Ages of the bulge globular clusters NGC 6522 and NGC 6626 (M28) from HST proper-motion-cleaned color–magnitude diagrams

Bulge globular clusters (GCs) with metallicities [Fe/H]−1.0 and blue horizontal branches are candidates to harbor the oldest populations in the Galaxy. Based on the analysis of HST proper-motion-cleaned color–magnitude diagrams in filters F435W and F625W, we determine physical parameters for the old bulge GCs NGC 6522 and NGC 6626 (M28), both with well-defined blue horizontal branches. We compare these results with similar data for the inner halo cluster NGC 6362. These clusters have similar metallicities (−1.3[Fe/H]−1.0) obtained from high-resolution spectroscopy. We derive ages, distance moduli, and reddening values by means of statistical comparisons between observed and synthetic fiducial lines employing likelihood statistics and the Markov chain Monte Carlo method. The synthetic fiducial lines were generated using α-enhanced BaSTI and Dartmouth stellar evolutionary models, adopting both canonical (Y∼0.25) and enhanced (Y∼0.30–0.33) helium abundances. RR Lyrae stars were employed to determine the HB magnitude level, providing an independent indicator to constrain the apparent distance modulus and the helium enhancement. The shape of the observed fiducial line could be compatible with some helium enhancement for NGC 6522 and NGC 6626, but the average magnitudes of RR Lyrae stars tend to rule out this hypothesis. Assuming canonical helium abundances, BaSTI and Dartmouth models indicate that all three clusters are coeval, with ages between ∼12.5 and 13.0 Gyr. The present study also reveals that NGC 6522 has at least two stellar populations, since its CMD shows a significantly wide subgiant branch compatible with 14%±2% and 86%±5% for first and second generations, respectively

Osmotic Dehydration as a Tool for Insdustrialization of Jabuticaba Peel (Myrciaria jabuticaba)

This study evaluated the osmotic dehydration of jabuticaba peel for use as a by-product, with development of new food products. Response surface methodology was used, considering temperature and sucrose concentration as independent variables, assessing their effects on water loss, solid gain, mass loss, and solid gain rate. Sucrose concentration had a greater influence on osmotic process. Temperature increase is necessary in osmotic dehydration, once it leads to tissue softening, which is essential for dehydration of jabuticaba peel. Therefore, the best osmotic dehydration conditions were set at 60°C and 70 °Brix. With respect to the physicochemical characterization of the bioactive compounds of dehydrated jabuticaba peel, considerable amounts of sugars, anthocyanins, and phenolic compounds were observed, besides the antioxidant potential. Thus, dehydration of jabuticaba peel is a viable alternative to minimize the waste generated during harvest, being a product with high nutritional value

Topical essential fatty acid oil on wounds: local and systemic effects

FAPESP - FUNDAÇÃO DE AMPARO À PESQUISA DO ESTADO DE SÃO PAULOFUNADERM - FUNDO DE APOIO À DERMATOLOGIA DE SÃO PAULOCAPES - COORDENAÇÃO DE APERFEIÇOAMENTO DE PESSOAL E NÍVEL SUPERIORBackground The use of medicinal plants and their derivatives is increasing, and approximately one-third of all traditional herbal medicines are intended for wound treatment. Natural products used in these treatments include vegetable oils, which are rich in essential fatty acids. Once in contact with an ulcerative surface, the oil reaches the blood and lymphatic vessels, thus eliciting systemic effects. ObjectiveThis study evaluated the local and possible systemic effects of essential fatty acids (sunflower oil) applied topically to rat wounds. Methods Cutaneous punch wounds (6 mm) were produced on the dorsa of 30 rats. Saline (SS), mineral oil (MO) or essential fatty acid (EFA) solutions were applied topically. Healing was evaluated after 2, 4 and 10 days (n = 5 per group) by visual and histological/morphometric examination, second harmonic generation (SHG) microscopy, and cytokine and growth factor quantification in the scar tissue (real-time PCR) and in serum (ELISA). Results MO/EFA-treated animals had higher IGF-1, leptin, IL-6 and IFN-gamma mRNA expression and lower serum IL-6 levels than the control (SS/MO) animals. SHG analysis showed no difference in collagen density between the animals treated with MO and EFA. Conclusion EFA treatment induces topical (observed by local IGF-1, leptin, IL-6 and IFN-gamma production) and systemic effects, lowering IL-6 levels in the serum. As the oil is widely used to shorten ulcer healing time, studies are needed to evaluate the treatment safety and possible undesired effects.141115FAPESP - FUNDAÇÃO DE AMPARO À PESQUISA DO ESTADO DE SÃO PAULOFUNADERM - FUNDO DE APOIO À DERMATOLOGIA DE SÃO PAULOCAPES - COORDENAÇÃO DE APERFEIÇOAMENTO DE PESSOAL E NÍVEL SUPERIORFAPESP - FUNDAÇÃO DE AMPARO À PESQUISA DO ESTADO DE SÃO PAULOFUNADERM - FUNDO DE APOIO À DERMATOLOGIA DE SÃO PAULOCAPES - COORDENAÇÃO DE APERFEIÇOAMENTO DE PESSOAL E NÍVEL SUPERIOR07/59319-5015/2014043/201601P-04520-201

