cometadata/datacite-titles-descriptions-related-identifiers huggingface dataset:
DOI: 10.25549/examiner-c44-102822
title: Tuna Industry crisis, 1952

description: 17 images. Tuna Industry crisis, 10 January 1952. Tony Barcott (President, Fishermen's Cooperation Association); Pete Framengo (American Beauty); John Gargas (City of Los Angeles); Andy Rufkin (Long Island); Pete Akalovich (Betsy Ross); John J. Evich (Claremont); John Stanovich (Golden West); John Burich (Zepher).; Caption slip reads: "Photographer: Paegel. Date: 1952-01-10. Reporter: Baker. Assignment: Tuna Industry Crisis. 26, 13, 14: Empty packing table at a Terminal Island Cannery. Capt. John Gargas of City of Los Angeles at table eating with crew. Other pictures are general views of the fleet. View of crewmen sitting on nets talking over situation on the stern of Purse Seiner, with fleet in background. 18: Idle Purse Seiner tied up at Fishermen's Wharf, San Pedro. 45: Crewmen preparing and checking tuna nets. 25: Purse Seiner skippers, l to r: Tony Barcott, president, Fishermen's Cooperative Association; Pete Framengo, American Beauty; John Gargas, City of Los Angeles; Andy Rufkin, Long Island; Pete Akalovich, Betsy Ross; John J. Evich, Claremont; John Stanovich, Golden West; John Burich, Zephyr".
DOI: 10.25549/examiner-c44-14120
title: Ditch cave in (Hollywood Hills), 1951

description: 19 images. Ditch cave in (Hollywood Hills), 31 July 1951. A.G. Crawford (foreman injured); Sam Dykes; Alfredo Gonzales (victim); Leonard Santos (victim); Ray Campuzano (fireman); Father John J. Devlin (gives last rites).
DOI: 10.25549/examiner-c44-54457
title: Model of Beverly Hilton Hotel, 1954

description: 3 images. Model of Beverly Hilton Hotel, 8 June 1954. Arthur E. Elmiger -- General Manager of new hotel, with model.; Caption slip reads: "Photographer: McCarty. Date: 06-08. Reporter: Massard. Assignment: New hotel. 27/28/29: Arthur E. Elmiger, Gen. Mgr. of the new 'Beverly Hilton' hotel to be, and model of hotel".
DOI: 10.25549/examiner-c44-14759
title: Luther Scherer wedding, 1951

description: 16 images. Luther Scherer wedding, 30 July 1951. Lieutenant Governor Clifford Jones (of Nevada, best man); Luther B. "Tudor" Scherer (groom); Leveeda Marie Varley (bride); Mrs. Henry Van Dyke (matron of honor); Fred Soly (host); Miss Lolly Scherer (daughter of groom); Ted Mossman; Deputy Sheriff Gy Robinson; Mrs. George Skylstead; Emma Davis; Lew Cook; Mrs. P.R. Orlich.; More descriptive information with originals.
DOI: 10.26188/25458967.v2
title: SOLID-M Instantiation Example

description: SOLID-M is a quality framework for conceptual models learned from data.his dataset provides a SOLID-M instantiation example for analyzing the quality of agent-based Petri net models discovered from data by the Agent Miner algorithm.In this example, we specify the six SOLID-M modeling artifact sets and propose possible characteristics and measures for each of the eight SOLID-M quality aspects calculated over the specified sets.
DOI: 10.25549/examiner-c44-20093
title: Traffic accident (West Adams and 12th Avenue), 1951

