Itgb1) in radiation-induced tissue injury and elucidate its underlying molecular mechanisms. Methods Differentially expressed genes associated with radiation injury were identified from the Gene Expression Omnibus (GEO) microarray database through bioinformatics analysis, followed by enrichment analysis to determine core hub genes. In vitro, Itgb1 was silenced using siRNA transfection in human chronic myeloid leukemia (K562) and mouse alveolar epithelial (MLE-12) cells. Protein expression was assessed by Western blot, while cell proliferation, apoptosis, and reactive oxygen species (ROS) levels were quantified by flow cytometry following Itgb1 inhibition. In vivo, C57BL/6 mice (n=5 per group) were divided into 4 experimental groups: Control (intraperitoneal injection of PBS without irradiation), RGD (intraperitoneal injection of RGD 10 mg/kg without irradiation), IR+PBS (8 Gy 60Co γ-ray total body irradiation with PBS), and IR+RGD (intraperitoneal injection of RGD 10 mg/kg, 2 h prior to 8 Gy 60Co γ-ray total body irradiation). Bronchoalveolar lavage fluid (BALF) was collected for macrophage analysis. Lung and intestine tissues were subjected to hematoxylin-eosin (H&E) staining and immunofluorescence (IF) examination. Peripheral blood samples were analyzed to evaluate hematopoietic function. Results Bioinformatics analysis identified Itgb1 as a hub gene in radiation-induced injury. Western blot analysis demonstrated significant upregulation of Itgb1 protein following irradiation. In K562 cells, Itgb1 expression peaked at 12 h post-irradiation (t= 3.07, P < 0.01) and declined by 24 h, whereas MLE-12 cells exhibited sustained elevation at both time points (t = 10.44, P < 0.0001). Itgb1 silencing significantly exacerbated radiation-induced cellular damage. In K562 cells, knockdown reduced S-phase proliferation from 52.49% to 36.41% (t = 9.64, P < 0.01), increased apoptosis (t = 11.36, P < 0.001), and elevated ROS levels (t =3.62, P < 0.05). Comparable effects were observed in MLE-12 cells: reduced proliferation (46.82% to 37.98%, t = 12.78, P < 0.0001), enhanced apoptosis (t = 10.16, P < 0.0001), and increased ROS (t = 5.58, P < 0.0001). In vivo, Itgb1 inhibition aggravated radiation-induced pulmonary, intestinal and hematopoietic injuries, characterized by increased inflammatory infiltration, alveolar septal thickening, and decreased peripheral blood cell counts (t = 2.34, P < 0.01). These findings indicate that Itgb1 functions as a protective factor against radiation injury. Conclusions This study elucidates Itgb1 critical radioprotective role, where compensatory upregulation constitutes an endogenous defense mechanism, while its deficiency exacerbates injury through amplified apoptosis and inflammation, highlighting its clinical utility as a therapeutic target.

The evolving geopolitical landscape has heightened the probability of nuclear incidents, including accidental release or deliberate detonation, which can cause acute, life-threatening radiation injury to large populations. High-dose ionizing radiation (IR) is highly likely to cause radiation injury to the intestines and lead to intestinal radiation sickness. This study systematically explored the protective effect of cobalt chloride (CoCl2) on intestinal radiation injury and its preliminary mechanism from multiple levels, including cells, intestinal tissues, intestinal organoids, and live mice. The results showed that CoCl2 pretreatment could significantly enhance the radiation tolerance of mice, not only greatly improving the survival rate and multiple indicators such as intestinal injury score, but also maintaining the integrity of the small intestinal epithelial villi structure. At the same time, it promotes the proliferation and differentiation of intestinal organoids, inhibits the apoptosis of intestinal epithelial cells, and enhances the expression of barrier protection genes, thereby enhancing the intestinal resistance to radiation injury. Mechanism studies have shown that CoCl2 can up-regulate the expression of hypoxia-inducible factor-2 α (HIF-2α) via hypoxia-mimetic action and activate downstream signaling pathways related to cell proliferation, anti-apoptosis, and angiogenesis. This study initially clarified the mechanism by which CoCl2 protects the intestinal tract from radiation injury, providing a scientific basis and strategic support for the development of new radiation protection targets. Its in-depth research and application transformation are expected to play an important role in the future field of nuclear radiation protection.