AVALIAÇÃO DA ATIVIDADE ANTIOXIDANTE IN VITRO DE CAGAITA MADURA.

Introdução e objetivos: Eugenia dysenterica DC. (Myrtaceae), popularmente conhecida como cagaita, é uma frutífera nativa do cerrado. Seus frutos podem ser consumidos in natura ou processados. A polpa de cagaita apresenta elevada concentração de ácidos linoleico e linolênico, vitamina C e compostos antioxidantes. Os métodos in vitro de avaliação da capacidade antioxidante tornaram-se importante ferramenta pela crescente busca por novos antioxidantes naturais, com aplicação nas indústrias de alimentos, cosméticos, farmacêuticase na prática clínica¹. Objetivou-se com este trabalho determinar a atividade antioxidante in vitro do fruto de cagaita madura por meio de três diferentes extratos: aquoso, etéreo e etanólico. Metodologia: A atividade antioxidante foi determinada pelo método do DPPH (2,2 difenil-1-picrilhidrazil), segundo Brand-Williamset al. (1995)² com modificações de Borguini (2006)³. A leitura foi realizada no comprimento de onda à 517 nm e os resultados foram expressos em % de descoloração do DPPH. Resultados e discussão: O processo de extração, utilizando solventes com diferentes polaridades, possibilitou a extração de substâncias antioxidantes em quantidades variadas. Observou-se que o extrato aquoso exibiu maior potencial de antioxidante, com valor médio de 27,07±0,73% de descoloração do DPPH, quando comparados aos extratos etéreo (23,43±0,87) e etanólico (14,75±2,73). Segundo Pellegrini et al. (2007)4 e Melo et al. (2008)5, a solubilidade, em determinado solvente, é característica peculiar do fitoquímico, o que justifica a inexistência de um procedimento universal de extração em função da diversidade estrutural e sensibilidade dos compostos antioxidantes às condições de extração. Conclusão: Por meio dos resultados apresentados, pode-se concluir que a cagaita madura possui substâncias com capacidade antioxidante eficaz como fruto do cerrado e maior extração no extrato aquoso

QUANTIFICAÇÃO DE COMPOSTOS FENÓLICOS PRESENTES NA CAGAITA (Eugenia dysenterica DC.), A PARTIR DOS EXTRATOS ETÉREO, ETANÓLICO E AQUOSO

O Centro-Oeste é dominado pelo bioma Cerrado, no qual possui diversas espécies frutíferas nativas, dentre elas, a cagaiteira. A cagaiteira cujo fruto é a cagaita (Eugenia dysenterica DC.) pertence à família das Mirtáceas, seus frutos são ligeiramente ácidos de cor amarelo-clara. Na maioria dos vegetais, os compostos fenólicos constituem os antioxidantes mais abundantes1, desempenhando papel importante nos processos de inibição do risco das doenças cardiovasculares e atuando sobre o estresse oxidativo2. Desta forma, este trabalho teve como objetivo quantificar o teor de compostos fenólicos presentes na cagaita, através dos extratos etéreo, etanólico e aquoso. Os frutos foram coletados no município de Abadia-GO, e as análises foram realizadas na Faculdade de Farmácia/UFG. O teor de compostos fenólicos, nos três extratos foram determinados em espectrofotômetro, a 750 nm, utilizando o reagente Folin-Ciocalteau, segundo Waterhouse (2002). A quantificação foi baseada no estabelecimento da curva padrão de ácido gálico (EAG), na faixa de 5 a 50 mg.L-1. Os resultados foram expressos em mg de (EAG)/100g de amostra. Nos três extratos foram avaliados os teores de compostos fenólicos na cagaita verde (colhida 10 dias após antese) e na cagaita madura (37 dias após antese). No extrato étereo a quantidade de compostos fenólicos aumentou 11,398 mg de (EAG)/100g de amostra do fruto verde para o maduro. Já nos extratos etanólico e aquoso, os compostos fenólicos tiveram redução de 17,934 e 14,204 mg de (EAG)/100g de amostra, porém o extrato etanólico extraiu a maior quantidade de compostos fenólicos, 382,178 mg de (EAG)/100g de amostra. Conclui-se que a cagaita apresenta satisfatória quantidade de compostos fenólicos quando o fruto ainda está verde, visto que o extrato etanólico extraiu maior quantidade deste composto com o fruto colhido com 10 dias

