cometadata/datacite-titles-descriptions-related-identifiers huggingface dataset:
DOI: 10.3535/36s-03c-bf2
title: Argynnis paphia (Linnaeus, 1758)

description: Digital Specimen for the physical specimen hosted at Finnish Museum of Natural History.
DOI: 10.6084/m9.figshare.28049876
title: N6-methyladenosine modification of THBS1 induced by affluent WTAP promotes Graves’ ophthalmopathy progression through glycolysis to affect Th17/Treg balance

description: Graves’ ophthalmopathy (GO) obvious manifestation is the imbalance of Th17/Treg. N6-methyladenosine (m6A) methylation is an important regulator of Th17/Treg balance. However, few reports narrate how m6A regulators mediate the role of genes in GO progression. We explored the m6A modification of THBS1 mediated by WTAP, and the mechanism by which THBS1 regulated glycolysis and Th17/Treg balance. A total of 12 peripheral blood (4 GO samples, 4 GH samples, and 4 health samples) were collected to measure the percentage of Th17/Treg in monocytes by flow cytometry. RNA sequencing (RNA-seq) combined with MeRIP sequencing (MeRIP-seq) was used to screen differentially expressed and methylated genes. MeRIP-qPCR was performed to evaluate the m6A abundance of THBS1 after WTAP silencing. Glycolysis of CD4<sup>+</sup> T cells was reflected by the lactate content and glucose uptake. The number of Th17 cells was increased in GO peripheral blood, whereas the Treg cells decreased. RNA-seq acquired 679 differentially expressed genes (308 up-regulated, and 371 down-regulated) in the CD4<sup>+</sup> T cells of GO compared to healthy control. MeRIP-seq identified 3277 m6A peaks between the GO group and the healthy control group, corresponding with 2744 genes (1143 hypermethylated and 1601 hypomethylated). Combined analysis of RNA-seq and MeRIP-seq showed 81 hypermethylated and up-regulated genes. Among the six candidate genes in the PI3K-signaling pathway, THBS1 was the most significantly differentially expressed and hypermethylated. THBS1 silencing resulted in decreased lactate content and glucose uptake in CD4<sup>+</sup> T cells. WTAP was significantly upregulated in CD4<sup>+</sup> T cells of GO, and WTAP silencing significantly reduced m6A abundance and expression of THBS1. Upregulated and hypermethylated THBS1 mediated by WTAP promoted glycolysis of CD4<sup>+</sup> T cells, affected Th17/Treg balance, and facilitated GO progression. We provided a novel potential target for GO treatment and revealed the molecular mechanism of WTAP and THBS1 in GO under the m6A perspective.
DOI: 10.6084/m9.figshare.28049876.v1
title: N6-methyladenosine modification of THBS1 induced by affluent WTAP promotes Graves’ ophthalmopathy progression through glycolysis to affect Th17/Treg balance