description: 9 images. Traffic accident (West Adams Boulevard and 12th Avenue), 05 September 1951. Mrs. Julian Raymond; Leo Lomeli; Doris Hilton -- 22 years (model) victim; Officer A.R. McCartney; Robert F. Lee -- 38 years.; Caption slip reads: "Photographer: McCarty. Date: 1951-09-05. Reporter: Rose. Assignment: Traffic Accident -- West Adams and 12th Avenue. Left to Right: Mrs. Julian Raymond and Leo Lomeli squat to comfort traffic accident victim, Doris Hilton, 22, model. Officer A.R. McCartney gives toximeter baloon test to Miss Hilton's companion, Robert F. Lee, 38, sales manager, who was booked, University Station for drunk driving. General view of Lee's car on side against parked car with Miss Hilton lying in foreground. University Station Detective P.C. Barone inspects Lee's car on its side".
DOI: 10.25549/examiner-c44-13386
title: Mosquitos, 1951

description: 17 images. Mosquitos, July 18, 1951. Val Wright (senior sanitary inspector); Stanley Marlin (director of Bureau of Sanitation, County Health Department); Susan Pederson -- 11 1/2 months; Mrs. Phyllis Pederson.; More descriptive information with originals.
DOI: 10.25549/examiner-c44-102581
title: New Officers of Las Damas Pan Americanas, 1952

description: 3 images. New Officers of Las Damas Pan Americanas, 26 June 1952. Mrs. Fernando Figueroa; Mrs. Enrique de La Vaga; Mrs. James C. Quinn. (Sleeve reads: S-9697).; Caption slip reads: "Photographer: Lapp. Date: 1952-06-26. Assignment: Society. 17/39/40: Mrs. Fernando Figueroa, new pres.; Mrs. Enrique de La Vega; & Mrs. James C. Quinn, founder & Pres Emeritus".; Supplementary material reads: "Photo assignment for Thursday June 26 at 1 p.m. Rush negs. in. Pls. go to home of Mrs. Enrique de la Vega, 636 South Plymouth Blvd., get shots of new officers of Las Damas Pan Americanas. Candid, both three and four cols., not more than three people in three, four or five in four col. Try and include Mrs. De La Vega. Wet negs. to me. Thanks, Carter Ludlow".
DOI: 10.25549/examiner-c44-14635
title: Pedestrian vs auto (Pico and Westwood), 1951

description: 4 images. Pedestrian vs auto (Pico and Westwood), 4 August 1951. Mrs. Clydeam Topham (victim and her dog) killed; Officer George Adams.
DOI: 10.15468/dl.tzc4n6
title: Occurrence Download

description: A dataset containing 6636 species occurrences available in GBIF matching the query:
{
 "TaxonKey" : [
 "is one of (Eragrostis tenella (L.) P.Beauv. ex Roem. & Schult.)"
 ]
}

 The dataset includes 6636 records from 244 constituent datasets; see https://api.gbif.org/v1/occurrence/download/0017716-240506114902167/datasets/export for details.
 
Data from some individual datasets included in this download may be licensed under less restrictive terms.
DOI: 10.25549/examiner-c44-11757
title: School board, 1951

description: 9 images. School board, July 2, 1951. Mrs. Eleanor Allen (new president); Arthur F. Gardner (new member); Paul Burke; Dr. Alexander Stoddard; Olin E. Darby.; More descriptive information with originals.
DOI: 10.25549/examiner-c44-11475
title: Sloat inquest, 1951

description: 23 images. Sloat inquest, July 5, 1951. Helen Sloat; Marian Wright; Leo Kubic (brother of Helen); John Harrison (officer); Arthur Collins (inquest reporter); Rosemary Connor; Deputy Sheriff Josephine Uttke.; More descriptive information with originals.
DOI: 10.6084/m9.figshare.25606234
title: Repression of YEATS2 induces cellular senescence in hepatocellular carcinoma and inhibits tumor growth