Bartonella Clarridgeiae Bacteremia Detected In An Asymptomatic Blood Donor

Human exposure to Bartonella clarridgeiae has been reported only on the basis of antibody detection. We report for the first time an asymptomatic human blood donor infected with B. clarridgeiae, as documented by enrichment blood culture, PCR, and DNA sequencing.531352356Maggi, R.G., Duncan, A.W., Breitschwerdt, E.B., Novel chemically modified liquid medium that will support the growth of seven Bartonella species (2005) J Clin Microbiol, 43, pp. 2651-2655. , http://dx.doi.org/10.1128/JCM.43.6.2651-2655.2005Drummond, M.R., Pitassi, L.H., Lania, B.G., Dos Santos, S.R., Gilioli, R., Velho, P.E., Detection of Bartonella henselae in defibrinated sheep blood used for culture media supplementation (2011) Braz J Microbiol, 42, pp. 430-432. , http://dx.doi.org/10.1590/S1517-83822011000200003Altschul, S.F., Gish, W., Miller, W., Myers, E.W., Lipman, D.J., Basic local alignment search tool (1990) J Mol Biol, 215, pp. 403-410Dalton, M.J., Robinson, L.E., Cooper, J., Regnery, R.L., Olson, J.G., Childs, J.E., Use of Bartonella antigens for serologic diagnosis of cat-scratch disease at a national referral center (1995) Arch Intern Med, 155, pp. 1670-1676Breitschwerdt, E.B., Maggi, R.G., Chomel, B.B., Lappin, M.R., Bartonellosis: An emerging infectious disease of zoonotic importance to animals and human beings (2010) J Vet Emerg Crit Care (San Antonio), 20, pp. 8-30. , http://dx.doi.org/10.1111/j.1476-4431.2009.00496.xChamberlin, J., Laughlin, L.W., Romero, S., Solorzano, N., Gordon, S., Andre, R.G., Pachas, P., Watts, D., Epidemiology of endemic Bartonella bacilliformis: A prospective cohort study in a Peruvian mountain valley community (2002) J Infect Dis, 186, pp. 983-990. , http://dx.doi.org/10.1086/344054Maggi, R.G., Ericson, M., Mascarelli, P.E., Bradley, J.M., Breitschwerdt, E.B., Bartonella henselae bacteremia in a mother and son potentially associated with tick exposure (2013) Parasit Vectors, 6, p. 101. , http://dx.doi.org/10.1186/1756-3305-6-101Scott, M.A., McCurley, T.L., Vnencak-Jones, C.L., Hager, C., McCoy, J.A., Anderson, B., Collins, R.D., Edwards, K.M., Cat scratch disease: Detection of Bartonella henselae DNA in archival biopsies from patients with clinically, serologically, and histologically defined disease (1996) Am J Pathol, 149, pp. 2161-2167Slater, L.N., Welch, D.F., Min, K.W., Rochalimaea henselae causes bacillary angiomatosis and peliosis hepatis (1992) Arch Intern Med, 152, pp. 602-606Sander, A., Zagrosek, A., Bredt, W., Schiltz, E., Piemont, Y., Lanz, C., Dehio, C., Characterization of Bartonella clarridgeiae flagellin (FlaA) and detection of antiflagellin antibodies in patients with lymphadenopathy (2000) J Clin Microbiol, 38, pp. 2943-2948Kordick, D.L., Hilyard, E.J., Hadfield, T.L., Wilson, K.H., Steigerwalt, A.G., Brenner, D.J., Breitschwerdt, E.B., Bartonella clarridgeiae, a newly recognized zoonotic pathogen causing inoculation papules, fever, and lymphadenopathy (cat scratch disease) (1997) J Clin Microbiol, 35, pp. 1813-1818Margileth, A.M., Baehren, D.F., Chest-wall abscess due to cat-scratch disease (CSD) in an adult with antibodies to Bartonella clarridgeiae: Case report and review of the thoracopulmonary manifestations of CSD (1998) Clin Infect Dis, 27, pp. 353-357. , http://dx.doi.org/10.1086/514671Chomel, B.B., Mac Donald, K.A., Kasten, R.W., Chang, C.C., Wey, A.C., Foley, J.E., Thomas, W.P., Kittleson, M.D., Aortic valve endocarditis in a dog due to Bartonella clarridgeiae (2001) J Clin Microbiol, 39, pp. 3548-3554. , http://dx.doi.org/10.1128/JCM.39.10.3548-3554.2001Gillespie, T.N., Washabau, R.J., Goldschmidt, M.H., Cullen, J.M., Rogala, A.R., Breitschwerdt, E.B., Detection of Bartonella henselae and Bartonella clarridgeiae DNA in hepatic specimens