PURPOSE:Ionizing radiation (IR) has been shown to induce epithelial-mesenchymal transition (EMT) of alveolar epithelial cells (AECs), which is a critical cause of radiation-induced pulmonary fibrosis (RIPF). In this study, we investigated the role and molecular mechanisms of musashi2 (MSI2), an RNA-binding protein, in IR-induced EMT of AECs for aiming at potential therapeutic strategies to prevent RIPF. MATERIALS AND METHODS:Changes in the expression levels of MSI2 and EMT markers (E-cadherin, N-cadherin, and Vimentin) induced by IR in AECs were detected by western blot (WB). Then, the effect of MSI2 on IR-induced EMT of AECs was investigated by observing morphological changes and detecting expression of MSI2 and EMT markers by WB and immunofluorescence (IF). RNA-Seq analysis, WB and RT-qPCR were used to identify the targets of MSI2. RESULTS:We observed that IR could cause a significant increase of MSI2 protein expression, a down-regulation of E-cadherin and an up-regulation of Vimentin and N-cadherin in AECs (MLE-12 and RLE-6TN cells). We also revealed that MSI2 was involved in regulating the alteration of morphology and EMT-related markers in AECs after irradiation, suggesting the occurrence of EMT regulated by MSI2. Moreover, we found the mechanism of MSI2 participating in EMT by regulating the expression of transcription factor ZEB1, acting as a downstream target of MSI2 in IR-induced EMT of AECs. CONCLUSIONS:Our study unveils the critical role of MSI2 in IR-induced EMT of AECs and preliminarily elucidates its molecular mechanisms, providing new insights into the process of IR-induced pulmonary fibrosis.

选取2021年1—9月在我院泌尿外科门诊进行体外冲击波碎石的86例患者为研究对象,探讨基于IKAP理论所构建的延续性护理模式在门诊体外冲击波碎石术患者中的应用.实践表明,对体外冲击波碎石术后患者实施IKAP延续性护理模式,能有效提升患者依从性,降低术后并发症,显著提高临床治疗效果.

Radiation injury is a common side effect of nuclear and radiation accidents as well as clinical oncologic radiotherapy. The organism undergoes a series of pathological responses after irradiation, especially in the short term, accompanied by an intense inflammatory storm [1], and effective targets for intervention have not been identified [2]. In this study, we screened differential genes in gene microarray data from the GEO database and then identified the core gene Itgb1 by enrichment analysis. Subsequently, the expression of Itgb1 was knocked down by siRNA interference and was functionally blocked by RGD, a Itgb1 inhibitor. Next, the proliferation and apoptosis of irradiated cells was detected, and injury of lung tissues and hemopoietic system were also investigated. As a result, knockdown of Itgb1 protected pulmonary epithelial cells and blood cell from irradiation, and RGD remitted the irradiation-induced lung injury and hematopoietic injury. This study suggests that Itgb1 plays a key role in radiation injury and provides new ideas for the prevention and treatment of radiation therapy.

