基于模糊物元模型的用频方案评估

提出了一种用频方案评估的方法,该方法建立了一套涵盖需求匹配性、方案经济性、方案抗扰性的用频方案评估指标体系,并利用基于模糊物元模型实现了多目标用频方案评估.仿真试验结果表明：该指标体系易于量化分析,采用模糊元方法直观地反映用频方案对不同目标的实现程度,能够较为客观地对用频方案进行评估.这对用频辅助决策有重要的应用价值.     

一种电磁环境量化分析方法

提出了一种电磁环境量化分析的新方法.该方法充分考虑了电磁环境信号的极化方式、调制方式,给出了极化因子、调制因子的内涵和定义基于不同极化方式、调制方式之间影响特性的理论分析和仿真,给出了典型电磁环境的极化因子、调制因子及其变化特性.所得成果为深入研究复杂电磁环境的量化分析和评估方法提供了积极的理论探索.     

区域频谱资源数据融合方法

为实现高效的数据融合,提出了一种多源频谱资源数据融合方法.该方法将多个监测节点的频谱可用资源评估信息进行融合,利用意见形成理论,对关心地域的频谱资源可用性进行评估,为频谱动态管理提供资源状态信息.通过对不同网络规模的仿真分析,结果表明：在意见形成理论的基础上,通过设定“骨干”节点,缩减了50%的融合时间;在网络节点不超过100个的情况下,通过30轮次的沟通即可完成频谱资源数据的融合.     

松茸多糖对乳酸菌发酵及酸奶品质的影响

以松茸多糖为研究对象,通过测定酸奶的滴定酸度、持水力、质构、乳酸菌活菌数、感官等指标,研究松茸多糖对保加利亚乳杆菌和嗜热链球菌两种乳酸菌的发酵及酸奶品质的影响。结果表明:松茸多糖对乳酸菌的影响呈倒\     

晋西北酸粥发酵过程中微生物基因组DNA提取方法的比较

为了找到一种简单高效的晋西北酸粥发酵过程中微生物基因组DNA提取方法,本文采取对提取的微生物基因组DNA进行浓度测定的方法,比较了溶菌酶-SDS-蛋白酶K法、改良CTAB法和改良CTAB-溶菌酶法三种方法的提取效果。结果表明:溶菌酶-SDS-蛋白酶K法效果最好,可以获得质量较高的微生物基因组DNA,DNA浓度为1657.53 ng/μL;改良CTAB-溶菌酶法比溶菌酶-SDS-蛋白酶K法效果差,DNA浓度为1308.08 ng/μL;改良CTAB法对微生物基因组DNA的提取效果比溶菌酶-SDS-蛋白酶K法更差,DNA浓度为1098.36 ng/μL。以提取到的微生物基因组总DNA为模板,进行16S r DNA基因的PCR扩增,在回收产物中目的条带清晰,表明提取到的微生物基因组DNA含量高、结构完整。整体实验结果表明,溶菌酶-SDS-蛋白酶K法对于提取晋西北酸粥发酵过程中微生物基因组DNA效果最好。      

乳酸菌氧化锆珠破壁方法的优化及适用性研究

本实验旨在优化氧化锆珠破壁方法,以期筛选出较佳的破壁条件,提高蛋白得率。实验在菌体重量、研磨buffer和研磨时间这3方面对该破壁方法进行了优化,并通过SDS-PAGE来分析其破壁效果。在优化后的条件下,同时对6株乳酸菌进行破壁处理并通过SDS-PAGE来分析其破壁效果。结果表明:在菌体重量、研磨buffer、锆珠三者的加入比例（W/V/W）为0.013 g∶300μL∶1 g的条件下,研磨15 min,提取的蛋白图谱条带清晰,丰度高;RIPA、PBS、PENP、GUS作为研磨buffer时,提取的蛋白图谱条带清晰且丰度高,而8 mol/L尿素作为研磨buffer时,图谱条带模糊且丰度低;6株乳酸菌经该方法破壁处理后,蛋白图谱条带均具有较高的丰度和清晰度。因此,对于乳酸菌的破壁,氧化锆珠破壁法具有快速、高效的优点。      

Emerging Potential Mechanism and Therapeutic Target of Ferroptosis in PDAC: A Promising Future

Pancreatic cancer (PC) is a devastating malignant tumor of gastrointestinal (GI) tumors characterized by late diagnosis, low treatment success and poor prognosis. The most common pathological type of PC is pancreatic ductal adenocarcinoma (PDAC), which accounts for approximately 95% of PC. PDAC is primarily driven by the Kirsten rat sarcoma virus (KRAS) oncogene. Ferroptosis was originally described as ras-dependent cell death but is now defined as a regulated cell death caused by iron accumulation and lipid peroxidation. Recent studies have revealed that ferroptosis plays an important role in the development and therapeutic response of tumors, especially PDAC. As the non-apoptotic cell death, ferroptosis may minimize the emergence of drug resistance for clinical trials of PDAC. This article reviews what has been learned in recent years about the mechanisms of ferroptosis in PDAC, introduces the association between ferroptosis and the KRAS target, and summarizes several potential strategies that are capable of triggering ferroptosis to suppress PDAC progression.     