description: Hepatocellular carcinoma (HCC) stands as the third leading cause of cancer-related fatalities globally. In this study, we observed a significant increase in the expression level of the <i>YEATS2</i> gene in HCC patients, and it is negatively correlated with the patients’ survival rate. While we have previously identified the association between YEATS2 and the survival of pancreatic cancer cells, the regulatory mechanisms and significance in HCC are still to be fully elucidated. Our study shows that knockdown (KD) of YEATS2 expression leads to DNA damage, which in turn results in an upregulation of γ-H2A.X expression and activation of the canonical senescence-related pathway p53/p21Cip1. Moreover, our transcriptomic analysis reveals that YEATS2 KD cells can enhance the expression of p21Cip1 via the c-Myc/miR-93-5p pathway, consequently fostering the senescence of HCC cells. The initiation of cellular senescence through dual-channel activation suggests that YEATS2 plays a pivotal regulatory role in the process of cell proliferation. Ultimately, our <i>in vivo</i> research utilizing a nude mouse tumor model revealed a notable decrease in both tumor volume and weight after the suppression of YEATS2 expression. This phenomenon is likely attributable to the attenuation of proliferative cell activity, coupled with a concurrent augmentation in the population of natural killer (NK) cells. In summary, our research results have supplemented the understanding of the regulatory mechanisms of HCC cell proliferation and indicated that targeting YEATS2 may potentially inhibit liver tumor growth.
DOI: 10.25549/examiner-c44-9037
title: Arthur Lake and wife leave for New York, 1951

description: 6 images. Arthur Lake and wife leave for New York, May 10, 1951. Stephen Slesinger; Arthur Lake; Mrs. Arthur Lake.
DOI: 10.6084/m9.figshare.25539510
title: Homologous recombination contributes to the repair of acetaldehyde-induced DNA damage

description: Acetaldehyde, a chemical that can cause DNA damage and contribute to cancer, is prevalently present in our environment, e.g. in alcohol, tobacco, and food. Although aldehyde potentially promotes crosslinking reactions among biological substances including DNA, RNA, and protein, it remains unclear what types of DNA damage are caused by acetaldehyde and how they are repaired. In this study, we explored mechanisms involved in the repair of acetaldehyde-induced DNA damage by examining the cellular sensitivity to acetaldehyde in the collection of human TK6 mutant deficient in each genome maintenance system. Among the mutants, mismatch repair mutants did not show hypersensitivity to acetaldehyde, while mutants deficient in base and nucleotide excision repair pathways or homologous recombination (HR) exhibited higher sensitivity to acetaldehyde than did <i>wild-type</i> cells. We found that acetaldehyde-induced RAD51 foci representing HR intermediates were prolonged in HR-deficient cells. These results indicate a pivotal role of HR in the repair of acetaldehyde-induced DNA damage. These results suggest that acetaldehyde causes complex DNA damages that require various types of repair pathways. Mutants deficient in the removal of protein adducts from DNA ends such as <i>TDP1</i><sup>−/−</sup> and <i>TDP2</i><sup>−/−</sup> cells exhibited hypersensitivity to acetaldehyde. Strikingly, the double mutant deficient in both TDP1 and RAD54 showed similar sensitivity to each single mutant. This epistatic relationship between <i>TDP1</i><sup>−/−</sup> and <i>RAD54</i><sup>−/−</sup> suggests that the protein-DNA adducts generated by acetaldehyde need to be removed for efficient repair by HR. Our study would help understand the molecular mechanism of the genotoxic and mutagenic effects of acetaldehyde.
DOI: 10.6084/m9.figshare.25539510.v1
title: Homologous recombination contributes to the repair of acetaldehyde-induced DNA damage

