cometadata/datacite-titles-descriptions-related-identifiers huggingface dataset:
DOI: 10.13130/rd_unimi/zaucgl/mkk11x
title: Febbraio_1921_Pagina_098.jpg

description: Bulletin of 1921/02/17
DOI: 10.13130/rd_unimi/zaucgl/tyxl6c
title: Febbraio_1921_Pagina_099.jpg

description: Bulletin of 1921/02/17
DOI: 10.13130/rd_unimi/zaucgl/kmmyqt
title: Febbraio_1921_Pagina_100.jpg

description: Bulletin of 1921/02/17
DOI: 10.13130/rd_unimi/zaucgl/mrvicx
title: Febbraio_1921_Pagina_101.jpg

description: Bulletin of 1921/02/17
DOI: 10.13130/rd_unimi/zaucgl/vvsktb
title: Febbraio_1921_Pagina_102.jpg

description: Bulletin of 1921/02/17
DOI: 10.13130/rd_unimi/zaucgl/l7dox8
title: Febbraio_1921_Pagina_104.jpg

description: Bulletin of 1921/02/18
DOI: 10.13130/rd_unimi/zaucgl/tbdjt6
title: Febbraio_1921_Pagina_103.jpg

description: Bulletin of 1921/02/18
DOI: 10.13130/rd_unimi/zaucgl/4zhwvz
title: Febbraio_1921_Pagina_105.jpg

description: Bulletin of 1921/02/18
DOI: 10.13130/rd_unimi/zaucgl/tznc0g
title: Febbraio_1921_Pagina_106.jpg

description: Bulletin of 1921/02/18
DOI: 10.13130/rd_unimi/zaucgl/7enf1g
title: Febbraio_1921_Pagina_108.jpg

description: Bulletin of 1921/02/18
DOI: 10.13130/rd_unimi/zaucgl/q5pbx5
title: Febbraio_1921_Pagina_107.jpg

description: Bulletin of 1921/02/18
DOI: 10.13130/rd_unimi/zaucgl/cckh9v
title: Febbraio_1921_Pagina_109.jpg

description: Bulletin of 1921/02/19
DOI: 10.13130/rd_unimi/zaucgl/11fiyp
title: Febbraio_1921_Pagina_110.jpg

description: Bulletin of 1921/02/19
DOI: 10.13130/rd_unimi/zaucgl/ffzv1b
title: Febbraio_1921_Pagina_111.jpg

description: Bulletin of 1921/02/19
DOI: 10.13130/rd_unimi/zaucgl/ll1myr
title: Febbraio_1921_Pagina_112.jpg

description: Bulletin of 1921/02/19
DOI: 10.13130/rd_unimi/zaucgl/cw5my8
title: Febbraio_1921_Pagina_113.jpg

description: Bulletin of 1921/02/19
DOI: 10.13130/rd_unimi/zaucgl/owvjep
title: Febbraio_1921_Pagina_114.jpg

description: Bulletin of 1921/02/19
DOI: 10.13130/rd_unimi/zaucgl/lnopxw
title: Febbraio_1921_Pagina_115.jpg

description: Bulletin of 1921/02/20
DOI: 10.26165/juelich-data/zgri44
title: toluene+o-xylene+1-pentene + OH - Instruments intercomparison - 2015-10-12

description: toluene+o-xylene+1-pentene + OH - Instruments intercomparison - 2015-10-12Chamber information:actris_nf: Yinstitute: FZJirradiation: Natural sunlightlink: https://www.eurochamp.org/simulation-chambers/SAPHIRname: SAPHIRvolume: 270 m3wallMaterial: FEP filmExperimental conditions:date: '2015-10-12'lightSource: Natural sunlightprojectName: kOHCompreactiveSpecies: OHtype: Instruments intercomparisonMolecules:- name: toluene- name: o-xylene- name: 1-pentene
DOI: 10.13130/rd_unimi/zaucgl/go8klk
title: Febbraio_1921_Pagina_117.jpg