description: Graves’ ophthalmopathy (GO) obvious manifestation is the imbalance of Th17/Treg. N6-methyladenosine (m6A) methylation is an important regulator of Th17/Treg balance. However, few reports narrate how m6A regulators mediate the role of genes in GO progression. We explored the m6A modification of THBS1 mediated by WTAP, and the mechanism by which THBS1 regulated glycolysis and Th17/Treg balance. A total of 12 peripheral blood (4 GO samples, 4 GH samples, and 4 health samples) were collected to measure the percentage of Th17/Treg in monocytes by flow cytometry. RNA sequencing (RNA-seq) combined with MeRIP sequencing (MeRIP-seq) was used to screen differentially expressed and methylated genes. MeRIP-qPCR was performed to evaluate the m6A abundance of THBS1 after WTAP silencing. Glycolysis of CD4<sup>+</sup> T cells was reflected by the lactate content and glucose uptake. The number of Th17 cells was increased in GO peripheral blood, whereas the Treg cells decreased. RNA-seq acquired 679 differentially expressed genes (308 up-regulated, and 371 down-regulated) in the CD4<sup>+</sup> T cells of GO compared to healthy control. MeRIP-seq identified 3277 m6A peaks between the GO group and the healthy control group, corresponding with 2744 genes (1143 hypermethylated and 1601 hypomethylated). Combined analysis of RNA-seq and MeRIP-seq showed 81 hypermethylated and up-regulated genes. Among the six candidate genes in the PI3K-signaling pathway, THBS1 was the most significantly differentially expressed and hypermethylated. THBS1 silencing resulted in decreased lactate content and glucose uptake in CD4<sup>+</sup> T cells. WTAP was significantly upregulated in CD4<sup>+</sup> T cells of GO, and WTAP silencing significantly reduced m6A abundance and expression of THBS1. Upregulated and hypermethylated THBS1 mediated by WTAP promoted glycolysis of CD4<sup>+</sup> T cells, affected Th17/Treg balance, and facilitated GO progression. We provided a novel potential target for GO treatment and revealed the molecular mechanism of WTAP and THBS1 in GO under the m6A perspective.
DOI: 10.13130/rd_unimi/tdflym/g3siza
title: Novembre_1899_Pagina_070.jpg

description: Bulletin of 1899/11/18
DOI: 10.13130/rd_unimi/tdflym/mcbjbe
title: Novembre_1899_Pagina_071.jpg

description: Bulletin of 1899/11/18
DOI: 10.3535/853-5mm-7sg
title: Patania Moore, 1888

description: Digital Specimen for the physical specimen hosted at Finnish Museum of Natural History.
DOI: 10.6084/m9.figshare.28448561
title: Anti-perilipin-1 autoantibodies in autoimmune Addison’s disease and related endocrine disorders

description: Immune-mediated lipodystrophy syndromes are rare autoimmune disorders characterized by complete or partial destruction of adipocytes in the body. Recently, autoantibodies against perilipin-1 (PLIN1-autoAbs) have been linked to lipodystrophy. Since various perilipins are expressed in the adrenal cortex and ovaries, we asked whether PLIN1-autoAbs were present in patients with adrenal dysfunction and other autoimmune endocrinopathies. Using a sensitive radiobinding immune assay we analyzed anti-PLIN1-autoAbs in 521 patients with endocrinopathies including Sjögren’s syndrome. We identified 22 (4.2%) PLIN1-autoAbs positive patients, of whom 15% had autoimmune polyendocrine syndrome type 1 (4/27), 4% autoimmune Addison’s disease and/or autoimmune polyendocrine syndrome type 2 (11/274), 8% type 1 diabetes patients (4/53), and 2% Sjögren’s syndrome patients (1/50). However, none of them had known lipodystrophy. In conclusion, PLIN1-autoAbs are found in subgroups of autoimmune endocrinopathies and indicate autoimmunity against adipose tissue, but their pathogenic role if any, remains to be defined. Investigating their role in disease progression and their potential as therapeutic targets could pave the way for novel interventions in autoimmune endocrine diseases.
DOI: 10.6084/m9.figshare.28448561.v1
title: Anti-perilipin-1 autoantibodies in autoimmune Addison’s disease and related endocrine disorders