from two dogs with hepatic disease (2003) J Am Vet Med Assoc, 222, pp. 47-51. , http://dx.doi.org/10.2460/javma.2003.222.47, 35Robinson, M.T., Hillman, T., Langton, D.A., Shaw, S.E., Bartonella clarridgeiae in a cat in the UK (2009) Vet Rec, 164, pp. 58-59. , http://dx.doi.org/10.1136/vr.164.2.58Sykes, J.E., Westropp, J.L., Kasten, R.W., Chomel, B.B., Association between Bartonella species infection and disease in pet cats as determined using serology and culture (2010) J Feline Med Surg, 12, pp. 631-636. , http://dx.doi.org/10.1016/j.jfms.2010.04.003Fouch, B., Coventry, S., A case of fatal disseminated Bartonella henselae infection (cat-scratch disease) with encephalitis (2007) Arch Pathol Lab Med, 131, pp. 1591-1594Boudebouch, N., Sarih, M., Beaucournu, J.C., Amarouch, H., Hassar, M., Raoult, D., Parola, P., Bartonella clarridgeiae, B. Henselae, and Rickettsia felis in fleas from Morocco (2011) Ann Trop Med Parasitol, 105, pp. 493-498. , http://dx.doi.org/10.1179/1364859411Y.0000000038Kordick, D.L., Brown, T.T., Shin, K., Breitschwerdt, E.B., Clinical and pathologic evaluation of chronic Bartonella henselae or Bartonella clarridgeiae infection in cats (1999) J Clin Microbiol, 37, pp. 1536-1547Chomel, B.B., Carlos, E.T., Kasten, R.W., Yamamoto, K., Chang, C.C., Carlos, R.S., Abenes, M.V., Pajares, C.M., Bartonella henselae and Bartonella clarridgeiae infection in domestic cats from the Philippines (1999) Am J Trop Med Hyg, 60, pp. 593-597Dehio, C., Bartonella interactions with endothelial cells and erythrocytes (2001) Trends Microbiol, 9, pp. 279-285. , http://dx.doi.org/10.1016/S0966-842X(01)02047-9Dehio, C., Meyer, M., Berger, J., Schwarz, H., Lanz, C., Interaction of Bartonella henselae with endothelial cells results in bacterial aggregation on the cell surface and the subsequent engulfment and internalisation of the bacterial aggregate by a unique structure, the invasome (1997) J Cell Sci, 110 (18), pp. 2141-2154Braga Mdo, S., Diniz, P.P., André, M.R., Bortoli, C.P., Machado, R.Z., Molecular characterisation of Bartonella species in cats from São Luís, state of Maranhão, North-Eastern Brazil (2012) Mem Inst Oswaldo Cruz, 107, pp. 772-777. , http://dx.doi.org/10.1590/S0074-02762012000600011Eremeeva, M.E., Gerns, H.L., Lydy, S.L., Goo, J.S., Ryan, E.T., Mathew, S.S., Ferraro, M.J., Koehler, J.E., Bacteremia, fever, and splenomegaly caused by a newly recognized Bartonella species (2007) N Engl J Med, 356, pp. 2381-2387. , http://dx.doi.org/10.1056/NEJMoa065987Chomel, B.B., Boulouis, H.J., Breitschwerdt, E.B., Kasten, R.W., Vayssier-Taussat, M., Birtles, R.J., Koehler, J.E., Dehio, C., Ecological fitness and strategies of adaptation of Bartonella species to their hosts and vectors (2009) Vet Res, 40, p. 29. , http://dx.doi.org/10.1051/vetres/2009011Breitschwerdt, E.B., Maggi, R.G., Duncan, A.W., Nicholson, W.L., Hegarty, B.C., Woods, C.W., Bartonella species in blood of immunocompetent persons with animal and arthropod contact (2007) Emerg Infect Dis, 13, pp. 938-941. , http://dx.doi.org/10.3201/eid1306.061337Carson, J.L., Grossman, B.J., Kleinman, S., Tinmouth, A.T., Marques, M.B., Fung, M.K., Holcomb, J.B., Djulbegovic, B., Red blood cell transfusion: A clinical practice guideline from the AABB (2012) Ann Intern Med, 157, pp. 49-58. , http://dx.doi.org/10.7326/0003-4819-157-1-201206190-00429Ramirez-Arcos, S., Goldman, M., Blajchman, M., Bacterial contamination (2012) Transfusion Reaction, 4, pp. 153-189. , Popovsky MA (ed), American Association Of Blood Banks, Bethesda, MDVamvakas, E.C., Blajchman, M.A., Transfusion-related mortality: The ongoing risks of allogeneic blood transfusion and the available strategies for their prevention (2009) Blood, 113, pp. 3406-3417. , http://dx.doi.org/10.1182/blood-2008-10-167643Magalhães, R.F., Cintra, M.L., Barjas-Castro, M.L., Del