description: Bulletin of 1921/02/20
DOI: 10.13130/rd_unimi/zaucgl/qlkony
title: Febbraio_1921_Pagina_116.jpg

description: Bulletin of 1921/02/20
DOI: 10.13130/rd_unimi/zaucgl/qxcdvl
title: Febbraio_1921_Pagina_118.jpg

description: Bulletin of 1921/02/20
DOI: 10.13130/rd_unimi/zaucgl/ihzdji
title: Febbraio_1921_Pagina_119.jpg

description: Bulletin of 1921/02/20
DOI: 10.13130/rd_unimi/zaucgl/daztxy
title: Febbraio_1921_Pagina_120.jpg

description: Bulletin of 1921/02/20
DOI: 10.6084/m9.figshare.30217006
title: The GABBR1/miR-19b-3p/WNT2B axis regulates insulin resistance and liver injury in diabetes with viral infection: mechanistic and therapeutic insights

description: Insulin resistance (IR) is the main feature of type 2 diabetes mellitus. Furthermore, viral infection can aggravate the abnormal glucose metabolism in diabetic patients. GABBR1 can maintain normal glucose homeostasis, but its specific role in diabetes is not clear. We investigated the function of the GABBR1/miR-19b-3p/WNT2B axis <i>in vitro</i> and <i>in vivo</i>. miR-19b-3p and GABBR1 were overexpressed or knocked down in AML12 cells. Subsequently, these cells were treated with palmitic acid (PA) to induce damage or poly I : C to mimic viral infection. The degree of AML12 cell damage was assessed using the CCK-8 assay; inflammation levels were measured using ELISA; and IR indexes were determined using the Immunofluorescence kit and Western blot assay. The diabetic mice model was established to evaluate liver injury and IR. PA and poly I : C can reduce the activity of AML12 cells, increase apoptosis and inflammatory factor contents, weaken the ability of glucose uptake and consumption, enhance the production capacity, and reduce the level of GLUT4. GABBR1 mediates the targeted regulation of WNT2B by miR-19b-3p. PA and poly I : C also increased ALT, AST, inflammatory factors and miR-19b-3p levels, and decreased GABBR1 and WNT2B expression of mice. Liver cells showed swelling and many spherical lipid droplets. After miR-19b-3p knockdown and GABBR1 overexpression, the degree of liver injury and IR in AML12 cells and mice were alleviated. GABBR1 regulates miR-19b-3p/WNT2B axis to reduce liver injury, IR and inflammatory response, and improve the comorbidity of diabetes and viral infection. This pathway represents a potential therapeutic target for mitigating the comorbidity of diabetes and viral infection.
DOI: 10.6084/m9.figshare.30217006.v1
title: The GABBR1/miR-19b-3p/WNT2B axis regulates insulin resistance and liver injury in diabetes with viral infection: mechanistic and therapeutic insights

description: Insulin resistance (IR) is the main feature of type 2 diabetes mellitus. Furthermore, viral infection can aggravate the abnormal glucose metabolism in diabetic patients. GABBR1 can maintain normal glucose homeostasis, but its specific role in diabetes is not clear. We investigated the function of the GABBR1/miR-19b-3p/WNT2B axis <i>in vitro</i> and <i>in vivo</i>. miR-19b-3p and GABBR1 were overexpressed or knocked down in AML12 cells. Subsequently, these cells were treated with palmitic acid (PA) to induce damage or poly I : C to mimic viral infection. The degree of AML12 cell damage was assessed using the CCK-8 assay; inflammation levels were measured using ELISA; and IR indexes were determined using the Immunofluorescence kit and Western blot assay. The diabetic mice model was established to evaluate liver injury and IR. PA and poly I : C can reduce the activity of AML12 cells, increase apoptosis and inflammatory factor contents, weaken the ability of glucose uptake and consumption, enhance the production capacity, and reduce the level of GLUT4. GABBR1 mediates the targeted regulation of WNT2B by miR-19b-3p. PA and poly I : C also increased ALT, AST, inflammatory factors and miR-19b-3p levels, and decreased GABBR1 and WNT2B expression of mice. Liver cells showed swelling and many spherical lipid droplets. After miR-19b-3p knockdown and GABBR1 overexpression, the degree of liver injury and IR in AML12 cells and mice were alleviated. GABBR1 regulates miR-19b-3p/WNT2B axis to reduce liver injury, IR and inflammatory response, and improve the comorbidity of diabetes and viral infection. This pathway represents a potential therapeutic target for mitigating the comorbidity of diabetes and viral infection.
DOI: 10.6084/m9.figshare.30418115.v2
title: Transcriptional cyclin-dependent kinases Cdk8 and Cdk19 are required for normal macrophage differentiation