Background and Aims Reducing reactive oxygen species (ROS) production has proven an effective way for alleviating oxidative stress during ischemia-reperfusion injury (IRI). Moreover, inhibition of Rac1 could reduce ROS production and prevent oxidative stress injury. Previous studies have suggested a positive interactivation feedback loop between Rac1 and hypoxia-inducible factor (HIF)-1α, the latter being up-regulated early during ischemia. The positive inter-activation between Rac1 and HIF-1α would aggravate ROS production, thereby promoting IRI. This study was designed to verify the effects of Rac1 inhibition on hepatic IRI both at animal and cellular levels and to explore the interaction between Rac1 and HIF-1α during hepatic IRI. Methods C57B/6 mice and AML-12 cells were used for the construction of hepatic IRI animal and cell models. Rac1 inhibition was achieved by NSC23766 (a specific Rac1 inhibitor). Lentiviral vectors were used for Rac1 knockdown. At designated time points, serum and liver tissues were collected from the mice and treated cells were collected for further analysis. Results NSC23766 treatment significantly alleviated the hepatic IRI in mice, manifesting as lower vacuolation score and less apoptosis cells, lower ROS and serum/liver alanine aminotransferase/aspartate aminotransferase levels, and fewer activated inflammatory cells. IRI of AML-12 was also alleviated by 50 µM NSC23766 or Rac1-knockdown, manifesting as reduced cell apoptosis, less extensive interruption of mitochondrial membrane potential, down-regulation of apoptosis, and effects on DNA damage-related proteins. Interestingly, Rac1 knockdown also down-regulated the expression level of HIF-1α. Conclusions Our study supports a protective effect of Rac1 inhibition on hepatic IRI. Aside from the classic topics of reducing ROS production and oxidative stress, our study showed an interaction between Rac1 and HIF-1α signaling during hepatic IRI.

The lung is one of the most sensitive tissues to ionizing radiation, thus, radiation-induced lung injury (RILI) stays a key dose-limiting factor of thoracic radiotherapy. However, there is still little progress in the effective treatment of RILI. Ras-related C3 botulinum toxin substrate1, Rac1, is a small guanosine triphosphatases involved in oxidative stress and apoptosis. Thus, Rac1 may be an important molecule that mediates radiation damage, inhibition of which may produce a protective effect on RILI. By establishing a mouse model of radiation-induced lung injury and orthotopic lung tumor-bearing mouse model, we detected the role of Rac1 inhibition in the protection of RILI and suppression of lung tumor. The results showed that ionizing radiation induces the nuclear translocation of Rac1, the latter then promotes nuclear translocation of P53 and prolongs the residence time of p53 in the nucleus, thereby promoting the transcription of Trp53inp1 which mediates p53-dependent apoptosis. Inhibition of Rac1 significantly reduce the apoptosis of normal lung epithelial cells, thereby effectively alleviating RILI. On the other hand, inhibition of Rac1 could also significantly inhibit the growth of lung tumor, increase the radiation sensitivity of tumor cells. These differential effects of Rac1 inhibition were related to the mutation and overexpression of Rac1 in tumor cells.

Abstract Background radiation-induced intestinal injury (RIII) is an important cause of death in nuclear accidents and common complication after radiotherapy in patients with pelvic, abdominal, or retroperitoneal tumors. Up to now there is no effective means to prevent or treat RIII due to its complex mechanism, in which the death of intestinal cells is the main reason. Recently, GSDMD-mediated pyroptosis was identified as an important type of cell death and play a role in many diseases. However, the effect of pyroptosis on RIII is still unclear. Method using GSDMD knockout mice, the role of pyroptosis in the RIII was investigated. By detecting the release of LDH, expression of GSDMD, Caspase-11, Caspase-1 and absorption rate of SYTOX Green, the pyroptosis of radiated Mode-k cells was determined, simultaneously the common pyroptosis induced by LPS was conducted as positive control. Further, the upstream of GSDMD were screened by predictive analysis of transcription factors combing RNA-seq. Results we showed that GSDMD-mediated pyroptosis is involved in the process of RIII, and unexpectedly found that radiation induced a delayed pyroptosis that is substantially different from common pyroptosis induced by such as LPS. Further investigation revealed that radiation-induced DNA damage up-regulated the expression of P53, which subsequently transcribes GSDMD. In addition, the up-regulated GSDMD led to pyroptosis simultaneously promoting Ca2+ influx that afterwards enhanced apoptosis induced by radiation. Finally, targeting GSDMD, disulfiram displayed a potential protection for RIII. Conclusion radiation could induce delayed pyroptosis in the intestinal epithelial cell that is greatly different from common pyroptosis. During that process, GSDMD was cleaved and had inducible high expression which was mainly mediated by P53 transcription.

