蜗牛酶对原生质体游离的影响

用10科11种双子叶植物的营养器官,在含1mg/L 2,4—D的MS固体培养基上诱导形成愈伤组织。取其生长旺盛的区域进行原生质体游离,并采用未经处理的相应植物的新鲜叶或茎作对照。研究结果表明,蜗牛酶对愈伤组织的原生质体游离具有明显的促进作用,而对照却无此效应。还研究了两种植物愈伤组织的继代天数和不同的酶组合对原生质体游离的影响。     

大鼠出生后脑内钙调神经磷酸酶的研究

本文用BA-ELISA.immunoblotting及酶活力测定等方法,研究了大鼠脑中钙调神经磷酸酶在大鼠出生后的变化情况。结果表明,钙调神经磷酸酶的含量在大鼠出生后第二周和第三周显著增加,其活力也在出生后第二周达到顶峰。钙调神经磷酸酶这种有规律的变化与脑中突触形成在时间上是一致的,暗示钙调神经磷酸酶可能参与突触功能的调节。     

岭南垛基果林湿地土壤碳组分特征

岭南垛基果林湿地是珠三角地区典型的湿地类型之一,其对土壤碳汇的贡献值得关注。为探讨果林种植类型对土壤有机碳的影响,对广州垛基果林湿地内种植黄皮(Clausenalansium)(HP),龙眼(Dimocarpuslongan)(LY)、杨桃(Averrhoa carambola)(YT),龙眼和黄皮间种(LH),杨桃、龙眼和黄皮间种(YLH)共5种种植类型下的表层(0～20 cm)土壤碳组分进行研究。结果表明,不同的植被类型对土壤的总有机碳(SOC)、可溶性有机碳(DOC)、微生物生物量碳(MBC)、易氧化有机碳(ROC)、惰性碳(NLC)含量都有影响,LY的SOC含量最高(22.6 g/kg),显著高于YLH (P<0.05),且NLC含量显著高于LH和YLH (P<0.05)。NLC含量与土壤养分呈正相关,与土壤容重呈负相关。YT的MBC含量显著高于LY、HP、LH (P<0.05),且MBC/SOC显著高于HP、LY(P<0.05)。YLH模式下,土壤DOC含量和DOC/SOC显著高于其他植被类型(P<0.05)。LH的ROC/SOC显著高于HP和L...     

四川缙云山森林群落林窗边缘效应的研究

 本文运用Shannon—Wiener物种多样性指数、Simpson生态优势度指标以及边缘效应强度指数,对缙云山亚热带森林群落林窗的边缘效应现象进行了初步研究。29个林窗样地不同部位上述指标的测定表明用物种多样性指数拟合边缘效应测度通式,缙云山亚热带森林群落林窗的边缘效应强度值为1—3左右;而用生态优势度值拟合边缘效应强度测式,则上述边缘效应强度值为0.1一1.2左右。研究表明林窗边缘区由于边缘效应的作用有增大物种多样性的趋势。而林窗面积、所处坡向以及林窗所在的森林群落类型,都对处于不同发育阶段的林窗的边缘效应强度具有影响。在此基础上,本文对林窗边缘效应强度的变化规律、效应性质、测定意义以及对森林营造和优化管理上的作用进行了一定探讨。     

Bisphenol S induces oxidative stress-mediated impairment of testosterone synthesis by inhibiting the Nrf2/HO-1 signaling pathway

Bisphenol S (BPS) is an environmental endocrine disruptor widely used in industrial production. BPS induces oxidative stress and exhibits male reproductive toxicity in mice, but the mechanisms by which BPS impairs steroid hormone synthesis are not fully understood. Nuclear factor erythroid 2-related factor 2(Nrf2)/HO-1 signaling is a key pathway in improving cellular antioxidant defense capacities. Therefore, this study explored the effects of exposure to BPS on testosterone synthesis in adult male mice and its mechanisms with regard to the Nrf2/HO-1 signaling pathway. Adult male C57BL/6 mice were orally exposed to BPS (2, 20, and 200 mg/kg BW) with sesame oil as a vehicle (0.1 ml/10 g BW) per day for 28 consecutive days. The results showed that compared with the control group, serum testosterone levels were substantially reduced in the 20 and 200 mg/kg BPS treatment groups, and testicular testosterone levels were reduced in all BPS treatment groups. These changes were accompanied by a prominent decrease in the expression levels of testosterone synthesis-related enzymes (STAR, CYP11A1, CYP17A1, HSD3B1, and HSD17B3) in the mouse testis. In addition, BPS induced oxidative stress in the testis by upregulating the messenger RNA and protein levels of Keap1 and downregulating the levels of Nrf2, HO-1, and downstream antioxidant enzymes (CAT, SOD1, and Gpx4). In summary, our results indicate that exposure of adult male mice to BPS can inhibit Nrf2/HO-1 signaling and antioxidant enzyme activity, which induces oxidative stress and thereby may impair testosterone synthesis in testicular tissues, leading to reproductive damage.     