description: Cyclin-dependent kinases CDK8 and CDK19 together with their activating partner, cyclin C, regulate gene expression as a part of the Mediator complex and by phosphorylating DNA sequence-specific transcription factors. Here, we investigated the <i>in vivo</i> requirement for Cdk8 and Cdk19 in hematopoiesis by generating double knockout (DKO) mice lacking Cdk8 and Cdk19 expression in hematopoietic cells. DKO mice displayed relatively normal hematopoiesis and largely unperturbed gene expression in the bone marrow, indicating that the Mediator kinases are not essential for the regulation of gene expression during hematopoiesis. However, DKO mice showed an expansion of splenic macrophages. Bone marrow-derived DKO macrophages displayed an increased expression levels of both M1-like and M2-like markers, altered cytokine secretion, deregulated gene expression, precocious cell cycle exit and impaired Fc-mediated phagocytosis. Our findings reveal a highly cell type-specific role of Cdk8/19 in gene transcription during hematopoiesis.
DOI: 10.13130/rd_unimi/zaucgl/deyq4l
title: Febbraio_1921_Pagina_122.jpg

description: Bulletin of 1921/02/21
DOI: 10.13130/rd_unimi/zaucgl/opwfon
title: Febbraio_1921_Pagina_121.jpg

description: Bulletin of 1921/02/21
DOI: 10.6084/m9.figshare.30418115
title: Transcriptional cyclin-dependent kinases Cdk8 and Cdk19 are required for normal macrophage differentiation

description: Cyclin-dependent kinases CDK8 and CDK19 together with their activating partner, cyclin C, regulate gene expression as a part of the Mediator complex and by phosphorylating DNA sequence-specific transcription factors. Here, we investigated the <i>in vivo</i> requirement for Cdk8 and Cdk19 in hematopoiesis by generating double knockout (DKO) mice lacking Cdk8 and Cdk19 expression in hematopoietic cells. DKO mice displayed relatively normal hematopoiesis and largely unperturbed gene expression in the bone marrow, indicating that the Mediator kinases are not essential for the regulation of gene expression during hematopoiesis. However, DKO mice showed an expansion of splenic macrophages. Bone marrow-derived DKO macrophages displayed an increased expression levels of both M1-like and M2-like markers, altered cytokine secretion, deregulated gene expression, precocious cell cycle exit and impaired Fc-mediated phagocytosis. Our findings reveal a highly cell type-specific role of Cdk8/19 in gene transcription during hematopoiesis.
DOI: 10.6084/m9.figshare.30418115.v1
title: Transcriptional cyclin-dependent kinases Cdk8 and Cdk19 are required for normal macrophage differentiation

