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Immune response to SARS-CoV-2 variants after immunization with different vaccines in Mexico
- Erika Garay, Sean P. J. Whelan, Rebecca M. DuBois, Sara M. O’Rourke, Angel Eduardo Salgado-Escobar, José Esteban Muñoz-Medina, Carlos F. Arias, Susana López
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- Journal:
- Epidemiology & Infection / Volume 152 / 2024
- Published online by Cambridge University Press:
- 05 February 2024, e30
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There is limited information on the antibody responses against severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) in subjects from developing countries with populations having a high incidence of co-morbidities. Here, we analysed the immunogenicity of homologous schemes using the ChAdOx1-S, Sputnik V, or BNT162b2 vaccines and the effect of a booster dose with ChAdOx1-S in middle-aged adults who were seropositive or seronegative to the SARS-CoV-2 spike protein before vaccination. The study was conducted post-vaccination with a follow-up of 4 months for antibody titre using enzyme-linked immunosorbent assay (ELISA) and pseudovirus (PV) neutralization assays (PNAs). All three vaccines elicited a superior IgG anti-receptor-binding domain (RBD) and neutralization response against the Alpha and Delta variants when administered to individuals with a previous infection by SARS-CoV-2. The booster dose spiked the neutralization activity among individuals with and without a prior SARS-CoV-2 infection. The ChAdOx1-S vaccine induced weaker antibody responses in infection-naive subjects. A follow-up of 4 months post-vaccination showed a drop in antibody titre, with about 20% of the infection-naive and 100% of SARS-CoV-2 pre-exposed participants with detectable neutralization capacity against Alpha pseudovirus (Alpha-PV) and Delta PV (Delta-PV). Our observations support the use of different vaccines in a country with high seroprevalence at the vaccination time.
Chapter 31 - Tyrosinemia in Children
- from Section IV - Metabolic Liver Disease
- Edited by Frederick J. Suchy, Ronald J. Sokol, William F. Balistreri
- Edited in association with Jorge A. Bezerra, Cara L. Mack, Benjamin L. Shneider
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- Book:
- Liver Disease in Children
- Published online:
- 19 January 2021
- Print publication:
- 18 March 2021, pp 548-569
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Summary
Hepatorenal tyrosinemia1 is a severe inborn error of metabolism that can affect numerous organs, particularly the liver, kidneys, and peripheral nerves. In the first accounts of patients with features typical of tyrosinemia in the 1950s, almost all died of liver disease in infancy and childhood [1]. However, tyrosinemia is highly variable and rare case reports described surviving affected adults. Since the identification of tyrosinemia, its clinical course has been improved successively by the introduction of diet therapy, neonatal screening, liver transplantation and treatment with nitisinone (NTBC, 2-(2-nitro-4-trifluoromethyl benzoyl)-1,3-cyclohexanedione) [2]. Tyrosinemia raises questions in liver biology, biochemical and population genetics, cell biology, oncology, and public health.
Zygosity Differences in Height and Body Mass Index of Twins From Infancy to Old Age: A Study of the CODATwins Project