description: Immune-mediated lipodystrophy syndromes are rare autoimmune disorders characterized by complete or partial destruction of adipocytes in the body. Recently, autoantibodies against perilipin-1 (PLIN1-autoAbs) have been linked to lipodystrophy. Since various perilipins are expressed in the adrenal cortex and ovaries, we asked whether PLIN1-autoAbs were present in patients with adrenal dysfunction and other autoimmune endocrinopathies. Using a sensitive radiobinding immune assay we analyzed anti-PLIN1-autoAbs in 521 patients with endocrinopathies including Sjögren’s syndrome. We identified 22 (4.2%) PLIN1-autoAbs positive patients, of whom 15% had autoimmune polyendocrine syndrome type 1 (4/27), 4% autoimmune Addison’s disease and/or autoimmune polyendocrine syndrome type 2 (11/274), 8% type 1 diabetes patients (4/53), and 2% Sjögren’s syndrome patients (1/50). However, none of them had known lipodystrophy. In conclusion, PLIN1-autoAbs are found in subgroups of autoimmune endocrinopathies and indicate autoimmunity against adipose tissue, but their pathogenic role if any, remains to be defined. Investigating their role in disease progression and their potential as therapeutic targets could pave the way for novel interventions in autoimmune endocrine diseases.
DOI: 10.13130/rd_unimi/tdflym/ytvdbz
title: Novembre_1899_Pagina_072.jpg

description: Bulletin of 1899/11/18
DOI: 10.3535/49h-plm-9kb
title: Dahlica (Dahlica) charlottae (Meier, 1957)

description: Digital Specimen for the physical specimen hosted at Finnish Museum of Natural History.
DOI: 10.3535/h20-q00-wd1
title: Autographa gamma (Linnaeus, 1758)

description: Digital Specimen for the physical specimen hosted at Finnish Museum of Natural History.
DOI: 10.6084/m9.figshare.30254724
title: Immunogenic self-DNA drives neuropsychiatric systemic lupus erythematosus in conventional genetic background mice

description: Neuropsychiatric systemic lupus erythematosus (NPSLE) represents a significant and growing challenge in both clinical practice and research, with its mechanistic investigation hindered by the lack of reliable animal models. Over the past two decades, we have established that immunogenic self-DNA can induce SLE disease model, which has been widely utilized in the academic community. To modify the doses of immunogenic self-DNA, validate the induction of SLE disease, and systematically characterize the resulting neuropsychiatric manifestations, aiming to provide an optimal model for NPSLE. Conventional genetic background BALB/c mice were immunized with 75 µg of immunogenic self-DNA. Based on the criteria and diagnostic recommendations from the ACR and EULAR, we conducted neurobehavioral experiments to assess the neuropsychiatric manifestations of clinical NPSLE patients. Whole-cell patch-clamp electrophysiological recordings were performed on mouse brain slices to assess electroencephalographic (EEG) abnormalities associated with NPSLE. Cerebrospinal fluid (CSF) abnormalities were evaluated by measuring inflammatory factors in the CSF. Additionally, histopathological analyses were conducted to evaluate MRI abnormalities in self-DNA immunized mice. Self-DNA immunized mice developed progressive cognitive impairments, exhibiting spatial and working memory deficits from week 8 post-immunization, which worsened by week 12, alongside the emergence of anxiety-like and depression-like behaviors. In parallel, electrophysiological analysis revealed synaptic transmission deficits and reduced neuronal excitability beginning at week 8, further deteriorating by week 12. Of note, blood-brain barrier (BBB) disruption was observed at 4–8 weeks post immunization, which was evidenced by IgG leakage and FITC-dextran extravasation. Such BBB disruption was accompanied by elevated pro-inflammatory cytokines (IL-1β, IL-6, TNF-α, IL-10), resembling neuropsychiatric lupus pathology. Finally, histologically, hippocampal neuronal loss and dendritic spine reduction in CA1, CA3, and DG subregions were observed, providing structural correlates for the observed memory deficits in self-DNA immunized mice. This model induced by immunogenic self-DNA recapitulated the neurological manifestations observed in clinical patients, rendering it a robust model for the research of NPSLE.
DOI: 10.6084/m9.figshare.30254724.v1
title: Immunogenic self-DNA drives neuropsychiatric systemic lupus erythematosus in conventional genetic background mice