Radiation-induced intestinal injury (RIII) is a common complication after radiation therapy in patients with pelvic, abdominal, or retroperitoneal tumours. Recently, in the model of DSS (Dextran Sulfate Sodium Salt) -induced intestinal inflammatory injury, it has been found in the study that transgenic mice expressing hVDR in IEC (Intestinal Epithelial Cell) manifest highly anti-injury properties in colitis, suggesting that activated VDR in the epithelial cells of intestine may inhibit colitis by protecting the mucosal epithelial barrier. In this study, we investigated the effect of the expression and regulation of VDR on the protection of RIII, and the radiosensitivity in vitro experiments, and explored the initial mechanism of VDR in regulating radiosensitivity of IEC. As a result, we found that the expression of VDR in intestinal tissues and cells in mice can be induced by ionizing radiation. VDR agonists are able to prolong the average survival time of mice after radiation and reduce the radiation-induced intestinal injury. For lack of vitamin D, the radiosensitivity of intestinal epithelial cells in mice increased, which can be reduced by VDR activation. Ensuing VDR activation, the radiation-induced intestinal stem cells damage is decreased, and the regeneration and differentiation of intestinal stem cells is promoted as well. Finally, on the basis of sequencing analysis, we validated and found that VDR may target the HIF/PDK1 pathway to mitigate RIII. We concluded that agonism or upregulation of VDR expression attenuates radiation-induced intestinal damage in mice and promotes the repair of epithelial damage in intestinal stem cells.

为了保证防原医学实践课教学授课的顺利进行,海军军医大学舰船辐射医学防护教研室借助核应急医学救援虚拟仿真实践教学平台,开展了基于虚拟仿真的防原医学线上小班实践教学活动,针对教学设计、教学过程、教学效果等进行了一系列有益的探索,并与以往线下授课的实践教学效果进行对比,发现基于虚拟仿真的防原医学线上实践教学能够克服现场实践教学无法开展的不足,有效满足实践教学需求.课程结束后通过与学员和主讲教员进行交流发现,基于虚拟仿真的线上实践教学比现场实践教学更能调动学员积极性,在切实提高了学员操作能力与协作能力的同时,取得了非常好的实践教学效果.

Damage of Intestinal Stem Cells (ISCs) is the main cause of radiation induced-intestinal injury (RIII). Recently, hypoxia Inducible factor (HIF) was verified to be critical for promoting proliferation of ISCs, which suggested a protective role of HIF in the RIII. Thus, we investigated the effect of FG-4592, a novel up-regulator of HIF, on the protection of RIII. With/without FG-4592 treatment, the abdomen of mice was radiated, and intestinal injury was assessed. Especially, by intestinal organoid culture, the multiplication capacity and differentiation features of ISCs were detected. As a result, FG-4592, a novel up-regulator of HIF could remit RIII and promote regeneration and differentiation of ISCs after radiation, which were depended on HIF-2 rather than HIF-1.

防原医学是军事预防医学中的重要组成部分.在新时期新型军事医学人才培养需求的要求下,防原医学从注重理论教学转移到注重核应急医学救援的实践教学上来.通过创新性地建立"三位一体"的实践能力培养模式,更加注重学员互相协作和综合分析解决问题的综合能力培养,让学员系统性参与核应急医学救援教学实践,切实提高了学员的核应急医学救援能力与综合训练效果,增进了学员的协作能力和创新意识,取得了非常好的实践教学效果.

Severe ionizing radiation causes the acute lethal damage of haematopoietic system and gastrointestinal tract. Here, we found CL429, the novel chimeric TLR2/NOD2 agonist, exhibited significant radioprotective effects in mice. CL429 increased mice survival, protected mice against the lethal damage of haematopoietic system and gastrointestinal tract. CL429 was more effective than equivalent amounts of monospecific (TLR2 or NOD2) and combination (TLR2 + NOD2) of molecules in preventing radiation-induced death. The radioprotection of CL429 was mainly mediated by activating TLR2 and partially activating NOD2. CL429-induced radioprotection was largely dependent on the activation of TLR2-MyD88-NF-kappa B signalling pathway. In conclusion, the data suggested that the co-activation of TLR2 and NOD2 could induce significant synergistic radioprotective effects and CL429 might be a potential high-efficiency selective agent.

