Cyanobacterial blooms are an omnipresent and well-known result of eutrophication and climate change in aquatic systems. Cyanobacteria produce a plethora of toxic secondary metabolites that affect humans, animals and ecosystems. Many cyanotoxins primarily affect the grazers of phytoplankton, e.g., . The neurotoxin anatoxin-α has been reported world-wide; despite its potency, anatoxin-α and its effects on have not been thoroughly investigated. Here, we investigated the effects of the anatoxin-α-producing on life-history parameters and gene expression of nicotine-acetylcholine receptors (NAR), the direct targets of anatoxin-α, using several clones. We used juvenile somatic growth rates as a measure of fitness and analyzed gene expression by qPCR. Exposure to 100% reduced the clones' growth rates and caused an up-regulation of NAR gene expression. When 50% of the food consisted of , none of the clones were reduced in growth and only one of them showed an increase in NAR gene expression. We demonstrate that this increased NAR gene expression can be maternally transferred and that offspring from experienced mothers show a higher growth rate when treated with 50% compared with control offspring. However, the addition of further (anthropogenic) stressors might impair 's adaptive responses to anatoxin-α. Especially the presence of certain pollutants (i.e., neonicotinoids), which also target NARs, might reduce 's capability to cope with anatoxin-α.
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http://dx.doi.org/10.3390/toxins13050326 | DOI Listing |
J Transl Med
January 2025
Department of Gynecology, The Fourth Hospital of Hebei Medical University, No.12 Jiankang Road, Shijiazhuang, 050000, Hebei, China.
Background: Immune cells within tumor tissues play important roles in remodeling the tumor microenvironment, thus affecting tumor progression and the therapeutic response. The current study was designed to identify key markers of plasma cells and explore their role in high-grade serous ovarian cancer (HGSOC).
Methods: We utilized single-cell sequencing data from the Gene Expression Omnibus (GEO) database to identify key immune cell types within HGSOC tissues and to extract related markers via the Seurat package.
Cell Div
January 2025
Department of Nuclear Medicine, The Affiliated Cancer Hospital of Xiangya School of Medicine, Central South university/Hunan Cancer Hospital, No. 283 Tongzipo Road, Yuelu District, Changsha, 410013, Hunan, P.R. China.
Background: Zinc finger protein 169 (ZNF169) plays a key role in cancer development. However, the specific role of ZNF169 in the tumorigenesis of thyroid carcinoma (THCA) remains poorly understood.
Methods: The expression of ZNF169 was measured using immunohistochemistry, RT-qPCR, and western blot.
BMC Pharmacol Toxicol
January 2025
Yantai Affiliated Hospital of Binzhou Medical University, Yantai, Shandong, 264100, PR China.
Background: Alzheimer's disease (AD), a hallmark of age-related cognitive decline, is defined by its unique neuropathology. Metabolic dysregulation, particularly involving glutamine (Gln) metabolism, has emerged as a critical but underexplored aspect of AD pathophysiology, representing a significant gap in our current understanding of the disease.
Methods: To investigate the involvement of GlnMgs in AD, we conducted a comprehensive bioinformatic analysis.
BMC Biol
January 2025
The Jackson Laboratory for Genomic Medicine, Farmington, CT, 06032, USA.
Background: The microbiome regulates the respiratory epithelium's immunomodulatory functions. To explore how the microbiome's biodiversity affects microbe-epithelial interactions, we screened 58 phylogenetically diverse microbes for their transcriptomic effect on human primary bronchial air-liquid interface (ALI) cell cultures.
Results: We found distinct species- and strain-level differences in host innate immunity and epithelial barrier response.
Breast Cancer Res
January 2025
Guangdong Provincial Key Laboratory of Malignant Tumor Epigenetics and Gene Regulation, Sun Yat-Sen Memorial Hospital, Sun Yat-Sen University, Guangzhou, 510120, China.
Background: CDK4/6 inhibitors have significantly improved the survival of patients with HR-positive/HER2-negative breast cancer, becoming a first-line treatment option. However, the development of resistance to these inhibitors is inevitable. To address this challenge, novel strategies are required to overcome resistance, necessitating a deeper understanding of its mechanisms.
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