description: Neuropsychiatric systemic lupus erythematosus (NPSLE) represents a significant and growing challenge in both clinical practice and research, with its mechanistic investigation hindered by the lack of reliable animal models. Over the past two decades, we have established that immunogenic self-DNA can induce SLE disease model, which has been widely utilized in the academic community. To modify the doses of immunogenic self-DNA, validate the induction of SLE disease, and systematically characterize the resulting neuropsychiatric manifestations, aiming to provide an optimal model for NPSLE. Conventional genetic background BALB/c mice were immunized with 75 µg of immunogenic self-DNA. Based on the criteria and diagnostic recommendations from the ACR and EULAR, we conducted neurobehavioral experiments to assess the neuropsychiatric manifestations of clinical NPSLE patients. Whole-cell patch-clamp electrophysiological recordings were performed on mouse brain slices to assess electroencephalographic (EEG) abnormalities associated with NPSLE. Cerebrospinal fluid (CSF) abnormalities were evaluated by measuring inflammatory factors in the CSF. Additionally, histopathological analyses were conducted to evaluate MRI abnormalities in self-DNA immunized mice. Self-DNA immunized mice developed progressive cognitive impairments, exhibiting spatial and working memory deficits from week 8 post-immunization, which worsened by week 12, alongside the emergence of anxiety-like and depression-like behaviors. In parallel, electrophysiological analysis revealed synaptic transmission deficits and reduced neuronal excitability beginning at week 8, further deteriorating by week 12. Of note, blood-brain barrier (BBB) disruption was observed at 4–8 weeks post immunization, which was evidenced by IgG leakage and FITC-dextran extravasation. Such BBB disruption was accompanied by elevated pro-inflammatory cytokines (IL-1β, IL-6, TNF-α, IL-10), resembling neuropsychiatric lupus pathology. Finally, histologically, hippocampal neuronal loss and dendritic spine reduction in CA1, CA3, and DG subregions were observed, providing structural correlates for the observed memory deficits in self-DNA immunized mice. This model induced by immunogenic self-DNA recapitulated the neurological manifestations observed in clinical patients, rendering it a robust model for the research of NPSLE.
DOI: 10.6084/m9.figshare.30437414
title: High glucose promotes O-GlcNAcylation of ACSL4 to induce ferroptosis of renal tubular epithelial cell

description: O-linked N-acetylglucosamine (O-GlcNAc) glycosylation represents a prevalent post-translational modification of proteins. Accumulating evidence indicates that dysregulated O-GlcNAcylation can induce glucose toxicity and plays critical roles in the pathogenesis of diabetic nephropathy (DN). Human kidney proximal tubular epithelial HK-2 cells were exposed to high glucose (HG) conditions to establish DN cellular models. Co-immunoprecipitation (Co-IP) combined with western blot analysis was employed to assess the expression levels of O-GlcNAc, O-GlcNAc transferase (OGT), O-GlcNAcase (OGA), ACSL4, and ferroptosis-associated proteins. Cell viability was evaluated using the CCK-8 assay, while cell death was analyzed through DAPI/propidium iodide (PI) double staining. Ferroptosis was assessed by measuring intracellular iron accumulation, glutathione (GSH) content, and reactive oxygen species (ROS) levels. Additionally, <i>in vivo</i> experiments were conducted using male C57BL/6J mice divided into four groups: control, DN, DN+shOGT, and DN+shNC. DN was induced by a high-fat diet (HFD) followed by streptozotocin (STZ) injection. OGT was specifically knocked down in the kidneys using AAV-shOGT. Kidney tissues were analyzed for pathological changes, O-GlcNAcylation levels, and ferroptosis markers. Our findings demonstrated that O-GlcNAc and OGT expressions were significantly upregulated in HG-treated HK-2 cells. OGT knockdown effectively attenuated HG-induced ferroptosis. Importantly, ACSL4 protein levels exhibited strong positive correlation with OGT expression. Subsequent investigation revealed direct interaction between ACSL4 and OGT. O-GlcNAcylation modification was found to enhance ACSL4 protein stability. Moreover, overexpression of ACSL4 counteracted the protective effects of OGT knockdown against ferroptosis. Additionally, OGT knockdown reversed the high iron concentration, ROS, and MDA levels, and restored GSH and SOD levels in DN mice. O-GlcNAc, OGT, and ACSL4 levels, which were markedly increased in the DN group, were downregulated by OGT knockdown treatment <i>in vivo</i>. Collectively, these results demonstrate that high glucose promotes OGT-mediated O-GlcNAcylation of ACSL4, thereby stabilizing this enzyme and facilitating ferroptosis progression in DN.
DOI: 10.6084/m9.figshare.30437414.v1
title: High glucose promotes O-GlcNAcylation of ACSL4 to induce ferroptosis of renal tubular epithelial cell