description: Cyclin-dependent kinases CDK8 and CDK19 together with their activating partner, cyclin C, regulate gene expression as a part of the Mediator complex and by phosphorylating DNA sequence-specific transcription factors. Here, we investigated the <i>in vivo</i> requirement for Cdk8 and Cdk19 in hematopoiesis by generating double knockout (DKO) mice lacking Cdk8 and Cdk19 expression in hematopoietic cells. DKO mice displayed relatively normal hematopoiesis and largely unperturbed gene expression in the bone marrow, indicating that the Mediator kinases are not essential for the regulation of gene expression during hematopoiesis. However, DKO mice showed an expansion of splenic macrophages. Bone marrow-derived DKO macrophages displayed an increased expression levels of both M1-like and M2-like markers, altered cytokine secretion, deregulated gene expression, precocious cell cycle exit and impaired Fc-mediated phagocytosis. Our findings reveal a highly cell type-specific role of Cdk8/19 in gene transcription during hematopoiesis.
DOI: 10.13130/rd_unimi/zaucgl/q7rmkj
title: Febbraio_1921_Pagina_123.jpg

description: Bulletin of 1921/02/21
DOI: 10.6084/m9.figshare.30550403
title: Mitophagy suppression via lncRNA H19 silencing: a novel strategy to overcome cisplatin resistance in lung adenocarcinoma

description: Cisplatin (DDP) resistance substantially compromises treatment efficacy in lung adenocarcinoma (LUAD). This study investigates the role of mitochondrial long non-coding RNA (lncRNA) H19 in mediating DDP resistance. High-throughput sequencing and RT-qPCR analyses revealed pronounced H19 upregulation in DDP-resistant A549 (A549/DDP) cells relative to parental A549 cells. Subcellular localization studies indicated that H19 is primarily nuclear in A549 cells but translocates to mitochondria in A549/DDP cells. Functional assays demonstrated that H19 silencing in resistant cells attenuated chemoresistance, suppressed proliferation, migration, invasion, and colony formation in vitro, and delayed tumor growth in vivo. H19 knockdown impaired mitophagy and promoted apoptosis, mirroring autophagy inhibition and restoring DDP sensitivity. In contrast, H19 overexpression in A549 cells did not significantly alter mitophagy or cellular behavior. Furthermore, H19 silencing induced its relocalization from mitochondria back to the nucleus in resistant cells, while overexpression did not affect its nuclear localization. These findings establish that H19 translocation to mitochondria promotes DDP resistance, and its downregulation reverses this process by inhibiting mitophagy and resensitizing cells to DDP. As a nucleus-encoded mitochondria-associated lncRNA (ntmtlncRNA), H19 mediates intercompartmental communication, highlighting its potential as a therapeutic target for overcoming DDP resistance in LUAD.
DOI: 10.6084/m9.figshare.30550403.v1
title: Mitophagy suppression via lncRNA H19 silencing: a novel strategy to overcome cisplatin resistance in lung adenocarcinoma

description: Cisplatin (DDP) resistance substantially compromises treatment efficacy in lung adenocarcinoma (LUAD). This study investigates the role of mitochondrial long non-coding RNA (lncRNA) H19 in mediating DDP resistance. High-throughput sequencing and RT-qPCR analyses revealed pronounced H19 upregulation in DDP-resistant A549 (A549/DDP) cells relative to parental A549 cells. Subcellular localization studies indicated that H19 is primarily nuclear in A549 cells but translocates to mitochondria in A549/DDP cells. Functional assays demonstrated that H19 silencing in resistant cells attenuated chemoresistance, suppressed proliferation, migration, invasion, and colony formation in vitro, and delayed tumor growth in vivo. H19 knockdown impaired mitophagy and promoted apoptosis, mirroring autophagy inhibition and restoring DDP sensitivity. In contrast, H19 overexpression in A549 cells did not significantly alter mitophagy or cellular behavior. Furthermore, H19 silencing induced its relocalization from mitochondria back to the nucleus in resistant cells, while overexpression did not affect its nuclear localization. These findings establish that H19 translocation to mitochondria promotes DDP resistance, and its downregulation reverses this process by inhibiting mitophagy and resensitizing cells to DDP. As a nucleus-encoded mitochondria-associated lncRNA (ntmtlncRNA), H19 mediates intercompartmental communication, highlighting its potential as a therapeutic target for overcoming DDP resistance in LUAD.
DOI: 10.13130/rd_unimi/zaucgl/w462gd
title: Febbraio_1921_Pagina_124.jpg

