43 research outputs found
The Ursinus Weekly, October 5, 1972
No full textJerrold Schecter speaks on China: Mao in control • Ursinus administration appoints twelve new faculty members for coming year • Voting deadline nears; Have you registered? • News editors hope for expansion and diversity • Editorial: A falling star? • Focus: Andrea Turner • Ursinus receives a big fat government grant • Coordinating the freshmen, or Thank God for the relay races • Tired of classes? • Harriers upset by DelVal; Win streak ends • Soccer team impressive in Villanova victory • New coach takes over • Gridders drop first two to F&M, Lebanon Valley • Sports buffs\u27 corner • Sports scoreboardhttps://digitalcommons.ursinus.edu/weekly/1086/thumbnail.jp
Subchronic toxicity of 2,4,4'-trichlorobiphenyl in the rat liver: an ultrastructural and biochemical study
No full text2,4,4'-Trichlorobiphenyl or PCB congener 28 was given to Sprague-Dawley weanling rats and the experimental diets were prepared by mixing the congener in 4% corn oil. The congener was administered to animals placed in four groups, each comprising 10 males or females. The diets contained 0.05, 0.5, 5, or 50 ppm congener. The fifth or control group comprised animals that received diets mixed with corn oil. Thirteen weeks after commencement of dosing, animals were euthanized and liver specimens were harvested from the animals and prepared for electron microscopy and biochemical analyses. The hepatocyte architectural modifications included an augmentation of SER profiles and an elevation of peroxisome numbers in animals regardless of gender, and mitochondrial abnormalities in the females only. Mitochondrial aberrations consisted of abnormal shapes and cristae in atypical orientation. The alterations were revealed in animals of the 5- and 50-ppm groups and were more extensive in the females. Ethoxyresorufin-O-de-ethylase activity was significantly high in the animals of the 50-ppm group. The results suggest that the female rats were more sensitive than the males to congener 28, and the no observable adverse effect level (NOAEL) was believed to be 0.5 ppm for the congener.PT: J; CR: ALLEN JR, 1973, ARCH ENV CONTAM TOXI, V1, P265 BAUMANN M, 1983, ARCH ENVIRON CON TOX, V12, P509 CADOGAN JIG, 1962, J CHEM SOC, P4257 CHU I, 1994, FUND APPL TOXICOL, V22, P457 CHUI YC, 1985, TOXICOL APPL PHARM, V81, P287 COCHIN J, 1959, J PHARMACOL EXP THER, V125, P105 COLLINS WT, 1980, AM J PATHOL, V99, P125 CROSS PC, 1993, CELL TISSUE ULTRASTR, P26 DURHAM SK, 1989, TOXICOL PATHOL, V17, P536 DURHAM SK, 1989, TOXICOL PATHOL, V17, P782 ELANGBAM CS, 1991, B ENVIRON CONTAM TOX, V47, P321 FAWCETT DW, 1994, TXB HISTOLOGY, P668 FISHBEIN L, 1974, ANNU REV PHARMACOL, V14, P139 GHADIALLY FN, 1988, ULTRASTRUCT PATHOL, V1, P191 GILLETTE DM, 1987, FUND APPL TOXICOL, V8, P5 GRISHAM JW, 1994, AM J PATHOL, V144, P849 HANSELL MM, 1974, TOXICOL APPL PHARM, V28, P418 HARKNESS MR, 1993, SCIENCE, V259, P503 HARRIS C, 1984, ARCH ENVIRON CON TOX, V13, P715 HEINOMEN T, 1982, TOXICOLOGY, V22, P297 HINKLE PC, 1994, LIVER BIOL PATHOBIOL, P309 HINTON DE, 1978, VIRCHOWS ARCH