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Article ; Online: Opposing p53 and mTOR/AKT promote an in vivo switch from apoptosis to senescence upon telomere shortening in zebrafish.

El Maï, Mounir / Marzullo, Marta / de Castro, Inês Pimenta / Ferreira, Miguel Godinho

2020 Volume 9

Abstract: Progressive telomere shortening during lifespan is associated with restriction of cell proliferation, genome instability and aging. Apoptosis and senescence are the two major outcomes upon irreversible cellular damage. Here, we show a transition of these ...

Abstract	Progressive telomere shortening during lifespan is associated with restriction of cell proliferation, genome instability and aging. Apoptosis and senescence are the two major outcomes upon irreversible cellular damage. Here, we show a transition of these two cell fates during aging of telomerase deficient zebrafish. In young telomerase mutants, proliferative tissues exhibit DNA damage and p53-dependent apoptosis, but no senescence. However, these tissues in older animals display loss of cellularity and senescence becomes predominant. Tissue alterations are accompanied by a pro-proliferative stimulus mediated by AKT signaling. Upon AKT activation, FoxO transcription factors are phosphorylated and translocated out of the nucleus. This results in reduced SOD2 expression causing an increase of ROS and mitochondrial dysfunction. These alterations induce p15/16 growth arrest and senescence. We propose that, upon telomere shortening, early apoptosis leads to cell depletion and insufficient compensatory proliferation. Following tissue damage, the mTOR/AKT is activated causing mitochondrial dysfunction and p15/16-dependent senescence.
MeSH term(s)	Aging ; Animals ; Apoptosis/genetics ; Cell Proliferation ; Cellular Senescence/genetics ; DNA Damage ; Female ; Male ; Mitochondria ; Mutation ; Phosphorylation ; Proto-Oncogene Proteins c-akt/genetics ; Proto-Oncogene Proteins c-akt/metabolism ; Reactive Oxygen Species/metabolism ; Signal Transduction ; TOR Serine-Threonine Kinases/genetics ; TOR Serine-Threonine Kinases/metabolism ; Telomerase/genetics ; Telomerase/metabolism ; Telomere/metabolism ; Telomere Shortening/genetics ; Tumor Suppressor Protein p53/genetics ; Tumor Suppressor Protein p53/metabolism ; Zebrafish/genetics ; Zebrafish/physiology
Chemical Substances	Reactive Oxygen Species ; Tumor Suppressor Protein p53 ; TOR Serine-Threonine Kinases (EC 2.7.1.1) ; Proto-Oncogene Proteins c-akt (EC 2.7.11.1) ; Telomerase (EC 2.7.7.49)
Language	English
Publishing date	2020-05-19
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2687154-3
ISSN	2050-084X ; 2050-084X
ISSN (online)	2050-084X
ISSN	2050-084X
DOI	10.7554/eLife.54935
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Opposing p53 and mTOR/AKT promote an in vivo switch from apoptosis to senescence upon telomere shortening in zebrafish

Mounir El Maï / Marta Marzullo / Inês Pimenta de Castro / Miguel Godinho Ferreira

eLife, Vol

2020 Volume 9

Abstract	Progressive telomere shortening during lifespan is associated with restriction of cell proliferation, genome instability and aging. Apoptosis and senescence are the two major outcomes upon irreversible cellular damage. Here, we show a transition of these two cell fates during aging of telomerase deficient zebrafish. In young telomerase mutants, proliferative tissues exhibit DNA damage and p53-dependent apoptosis, but no senescence. However, these tissues in older animals display loss of cellularity and senescence becomes predominant. Tissue alterations are accompanied by a pro-proliferative stimulus mediated by AKT signaling. Upon AKT activation, FoxO transcription factors are phosphorylated and translocated out of the nucleus. This results in reduced SOD2 expression causing an increase of ROS and mitochondrial dysfunction. These alterations induce p15/16 growth arrest and senescence. We propose that, upon telomere shortening, early apoptosis leads to cell depletion and insufficient compensatory proliferation. Following tissue damage, the mTOR/AKT is activated causing mitochondrial dysfunction and p15/16-dependent senescence.
Keywords	telomeres ; apoptosis ; senescence ; p53 ; AKT ; aging ; Medicine ; R ; Science ; Q ; Biology (General) ; QH301-705.5
Subject code	610
Language	English
Publishing date	2020-05-01T00:00:00Z
Publisher	eLife Sciences Publications Ltd
Document type	Article ; Online
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Article ; Online: Telomeres in aging and disease: lessons from zebrafish.