Negro, G.M., Okay, T.S., Velho, P.E., Blood donor infected with Bartonella henselae (2010) Transfus Med, 20, pp. 280-282. , http://dx.doi.org/10.1111/j.1365-3148.2010.01001.xMagalhães, R.F., Pitassi, L.H., Salvadego, M., De Moraes, A.M., Barjas-Castro, M.L., Velho, P.E., Bartonella henselae survives after the storage period of red blood cell units: Is it transmissible by transfusion? (2008) Transfus Med, 18, pp. 287-291. , http://dx.doi.org/10.1111/j.1365-3148.2008.00871.xLin, J.W., Chen, C.M., Chang, C.C., Unknown fever and back pain caused by Bartonella henselae in a veterinarian after a needle puncture: A case report and literature review (2011) Vector Borne Zoonotic Dis, 11, pp. 589-591. , http://dx.doi.org/10.1089/vbz.2009.0217Oliveira, A.M., Maggi, R.G., Woods, C.W., Breitschwerdt, E.B., Suspected needle stick transmission of Bartonella vinsonii subspecies berkhoffii to a veterinarian (2010) J Vet Intern Med, 24, pp. 1229-1232. , http://dx.doi.org/10.1111/j.1939-1676.2010.0563.xOhl, M.E., Spach, D.H., Bartonella quintana and urban trench fever (2000) Clin Infect Dis, 31, pp. 131-135. , http://dx.doi.org/10.1086/313890Daly, J.S., Worthington, M.G., Brenner, D.J., Moss, C.W., Hollis, D.G., Weyant, R.S., Steigerwalt, A.G., O'Connor, S.P., Rochalimaea elizabethae sp. Nov. Isolated from a patient with endocarditis (1993) J Clin Microbiol, 31, pp. 872-881Oksi, J., Rantala, S., Kilpinen, S., Silvennoinen, R., Vornanen, M., Veikkolainen, V., Eerola, E., Pulliainen, A.T., Cat scratch disease caused by Bartonella grahamii in an immunocompromised patient (2013) J Clin Microbiol, 51, pp. 2781-2784. , http://dx.doi.org/10.1128/JCM.00910-13Breitschwerdt, E.B., Mascarelli, P.E., Schweickert, L.A., Maggi, R.G., Hegarty, B.C., Bradley, J.M., Woods, C.W., Hallucinations, sensory neuropathy, and peripheral visual deficits in a young woman infected with Bartonella koehlerae (2011) J Clin Microbiol, 49, pp. 3415-3417. , http://dx.doi.org/10.1128/JCM.00833-11Raoult, D., Roblot, F., Rolain, J.M., Besnier, J.M., Loulergue, J., Bastides, F., Choutet, P., First isolation of Bartonella alsatica from a valve of a patient with endocarditis (2006) J Clin Microbiol, 44, pp. 278-279. , http://dx.doi.org/10.1128/JCM.44.1.278-279.2006Welch, D.F., Carroll, K.C., Hofmeister, E.K., Persing, D.H., Robison, D.A., Steigerwalt, A.G., Brenner, D.J., Isolation of a new subspecies, Bartonella vinsonii subsp. Arupensis, from a cattle rancher: Identity with isolates found in conjunction with Borrelia burgdorferi and Babesia microti among naturally infected mice (1999) J Clin Microbiol, 37, pp. 2598-2601Probert, W., Louie, J.K., Tucker, J.R., Longoria, R., Hogue, R., Moler, S., Graves, M., Fritz, C.L., Meningitis due to a "Bartonella washoensis"-like human pathogen (2009) J Clin Microbiol, 47, pp. 2332-2335. , http://dx.doi.org/10.1128/JCM.00511-09Kosoy, M., Morway, C., Sheff, K.W., Bai, Y., Colborn, J., Chalcraft, L., Dowell, S.F., Petersen, L.R., Bartonella tamiae sp. Nov., a newly recognized pathogen isolated from three human patients from Thailand (2008) J Clin Microbiol, 46, pp. 772-775. , http://dx.doi.org/10.1128/JCM.02120-07Maggi, R.G., Kosoy, M., Mintzer, M., Breitschwerdt, E.B., Isolation of Candidatus Bartonella melophagi from human blood (2009) Emerg Infect Dis, 15, pp. 66-68. , http://dx.doi.org/10.3201/eid1501.081080Lin, E.Y., Tsigrelis, C., Baddour, L.M., Lepidi, H., Rolain, J.M., Patel, R., Raoult, D., Candidatus Bartonella mayotimonensis and endocarditis (2010) Emerg Infect Dis, 16, pp. 500-503. , http://dx.doi.org/10.3201/eid1603.081673Breitschwerdt, E.B., Maggi, R.G., Cadenas, M.B., De Paiva Diniz, P.P., A groundhog, a novel Bartonella sequence, and my father's death (2009) Emerg Infect Dis, 15, pp. 2080-2086. , http://dx.doi.org/10.3201/eid1512.AD151