B, V27, P279 JONSSON HT, 1981, ARCH ENV CONTAM TOXI, V10, P171 KASZA L, 1978, J ENVIRON PATHOL TOX, V1, P241 KIMBROUGH RD, 1972, ARCH ENVIRON HEALTH, V25, P354 LAZAROW PB, 1982, LIVER BIOL PATHOBIOL, P27 LIN FS, 1979, ARCH ENV CONTAM TOXI, V8, P321 LIPPINCOTTSCHWA.J, 1994, LIVER BIOL PATHOBIOL, P215 LUBET RA, 1985, MUTAT RES, V142, P127 MACLELLAN K, 1994, J SUBMICR CYTOL PATH, V26, P279 MANNELLA CA, 1993, J STRUCT BIOL, V108, P227 NISHIHARA Y, 1985, BRIT J IND MED, V42, P128 NISHIZUMI M, 1970, ARCH ENVIRON HEALTH, V21, P620 ROSS MH, 1989, HISTOLOGY TEXT ATLAS, P17 SAFE SH, 1994, CRIT REV TOXICOL, V24, P87 SATO T, 1968, J ELECTRON MICROSC, V17, P158 SCHECTER A, 1984, BANBURY REPORT, V18, P177 SCHECTER A, 1985, ENVIRON HEALTH PERSP, V60, P241 SCHENKMAN JB, 1967, MOL PHARMACOL, V3, P113 SINGH A, 1981, PATHOLOGY, V13, P487 STOTZ IJ, 1978, B ENVIRON CONTAM TOX, V19, P319 TONER PG, 1992, OXFORD TXB PATHOLOGY, V1, P173 WEISS L, 1988, CELL TISSUE BIOL TXB, P1; NR: 43; TC: 7; J9: ULTRASTRUCT PATHOL; PG: 10; GA: UL536Source type: Electronic(1
Toxicity of PCB 105 in the rat liver: an ultrastructural and biochemical study
No full textPCB 105 (2,3,3',4,4'-pentachlorobiphenyl) congener was fed to weanling Sprague-Dawley rats in a diet combined with 4% corn oil. The animals were distributed randomly into 10 groups, each of which contained 10 males and 10 females, and rats in 8 groups received diets containing PCB at concentrations of 0.05, 0.5, 5, and 50 ppm. Animals in the other 2 groups served as controls. After 13 weeks, the animals were humanely killed and liver samples were obtained and prepared for transmission electron microscopy. Ultrastructural alterations revealed in the hepatocytes of animals fed the PCB included smooth endoplasmic reticulum proliferation, atypical mitochondrial cristae, and augmentation of peroxisome numbers (in animals fed high PCB concentrations). Biochemical alterations were estimated by using hepatic microsomal pentoxyresorufin-O-dealkylase (PROD) and ethoxyresorufin-O-deethylase (EROD) activities. A dose-dependent increase in EROD and PROD activities was discovered; only in the animals of highest PCB dose group, however, was EROD found to be significant (p < .05). Based on our previous work, this congener is relatively less toxic than PCB 126, 118, and 153 and is similar in toxicity to 156.PT: J; CR: BICKERS DR, 1972, RES COMMUN PATHOL PH, V3, P505 BURKE MD, 1985, BIOCHEM PHARMACOL, V34, P3337 CHEVILLE NF, 1994, ULTRASTRUCT PATHOL, P40 CHU I, 1995, FUND APPL TOXICOL, V26, P282 CHU I, 1996, J APPL TOXICOL, V16, P121 CHUI YC, 1985, TOXICOL APPL PHARM, V81, P287 CUERVO AM, 1996, SCIENCE, V273, P501 FAWCETT DW, 1994, TXB HISTOLOGY, P23 FISHBEIN L, 1974, ANNU REV PHARMACOL, V14, P139 GHADIALLY FN, 1988, ULTRASTRUCT PATHOL, V1, P192 GILLETTE DM, 1987, FUND APPL TOXICOL, V8, P5 GRANT DL, 1971, B ENVIRON CONTAM TOX, V6, P120 GREENE WB, 1973, PESTICIDES ENV CONTI, P137 HANSELL MM, 1974, TOXICOL APPL PHARM, V28, P418 HARRIS C, 1984, ARCH ENVIRON CON TOX, V13, P715 JONSSON HT, 1981, ARCH ENV CONTAM TOXI, V10, P171 KASZA L, 1976, J TOXICOL ENV HLTH, V1, P689 KASZA