description: Acetaldehyde, a chemical that can cause DNA damage and contribute to cancer, is prevalently present in our environment, e.g. in alcohol, tobacco, and food. Although aldehyde potentially promotes crosslinking reactions among biological substances including DNA, RNA, and protein, it remains unclear what types of DNA damage are caused by acetaldehyde and how they are repaired. In this study, we explored mechanisms involved in the repair of acetaldehyde-induced DNA damage by examining the cellular sensitivity to acetaldehyde in the collection of human TK6 mutant deficient in each genome maintenance system. Among the mutants, mismatch repair mutants did not show hypersensitivity to acetaldehyde, while mutants deficient in base and nucleotide excision repair pathways or homologous recombination (HR) exhibited higher sensitivity to acetaldehyde than did <i>wild-type</i> cells. We found that acetaldehyde-induced RAD51 foci representing HR intermediates were prolonged in HR-deficient cells. These results indicate a pivotal role of HR in the repair of acetaldehyde-induced DNA damage. These results suggest that acetaldehyde causes complex DNA damages that require various types of repair pathways. Mutants deficient in the removal of protein adducts from DNA ends such as <i>TDP1</i><sup>−/−</sup> and <i>TDP2</i><sup>−/−</sup> cells exhibited hypersensitivity to acetaldehyde. Strikingly, the double mutant deficient in both TDP1 and RAD54 showed similar sensitivity to each single mutant. This epistatic relationship between <i>TDP1</i><sup>−/−</sup> and <i>RAD54</i><sup>−/−</sup> suggests that the protein-DNA adducts generated by acetaldehyde need to be removed for efficient repair by HR. Our study would help understand the molecular mechanism of the genotoxic and mutagenic effects of acetaldehyde.
DOI: 10.6084/m9.figshare.25606234.v1
title: Repression of YEATS2 induces cellular senescence in hepatocellular carcinoma and inhibits tumor growth

description: Hepatocellular carcinoma (HCC) stands as the third leading cause of cancer-related fatalities globally. In this study, we observed a significant increase in the expression level of the <i>YEATS2</i> gene in HCC patients, and it is negatively correlated with the patients’ survival rate. While we have previously identified the association between YEATS2 and the survival of pancreatic cancer cells, the regulatory mechanisms and significance in HCC are still to be fully elucidated. Our study shows that knockdown (KD) of YEATS2 expression leads to DNA damage, which in turn results in an upregulation of γ-H2A.X expression and activation of the canonical senescence-related pathway p53/p21Cip1. Moreover, our transcriptomic analysis reveals that YEATS2 KD cells can enhance the expression of p21Cip1 via the c-Myc/miR-93-5p pathway, consequently fostering the senescence of HCC cells. The initiation of cellular senescence through dual-channel activation suggests that YEATS2 plays a pivotal regulatory role in the process of cell proliferation. Ultimately, our <i>in vivo</i> research utilizing a nude mouse tumor model revealed a notable decrease in both tumor volume and weight after the suppression of YEATS2 expression. This phenomenon is likely attributable to the attenuation of proliferative cell activity, coupled with a concurrent augmentation in the population of natural killer (NK) cells. In summary, our research results have supplemented the understanding of the regulatory mechanisms of HCC cell proliferation and indicated that targeting YEATS2 may potentially inhibit liver tumor growth.
DOI: 10.25549/examiner-c44-9803
title: Arrival, 1951

description: 4 images. Arrival, May 11, 1951. Cecil Douglas Horsley (Right Reverend); John M. Krumm (Dean of St. Paul's).
DOI: 10.6084/m9.figshare.25504689
title: Identification and validation of key miRNAs and a microRNA-mRNA regulatory network associated with liver cancer

description: MiRNAs play crucial regulatory roles in the growth and development of tumor cells by serving as carriers of post-transcriptional regulatory information derived from genes. Investigating the potential function and clinical significance of miRNA-mediated mRNA regulatory networks in liver cancer can offer novel insights and therapeutic strategies for the treatment of this disease. We identified 300 differentially expressed miRNAs, and five miRNAs were identified to be correlated with overall survival and could be used as an independent prognostic. GO enrichment analysis mainly included carboxylic acid biosynthesis, organic acid biosynthesis, peroxisomal membrane, microsomal membrane, DNA binding, C-acyltransferase activity, etc. KEGG enrichment analysis showed that the pathways of target genes related to liver cancer were mainly focused on butyric acid metabolism and partial amino acid metabolism. Eight of the top 10 HUB genes were associated with prognosis, and the expression of four genes was positively correlated with prognosis, of which ABAT, BHMT, and SHMT1 were target genes of hsa-miR-5003-3p. MiR-5003-3p inhibits ABAT/BHMT/SHMT1 expression, thereby promoting liver cancer development. Overall, our study provides new ideas for the treatment of liver cancer, and these five miRNAs may be independent prognostic biomarkers and therapeutic targets for liver cancer patients. And miR-5003-3p may be a critical factor in the mechanism of liver cancer development.
DOI: 10.6084/m9.figshare.25620468.v1
title: SIRT3 suppression resulting from the enhanced β-catenin signaling drives glycolysis and promotes hypoxia-induced cell growth in hepatocellular carcinoma cells