description: O-linked N-acetylglucosamine (O-GlcNAc) glycosylation represents a prevalent post-translational modification of proteins. Accumulating evidence indicates that dysregulated O-GlcNAcylation can induce glucose toxicity and plays critical roles in the pathogenesis of diabetic nephropathy (DN). Human kidney proximal tubular epithelial HK-2 cells were exposed to high glucose (HG) conditions to establish DN cellular models. Co-immunoprecipitation (Co-IP) combined with western blot analysis was employed to assess the expression levels of O-GlcNAc, O-GlcNAc transferase (OGT), O-GlcNAcase (OGA), ACSL4, and ferroptosis-associated proteins. Cell viability was evaluated using the CCK-8 assay, while cell death was analyzed through DAPI/propidium iodide (PI) double staining. Ferroptosis was assessed by measuring intracellular iron accumulation, glutathione (GSH) content, and reactive oxygen species (ROS) levels. Additionally, <i>in vivo</i> experiments were conducted using male C57BL/6J mice divided into four groups: control, DN, DN+shOGT, and DN+shNC. DN was induced by a high-fat diet (HFD) followed by streptozotocin (STZ) injection. OGT was specifically knocked down in the kidneys using AAV-shOGT. Kidney tissues were analyzed for pathological changes, O-GlcNAcylation levels, and ferroptosis markers. Our findings demonstrated that O-GlcNAc and OGT expressions were significantly upregulated in HG-treated HK-2 cells. OGT knockdown effectively attenuated HG-induced ferroptosis. Importantly, ACSL4 protein levels exhibited strong positive correlation with OGT expression. Subsequent investigation revealed direct interaction between ACSL4 and OGT. O-GlcNAcylation modification was found to enhance ACSL4 protein stability. Moreover, overexpression of ACSL4 counteracted the protective effects of OGT knockdown against ferroptosis. Additionally, OGT knockdown reversed the high iron concentration, ROS, and MDA levels, and restored GSH and SOD levels in DN mice. O-GlcNAc, OGT, and ACSL4 levels, which were markedly increased in the DN group, were downregulated by OGT knockdown treatment <i>in vivo</i>. Collectively, these results demonstrate that high glucose promotes OGT-mediated O-GlcNAcylation of ACSL4, thereby stabilizing this enzyme and facilitating ferroptosis progression in DN.
DOI: 10.13130/rd_unimi/tdflym/n7wntb
title: Novembre_1899_Pagina_073.jpg

description: Bulletin of 1899/11/19
DOI: 10.3535/3jm-9bd-dgv
title: Ochlodes Scudder, 1872

description: Digital Specimen for the physical specimen hosted at Finnish Museum of Natural History.
DOI: 10.6084/m9.figshare.30296187
title: Multi-omics identification of RNASE6 as an immune regulatory RNA-binding protein associated with melanoma metastasis