L, 1978, J ENVIRON PATHOL TOX, V1, P241 KIMBROUGH RD, 1972, ARCH ENVIRON HEALTH, V25, P354 KIMBROUGH RD, 1987, ANNU REV PHARMACOL, V27, P87 LIN FS, 1979, ARCH ENV CONTAM TOXI, V8, P321 LODISH H, 1995, MOL CELL BIOL, P173 LUBET RA, 1985, MUTAT RES, V142, P127 MACLELLAN K, 1994, HISTOL HISTOPATHOL, V9, P453 MACLELLAN K, 1994, HISTOL HISTOPATHOL, V9, P461 MACLELLAN K, 1994, J SUBMICR CYTOL PATH, V26, P279 MASTERS C, 1995, PEROXISONE VITAL ORG, V2, P203 NISHIHARA Y, 1985, BRIT J IND MED, V42, P128 NISHIHARA Y, 1986, BIOCHEM PHARMACOL, V35, P3335 NISHIZUMI M, 1970, ARCH ENVIRON HEALTH, V21, P620 NORBACK DH, 1972, ENVIRON HEALTH PERSP, V1, P137 PENG J, 1995, MICROSCOPY MICROANAL, P994 PENG J, 1995, THESIS U EDWARD ISLA RAO MS, 1991, HEPATOTOXICOLOGY, P621 RENDER JA, 1982, TOXICOL APPL PHARM, V62, P428 SAFE S, 1984, CRC CRIT R TOXICOL, V13, P319 SAFE SH, 1994, CRIT REV TOXICOL, V24, P87 SATO T, 1968, J ELECTRON MICROSC, V17, P158 SCHECTER A, 1984, BANBURY REPORT, V18, P177 SCHECTER A, 1985, ENVIRON HEALTH PERSP, V60, P241 SEGLEN PO, 1992, EXPERIENTIA, V48, P158 SINGH A, 1981, PATHOLOGY, V13, P487 SINGH A, 1996, ULTRASTRUCT PATHOL, V20, P275 STAUBLI W, 1969, J CELL BIOL, V42, P92 VOS JG, 1972, TOXICOL APPL PHARM, V23, P536 WEISS L, 1988, TISSUE BIOL TXB HIST, P1; NR: 46; TC: 4; J9: ULTRASTRUCT PATHOL; PG: 9; GA: WP181Source type: Prin
PCB congener 77-induced ultrastructural alterations in the rat liver: a quantitative study
No full textLiver alterations were estimated morphometrically in male and female Sprague-Dawley rats that were fed PCB congener 77 (3,3',4,4'-tetrachlorobiphenyl) in concentrations of 0.01, 0.1, 1, 10 ppm or corn oil in diets for 13 weeks. A dose-dependent increase in the volume of smooth endoplasmic reticulum (SER) and an elevation in the volume of mitochondria following administration of the highest congener concentration (10 ppm) were estimated in the female rats. Hepatocytes of the male rats contained a significantly greater baseline volume of both SER and mitochondria compared to that in the females. A statistically significant (P < 0.05) change in the volumes of either SER or mitochondria in the PCB-fed males was not revealed. The authors concluded that the increase in mitochondrial volume was probably a necessary cellular adaptation to meet the heightened energy demands required by the SER to detoxify the PCB. The use of morphometric rather than a descriptive methodology allowed for a better determination of the hepatic alterations induced by PCB 77. (C) 1998 Elsevier Science Ireland Ltd. All rights reserved.PT: J; CR: AHLBORG UG, 1994, CHEMOSPHERE, V28, P1049 CHU I, 1995, FUND APPL TOXICOL, V26, P282 CLARKE DW, 1984, CAN J PHYSIOL PHARM, V62, P1253 DEVITO MJ, 1993, FUND APPL TOXICOL, V20, P125 DURHAM SK, 1989, TOXICOL PATHOL, V17, P782 GHADIALLY FN, 1988, ULTRASTRUCT PATHOL, V2, P767 GILLETTE DM, 1987, FUND APPL TOXICOL, V8, P5 GUNDERSEN HJG, 1985, J MICROSC-OXFORD, V138, P127 HANSELL MM, 1974, TOXICOL APPL PHARM, V28, P418 HARRIS C, 1984, ARCH ENVIRON CON TOX, V13, P715 HUFF J, 1994, ANNU REV PHARMACOL, V34, P343 KASZA L, 1978, J ENVIRON PATHOL