- Aline Jelenkovic, Yoshie Yokoyama, Reijo Sund, Chika Honda, Leonie H Bogl, Sari Aaltonen, Fuling Ji, Feng Ning, Zengchang Pang, Juan R. Ordoñana, Juan F. Sánchez-Romera, Lucia Colodro-Conde, S. Alexandra Burt, Kelly L. Klump, Sarah E. Medland, Grant W. Montgomery, Christian Kandler, Tom A. McAdams, Thalia C. Eley, Alice M. Gregory, Kimberly J. Saudino, Lise Dubois, Michel Boivin, Adam D. Tarnoki, David L. Tarnoki, Claire M. A. Haworth, Robert Plomin, Sevgi Y. Öncel, Fazil Aliev, Maria A. Stazi, Corrado Fagnani, Cristina D’Ippolito, Jeffrey M. Craig, Richard Saffery, Sisira H. Siribaddana, Matthew Hotopf, Athula Sumathipala, Fruhling Rijsdijk, Timothy Spector, Massimo Mangino, Genevieve Lachance, Margaret Gatz, David A. Butler, Gombojav Bayasgalan, Danshiitsoodol Narandalai, Duarte L Freitas, José Antonio Maia, K. Paige Harden, Elliot M. Tucker-Drob, Bia Kim, Youngsook Chong, Changhee Hong, Hyun Jung Shin, Kaare Christensen, Axel Skytthe, Kirsten O. Kyvik, Catherine A. Derom, Robert F. Vlietinck, Ruth J. F. Loos, Wendy Cozen, Amie E. Hwang, Thomas M. Mack, Mingguang He, Xiaohu Ding, Billy Chang, Judy L. Silberg, Lindon J. Eaves, Hermine H. Maes, Tessa L. Cutler, John L. Hopper, Kelly Aujard, Patrik K. E. Magnusson, Nancy L. Pedersen, Anna K. Dahl Aslan, Yun-Mi Song, Sarah Yang, Kayoung Lee, Laura A. Baker, Catherine Tuvblad, Morten Bjerregaard-Andersen, Henning Beck-Nielsen, Morten Sodemann, Kauko Heikkilä, Qihua Tan, Dongfeng Zhang, Gary E. Swan, Ruth Krasnow, Kerry L. Jang, Ariel Knafo-Noam, David Mankuta, Lior Abramson, Paul Lichtenstein, Robert F. Krueger, Matt McGue, Shandell Pahlen, Per Tynelius, Glen E. Duncan, Dedra Buchwald, Robin P. Corley, Brooke M. Huibregtse, Tracy L. Nelson, Keith E. Whitfield, Carol E. Franz, William S. Kremen, Michael J. Lyons, Syuichi Ooki, Ingunn Brandt, Thomas Sevenius Nilsen, Fujio Inui, Mikio Watanabe, Meike Bartels, Toos C. E. M. van Beijsterveldt, Jane Wardle, Clare H. Llewellyn, Abigail Fisher, Esther Rebato, Nicholas G. Martin, Yoshinori Iwatani, Kazuo Hayakawa, Joohon Sung, Jennifer R. Harris, Gonneke Willemsen, Andreas Busjahn, Jack H. Goldberg, Finn Rasmussen, Yoon-Mi Hur, Dorret I. Boomsma, Thorkild I. A. Sørensen, Jaakko Kaprio, Karri Silventoinen
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- Journal:
- Twin Research and Human Genetics / Volume 18 / Issue 5 / October 2015
- Published online by Cambridge University Press:
- 04 September 2015, pp. 557-570
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A trend toward greater body size in dizygotic (DZ) than in monozygotic (MZ) twins has been suggested by some but not all studies, and this difference may also vary by age. We analyzed zygosity differences in mean values and variances of height and body mass index (BMI) among male and female twins from infancy to old age. Data were derived from an international database of 54 twin cohorts participating in the COllaborative project of Development of Anthropometrical measures in Twins (CODATwins), and included 842,951 height and BMI measurements from twins aged 1 to 102 years. The results showed that DZ twins were consistently taller than MZ twins, with differences of up to 2.0 cm in childhood and adolescence and up to 0.9 cm in adulthood. Similarly, a greater mean BMI of up to 0.3 kg/m2 in childhood and adolescence and up to 0.2 kg/m2 in adulthood was observed in DZ twins, although the pattern was less consistent. DZ twins presented up to 1.7% greater height and 1.9% greater BMI than MZ twins; these percentage differences were largest in middle and late childhood and decreased with age in both sexes. The variance of height was similar in MZ and DZ twins at most ages. In contrast, the variance of BMI was significantly higher in DZ than in MZ twins, particularly in childhood. In conclusion, DZ twins were generally taller and had greater BMI than MZ twins, but the differences decreased with age in both sexes.