Nematode effector proteins: an emerging paradigm of parasitism

Phytonematodes use a stylet and secreted effectors to modify host cells and ingest nutrients to support their growth and development. The molecular function of nematode effectors is currently the subject of intense investigation. In this review, we summarize our current understanding of nematode effectors, with a particular focus on proteinaceous stylet-secreted effectors of sedentary endoparasitic phytonematodes, for which a wealth of information has surfaced in the past 10 yr. We provide an update on the effector repertoires of several of the most economically important genera of phytonematodes and discuss current approaches to dissecting their function. Lastly, we highlight the latest breakthroughs in effector discovery that promise to shed new light on effector diversity and function across the phylum Nematoda

Global age-sex-specific mortality, life expectancy, and population estimates in 204 countries and territories and 811 subnational locations, 1950–2021, and the impact of the COVID-19 pandemic: a comprehensive demographic analysis for the Global Burden of Disease Study 2021

Background: Estimates of demographic metrics are crucial to assess levels and trends of population health outcomes. The profound impact of the COVID-19 pandemic on populations worldwide has underscored the need for timely estimates to understand this unprecedented event within the context of long-term population health trends. The Global Burden of Diseases, Injuries, and Risk Factors Study (GBD) 2021 provides new demographic estimates for 204 countries and territories and 811 additional subnational locations from 1950 to 2021, with a particular emphasis on changes in mortality and life expectancy that occurred during the 2020–21 COVID-19 pandemic period. Methods: 22 223 data sources from vital registration, sample registration, surveys, censuses, and other sources were used to estimate mortality, with a subset of these sources used exclusively to estimate excess mortality due to the COVID-19 pandemic. 2026 data sources were used for population estimation. Additional sources were used to estimate migration; the effects of the HIV epidemic; and demographic discontinuities due to conflicts, famines, natural disasters, and pandemics, which are used as inputs for estimating mortality and population. Spatiotemporal Gaussian process regression (ST-GPR) was used to generate under-5 mortality rates, which synthesised 30 763 location-years of vital registration and sample registration data, 1365 surveys and censuses, and 80 other sources. ST-GPR was also used to estimate adult mortality (between ages 15 and 59 years) based on information from 31 642 location-years of vital registration and sample registration data, 355 surveys and censuses, and 24 other sources. Estimates of child and adult mortality rates were then used to generate life tables with a relational model life table system. For countries with large HIV epidemics, life tables were adjusted using independent estimates of HIV-specific mortality generated via an epidemiological analysis of HIV prevalence surveys, antenatal clinic serosurveillance, and other data sources. Excess mortality due to the COVID-19 pandemic in 2020 and 2021 was determined by subtracting observed all-cause mortality (adjusted for late registration and mortality anomalies) from the mortality expected in the absence of the pandemic. Expected mortality was calculated based on historical trends using an ensemble of models. In location-years where all-cause mortality data were unavailable, we estimated excess mortality rates using a regression model with covariates pertaining to the pandemic. Population size was computed using a Bayesian hierarchical cohort component