description: Bulletin of 1921/02/21
DOI: 10.6084/m9.figshare.30231579.v1
title: Astrocyte-derived stanniocalcin-1 orchestrates epileptogenesis through NF-κB-dependent neuroinflammation

description: Background: This study aimed to investigate the expression pattern of astrocyte-derived STC1 in TLE and elucidate the molecular mechanisms by which STC1 regulates neuroinflammation and seizures through the NF-κB signaling pathway. Methods: A TLE model was established by intrahippocampal injection of kainic acid (KA) in mice. STC1 expression levels and cellular localization in the hippocampus of TLE mice were examined. Adeno-associated virus-mediated gene overexpression and shRNA knockdown approaches were employed to investigate the effects of STC1 on neuroinflammatory responses, neuronal survival, and seizure activity. qRT-PCR and immunofluorescence methods were further utilized to evaluate inflammatory cytokine levels and NF-κB signaling pathway activity. Results: STC1 expression was upregulated in hippocampal tissues of TLE mice, with double immunofluorescence showing STC1 predominantly localized in GFAP-positive reactive astrocytes. STC1 overexpression significantly exacerbated KA-induced neuroinflammation, along with enhanced microglial activation. STC1 knockdown attenuated neuroinflammatory responses. Nissl staining and NeuN immunohistochemistry confirmed that STC1 aggravated KA-induced neuronal loss. STC1 overexpression promoted p65 phosphorylation and nuclear translocation, activating the NF-κB signaling pathway. Conclusion: This study reveals the molecular mechanism by which astrocyte-derived STC1 promotes TLE-associated neuroinflammation and neuronal injury through activation of the NF-κB signaling pathway, elucidating the crucial role of the astrocyte-STC1-NF-κB axis in epileptogenesis.
DOI: 10.6084/m9.figshare.30314592
title: The methyltransferase METTL3 promotes the progression of breast cancer cells via regulating EGF m6A modification

description: Ranking second out of new cancer cases, breast cancer (BRCA) is the leading cause of cancerous death among women globally. Methyltransferase-like 3 (METTL3), as the well-known N6‑methyladenosine (m6A) “writer” with catalytic function, regulates cancer progression through specific downstream targets, but its interplay with epidermal growth factor (EGF) signaling in BRCA is poorly defined. Here, we depict a METTL3-m6A-EGF axis in BRCA, where BRCA cell properties were affected by METTL3 through m6A-dependent expression of EGF. We observed the correlation between METTL3 expression in BRCA tissues and negative prognosis through bioinformatics analysis and RT-qPCR. <i>In vitro</i> lentiviral-mediated METTL3 knockdown suppressed proliferation and migration, while the <i>in vivo</i> tumor formation experiment in nude mice validated the tumor-promoting effect of METTL3. Hematoxylin-eosin staining and immunohistochemistry also showed the tumor-promoting effect of METTL3. Mechanistically, METTL3 stabilized EGF mRNA via m6A modification, as evidenced by MeRIP-qPCR and Western blotting. Notably, METTL3 maintains EGF/EGFR signaling, and its overexpression leads to insensitivity to gefitinib and adriamycin. We naturally conclude that METTL3 is a central epigenetic regulator of EGF-driven BRCA progression, providing a rationale for targeting METTL3 to overcome chemotherapeutic resistance.
DOI: 10.6084/m9.figshare.30314592.v1
title: The methyltransferase METTL3 promotes the progression of breast cancer cells via regulating EGF m6A modification

