The most damaging disease affecting citrus globally is Huanglongbing (HLB), primarily attributed to the infection by 'Candidatus Liberibacter asiaticus' (CaLas). Based on comparative transcriptome data, two cellulose synthase (CESA) genes responsive to CaLas infection induction were screened, and one gene cloned with higher differential expression level was selected and named CsCESA1. we verified the interaction between CsCESA1 and citrus exopolysaccharide 2 (CsEPS2) proteins. Subcellular localization in tobacco indicated that both CsCESA1 and CsEPS2 proteins are primarily located in the nucleus and cytoplasm. RT-qPCR analysis indicated that the expression levels of CsCESA1 and CsEPS2 were associated with variety tolerance, tissue site, and symptom development. Furthermore, we generated CsCESA1 and CsEPS2 silencing plants and obtained CsCESA1 and CsEPS2 silencing and overexpressing hairy roots. The analysis of hormone content and gene expression also showed that CsCESA1 and CsEPS2 are involved in transcriptional regulation of genes involved in systemic acquired resistance (SAR) response. In conclusion, our results suggested that CsCESA1 and CsEPS2 could serve as potential resistance genes for HLB disease, offering insights into the plant's defense mechanisms against HLB.

2025-03-01·Journal of Ethnopharmacology

The stems of Syringa oblata Lindl. exert cardioprotective effects against acute myocardial ischemia by inhibiting the TLR4/MyD88/NF-κB and NLRP3 inflammasome signaling pathways in mice

Article

作者: Kang, Lulu ; Shen, Yiru ; Ding, Qiuyuan ; Liu, Changxin ; Tai, Badalahu ; Zhang, Zefeng ; Yang, Guodong ; Chai, Xingyun ; Xu, Jixuan ; Gao, Xiaoli

ETHNOPHARMACOLOGICAL RELEVANCEThe stripped roots and stems of Syringa oblata Lindl. (SO), a Mongolian and Tibetan folk medicinal plant, are renowned for their traditional use against "Khii", pain relief, and heat clearing. It is used to treat cardiovascular diseases (CVDs), upset, insomnia, and other symptoms and is commonly used as a substitute for another plant known as S. pinnatifolia, which is used in Mongolian folk medicine.OBJECTIVEThis study analyzed the cardioprotective effect of SO against myocardial ischemia and the underlying mechanism through cardiac inflammation and the pyroptosis pathway.MATERIALS AND METHODSThis study developed an acute myocardial infarction (AMI) model by ligating the left anterior descending coronary artery (LAD) in mice. Additionally, the cardioprotective effect was determined via echocardiography, detection of creatine kinase-MB (CK-MB), lactate dehydrogenase (LDH), and cardiac troponin-I (cTnI) detection, and hematoxylin and eosin (HE) staining. Lipopolysaccharide (LPS) plus adenosine triphosphate (ATP) was used to stimulate RAW264.7 mouse monocyte macrophages to induce pyroptosis. The cell morphology was monitored by scanning electron microscopy. The underlying mechanisms were assessed via immunohistochemistry, immunofluorescence staining, and western blotting (WB).RESULTSSO (40-160 mg/kg) significantly decreased the values of left ventricular internal dimension diastole (LVID; d) and left ventricular internal dimension systole (LVID; s), increased the ejection fraction (EF) and fractional shortening (FS), reduced serum levels of CK-MB, LDH, and cTnI, and mitigated microstructural destruction of MI tissue. SO at concentrations of 1.25-10 μg/mL significantly inhibited nitrogen monoxide (NO) production. At 10 μg/mL, it strongly suppressed pyroptosis while maintaining the morphological features of RAW264.7 cells. These findings suggest that SO has significant anti-myocardial ischemic effects. Administration of SO (40-160 mg/kg) in mice significantly reduced interleukin-1β (IL-1β) and interleukin-18 (IL-18) levels, accompanied by decreased fluorescence intensities of the apoptosis speck-like protein containing a caspase recruitment domain (ASC), NOD-like receptor family pyrin domain-containing 3 (NLRP3), and cysteinyl aspartate-specific protease-1 (caspase-1) proteins. WB analysis revealed that SO (40-160 mg/kg) treatment reduced inflammatory protein levels, including toll-like receptor 4 (TLR4) and myeloid differentiation factor 88 (MyD88). Additionally, the phosphorylation levels of nuclear factor-kappa-B (NF-κB) and inhibitors of NF-kappa-Bα (IκBα) were suppressed. Moreover, levels of pyroptosis-related proteins, including ASC, caspase-1, NLRP3, and gasdermin D (GSDMD), were reduced.CONCLUSIONSSO may protect against myocardial ischemia through modulation of the TLR4/MyD88/NF-κB inflammatory pathway and suppression of NLRP3 inflammasome-mediated pyroptosis. This study demonstrates that SO alleviates AMI by mechanisms involving anti-inflammatory effects and pyroptosis inhibition, establishing an experimental basis for evaluating its therapeutic efficacy and clinical translation.