description: The precise mechanisms underlying the inhibitory effects of SIRT3, a mitochondrial sirtuin protein, on hepatocellular carcinoma (HCC) development, as well as its impact on mitochondrial respiration, remain poorly understood. We assessed sirtuins 3 (SIRT3) levels in HCC tissues and Huh7 cells cultured under hypoxic condition. We investigated the effects of SIRT3 on cell proliferation, glycolytic metabolism, mitochondrial respiration, mitophagy, and mitochondrial biogenesis in Huh7 cells. Besides, we explored the potential mechanisms regulating SIRT3 expression in hypoxically cultured Huh7 cells. Gradual reduction in SIRT3 expressions were observed in both adjacent tumor tissues and tumor tissues. Similarly, SIRT3 expressions were diminished in Huh7 cells cultured under hypoxic condition. Forced expression of SIRT3 attenuated the growth of hypoxically cultured Huh7 cells. SIRT3 overexpression led to a decrease in extracellular acidification rate while increasing oxygen consumption rate. SIRT3 downregulated the levels of hexokinase 2 and pyruvate kinase M2. Moreover, SIRT3 enhanced mitophagy signaling, as indicated by mtKeima, and upregulated key proteins involved in various mitophagic pathways while reducing intracellular reactive oxygen species levels. Furthermore, SIRT3 increased proxisome proliferator-activated receptor-gamma coactivator 1α levels and the amount of mitochondrial DNA in Huh7 cells. Notably, β-catenin expressions were elevated in Huh7 cells cultured under hypoxic condition. Antagonists and agonists of β-catenin respectively upregulated and downregulated SIRT3 expressions in hypoxically cultured Huh7 cells. The modulationsof glycolysis and mitochondrial respiration represent the primary mechanism through which SIRT3, suppressed by β-catenin, inhibits HCC cell proliferation.
DOI: 10.6084/m9.figshare.25504689.v1
title: Identification and validation of key miRNAs and a microRNA-mRNA regulatory network associated with liver cancer

description: MiRNAs play crucial regulatory roles in the growth and development of tumor cells by serving as carriers of post-transcriptional regulatory information derived from genes. Investigating the potential function and clinical significance of miRNA-mediated mRNA regulatory networks in liver cancer can offer novel insights and therapeutic strategies for the treatment of this disease. We identified 300 differentially expressed miRNAs, and five miRNAs were identified to be correlated with overall survival and could be used as an independent prognostic. GO enrichment analysis mainly included carboxylic acid biosynthesis, organic acid biosynthesis, peroxisomal membrane, microsomal membrane, DNA binding, C-acyltransferase activity, etc. KEGG enrichment analysis showed that the pathways of target genes related to liver cancer were mainly focused on butyric acid metabolism and partial amino acid metabolism. Eight of the top 10 HUB genes were associated with prognosis, and the expression of four genes was positively correlated with prognosis, of which ABAT, BHMT, and SHMT1 were target genes of hsa-miR-5003-3p. MiR-5003-3p inhibits ABAT/BHMT/SHMT1 expression, thereby promoting liver cancer development. Overall, our study provides new ideas for the treatment of liver cancer, and these five miRNAs may be independent prognostic biomarkers and therapeutic targets for liver cancer patients. And miR-5003-3p may be a critical factor in the mechanism of liver cancer development.
DOI: 10.6084/m9.figshare.25517083
title: REV7-p53 interaction inhibits ATM-mediated DNA damage signaling