TOX, V1, P241 KIMBROUGH RD, 1972, ARCH ENVIRON HEALTH, V25, P354 LIN FS, 1979, ARCH ENV CONTAM TOXI, V88, P321 MACLELLAN K, 1994, HISTOL HISTOPATHOL, V9, P453 MACLELLAN K, 1994, HISTOL HISTOPATHOL, V9, P461 MACLELLAN K, 1994, J SUBMICR CYTOL PATH, V26, P279 OKEY AB, 1990, PHARMACOL THERAPEUT, V45, P241 PARKINSON A, 1980, CHEM-BIOL INTERACT, V30, P217 PATTERSON DG, 1994, ENVIRON HEALTH PERSP, V102, P195 PENG J, 1997, TOXICOLOGY, V120, P171 SAFE SH, 1994, CRIT REV TOXICOL, V24, P87 SATO T, 1968, J ELECTRON MICROSC, V17, P158 SCHECTER A, 1984, BANBURY REPORT, V18, P177 SINGH A, 1981, PATHOLOGY, V13, P487 SINGH A, 1996, ULTRASTRUCT PATHOL, V20, P275 SINGH A, 1997, ULTRASTRUCT PATHOL, V21, P143 VOS JG, 1972, TOXICOL APPL PHARM, V23, P563 WASSERMANN D, 1979, TOXICOL EUR RES, V1, P159 WEIBEL ER, 1969, J CELL BIOL, V42, P68 WEISS L, 1988, CELL TISSUE BIOL TXB, P1; NR: 31; TC: 5; J9: TOXICOLOGY; PG: 7; GA: 104FDSource type: Electronic(1
Models as Social Actors in the Diffusion of AI Innovations: A Multilayer, Heterogeneous, Dynamic Network Perspective
No full textArtificial Intelligence (AI) has emerged as a crucial facet of contemporary technological innovation, influencing diverse domains. Consequently, understanding the diffusion and evolution of AI innovations is vital. Scholarly publications have commonly served as proxies for studying these AI innovations. However, previous studies on publication diffusion have largely overlooked the role of models, which is particularly integral for AI innovations as they bridge upstream datasets and downstream applications. Moreover, models form an interdependent network due to their combinational evolution. This paper addresses this gap, examining how the location, movement, and speed of model movement in that model network affect the dissemination of AI research. Using a four-layer network—author collaborations, paper citations, model dependencies, and keyword co-occurrences—we examine 345,383 AI papers from 2000 to 2022. This research aims to contribute to the diffusion of innovation literature and dynamic network analysis, offering several novel insights and advancements
Models as social actors in the diffusion of AI innovations: a multilayer, heterogeneous, dynamic network perspective
No full textArtificial Intelligence (AI) has emerged as a crucial facet of contemporary technological innovation, influencing diverse domains. Consequently, understanding the diffusion and evolution of AI innovations is vital. Scholarly publications have commonly served as proxies for studying these AI innovations. However, previous studies on publication diffusion have largely overlooked the role of models, which is particularly integral for AI innovations as they bridge upstream datasets and downstream applications. Moreover, models form an interdependent network due to their combinational evolution. This paper addresses this gap, examining how the location, movement, and speed of model movement in that model network affect the dissemination of AI research. Using a four-layer network—author collaborations, paper citations, model dependencies, and keyword co-occurrences—we examine 345,383 AI papers from 2000 to 2022. This research aims to contribute to the diffusion of innovation literature and dynamic network analysis, offering several novel insights and advancements