Carneiro, Madalena C / de Castro, Inês Pimenta / Ferreira, Miguel Godinho

Disease models & mechanisms

2016 Volume 9, Issue 7, Page(s) 737–748

Abstract: Age is the highest risk factor for some of the most prevalent human diseases, including cancer. Telomere shortening is thought to play a central role in the aging process in humans. The link between telomeres and aging is highlighted by the fact that ... ...

Abstract	Age is the highest risk factor for some of the most prevalent human diseases, including cancer. Telomere shortening is thought to play a central role in the aging process in humans. The link between telomeres and aging is highlighted by the fact that genetic diseases causing telomerase deficiency are associated with premature aging and increased risk of cancer. For the last two decades, this link has been mostly investigated using mice that have long telomeres. However, zebrafish has recently emerged as a powerful and complementary model system to study telomere biology. Zebrafish possess human-like short telomeres that progressively decline with age, reaching lengths in old age that are observed when telomerase is mutated. The extensive characterization of its well-conserved molecular and cellular physiology makes this vertebrate an excellent model to unravel the underlying relationship between telomere shortening, tissue regeneration, aging and disease. In this Review, we explore the advantages of using zebrafish in telomere research and discuss the primary discoveries made in this model that have contributed to expanding our knowledge of how telomere attrition contributes to cellular senescence, organ dysfunction and disease.
MeSH term(s)	Aging/metabolism ; Animals ; Disease ; Humans ; Models, Biological ; Telomerase/metabolism ; Telomere/metabolism ; Zebrafish/physiology
Chemical Substances	Telomerase (EC 2.7.7.49)
Language	English
Publishing date	2016-06-28
Publishing country	England
Document type	Journal Article ; Review ; Research Support, Non-U.S. Gov't
ISSN	1754-8411
ISSN (online)	1754-8411
DOI	10.1242/dmm.025130
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Article ; Online: Telomeres in aging and disease

Madalena C. Carneiro / Inês Pimenta de Castro / Miguel Godinho Ferreira

Disease Models & Mechanisms, Vol 9, Iss 7, Pp 737-

lessons from zebrafish

2016 Volume 748

Abstract	Age is the highest risk factor for some of the most prevalent human diseases, including cancer. Telomere shortening is thought to play a central role in the aging process in humans. The link between telomeres and aging is highlighted by the fact that genetic diseases causing telomerase deficiency are associated with premature aging and increased risk of cancer. For the last two decades, this link has been mostly investigated using mice that have long telomeres. However, zebrafish has recently emerged as a powerful and complementary model system to study telomere biology. Zebrafish possess human-like short telomeres that progressively decline with age, reaching lengths in old age that are observed when telomerase is mutated. The extensive characterization of its well-conserved molecular and cellular physiology makes this vertebrate an excellent model to unravel the underlying relationship between telomere shortening, tissue regeneration, aging and disease. In this Review, we explore the advantages of using zebrafish in telomere research and discuss the primary discoveries made in this model that have contributed to expanding our knowledge of how telomere attrition contributes to cellular senescence, organ dysfunction and disease.
Keywords	Aging ; Cancer ; Disease ; Telomerase ; Telomeres ; Zebrafish ; Medicine ; R ; Pathology ; RB1-214
Subject code	610
Language	English
Publishing date	2016-07-01T00:00:00Z
Publisher	The Company of Biologists
Document type	Article ; Online
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Article ; Online: Mitochondrial quality control and neurological disease: an emerging connection.

de Castro, Inês Pimenta / Martins, L Miguel / Tufi, Roberta

Expert reviews in molecular medicine

2010 Volume 12, Page(s) e12

Abstract: The human brain is a highly complex organ with remarkable energy demands. Although it represents only 2% of the total body weight, it accounts for 20% of all oxygen consumption, reflecting its high rate of metabolic activity. Mitochondria have a crucial ... ...