description: Ranking second out of new cancer cases, breast cancer (BRCA) is the leading cause of cancerous death among women globally. Methyltransferase-like 3 (METTL3), as the well-known N6‑methyladenosine (m6A) “writer” with catalytic function, regulates cancer progression through specific downstream targets, but its interplay with epidermal growth factor (EGF) signaling in BRCA is poorly defined. Here, we depict a METTL3-m6A-EGF axis in BRCA, where BRCA cell properties were affected by METTL3 through m6A-dependent expression of EGF. We observed the correlation between METTL3 expression in BRCA tissues and negative prognosis through bioinformatics analysis and RT-qPCR. <i>In vitro</i> lentiviral-mediated METTL3 knockdown suppressed proliferation and migration, while the <i>in vivo</i> tumor formation experiment in nude mice validated the tumor-promoting effect of METTL3. Hematoxylin-eosin staining and immunohistochemistry also showed the tumor-promoting effect of METTL3. Mechanistically, METTL3 stabilized EGF mRNA via m6A modification, as evidenced by MeRIP-qPCR and Western blotting. Notably, METTL3 maintains EGF/EGFR signaling, and its overexpression leads to insensitivity to gefitinib and adriamycin. We naturally conclude that METTL3 is a central epigenetic regulator of EGF-driven BRCA progression, providing a rationale for targeting METTL3 to overcome chemotherapeutic resistance.
DOI: 10.13130/rd_unimi/zaucgl/uqe4hg
title: Febbraio_1921_Pagina_125.jpg

description: Bulletin of 1921/02/21
DOI: 10.6084/m9.figshare.30231579
title: Astrocyte-derived stanniocalcin-1 orchestrates epileptogenesis through NF-κB-dependent neuroinflammation

description: Background: This study aimed to investigate the expression pattern of astrocyte-derived STC1 in TLE and elucidate the molecular mechanisms by which STC1 regulates neuroinflammation and seizures through the NF-κB signaling pathway. Methods: A TLE model was established by intrahippocampal injection of kainic acid (KA) in mice. STC1 expression levels and cellular localization in the hippocampus of TLE mice were examined. Adeno-associated virus-mediated gene overexpression and shRNA knockdown approaches were employed to investigate the effects of STC1 on neuroinflammatory responses, neuronal survival, and seizure activity. qRT-PCR and immunofluorescence methods were further utilized to evaluate inflammatory cytokine levels and NF-κB signaling pathway activity. Results: STC1 expression was upregulated in hippocampal tissues of TLE mice, with double immunofluorescence showing STC1 predominantly localized in GFAP-positive reactive astrocytes. STC1 overexpression significantly exacerbated KA-induced neuroinflammation, along with enhanced microglial activation. STC1 knockdown attenuated neuroinflammatory responses. Nissl staining and NeuN immunohistochemistry confirmed that STC1 aggravated KA-induced neuronal loss. STC1 overexpression promoted p65 phosphorylation and nuclear translocation, activating the NF-κB signaling pathway. Conclusion: This study reveals the molecular mechanism by which astrocyte-derived STC1 promotes TLE-associated neuroinflammation and neuronal injury through activation of the NF-κB signaling pathway, elucidating the crucial role of the astrocyte-STC1-NF-κB axis in epileptogenesis.
DOI: 10.13130/rd_unimi/zaucgl/evpxlv
title: Febbraio_1921_Pagina_126.jpg

description: Bulletin of 1921/02/21
DOI: 10.13130/rd_unimi/zaucgl/sxp0gf
title: Febbraio_1921_Pagina_128.jpg

description: Bulletin of 1921/02/22
DOI: 10.13130/rd_unimi/zaucgl/xm3rgo
title: Febbraio_1921_Pagina_127.jpg

description: Bulletin of 1921/02/22
DOI: 10.13130/rd_unimi/zaucgl/ttwpsp
title: Febbraio_1921_Pagina_129.jpg

description: Bulletin of 1921/02/22
DOI: 10.13130/rd_unimi/zaucgl/tmtnpf
title: Febbraio_1921_Pagina_130.jpg

description: Bulletin of 1921/02/22
DOI: 10.13130/rd_unimi/zaucgl/8naomz
title: Febbraio_1921_Pagina_131.jpg