Lactoferrin Ameliorates Ovalbumin-Induced Asthma in Mice through Reducing Dendritic-Cell-Derived Th2 Cell Responses

Asthma is a chronic respiratory disease with symptoms such as expiratory airflow narrowing and airway hyperresponsiveness (AHR). Millions of people suffer from asthma and are at risk of life-threatening conditions. Lactoferrin (LF) is a glycoprotein with multiple physiological functions, including antioxidant, anti-inflammatory, antimicrobial, and antitumoral activities. LF has been shown to function in immunoregulatory activities in ovalbumin (OVA)-induced delayed type hypersensitivity (DTH) in mice. Hence, the purpose of this study was to investigate the roles of LF in AHR and the functions of dendritic cells (DCs) and Th2-related responses in asthma. Twenty 8-week-old male BALB/c mice were divided into normal control (NC), ovalbumin (OVA)-sensitized, and OVA-sensitized with low dose of LF (100 mg/kg) or high dose of LF (300 mg/kg) treatment groups. The mice were challenged by intranasal instillation with 5% OVA on the 21st to 27th day after the start of the sensitization period. The AHR, cytokines in bronchoalveolar lavage fluid, and pulmonary histology of each mouse were measured. Serum OVA-specific IgE and IgG1 and OVA-specific splenocyte responses were further detected. The results showed that LF exhibited protective effects in ameliorating AHR, as well as lung inflammation and damage, in reducing the expression of Th2 cytokines and the secretion of allergen-specific antibodies, in influencing the functions of DCs, and in decreasing the level of Th2 immune responses in a BALB/c mouse model of OVA-induced allergic asthma. Importantly, we demonstrated that LF has practical application in reducing DC-induced Th2 cell responses in asthma. In conclusion, LF exhibits anti-inflammation and immunoregulation activities in OVA-induced allergic asthma. These results suggest that LF may act as a supplement to prevent asthma-induced lung injury and provide an additional agent for reducing asthma severity.     

Revealing Differential Expression of Phytohormones in Sorghum in Response to Aphid Attack Using the Metabolomics Approach

Sorghum (Sorghum bicolor) is an important multipurpose crop grown worldwide, but like many other crops, it is often threatened by insect pests. Sugarcane aphid (SCA, Melanaphis sacchari Zehntner), for example, is one of the most severe pests in sorghum, which causes plant damage and yield loss. The main objective of this study was to assess the effect of phytohormones on host plant resistance to aphid attack. Two sorghum genotypes, BTx623 (susceptible) and Tx2783 (resistant), were selected for a comparative analysis of differential expression of a group of phytohormones in response to aphid infestation. The quantification of phytohormones through LC-MS demonstrated higher levels of jasmonic acid (JA), salicylic acid (SA), abscisic acid (ABA), and auxins in the resistant genotype infested with SCA. The PCA plot supports the strong differential responses between resistant and susceptible genotypes, indicating a positive correlation between JA and ABA and a negative correlation between SA and auxins. Similarly, RT-PCR results of the phytohormones-related marker genes showed higher expression in the resistant genotype compared to the susceptible one. Furthermore, to corroborate the role of phytohormones in plant defense, the susceptible genotype was treated with SA, JA, and ABA. The exogenous application of SA and JA + ABA significantly reduced plant mortality, aphid number, and damage in the susceptible genotype, suggesting a strong correlation between phytohormones and plant survival. Our findings indicate that phytohormones play positive roles in plant defense against aphids and provide new insights into the molecular mechanisms operating in plants for self-protection. These findings could also stimulate further research into the mystery about the regulation of phytohormone production during plant interaction with aphids.     

Regulation of Epstein-Barr Virus Minor Capsid Protein BORF1 by TRIM5α

TRIM5α is a host anti-retroviral restriction factor that destroys human immunodeficiency virus (HIV) virions and triggers innate immune signaling. TRIM5α also mediates the autophagic degradation of target proteins via TRIMosome formation. We previously showed that TRIM5α promotes Epstein-Barr virus (EBV) Rta ubiquitination and attenuates EBV lytic progression. In this study, we sought to elucidate whether TRIM5α can interact with and induce the degradation of EBV capsid proteins. Glutathione S-transferase (GST) pulldown and immunoprecipitation assays were conducted to identify interacting proteins, and mutants were generated to investigate key binding domains and ubiquitination sites. Results showed that TRIM5α binds directly with BORF1, an EBV capsid protein with a nuclear localization signal (NLS) that enables the transport of EBV capsid proteins into the host nucleus to facilitate capsid assembly. TRIM5α promotes BORF1 ubiquitination, which requires the surface patch region in the TRIM5α PRY/SPRY domain. TRIM5α expression also decreases the stability of BORF1(6KR), a mutant with all lysine residues mutated to arginine. However, chloroquine treatment restores the stability of BORF1(6KR), suggesting that TRIM5α destabilizes BORF1 via direct recognition of its substrate for autophagic degradation. These results reveal novel insights into the antiviral impact of TRIM5α beyond retroviruses.