Abstract	The human brain is a highly complex organ with remarkable energy demands. Although it represents only 2% of the total body weight, it accounts for 20% of all oxygen consumption, reflecting its high rate of metabolic activity. Mitochondria have a crucial role in the supply of energy to the brain. Consequently, their deterioration can have important detrimental consequences on the function and plasticity of neurons, and is thought to have a pivotal role in ageing and in the pathogenesis of several neurological disorders. Owing to their inherent physiological functions, mitochondria are subjected to particularly high levels of stress and have evolved specific molecular quality-control mechanisms to maintain the mitochondrial components. Here, we review some of the most recent advances in the understanding of mitochondrial stress-control pathways, with a particular focus on how defects in such pathways might contribute to neurodegenerative disease.
MeSH term(s)	Brain/metabolism ; Brain/pathology ; Brain/physiopathology ; Humans ; Metabolic Networks and Pathways ; Mitochondria/metabolism ; Mitochondrial Proteins/metabolism ; Models, Biological ; Neurodegenerative Diseases/metabolism ; Neurodegenerative Diseases/pathology ; Neurodegenerative Diseases/physiopathology ; Oxidative Stress
Chemical Substances	Mitochondrial Proteins
Language	English
Publishing date	2010-04-19
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ISSN	1462-3994
ISSN (online)	1462-3994
DOI	10.1017/S1462399410001456
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Article ; Online: Mitochondrial quality control and Parkinson's disease: a pathway unfolds.

de Castro, Inês Pimenta / Martins, L Miguel / Loh, Samantha Hui Yong

Molecular neurobiology

2010 Volume 43, Issue 2, Page(s) 80–86

Abstract: Recent findings from genetic studies suggest that defective mitochondrial quality control may play an important role in the development of Parkinson's disease (PD). Such defects may result in the impairment of neuronal mitochondria, which leads to both ... ...

Abstract	Recent findings from genetic studies suggest that defective mitochondrial quality control may play an important role in the development of Parkinson's disease (PD). Such defects may result in the impairment of neuronal mitochondria, which leads to both synaptic dysfunction and cell death and results in neurodegeneration. Here, we review state-of-the-art knowledge of how pathways affecting mitochondrial quality control might contribute to PD, with a particular emphasis on the molecular mechanisms employed by PTEN-induced putative kinase 1 (PINK1), HtrA2 and Parkin to regulate mitochondrial quality control.
MeSH term(s)	Animals ; Disease Models, Animal ; Humans ; Mitochondria/metabolism ; Mitochondria/pathology ; Neurons/metabolism ; Neurons/pathology ; Parkinson Disease/enzymology ; Parkinson Disease/genetics ; Parkinson Disease/metabolism ; Parkinson Disease/pathology ; Protein Kinases/metabolism
Chemical Substances	Protein Kinases (EC 2.7.-) ; PTEN-induced putative kinase (EC 2.7.11.1)
Language	English
Publishing date	2010-12-01
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	645020-9
ISSN	1559-1182 ; 0893-7648
ISSN (online)	1559-1182
ISSN	0893-7648
DOI	10.1007/s12035-010-8150-4
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Article: Mitochondrial Quality Control and Parkinson's Disease: A Pathway Unfolds