2025-02-01·Transactions of the Institute of Measurement and Control

Distributed finite-time adaptive consensus output-feedback control of multi-agent systems under switching topologies

作者: Guan, Shiwen ; Pang, Hongbo ; Li, Chensong

The paper investigates the finite-time adaptive consensus control of nonlinear multi-agent systems (MASs) by output-feedback. During the process of control design, the fuzzy logic system (FLS) is employed to approximate nonlinear function, as well as constructing a fuzzy state observer to estimate unmeasured states. Combining the dynamic surface control (DSC) with adaptive backstepping method conquers the complexity explosion issue. Then, semi-global practical finite-time stability (SGPFS) for closed-loop system is obtained under arbitrary switching communication topologies. All the signals of the overall system are uniformly ultimately bounded (UUB). Finally, the availability of developed control approach will be demonstrated through a simulation.

项与内蒙古民族大学相关的新闻（医药）

2022-07-22

·GlobeNewswire-Health Care

Immune Therapeutics, Inc. Appoints Dr. Stephen Wilson as Chief Executive Officer

ORLANDO, FL, July 22, 2022 (GLOBE NEWSWIRE) -- Immune Therapeutics, Inc. (OTC Pink: IMUN) (“Immune” or “IMUN”), a specialty pharmaceutical company involved in the acquisition, development and commercialization of pharmaceutical and biotechnology products that have a short and well-defined path to market, is pleased to announce the appointment of Dr. Stephen “Steve” Wilson as Immune’s Chief Executive Officer (CEO), President, and interim Chief Financial Officer (CFO) effective July 19, 2022; he will continue to serve as a member of the Company’s Board of Directors. Dr. Wilson brings over 20 years of experience in biomedical research, executive management, and corporate governance. He is a trained immunologist. In addition, he is, among other things, an Associate Clinical Professor at the University of California, San Diego, and he previously served as the Chief Operating Officer at the La Jolla Institute for Immunology as it grew to become an international powerhouse. Immune also announced that Kevin Phelps has stepped down from his positions as the company’s CFO, President, and CEO, but he will remain a member of Immune’s Board of Directors. The appointment of Dr. Wilson as Immune’s CEO, President, and interim CFO is expected to further strengthen IMUN’s global executive leadership team to drive its next phase of growth and operational success within a new operational model, initially focused on regulatory approval and commercialization of existing assets that treat patients with inflammatory disease. Dr. Wilson stated, “Our strategy is to lever the global need for affordable and effective therapeutics and modern financial tools; this hinges on acquisition, development and commercialization of pharmaceutical and biotechnology products that have a short and well-defined path to market. We have assets that fit this profile, and our business objectives fit immediate patient needs. Going forward, we will take a measured portfolio approach to investment, development and commercialization that will mandate each additional program be hyper focused, capital efficient and small-scale with clear paths to regulatory approval. Financing these programs through modern investment vehicles and partnerships, we plan to deploy in markets that include, but are not dependent upon, US commercialization.” Forward Looking Statement This press release may contain information about our views of future expectations, plans and prospects that constitute forward-looking statements. All forward-looking statements are based on management’s beliefs, assumptions, and expectations of Immune’s future economic performance, taking into account the information currently available to it. These statements are not statements of historical fact. Although Immune believes the expectations reflected in such forward-looking statements are based on reasonable assumptions, it can give no assurance that its expectations will be attained. Immune does not undertake any duty to update any statements contained herein (including any forward-looking statements), except as required by law. No assurances can be made that Immune will successfully acquire its acquisition targets. Forward-looking statements are subject to a number of factors, risks, and uncertainties, some of which are not currently known to us, that may cause Immune’s actual results, performance, or financial condition to be materially different from the expectations of future results, performance, or financial position. Actual results may differ materially from the expectations discussed in forward-looking statements. Factors that could cause actual results to differ materially from expectations include general industry considerations, regulatory changes, changes in local or national economic conditions and other risks set forth in “Risk Factors” included in our filings with the Securities and Exchange Commission. Disclaimer The information provided in this press release is intended for general knowledge only and is not a substitute for professional medical advice or treatment for specific medical conditions. Always seek the advice of your physician or other qualified health care provider with any questions you may have regarding a medical condition. This information is not intended to diagnose, treat, cure or prevent any disease. Contact Data Dr. Stephen WilsonCEOir@immunetherapeutics.com 1-888-391-9355

合作并购

100 项与内蒙古民族大学相关的药物交易

登录后查看更多信息

100 项与内蒙古民族大学相关的转化医学

登录后查看更多信息