Play’s the Thing: Community Adventure Play Experiences
No full textThe authors conducted a participatory action community-based research project that included the development, implementation and evaluation of 36 Community Adventure Play Experiences (CAPEs) in a variety of communities in the United States and abroad. In CAPEs, the emphasis is on free play created by children using “loose parts” that are readily available in their communities such as cardboard boxes, tires, fabric, recyclables, sand, wood, and water. During these play experiences children use their imaginations, and take the initiative to collaborate and problem-solve with found materials. Play facilitators ensure a safe physical and emotional space and assist children in their play as directed by the children. The authors studied CAPEs in rural, urban and peri-urban settings in the United States, Tanzania, Malawi, and Zimbabwe. As part of the investigation, they interviewed 225 caregivers and teachers in the United States, Tanzania, Malawi and Zimbabwe for information about their perceptions of CAPEs
PCB 118 induces ultrastructural alterations in the rat liver
No full textPolychlorinated biphenyls (PCBs) are ubiquitous environmental contaminants that bioaccumulate in the food chain and thus pose a health risk to humans and other animals. In this study, PCB 118 was added to the diets of Sprague Dawley rats for 13 weeks in concentrations of 2, 20, 200, 2000 p.p.b. to the females and 10, 100, 1000 and 10 000 p.p.b, to the males. The chemical was dissolved in corn oil; animals that served as the control received corn oil in the diets devoid of PCB. Use of transmission electron microscopy and stereology revealed significant (P < 0.05) elevation in the mean volume fraction of smooth reticulum profiles (20 p.p.b.), peroxisomes (200, 2600 p.p.b.) and lipid droplets (2000 p.p.b.) in the females. Hepatocytes from the males exhibited a significant increase in the mean volume fraction of lipid droplets at 10 000 p.p.b. (P < 0.05). Interactions between large quantity of estrogen and the PCB probably would account for more profound alterations in the liver of female Sprague-Dawley rats than in the males. (C) 2000 Elsevier Science Ireland Ltd. All rights reserved.PT: J; CR: BOLL M, 1998, XENOBIOTICA, V28, P479 BURSE VW, 1974, ARCH ENVIRON HEALTH, V29, P301 CASLEYSMITH JR, 1967, J R MICROSC SOC, V87, P463 CHU I, 1995, FUND APPL TOXICOL, V26, P282 CLARKE DW, 1984, CAN J PHYSIOL PHARM, V62, P1253 CONNELL BJ, 1998, J SUBMICR CYTOL PATH, V30, P157 CONNELL BJ, 1999, TOXICOLOGY, V136, P107 CULLEN JM, 1991, HEPATOTOXICOLOGY, P67 DAR E, 1992, ENVIRON RES, V59, P189 ESPEEL M, 1997, MICROSC RES TECHNIQ, V39, P453 GALLANT TL, 1999, P 165 ANN M AM ASS A, V165, A71 GHADIALLY FN, 1988, ULTRASTRUCT PATHOL, V2, P767 GILLETTE DM, 1987, FUND APPL TOXICOL, V8, P4 GILROY C, 1998, TOXICOLOGY, V127, P179 HARRIS C, 