de Castro, Inês Pimenta / Martins, L. Miguel / Loh, Samantha Hui Yong

Molecular neurobiology. 2011 Apr., v. 43, no. 2

2011

Abstract	Recent findings from genetic studies suggest that defective mitochondrial quality control may play an important role in the development of Parkinson's disease (PD). Such defects may result in the impairment of neuronal mitochondria, which leads to both synaptic dysfunction and cell death and results in neurodegeneration. Here, we review state-of-the-art knowledge of how pathways affecting mitochondrial quality control might contribute to PD, with a particular emphasis on the molecular mechanisms employed by PTEN-induced putative kinase 1 (PINK1), HtrA2 and Parkin to regulate mitochondrial quality control.
Keywords	mitochondria ; Parkinson disease
Language	English
Dates of publication	2011-04
Size	p. 80-86.
Publisher	Humana Press Inc
Publishing place	New York
Document type	Article
ZDB-ID	645020-9
ISSN	1559-1182 ; 0893-7648
ISSN (online)	1559-1182
ISSN	0893-7648
DOI	10.1007/s12035-010-8150-4
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Article ; Online: The 12 city HIV Surveillance Survey among MSM in Brazil 2016 using respondent-driven sampling: a description of methods and RDS diagnostics.

Kendall, Carl / Kerr, Ligia / Mota, Rosa Salani / Guimarães, Mark Drew Crosland / Leal, Andrea Fachel / Merchan-Hamann, Edgar / Dourado, Inês Costa / Veras, Maria Amélia / Brito, Ana Maria de / Pontes, Alexandre Kerr / Castro, Ana Rita Coimbra Motta / Macena, Raimunda Hermelinda Maia / Knauth, Daniela / Linda, Luana Costa / Oliveira, Lisangela Cristina / Cavalcante, Socorro / Camillo, Ana Cláudia / Bermudez, Ximena Pamela Diaz / Moreira, Regina Célia /

Benzaken, Adele Schwartz / Pereira, Gerson / Pascom, Ana Roberta Pati / Pimenta, Cristina / Grazina Johnston, Lisa

Revista brasileira de epidemiologia = Brazilian journal of epidemiology

2019 Volume 22, Page(s) e190004

Abstract: Introduction: This paper details the methods used in the second national Biological and Behavioral Surveillance Survey (BBSS) of HIV, syphilis, and hepatitis B and C among men who have sex with men in Brazil.: Methods: Respondent-driven sampling (RDS) ...

Abstract	Introduction: This paper details the methods used in the second national Biological and Behavioral Surveillance Survey (BBSS) of HIV, syphilis, and hepatitis B and C among men who have sex with men in Brazil. Methods: Respondent-driven sampling (RDS) was used in 12 cities in 2016. The targeted sample size was initiated with five to six seeds in each city. HIV, syphilis, and Hepatitis B and C rapid tests were offered to participants. RDS Analyst with Gile's successive sampling (SS) estimator was used to adjust results as recommended and a weight for each individual was generated for further analysis. Data for the 12 cities were merged and analyzed using Stata 14.0 complex survey data tools with each city treated as its own stratum. Results: Duration of data collection varied from 5.9 to 17.6 weeks. 4,176 men were recruited in the 12 cities. Two sites failed to achieve targeted sample size due to a six-month delay in local IRB approval. No city failed to reach convergence in our major outcome variable (HIV). Conclusion: The comprehensive BBSS was completed as planned and on budget. The description of methods here is more detailed than usual, due to new diagnostic tools and requirements of the new STROBE-RDS guidelines.
MeSH term(s)	Adult ; Brazil/epidemiology ; HIV Infections/diagnosis ; HIV Infections/epidemiology ; Health Surveys/methods ; Hepatitis B/diagnosis ; Hepatitis B/epidemiology ; Hepatitis C/diagnosis ; Hepatitis C/epidemiology ; Homosexuality, Male/statistics & numerical data ; Humans ; Male ; Population Surveillance ; Prevalence ; Self Report ; Surveys and Questionnaires ; Syphilis/diagnosis ; Syphilis/epidemiology
Language	English
Publishing date	2019-03-14
Publishing country	Brazil
Document type	Journal Article
ZDB-ID	2183366-7
ISSN	1980-5497 ; 1415-790X
ISSN (online)	1980-5497
ISSN	1415-790X
DOI	10.1590/1980-549720190004
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Article ; Online: MAMMALS IN PORTUGAL: A data set of terrestrial, volant, and marine mammal occurrences in Portugal.