description: REV7 is an abundant, multifunctional protein that is a known factor in cell cycle regulation and in several key DNA repair pathways including Trans-Lesion Synthesis (TLS), the Fanconi Anemia (FA) pathway, and DNA Double-Strand Break (DSB) repair pathway choice. Thus far, no direct role has been studied for REV7 in the DNA damage response (DDR) signaling pathway. Here we describe a novel function for REV7 in DSB-induced p53 signaling. We show that REV7 binds directly to p53 to block ATM-dependent p53 Ser15 phosphorylation. We also report that REV7 is involved in the destabilization of p53. These findings affirm REV7’s participation in fundamental cell cycle and DNA repair pathways. Furthermore, they highlight REV7 as a critical factor for the integration of multiple processes that determine viability and genome stability.
DOI: 10.6084/m9.figshare.25517083.v1
title: REV7-p53 interaction inhibits ATM-mediated DNA damage signaling

description: REV7 is an abundant, multifunctional protein that is a known factor in cell cycle regulation and in several key DNA repair pathways including Trans-Lesion Synthesis (TLS), the Fanconi Anemia (FA) pathway, and DNA Double-Strand Break (DSB) repair pathway choice. Thus far, no direct role has been studied for REV7 in the DNA damage response (DDR) signaling pathway. Here we describe a novel function for REV7 in DSB-induced p53 signaling. We show that REV7 binds directly to p53 to block ATM-dependent p53 Ser15 phosphorylation. We also report that REV7 is involved in the destabilization of p53. These findings affirm REV7’s participation in fundamental cell cycle and DNA repair pathways. Furthermore, they highlight REV7 as a critical factor for the integration of multiple processes that determine viability and genome stability.
DOI: 10.6084/m9.figshare.25620468
title: SIRT3 suppression resulting from the enhanced β-catenin signaling drives glycolysis and promotes hypoxia-induced cell growth in hepatocellular carcinoma cells

description: The precise mechanisms underlying the inhibitory effects of SIRT3, a mitochondrial sirtuin protein, on hepatocellular carcinoma (HCC) development, as well as its impact on mitochondrial respiration, remain poorly understood. We assessed sirtuins 3 (SIRT3) levels in HCC tissues and Huh7 cells cultured under hypoxic condition. We investigated the effects of SIRT3 on cell proliferation, glycolytic metabolism, mitochondrial respiration, mitophagy, and mitochondrial biogenesis in Huh7 cells. Besides, we explored the potential mechanisms regulating SIRT3 expression in hypoxically cultured Huh7 cells. Gradual reduction in SIRT3 expressions were observed in both adjacent tumor tissues and tumor tissues. Similarly, SIRT3 expressions were diminished in Huh7 cells cultured under hypoxic condition. Forced expression of SIRT3 attenuated the growth of hypoxically cultured Huh7 cells. SIRT3 overexpression led to a decrease in extracellular acidification rate while increasing oxygen consumption rate. SIRT3 downregulated the levels of hexokinase 2 and pyruvate kinase M2. Moreover, SIRT3 enhanced mitophagy signaling, as indicated by mtKeima, and upregulated key proteins involved in various mitophagic pathways while reducing intracellular reactive oxygen species levels. Furthermore, SIRT3 increased proxisome proliferator-activated receptor-gamma coactivator 1α levels and the amount of mitochondrial DNA in Huh7 cells. Notably, β-catenin expressions were elevated in Huh7 cells cultured under hypoxic condition. Antagonists and agonists of β-catenin respectively upregulated and downregulated SIRT3 expressions in hypoxically cultured Huh7 cells. The modulationsof glycolysis and mitochondrial respiration represent the primary mechanism through which SIRT3, suppressed by β-catenin, inhibits HCC cell proliferation.