Ionizing radiation is one of the common environmental carcinogens. miRNAs play critical roles in the processes of tumor occurrence, development, metastasis. However, the relationship between radiation-induced carcinogenesis and miRNA rarely reported. This study is aimed to investigate the effect of miRNAs on radiation-induced carcinogenesis. In this study we established the radiation-induced thymic lymphoma mice model. By using miRNA array of RTL tissue and predicting for miRNAs target genes, a miRNA-mRNA crosstalk network was established. Based on this network, we identified a critical miRNA, miR-486, which was the most down-regulated in the radiation-induced carcinogenesis. Then the function of miR-486 was confirmed by using knockout mice and cellular experiments. As a result, miR-486 could inhibit proliferation of mouse lymphoma cells by targeting IGF2BP3 mRNA. The adenovirus over-expression miR-486 vector reduced tumorigenesis in vivo . MiR-486 knockout mice have a strong tendency of radiation-induced carcinogenesis. In conclusion, miR-486 inhibits the proliferation of lymphoma cells and tumorigenesis induced by radiation through targeting IGF2BP3.

大规模网络开放课程(Massive Open Online Course,MOOC)是近年来发展迅速的一种网络授课形式,其具有大规模和开放性的特点,使得知识传播较传统教学形式更为迅速和广泛.特别是在当前军事职业教育全面推动的背景下,军队院校MOOC的引导性作用更为突出.本教研室的舰艇辐射医学防护课程作为我校首批MOOC建设项目,经过授课教员的共同努力,如期上线并收到业内专家和学员的广泛好评.本文就教研室在MOOC准备、制作、上线等过程中的情况做一个简单介绍,并对课程构建中出现的问题提出思考.

Objective:To screen the key miRNA downstream of TLR2 and explore the function of the miR-21.Methods:Wild type (WT) and TLR2 KO mice were irradiated with 60Co γ-ray to compare their survivals. The downstream miRNAs of TLR2 signaling pathway were screened by RNA sequence in BMCs, and their expressions were verified by QT-PCR. Cell lines with overexpression or knockdown of a miRNA were established to evaluate the function of miRNA. Results:The radiosensitivity of TLR2 KO mice was higher than that of TLR2 WT mice( χ2=4.490, 13.100, 7.928, P<0.05). The bone marrow transplantation experiment proved that the increased radiosensitivity of TLR2 KO mice was related to BMCs ( χ2=4.291, P<0.05). A total of 55 differentially expressed genes were screened by RNA sequence ([log2 Fold Change]>0.95, Q<0.05), of which 28 were up-regulated and 27 were down-regulated. QT-PCR assay determined that miR-21 was down-regulated in BMCs of TLR2 KO ( t=9.420, P<0.01) and MyD88 KO ( t=10.700, P<0.01) mice. It was proved by QT-PCR that the expressions of IL-6 ( t=13.790, P<0.05) and TNF-α ( t=14.280, P<0.05) were increased in a TLR2 dependent manner after PAM3CSK4 stimulation. Overexpression of miR-21 promoted viability of EL4 cells ( t=5.951, P<0.05) and NIH/3T3 cells ( t=4.786, P<0.05) and reduced BMCs apoptosis in WT ( t=4.842, P<0.05) and TLR2 KO ( t=10.520, P<0.05) mice after radiation. Inhibition of miR-21 decreased the viability of EL4 cells ( t=4.815, P<0.05) and NIH/3T3 cells ( t=4.042, P<0.05). Conclusions:miR-21 plays a key regulatory role in the process of TLR2 radioprotection, which may be related to the up-regulation of IL-6 and TNF-α.