Grilo, Clara / Afonso, Beatriz C / Afonso, Filipe / Alexandre, Marta / Aliácar, Sara / Almeida, Ana / Alonso, Ivan Prego / Álvares, Francisco / Alves, Paulo / Alves, Paulo Célio / Alves, Pedro / Amado, Anabela / Amendoeira, Vitor / Amorim, Francisco / da Silva Aparício, Guilherme / Araújo, Ricardo / Ascensão, Fernando / Augusto, Margarida / Bandeira, Victor /

Barbosa, A Márcia / Barbosa, Soraia / Barbosa, Sérgio / Barreiro, Silvia / Barros, Paulo / Barros, Tânia / Barros, Filomena / Basto, Mafalda / Bernardino, Joana / Bicho, Sara / Biedma, Luis Eduardo / Borges, Marta / Braz, Luis / Brito, José Carlos / Brito, Tiago / Cabral, João Alexandre / Calzada, Javier / Camarinha, Cláudia / Carapuço, Mafalda / Cardoso, Paulo / Carmo, Mário / Carrapato, Carlos / da Silva Carrilho, Maílis / Carvalho, Diogo Filipe T C S / Carvalho, Filipe / Carvalho, João / Castro, Diana / Castro, Guilherme / Castro, Joana / Castro, Luis Roma / Catry, Filipe Xavier / Cerveira, Ana M / Cid, André / Clarke, Rafael / Conde, Conceição / Conde, José / Costa, Jorge / Costa, Mafalda / Costa, Pedro / Costa, Cristina / do Couto, André Pedro / Craveiro, João / Dias, Marta / Dias, Sofia / Duarte, Beatriz / Duro, Virginia / Encarnação, Cláudia / Eufrázio, Sofia / Fael, António / Falé, João Salvador / Faria, Sandra / Fernandes, Carlos / Fernandes, Margarida / da Costa, Gonçalo Ferrão / Ferreira, Clara / Ferreira, Diogo F / Ferreira, Eduardo / Ferreira, Joaquim Pedro / Ferreira, João / Ferreira, Diana / Fonseca, Carlos / Fontes, Inês / Fragoso, Ricardo / Franco, Claudia / Freitas, Tamira / Gabriel, Sofia I / Gibb, Rory / Gil, Patricia / Gomes, Carla Patricia Jorge / Horta, Pedro / Gomes, Pedro / Gomes, Verónica / Grilo, Filipa / Guedes, Américo / Guilherme, Filipa / Gutiérrez, Iván / Harper, Henry / Herrera, José M / Hipólito, Dário / Infante, Samuel / Jesus, José / Jones, Kate E / Laborde, Marina I / de Oliveira, Luís Lamas / Leitão, Inês / Lemos, Rita / Lima, Cátia / Linck, Paloma / Lopes, Hugo / Lopes, Susana / López-Baucells, Adrià / Loureiro, Armando / Loureiro, Filipa / Lourenço, Rui / Lourenço, Sofia / Lucas, Paula / Magalhães, Ana / Maldonado, Cristina / Marcolin, Fabio / Marques, Sara / Marques, J Tiago / Marques, Carina / Marques, Paulo / Marrecas, Pedro Caetano / Martins, Frederico / Martins, Raquel / Mascarenhas, Miguel / Mata, Vanessa A / Mateus, Ana Rita / Matos, Milene / Medinas, Denis / Mendes, Tiago / Mendes, Gabriel / Mestre, Frederico / Milhinhas, Catarina / Mira, António / Monarca, Rita I / Monteiro, Norberto / Monteiro, Barbara / Monterroso, Pedro / Nakamura, Mónia / Negrões, Nuno / Nóbrega, Eva K / Nóvoa, Miguel / Nunes, Manuel / Nunes, Nuno Jardim / Oliveira, Flávio / Oliveira, José Miguel / Palmeirim, Jorge M / Pargana, João / Paula, Anabela / Paupério, Joana / Pedroso, Nuno M / Pereira, Guilherme / Pereira, Pedro F / Pereira, José / Pereira, Maria João Ramos / Petrucci-Fonseca, Francisco / Pimenta, Miguel / Pinto, Sara / Pinto, Nuno / Pires, Rosa / Pita, Ricardo / Pontes, Carlos / Quaresma, Marisa / Queirós, João / Queirós, Luís / Rainho, Ana / da Graça Ramalhinho, Maria / Ramalho, Patrícia / Raposeira, Helena / Rasteiro, Francisco / Rebelo, Hugo / Regala, Frederico Tátá / Reto, Dyana / Ribeiro, Sérgio Bruno / Rio-Maior, Helena / Rocha, Ricardo / Rocha, Rita Gomes / Rodrigues, Luísa / Román, Jacinto / Roque, Sara / Rosalino, Luís Miguel / do Rosário, Inês T / Rossa, Mariana / Russo, Danilo / Sá, Pedro / Sabino-Marques, Helena / Salgueiro, Vânia / Santos, Helena / Santos, Joana / Santos, João P V / Santos, Nuno / Santos, Sara / Santos, Carlos Pedro / Santos-Reis, Margarida / Serronha, Ana / Sierra, Pablo / Silva, Bruno / Silva, Carla S G M / Silva, Clara / Silva, Diogo / da Silva, Luís P / Silva, Ricardo / Silva, Carmen / da Silva Júnior, Flavio Manoel Rodrigues / Sousa, Pedro / Sousa-Guedes, Diana / Spadoni, Giulia / Tapisso, Joaquim T / Teixeira, Daniela / Teixeira, Sérgio / Teixeira, Nuno / Torres, Rita T / Travassos, Paulo / Vale-Gonçalves, Hélia / Cidraes-Vieira, Nuno / von Merten, Sophie / da Luz Mathias, Maria