The CODATwins Project: The Cohort Description of Collaborative Project of Development of Anthropometrical Measures in Twins to Study Macro-Environmental Variation in Genetic and Environmental Effects on Anthropometric Traits
- Karri Silventoinen, Aline Jelenkovic, Reijo Sund, Chika Honda, Sari Aaltonen, Yoshie Yokoyama, Adam D. Tarnoki, David L. Tarnoki, Feng Ning, Fuling Ji, Zengchang Pang, Juan R. Ordoñana, Juan F. Sánchez-Romera, Lucia Colodro-Conde, S. Alexandra Burt, Kelly L. Klump, Sarah E. Medland, Grant W. Montgomery, Christian Kandler, Tom A. McAdams, Thalia C. Eley, Alice M. Gregory, Kimberly J. Saudino, Lise Dubois, Michel Boivin, Claire M. A. Haworth, Robert Plomin, Sevgi Y. Öncel, Fazil Aliev, Maria A. Stazi, Corrado Fagnani, Cristina D’Ippolito, Jeffrey M. Craig, Richard Saffery, Sisira H. Siribaddana, Matthew Hotopf, Athula Sumathipala, Timothy Spector, Massimo Mangino, Genevieve Lachance, Margaret Gatz, David A. Butler, Gombojav Bayasgalan, Danshiitsoodol Narandalai, Duarte L. Freitas, José Antonio Maia, K. Paige Harden, Elliot M. Tucker-Drob, Kaare Christensen, Axel Skytthe, Kirsten O. Kyvik, Changhee Hong, Youngsook Chong, Catherine A. Derom, Robert F. Vlietinck, Ruth J. F. Loos, Wendy Cozen, Amie E. Hwang, Thomas M. Mack, Mingguang He, Xiaohu Ding, Billy Chang, Judy L. Silberg, Lindon J. Eaves, Hermine H. Maes, Tessa L. Cutler, John L. Hopper, Kelly Aujard, Patrik K. E. Magnusson, Nancy L. Pedersen, Anna K. Dahl Aslan, Yun-Mi Song, Sarah Yang, Kayoung Lee, Laura A. Baker, Catherine Tuvblad, Morten Bjerregaard-Andersen, Henning Beck-Nielsen, Morten Sodemann, Kauko Heikkilä, Qihua Tan, Dongfeng Zhang, Gary E. Swan, Ruth Krasnow, Kerry L. Jang, Ariel Knafo-Noam, David Mankuta, Lior Abramson, Paul Lichtenstein, Robert F. Krueger, Matt McGue, Shandell Pahlen, Per Tynelius, Glen E. Duncan, Dedra Buchwald, Robin P. Corley, Brooke M. Huibregtse, Tracy L. Nelson, Keith E. Whitfield, Carol E. Franz, William S. Kremen, Michael J. Lyons, Syuichi Ooki, Ingunn Brandt, Thomas Sevenius Nilsen, Fujio Inui, Mikio Watanabe, Meike Bartels, Toos C. E. M. van Beijsterveldt, Jane Wardle, Clare H. Llewellyn, Abigail Fisher, Esther Rebato, Nicholas G. Martin, Yoshinori Iwatani, Kazuo Hayakawa, Finn Rasmussen, Joohon Sung, Jennifer R. Harris, Gonneke Willemsen, Andreas Busjahn, Jack H. Goldberg, Dorret I. Boomsma, Yoon-Mi Hur, Thorkild I. A. Sørensen, Jaakko Kaprio
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- Journal:
- Twin Research and Human Genetics / Volume 18 / Issue 4 / August 2015
- Published online by Cambridge University Press:
- 27 May 2015, pp. 348-360
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For over 100 years, the genetics of human anthropometric traits has attracted scientific interest. In particular, height and body mass index (BMI, calculated as kg/m2) have been under intensive genetic research. However, it is still largely unknown whether and how heritability estimates vary between human populations. Opportunities to address this question have increased recently because of the establishment of many new twin cohorts and the increasing accumulation of data in established twin cohorts. We started a new research project to analyze systematically (1) the variation of heritability estimates of height, BMI and their trajectories over the life course between birth cohorts, ethnicities and countries, and (2) to study the effects of birth-related factors, education and smoking on these anthropometric traits and whether these effects vary between twin cohorts. We identified 67 twin projects, including both monozygotic (MZ) and dizygotic (DZ) twins, using various sources. We asked for individual level data on height and weight including repeated measurements, birth related traits, background variables, education and smoking. By the end of 2014, 48 projects participated. Together, we have 893,458 height and weight measures (52% females) from 434,723 twin individuals, including 201,192 complete twin pairs (40% monozygotic, 40% same-sex dizygotic and 20% opposite-sex dizygotic) representing 22 countries. This project demonstrates that large-scale international twin studies are feasible and can promote the use of existing data for novel research purposes.