Duvelisib attenuates bleomycin-induced pulmonary fibrosis via inhibiting the PI3K/Akt/mTOR signalling pathway

Idiopathic pulmonary fibrosis (IPF) is a chronic progressive interstitial lung disease that seriously threatens the health of patients. The pathogenesis of IPF is still unclear, and there is a lack of effective therapeutic drugs. Myofibroblasts are the main effector cells of IPF, leading to excessive deposition of extracellular matrix (ECM) and promoting the progression of fibrosis. Inhibiting the excessive activation and relieving autophagy blockage of myofibroblasts is the key to treat IPF. PI3K/Akt/mTOR pathway plays a key regulatory role in promoting fibroblast activation and autophagy inhibition in lung fibrosis. Duvelisib is a PI3K inhibitor that can simultaneously inhibit the activities of PI3K-δ and PI3K-γ, and is mainly used for the treatment of relapsed/refractory chronic lymphocytic leukaemia (CLL) and small lymphocytic lymphoma tumour (SLL). In this study, we aimed to examine the effects of Duvelisib on pulmonary fibrosis. We used a mouse model of bleomycin-induced pulmonary fibrosis to evaluate the effects of Duvelisib on pulmonary fibrosis in vivo and further explored the potential pharmacological mechanisms of Duvelisib in lung fibroblasts in vitro. The in vivo experiments showed that Duvelisib significantly alleviated bleomycin-induced collagen deposition and improved pulmonary function. In vitro and in vivo pharmacological experiments showed that Duvelisib dose-dependently suppressed lung fibroblast activation and improved autophagy inhibition by inhibiting the phosphorylation of PI3K, Akt and mTOR. Our results indicate that Duvelisib can alleviate the severity of pulmonary fibrosis and provide potential drugs for the treatment of pulmonary fibrosis.     

GPD1L inhibits renal cell carcinoma progression by regulating PINK1/Parkin-mediated mitophagy

Few approaches have been conducted in the treatment of renal cell carcinoma (RCC) after nephrectomy, resulting in a high mortality rate in urological tumours. Mitophagy is a mechanism of mitochondrial quality control that enables selective degradation of damaged and unnecessary mitochondria. Previous studies have found that glycerol-3-phosphate dehydrogenase 1-like (GPD1L) is associated with the progression of tumours such as lung cancer, colorectal cancer and oropharyngeal cancer, but the potential mechanism in RCC is still unclear. In this study, microarrays from tumour databases were analysed. The expression of GPD1L was confirmed by RT–qPCR and western blotting. The effect and mechanism of GPD1L were explored using cell counting kit 8, wound healing, invasion, flow cytometry and mitophagy-related experiments. The role of GPD1L was further confirmed in vivo. The results showed that GPD1L expression was downregulated and positively correlated with prognosis in RCC. Functional experiments revealed that GPD1L prevented proliferation, migration and invasion while promoting apoptosis and mitochondrial injury in vitro. The mechanistic results indicated that GPD1L interacted with PINK1, promoting PINK1/Parkin-mediated mitophagy. However, inhibition of PINK1 reversed GPD1L-mediated mitochondrial injury and mitophagy. Moreover, GPD1L prevented tumour growth and promoted mitophagy by activating the PINK1/Parkin pathway in vivo. Our study shows that GPD1L has a positive correlation with the prognosis of RCC. The potential mechanism involves interacting with PINK1 and regulating the PINK1/Parkin pathway. In conclusion, these results reveal that GPD1L can act as a biomarker and target for RCC diagnosis and therapy.     

底栖生物影响下的潮滩微地貌演化数值模拟

潮滩是海岸带湿地的主要类型之一,其中分布的底栖生物对生态环境具有重要的调节作用。潮滩底栖微藻、泥沙与水动力之间存在相互作用,影响潮滩微地貌形态,明晰底栖生物对潮滩微地貌的演化机制至关重要。以黄河三角洲潮滩湿地为研究区,通过构建潮滩微地貌动力模型,探究底栖生物对微地貌格局演化的作用机制,分析底栖生物对微地貌系统稳定性的影响。结果表明(1)底栖微藻生长与泥沙扩散、水流再分配过程交互作用驱动下,潮滩上可形成底栖微藻覆盖的高丘与积水洼地交替分布的规则性微地貌斑图;(2)微地貌斑图的形成提高了潮滩生态系统初级生产力和泥沙淤积高度;(3)底栖微藻与泥沙、水流的交互作用使得潮滩微地貌系统对侵蚀扰动呈现非线性响应行为,系统存在临界点,且在一定侵蚀率范围内存在双稳态;(4)黄河口泥螺入侵使得微地貌系统抵抗侵蚀扰动能力减小,且系统稳定性随泥螺生物量的增加而降低。     

青藏高原牧区家庭能源消费对生态环境和人体健康的影响研究现状与展望

探究家庭能源消费对生态环境和人体健康的研究是系统推进家庭能源绿色低碳转型和实现联合国2030可持续发展目标的关键。重点综述了目前家庭能源消费、影响因素及其对生态环境和居民健康影响的国际研究现状。目前研究不足主要聚焦在以下两个方面：一方面,影响家庭能源消费因素的贡献率和影响消费行为的驱动机制尚不清晰;另一方面,目前主要针对家庭能源消费或者生态系统或者环境或者居民健康其中的某一方面或者某两个方面开展研究,鲜有研究系统的考虑家庭能源消费对生态环境和人体健康影响的综合研究。基于上述研究现状,结合青藏高原的实际情况,提出未来需要在宏观层面和微观层面加强研究。宏观层面：(1)亟需厘清青藏高原家庭能源与生态环境和人体健康之间的内在联系与驱动机制,形成青藏高原牧区“家庭能源-生态效应-环境效应-健康效应”的理论分析框架;(2)构建模块化的牧区“能源-生态-环境-健康-经济”等多学科交叉的综合评估模型,形成完整的、系统的评估方法。微观层面：(1)迫切开展青藏高原家庭能源消费特征与变化规律的研究;(2)深入开展家庭能源消费特征和变化规律与生态系统的反馈机制与量化研究;(3)加强牧区室内空气污染物浓度测定,...