Ecology

2022 Volume 103, Issue 6, Page(s) e3654

Abstract: Mammals are threatened worldwide, with ~26% of all species being included in the IUCN threatened categories. This overall pattern is primarily associated with habitat loss or degradation, and human persecution for terrestrial mammals, and pollution, open ...

Abstract	Mammals are threatened worldwide, with ~26% of all species being included in the IUCN threatened categories. This overall pattern is primarily associated with habitat loss or degradation, and human persecution for terrestrial mammals, and pollution, open net fishing, climate change, and prey depletion for marine mammals. Mammals play a key role in maintaining ecosystems functionality and resilience, and therefore information on their distribution is crucial to delineate and support conservation actions. MAMMALS IN PORTUGAL is a publicly available data set compiling unpublished georeferenced occurrence records of 92 terrestrial, volant, and marine mammals in mainland Portugal and archipelagos of the Azores and Madeira that includes 105,026 data entries between 1873 and 2021 (72% of the data occurring in 2000 and 2021). The methods used to collect the data were: live observations/captures (43%), sign surveys (35%), camera trapping (16%), bioacoustics surveys (4%) and radiotracking, and inquiries that represent less than 1% of the records. The data set includes 13 types of records: (1) burrows \| soil mounds \| tunnel, (2) capture, (3) colony, (4) dead animal \| hair \| skulls \| jaws, (5) genetic confirmation, (6) inquiries, (7) observation of live animal (8), observation in shelters, (9) photo trapping \| video, (10) predators diet \| pellets \| pine cones/nuts, (11) scat \| track \| ditch, (12) telemetry and (13) vocalization \| echolocation. The spatial uncertainty of most records ranges between 0 and 100 m (76%). Rodentia (n =31,573) has the highest number of records followed by Chiroptera (n = 18,857), Carnivora (n = 18,594), Lagomorpha (n = 17,496), Cetartiodactyla (n = 11,568) and Eulipotyphla (n = 7008). The data set includes records of species classified by the IUCN as threatened (e.g., Oryctolagus cuniculus [n = 12,159], Monachus monachus [n = 1,512], and Lynx pardinus [n = 197]). We believe that this data set may stimulate the publication of other European countries data sets that would certainly contribute to ecology and conservation-related research, and therefore assisting on the development of more accurate and tailored conservation management strategies for each species. There are no copyright restrictions; please cite this data paper when the data are used in publications.
MeSH term(s)	Animals ; Carnivora ; Climate Change ; Ecosystem ; Mammals ; Portugal ; Rabbits ; Rodentia
Language	English
Publishing date	2022-04-12
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2010140-5
ISSN	1939-9170 ; 0012-9658
ISSN (online)	1939-9170
ISSN	0012-9658
DOI	10.1002/ecy.3654
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Article ; Online: HIV prevalence among men who have sex with men in Brazil: results of the 2nd national survey using respondent-driven sampling.