model. Life expectancy was calculated using age-specific mortality rates and standard demographic methods. Uncertainty intervals (UIs) were calculated for every metric using the 25th and 975th ordered values from a 1000-draw posterior distribution. Findings: Global all-cause mortality followed two distinct patterns over the study period: age-standardised mortality rates declined between 1950 and 2019 (a 62·8% [95% UI 60·5–65·1] decline), and increased during the COVID-19 pandemic period (2020–21; 5·1% [0·9–9·6] increase). In contrast with the overall reverse in mortality trends during the pandemic period, child mortality continued to decline, with 4·66 million (3·98–5·50) global deaths in children younger than 5 years in 2021 compared with 5·21 million (4·50–6·01) in 2019. An estimated 131 million (126–137) people died globally from all causes in 2020 and 2021 combined, of which 15·9 million (14·7–17·2) were due to the COVID-19 pandemic (measured by excess mortality, which includes deaths directly due to SARS-CoV-2 infection and those indirectly due to other social, economic, or behavioural changes associated with the pandemic). Excess mortality rates exceeded 150 deaths per 100 000 population during at least one year of the pandemic in 80 countries and territories, whereas 20 nations had a negative excess mortality rate in 2020 or 2021, indicating that all-cause mortality in these countries was lower during the pandemic than expected based on historical trends. Between 1950 and 2021, global life expectancy at birth increased by 22·7 years (20·8–24·8), from 49·0 years (46·7–51·3) to 71·7 years (70·9–72·5). Global life expectancy at birth declined by 1·6 years (1·0–2·2) between 2019 and 2021, reversing historical trends. An increase in life expectancy was only observed in 32 (15·7%) of 204 countries and territories between 2019 and 2021. The global population reached 7·89 billion (7·67–8·13) people in 2021, by which time 56 of 204 countries and territories had peaked and subsequently populations have declined. The largest proportion of population growth between 2020 and 2021 was in sub-Saharan Africa (39·5% [28·4–52·7]) and south Asia (26·3% [9·0–44·7]). From 2000 to 2021, the ratio of the population aged 65 years and older to the population aged younger than 15 years increased in 188 (92·2%) of 204 nations. Interpretation: Global adult mortality rates markedly increased during the COVID-19 pandemic in 2020 and 2021, reversing past decreasing trends, while child mortality rates continued to decline, albeit more slowly than in earlier years. Although COVID-19 had a substantial impact on many demographic indicators during the first 2 years of the pandemic, overall global health progress over the 72 years evaluated has been profound, with considerable improvements in mortality and life expectancy. Additionally, we observed a deceleration of global population growth since 2017, despite steady or increasing growth in lower-income countries, combined with a continued global shift of population age structures towards older ages. These demographic changes will likely present future challenges to health systems, economies, and societies. The comprehensive demographic estimates reported here will enable researchers, policy makers, health practitioners, and other key stakeholders to better understand and address the profound changes that have occurred in the global health landscape following the first 2 years of the COVID-19 pandemic, and longer-term trends beyond the pandemic

Global age-sex-specific mortality, life expectancy, and population estimates in 204 countries and territories and 811 subnational locations, 1950–2021, and the impact of the COVID-19 pandemic: a comprehensive demographic analysis for the Global Burden of Disease Study 2021