1984, ARCH ENVIRON CON TOX, V13, P715 HINTON DE, 1978, VIRCHOWS ARCH B, V27, P279 HUFF J, 1994, ANNU REV PHARMACOL, V34, P343 KEDDERIS GL, 1998, CIIT ACTIVITIES, V18, P1 KIMBROUGH RD, 1995, CRIT REV TOXICOL, V25, P133 LEMARCHAND Y, 1973, J BIOL CHEM, V248, P6862 LODISH L, 1995, MOL CELL BIOL, P170 MACLELLAN K, 1994, HISTOL HISTOPATHOL, V9, P461 MACLELLAN K, 1994, J SUBMICR CYTOL PATH, V26, P279 MARTUCCI CP, 1993, PHARMACOL THERAPEUT, V57, P237 MCFARLAND VA, 1989, ENVIRON HEALTH PERSP, V81, P225 NISHIZUMI M, 1970, ARCH ENVIRON HEALTH, V21, P620 ORCI L, 1973, NATURE, V244, P30 PARKINSON A, 1996, CASARETT DOULLS TOXI, P113 PENG J, 1995, P MICROSC MICROANAL, V1, P994 PENG J, 1997, TOXICOLOGY, V120, P171 RENDER JA, 1982, TOXICOL APPL PHARM, V62, P428 ROSS MH, 1995, HISTOLOGY TEXT ATLAS, P496 SAFA B, 1997, TOXICOL LETT, V90, P163 SAFE S, 1984, CRC CRIT R TOXICOL, V13, P319 SATO T, 1968, J ELECTRON MICROSC, V17, P158 SCHECTER A, 1984, BANBURY REPORT, V18, P177 SINGH A, 1975, EUR J CLIN INVEST, V5, P495 SINGH A, 1981, PATHOLOGY, V13, P487 SINGH A, 1996, ULTRASTRUCT PATHOL, V20, P275 SINGH A, 1997, ULTRASTRUCT PATHOL, V21, P143 SINGH A, 1999, IN PRESS J SUBMICROS UNDERWOOD EE, 1970, QUANTITATIVE STEREOL, P25 WASSERMANN D, 1979, TOXICOL EUR RES, V1, P159 WEIBEL ER, 1969, J CELL BIOL, V42, P68 ZUBAY GL, 1995, PRINCIPLES BIOCH, P412; NR: 45; TC: 2; J9: TOXICOLOGY; PG: 8; GA: 311PESource type: Electronic(1
PCB congener 126-induced ultrastructural alterations in the rat liver: a stereological study
No full textHepatocyte cytoplasmic alterations were morphometrically determined in male and female Sprague-Dawley rats fed PCB congener 126 (3,3',4,4',5-pentachlorobiphenyl) in concentrations of 0.1, 1.0, 10, 100 ppb or corn oil in diets for 13 weeks. A dose-dependent increase (P < 0.05) in the volume fraction of smooth endoplasmic reticulum (SER) and mitochondria was measured in the hepatocytes of the females. However, these cells of the male rats contained a significantly greater baseline volume fraction of SER compared to that in the females. Statistical differences were not detected in the volume fractions of rough endoplasmic reticulum, peroxisomes or lipid droplets of the hepatocytes in either the males or females. We conclude the increase in mitochondrial volume was a necessary cellular adaptation to meet the heightened energy demands by the SER to produce the necessary enzymes to detoxify the PCB. Morphometric analysis rather than a descriptive methodology allowed for a more accurate determination of the liver pathology induced by PCB 126. (C) 1999 Elsevier Science Ireland Ltd. All rights reserved.PT: J; CR: AHLBORG UG, 1994, CHEMOSPHERE, V28, P1049 BANDIERA S, 1982, CHEM-BIOL INTERACT, V39, P259 CHU I, 1994, FUND APPL TOXICOL, V22, P457 CLARKE DW, 1984, CAN J PHYSIOL PHARM, V62, P1253 DEVITO MJ, 1993, FUND APPL TOXICOL, V20, P125 GHADIALLY FN, 1988, ULTRASTRUCT PATHOL, V2, P767 GILLETTE DM, 1987, FUND APPL TOXICOL, V8, P4 GILROY C, 1998, TOXICOLOGY, V127, P179 HANSELL MM, 1974, TOXICOL APPL PHARM, V28, P418 HARRIS C, 1984, ARCH ENVIRON CON TOX, V13, P715 HONG CS, 1992, ECOTOX ENVIRON