description: Cutaneous melanoma is a highly invasive tumor. It enhances metastasis and resistance to immunotherapy <i>via</i> immunosuppressive mechanisms. Understanding RNA-binding proteins (RBPs) in melanoma’s immune alterations is limited. This study explores immune-regulatory RBPs in metastasis and clarifies RNASE6’s role in immune regulation. Utilizing the bulk RNA-seq datasets of melanoma, the immune status of the samples was assessed using CIBERSORT and ESTIMATE. WGCNA and five machine learning algorithms were employed to identify immune RBPs associated with metastasis. Further exploration of RNASE6 was mainly performed using COX, Kaplan-Meier survival analysis, and GSEA. Utilizing GWAS data, mendelian randomization was applied to demonstrate the causal relationship between RNASE6 and melanoma. Utilizing scRNA-seq dataset, the regulatory effect of RNASE6 on macrophages was validated through constructing a regulatory network. Finally, the key role of RNASE6 on macrophage polarization was validated through cell experiments. Using WGCNA and machine learning, we identified nine immune-related RBPs (CCDC86, CPEB3, EXO1, FASTKD2, MBNL1, RNASE6, RUVBL2, TLR8, URB2) associated with melanoma metastasis. Among these, RNASE6 emerged as a key regulator, with its expression highly positively correlated with M1 macrophage polarization and inhibition of metastasis. High RNASE6 expression was also correlated with improved prognosis and a better response to anti-PD-1 therapy. Mendelian randomization demonstrated that RNASE6 acts as a protective factor against melanoma. The regulatory network indicated that RNASE6 influences multiple macrophage polarization markers. Cell experiments confirmed the adverse effect of knocking down RNASE6 on M1 polarization of macrophages. We identified RNASE6 as an immune-regulatory RBP in melanoma, capable of influencing metastasis progression and immunotherapy outcomes by promoting M1 macrophage polarization.
DOI: 10.6084/m9.figshare.30296187.v1
title: Multi-omics identification of RNASE6 as an immune regulatory RNA-binding protein associated with melanoma metastasis

description: Cutaneous melanoma is a highly invasive tumor. It enhances metastasis and resistance to immunotherapy <i>via</i> immunosuppressive mechanisms. Understanding RNA-binding proteins (RBPs) in melanoma’s immune alterations is limited. This study explores immune-regulatory RBPs in metastasis and clarifies RNASE6’s role in immune regulation. Utilizing the bulk RNA-seq datasets of melanoma, the immune status of the samples was assessed using CIBERSORT and ESTIMATE. WGCNA and five machine learning algorithms were employed to identify immune RBPs associated with metastasis. Further exploration of RNASE6 was mainly performed using COX, Kaplan-Meier survival analysis, and GSEA. Utilizing GWAS data, mendelian randomization was applied to demonstrate the causal relationship between RNASE6 and melanoma. Utilizing scRNA-seq dataset, the regulatory effect of RNASE6 on macrophages was validated through constructing a regulatory network. Finally, the key role of RNASE6 on macrophage polarization was validated through cell experiments. Using WGCNA and machine learning, we identified nine immune-related RBPs (CCDC86, CPEB3, EXO1, FASTKD2, MBNL1, RNASE6, RUVBL2, TLR8, URB2) associated with melanoma metastasis. Among these, RNASE6 emerged as a key regulator, with its expression highly positively correlated with M1 macrophage polarization and inhibition of metastasis. High RNASE6 expression was also correlated with improved prognosis and a better response to anti-PD-1 therapy. Mendelian randomization demonstrated that RNASE6 acts as a protective factor against melanoma. The regulatory network indicated that RNASE6 influences multiple macrophage polarization markers. Cell experiments confirmed the adverse effect of knocking down RNASE6 on M1 polarization of macrophages. We identified RNASE6 as an immune-regulatory RBP in melanoma, capable of influencing metastasis progression and immunotherapy outcomes by promoting M1 macrophage polarization.
DOI: 10.13130/rd_unimi/tdflym/cj9q1n
title: Novembre_1899_Pagina_074.jpg

description: Bulletin of 1899/11/19
DOI: 10.3535/tbf-dk1-07j
title: Scopariinae

description: Digital Specimen for the physical specimen hosted at Finnish Museum of Natural History.