Kerr, Ligia / Kendall, Carl / Guimarães, Mark Drew Crosland / Salani Mota, Rosa / Veras, Maria Amélia / Dourado, Inês / Maria de Brito, Ana / Merchan-Hamann, Edgar / Pontes, Alexandre Kerr / Leal, Andréa Fachel / Knauth, Daniela / Castro, Ana Rita Coimbra Motta / Macena, Raimunda Hermelinda Maia / Lima, Luana Nepomuceno Costa / Oliveira, Lisangela Cristina / Cavalcantee, Maria do Socorro / Benzaken, Adele Schwartz / Pereira, Gerson / Pimenta, Cristina /

Pascom, Ana Roberta Pati / Bermudez, Ximena Pamela Diaz / Moreira, Regina Célia / Brígido, Luis Fernando Macedo / Camillo, Ana Cláudia / McFarland, Willi / Johnston, Lisa G

Medicine

2018 Volume 97, Issue 1S Suppl 1, Page(s) S9–S15

Abstract: This paper reports human immuno-deficiency virus (HIV) prevalence in the 2nd National Biological and Behavioral Surveillance Survey (BBSS) among men who have sex with men (MSM) in 12 cities in Brazil using respondent-driven sampling (RDS).Following ... ...

Abstract	This paper reports human immuno-deficiency virus (HIV) prevalence in the 2nd National Biological and Behavioral Surveillance Survey (BBSS) among men who have sex with men (MSM) in 12 cities in Brazil using respondent-driven sampling (RDS).Following formative research, RDS was applied in 12 cities in the 5 macroregions of Brazil between June and December 2016 to recruit MSM for BBSS. The target sample size was 350 per city. Five to 6 seeds were initially selected to initiate recruitment and coupons and interviews were managed online. On-site rapid testing was used for HIV screening, and confirmed by a 2nd test. Participants were weighted using Gile estimator. Data from all 12 cities were merged and analyzed with Stata 14.0 complex survey data analysis tools in which each city was treated as its own strata. Missing data for those who did not test were imputed HIV+ if they reported testing positive before and were taking antiretroviral therapy.A total of 4176 men were recruited in the 12 cities. The average time to completion was 10.2 weeks. The longest chain length varied from 8 to 21 waves. The sample size was achieved in all but 2 cities.A total of 3958 of the 4176 respondents agreed to test for HIV (90.2%). For results without imputation, 17.5% (95%CI: 14.7-20.7) of our sample was HIV positive. With imputation, 18.4% (95%CI: 15.4-21.7) were seropositive.HIV prevalence increased beyond expectations from the results of the 2009 survey (12.1%; 95%CI: 10.0-14.5) to 18.4%; CI95%: 15.4 to 21.7 in 2016. This increase accompanies Brazil's focus on the treatment to prevention strategy, and a decrease in support for community-based organizations and community prevention programs.
MeSH term(s)	Adult ; Brazil/epidemiology ; HIV Infections/epidemiology ; Homosexuality, Male/statistics & numerical data ; Humans ; Male ; Mass Screening/statistics & numerical data ; Prevalence ; Surveys and Questionnaires ; Young Adult
Language	English
Publishing date	2018-05-24
Publishing country	United States
Document type	Journal Article ; Observational Study
ZDB-ID	80184-7
ISSN	1536-5964 ; 0025-7974
ISSN (online)	1536-5964
ISSN	0025-7974
DOI	10.1097/MD.0000000000010573
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