核应急医学救援是国家核应急组织体系的重要组成部分,针对当前核应急医学救援任职教育中存在的问题,笔者所在的教研室结合近几年举办核应急医学救援任职教育培训班的实践,有针对性的提出了相应的改进措施并在实践中不断进行完善.核应急医学救援任职教育培训侧重岗位任职能力的提升,融入了虚拟仿真信息化教学,鼓励在职学员分享任职心得体会,变更原有的终结性考核为过程性考核,在核应急医学救援培训班中进行了探索与实践.结果发现新的改进措施不仅活跃了培训气氛,减轻了考试压力;还提高了学员的应用能力,对提升在职学员的核应急医学救援岗位任职能力发挥了重要作用.

Backgrounds: There is still little progress in the effective treatment of radiation-induced lung injury (RILI), a key dose-limiting factor for thoracic radiotherapy. Ras-related C3 botulinum toxin substrate1, Rac1, is a small guanosine triphosphatase involved in various mechanisms of radiation-induced damage and is over-expressed/mutated in various tumors. The gain-of-function mutation of Rac1 mediates tumor cells’ resistance to radiotherapy. Therefore, inhibiting Rac1 has the potential of protecting normal tissues from radiation-induced injury, and at the same time, sensitizing tumor to radiation therapy, which makes it a promising ideal target for radiation protection. To investigate the protective effects and mechanisms of Rac1 inhibition on RILI, and explore the possible mechanisms that mediate the differential effects of Rac1 inhibition on normal lung tissue and tumor cells. Methods: 60 Co radioactive source was used for ionizing radiation (IR). RILI mouse model was constructed. Influence of Rac1 inhibition which was achieved by Rac1-specific inhibitor, NSC23766, on RILI were studied by H & E and Masson staining, and immunohistochemical staining of vimentin, TGF-βand γ-H 2 AX. Normal mouse lung epithelial cell line, MLE-12, and mouse lung cancer cell line, LLC, were used to study the effects of Rac1 inhibition on the cellular level. RNA-seq analysis was used for screening differential gene expression caused by Rac1 knockdown. The molecular mechanisms of Rac1 inhibition were studied at the cellular level. Subcutaneous tumor-bearing nude mouse model and orthotopic lung tumor-bearing mouse model were constructed to verify the bidirectional effects of Rac1 inhibition in vivo. Results: RILI of mouse was alleviated by intraperitoneal injection of NSC23766. Rac1 inhibition/knockdown reduced the radiation-induced damage of MLE-12 while aggravated that of LLC. Rac1 translocated from cytoplasm to nucleus after radiation. Tumor protein p53-inducible nuclear protein 1, Trp53inp1, was down-regulated by Rac1 knockdown. In vivo study further proved the differential effects of Rac1 inhibition. Rac1 was over-expressed and mutated in LLC cells, and the expression level of Trp53inp1 significantly lower, compared with that of MLE-12. Conclusion: Rac1 inhibition reduced the radiation-induced damage of normal lung epithelial cells, thereby alleviating RILI of mouse. These effects were partially mediated by down-regulating the expression of Trp53inp1. However, Rac1 inhibition significantly increased the sensitivity of LLC to radiation damage and inhibited its growth. The over-expression and mutation of Rac1, and the significant low expression of Trp53inp1 in LLC, may be the fundamental reasons mediating the differential effects of Rac1 inhibition.

为了推动侧重核损伤救治能力培养的防原医学教学改革的不断深化,培养新型军事医学人才,对防原医学课程的考核方式进行了系统性的改革,在压缩理论考核比重而增加实践考核比重的同时,采用多样化的评价方式对学员进行过程性评价.为了评估此次课程考核方式改革的效果,以问卷调查的形式考察学员对教学考核效果的满意度、整体考核方案设置以及新增考核方式实施的意见和建议,进而分析与思考此次教学考核改革的策略,为进一步促进防原医学教学质量的提高探寻对策.