SAFE, V23, P118 KANNAN N, 1989, ARCH ENVIRON CON TOX, V18, P850 KASZA L, 1978, J ENVIRON PATHOL TOX, V1, P241 KIMBROUGH RD, 1972, ARCH ENVIRON HEALTH, V25, P354 LEECE B, 1985, J TOXICOL ENV HEALTH, V16, P379 LIN FS, 1979, ARCH ENV CONTAM TOXI, V88, P321 MACLELLAN K, 1994, HISTOL HISTOPATHOL, V9, P453 MACLELLAN K, 1994, HISTOL HISTOPATHOL, V9, P461 MACLELLAN K, 1994, J SUBMICR CYTOL PATH, V26, P279 MARTUCCI CP, 1993, PHARMACOL THERAPEUT, V57, P237 OKEY AB, 1990, PHARMACOL THERAPEUT, V45, P241 PARKINSON A, 1980, CHEM-BIOL INTERACT, V30, P217 PATTERSON DG, 1994, ENVIRON HEALTH PERSP, V102, P195 PENG J, 1997, TOXICOLOGY, V120, P171 POLAND A, 1977, MOL PHARMACOL, V13, P924 SAFE S, 1990, CRIT REV TOXICOL, V21, P51 SAFE SH, 1994, CRIT REV TOXICOL, V24, P87 SATO T, 1968, J ELECTRON MICROSC, V17, P158 SCHECTER A, 1984, BANBURY REPORT, V18, P177 SHAPIRO BH, 1995, INT J BIOCHEM CELL B, V27, P9 SINGH A, 1981, PATHOLOGY, V13, P487 SINGH A, 1996, ULTRASTRUCT PATHOL, V20, P275 SINGH A, 1997, ULTRASTRUCT PATHOL, V21, P143 SMITH LM, 1990, CHEMOSPHERE, V21, P1063 TANABE S, 1987, ENVIRON POLLUT, V47, P147 TEHSEEN WM, 1992, B ENVIRON CONTAM TOX, V48, P101 VANBIRGELEN APJM, 1994, TOXICOL APPL PHARM, V127, P209 VOS JG, 1972, TOXICOL APPL PHARM, V23, P563 WASSERMANN D, 1979, TOXICOL EUR RES, V1, P159 WEIBEL ER, 1969, J CELL BIOL, V42, P68 WEISS L, 1988, CELL TISSUE BIOL TXB, P1; NR: 41; TC: 4; J9: TOXICOLOGY; PG: 9; GA: 240XASource type: Electronic(1
The Valuation of Popular Theatre Performances: The Forgotten Success Story of Ljungby horn
No full textAlbert Ranft started as an actor in touring theatre companies in the 1880’s, but soon became responsible for one of the most important groups. Twenty-five years later, he ran a big company with about 2500 employees, owned theatres in Stockholm and Gothenburg as well as a couple of touring companies.His repertoire was based on popular entertainment plays, revues, operettas, historical plays, contemporary dramas etc. Simultaneously, his companies could offer ‘highbrow’ and ‘lowbrow’ productions. Even the actors could, during just one week, work in different genres. The way of programing was for Ranft an art form by itself, and sometimes he even acted in and directed the plays.In November 1893, at Stora Teatern in Gothenburg, he premiered a fairy tale play, and the staging was filled with spectacular effects. The play was, from the beginning, a stunning success with the production running for several hundred nights. Moreover, the production of Ljungby Horn became the ground stone for Ranft’s theatrical enterprise.The article describes how this success was established through mediatization and its base on rural oral history. The performance is analyzed and discussed as a popular theatre production (McConachie, Price, Röttger, Schecter). The author proposes that a more inclusive definition of popular theatre should be used; one which also takes into account the productions that had commercial success. Popular theatre needs to be included in theatre history writing to enable a better understanding of how the theatre system has developed.</jats:p