description: Bulletin of 1921/02/22
DOI: 10.13130/rd_unimi/zaucgl/dp5g1y
title: Febbraio_1921_Pagina_132.jpg

description: Bulletin of 1921/02/22
DOI: 10.13130/rd_unimi/zaucgl/xbriaw
title: Febbraio_1921_Pagina_133.jpg

description: Bulletin of 1921/02/23
DOI: 10.13130/rd_unimi/zaucgl/2ksj4l
title: Febbraio_1921_Pagina_134.jpg

description: Bulletin of 1921/02/23
DOI: 10.13130/rd_unimi/zaucgl/cpkdng
title: Febbraio_1921_Pagina_136.jpg

description: Bulletin of 1921/02/23
DOI: 10.13130/rd_unimi/zaucgl/pxt9eu
title: Febbraio_1921_Pagina_135.jpg

description: Bulletin of 1921/02/23
DOI: 10.13130/rd_unimi/zaucgl/1cwyyn
title: Febbraio_1921_Pagina_137.jpg

description: Bulletin of 1921/02/23
DOI: 10.13130/rd_unimi/zaucgl/2occcx
title: Febbraio_1921_Pagina_138.jpg

description: Bulletin of 1921/02/23
DOI: 10.13130/rd_unimi/zaucgl/yxq8t5
title: Febbraio_1921_Pagina_139.jpg

description: Bulletin of 1921/02/24
DOI: 10.13130/rd_unimi/zaucgl/aenoxm
title: Febbraio_1921_Pagina_140.jpg

description: Bulletin of 1921/02/24
DOI: 10.13130/rd_unimi/zaucgl/tnncqk
title: Febbraio_1921_Pagina_141.jpg

description: Bulletin of 1921/02/24
DOI: 10.13130/rd_unimi/zaucgl/tofrwb
title: Febbraio_1921_Pagina_142.jpg

description: Bulletin of 1921/02/24
DOI: 10.13130/rd_unimi/zaucgl/ekzrml
title: Febbraio_1921_Pagina_143.jpg

description: Bulletin of 1921/02/24
DOI: 10.13130/rd_unimi/zaucgl/adsz1i
title: Febbraio_1921_Pagina_144.jpg

description: Bulletin of 1921/02/24
DOI: 10.48657/52ft-7t14
title: Vallon de Nant weather station data 2023 - 2024
DOI: 10.13130/rd_unimi/zaucgl/e7ldfs
title: Febbraio_1921_Pagina_146.jpg

description: Bulletin of 1921/02/25
DOI: 10.13130/rd_unimi/zaucgl/yhe5o1
title: Febbraio_1921_Pagina_145.jpg

description: Bulletin of 1921/02/25
DOI: 10.13130/rd_unimi/zaucgl/cuzvrf
title: Febbraio_1921_Pagina_147.jpg

description: Bulletin of 1921/02/25
DOI: 10.13130/rd_unimi/zaucgl/iutokl
title: Febbraio_1921_Pagina_148.jpg

description: Bulletin of 1921/02/25
DOI: 10.13130/rd_unimi/zaucgl/tivl0i
title: Febbraio_1921_Pagina_149.jpg

description: Bulletin of 1921/02/25
DOI: 10.13130/rd_unimi/zaucgl/5e7dlz
title: Febbraio_1921_Pagina_151.jpg

description: Bulletin of 1921/02/26
DOI: 10.13130/rd_unimi/zaucgl/iounei
title: Febbraio_1921_Pagina_150.jpg

description: Bulletin of 1921/02/25
DOI: 10.13130/rd_unimi/zaucgl/z2f5xi
title: Febbraio_1921_Pagina_152.jpg

description: Bulletin of 1921/02/26
DOI: 10.13130/rd_unimi/zaucgl/eiz9me
title: Febbraio_1921_Pagina_153.jpg

description: Bulletin of 1921/02/26