Background Estimates of demographic metrics are crucial to assess levels and trends of population health outcomes. The profound impact of the COVID-19 pandemic on populations worldwide has underscored the need for timely estimates to understand this unprecedented event within the context of long-term population health trends. The Global Burden of Diseases, Injuries, and Risk Factors Study (GBD) 2021 provides new demographic estimates for 204 countries and territories and 811 additional subnational locations from 1950 to 2021, with a particular emphasis on changes in mortality and life expectancy that occurred during the 2020–21 COVID-19 pandemic period. Methods 22 223 data sources from vital registration, sample registration, surveys, censuses, and other sources were used to estimate mortality, with a subset of these sources used exclusively to estimate excess mortality due to the COVID-19 pandemic. 2026 data sources were used for population estimation. Additional sources were used to estimate migration; the effects of the HIV epidemic; and demographic discontinuities due to conflicts, famines, natural disasters, and pandemics, which are used as inputs for estimating mortality and population. Spatiotemporal Gaussian process regression (ST-GPR) was used to generate under-5 mortality rates, which synthesised 30 763 location-years of vital registration and sample registration data, 1365 surveys and censuses, and 80 other sources. ST-GPR was also used to estimate adult mortality (between ages 15 and 59 years) based on information from 31 642 location-years of vital registration and sample registration data, 355 surveys and censuses, and 24 other sources. Estimates of child and adult mortality rates were then used to generate life tables with a relational model life table system. For countries with large HIV epidemics, life tables were adjusted using independent estimates of HIV-specific mortality generated via an epidemiological analysis of HIV prevalence surveys, antenatal clinic serosurveillance, and other data sources. Excess mortality due to the COVID-19 pandemic in 2020 and 2021 was determined by subtracting observed all-cause mortality (adjusted for late registration and mortality anomalies) from the mortality expected in the absence of the pandemic. Expected mortality was calculated based on historical trends using an ensemble of models. In location-years where all-cause mortality data were unavailable, we estimated excess mortality rates using a regression model with covariates pertaining to the pandemic. Population size was computed using a Bayesian hierarchical cohort component model. Life expectancy was calculated using age-specific mortality rates and standard demographic methods. Uncertainty intervals (UIs) were calculated for every metric using the 25th and 975th ordered values from a 1000-draw posterior distribution. Findings Global all-cause mortality followed two distinct patterns over the study period: age-standardised mortality rates declined between 1950 and 2019 (a 62·8% [95% UI 60·5–65·1] decline), and increased during the COVID-19 pandemic period (2020–21; 5·1% [0·9–9·6] increase). In contrast with the overall reverse in mortality trends during the pandemic period, child mortality continued to decline, with 4·66 million (3·98–5·50) global deaths in children younger than 5 years in 2021 compared with 5·21 million (4·50–6·01) in 2019. An estimated 131 million (126–137) people died globally from all causes in 2020 and 2021 combined, of which 15·9 million (14·7–17·2) were due to the COVID-19 pandemic (measured by excess mortality, which includes deaths directly due to SARS-CoV-2 infection and those indirectly due to other social, economic, or behavioural changes associated with the pandemic). Excess mortality rates exceeded 150 deaths per 100 000 population during at least one year of the pandemic in 80 countries and territories, whereas 20 nations had a negative excess mortality rate in 2020 or 2021, indicating that all-cause mortality in these countries was lower during the pandemic than expected based on historical trends. Between 1950 and 2021, global life expectancy at birth increased by 22·7 years (20·8–24·8), from 49·0 years (46·7–51·3) to 71·7 years (70·9–72·5). Global life expectancy at birth declined by 1·6 years (1·0–2·2) between 2019 and 2021, reversing historical trends. An increase in life expectancy was only observed in 32 (15·7%) of 204 countries and territories between 2019 and 2021. The global population reached 7·89 billion (7·67–8·13) people in 2021, by which time 56 of 204 countries and territories had peaked and subsequently populations have declined. The largest proportion of population growth between 2020 and 2021 was in sub-Saharan Africa (39·5% [28·4–52·7]) and south Asia (26·3% [9·0–44·7]). From 2000 to 2021, the ratio of the population aged 65 years and older to the population aged younger than 15 years increased in 188 (92·2%) of 204 nations. Interpretation Global adult mortality rates markedly increased during the COVID-19 pandemic in 2020 and 2021, reversing past decreasing trends, while child mortality rates continued to decline, albeit more slowly than in earlier years. Although COVID-19 had a substantial impact on many demographic indicators during the first 2 years of the pandemic, overall global health progress over the 72 years evaluated has been profound, with considerable improvements in mortality and life expectancy. Additionally, we observed a deceleration of global population growth since 2017, despite steady or increasing growth in lower-income countries, combined with a continued global shift of population age structures towards older ages. These demographic changes will likely present future challenges to health systems, economies, and societies. The comprehensive demographic estimates reported here will enable researchers, policy makers, health practitioners, and other key stakeholders to better understand and address the profound changes that have occurred in the global health landscape following the first 2 years of the COVID-19 pandemic, and longer-term trends beyond the pandemic