Chapter 31 - Tyrosinemia
- from Section IV - Metabolic liver disease
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- By Grant Mitchell, Medical Genetic Division, Department of Pediatrics Saint Justine Medical Centre, University of Montreal, Montreal, Quebec, Canada, Pierre A. Russo, Anatomic Pathology, Children’s Hospital of Philadelphia, Philadelphia, PA, USA, Josée Dubois, CHU Saint Justine Medical Centre, University of Montreal, Montreal, Quebec, Canada, Fernando Alvarez, Division of Gastroenterology, Hepatology and Nutrition, CHU Saint Justine Medical Centre, Department of Pediatrics and Deaprtment of Microbiology and Immunology, University of Montreal, Montreal, Quebec, Canada
- Edited by Frederick J. Suchy, University of Colorado Medical Center, Ronald J. Sokol, University of Colorado Medical Center, William F. Balistreri
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- Book:
- Liver Disease in Children
- Published online:
- 05 March 2014
- Print publication:
- 20 February 2014, pp 526-545
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Summary
Introduction
Hepatorenal tyrosinemia is a fascinating inborn error of metabolism that can affect numerous organs, particularly the liver, kidneys, and peripheral nerves. (For simplicity, this chapter uses the generic term tyrosinemia to refer to hepatorenal tyrosinemia (also known as fumarylacetoacetate hydrolase deficiency, tyrosinemia type I or congenital tyrosinosis; MIM 27670). Other forms of hypertyrosinemia are referred to by their specific names.) The first report of a patient with elevated blood tyrosine was in 1932 [1]. Patients with a more typical clinical and biochemical picture of tyrosinemia were then described in the late 1950s [2]. Since then, more than 500 patients have been reported in the literature or enrolled in the International NTBC Trial (of 2-(2-nitro-4-trifluoromethyl benzoyl)-1,3-cyclohexanedione (nitisinone)). Previously, almost all patients died in infancy and early childhood, and only isolated case reports described affected adults. In the 50 years since the description of tyrosinemia, the course of the disease has been improved successively by the introduction of diet therapy, neonatal screening, and hepatic transplantation. The advent of liver and kidney transplantation as a definitive treatment revolutionized the outcome [3]. Recently, the availability of nitisinone, a chemical commercialized as Orfadin (Swedish Orphan International, Stockholm, Sweden), has provided hope for a non-surgical solution for some patients [4]. On a fundamental level, tyrosinemia raises questions in hepatology, biochemical and population genetics, cell biology, oncology, and public health.
Pathophysiology
Tyrosinemia is caused by a deficiency of fumarylacetoacetate hydrolase (FAH; EC 3.7.1.2), the last enzyme of tyrosine degradation (Figure 31.1a). The site of the primary metabolic block in tyrosinemia was elegantly deduced by Lindblad et al. in 1977 [5] and subsequently confirmed enzymatically by others [6]. The enzyme is a 419 amino acid residue cytosolic homodimer present in the liver and to some extent in the kidney, lymphocytes, erythrocytes, fibroblasts, and chorionic villi [7]. Human liver FAH cDNAs (GenBank NM000137) and the human gene FAH have been cloned and sequenced and the human gene mapped to chromosome 15q23-q25 [8]. Early studies of tyrosinemia showed that other enzymes of tyrosine degradation, particularly 4-hydroxyphenylpyruvate dioxygenase (4HPPD), are reduced in tyrosinemic liver. These changes have subsequently been shown to be secondary to the deficiency of FAH.
29 - Tyrosinemia
- from SECTION IV - METABOLIC LIVER DISEASE
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- By Grant A. Mitchell, M.D., Professor, Department of Pediatrics, CHU Sainte-Justine and Université de Montréal, Montréal, Québec, Canada, Pierre A. Russo, M.D., Professor of Pathology and Pediatrics, Department of Pathology and Laboratory Medicine, Children's Hospital of Philadelphia, Philadelphia, Pennsylvania, Josée Dubois, M.D., F.R.C.P., Professor of Radiology, Department of Radiology, CHU Sainte-Justine and Université de Montréal, Montréal, Québec, Canada, Fernando Alvarez, M.D., Professor of Pediatrics, Department of Pediatric Gastroenterology, CHU Sainte-Justine and Université de Montréal, Montréal, Québec, Canada
- Edited by Frederick J. Suchy, Mount Sinai School of Medicine, New York, Ronald J. Sokol, University of Colorado, Denver, William F. Balistreri, University of Cincinnati
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- Book:
- Liver Disease in Children
- Published online:
- 18 December 2009
- Print publication:
- 07 May 2007, pp 694-713
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Summary
Hepatorenal tyrosinemia is a fascinating inborn error of metabolism that can affect numerous organs, particularly the liver, kidneys, and peripheral nerves. The first report of a patient with elevated blood tyrosine was by Medes in 1932 [1]. Patients with a more typical clinical and biochemical picture of tyrosinemia were then described in the late 1950s [2–5]. Since then, more than 500 patients have been reported in the literature [6–8] or enrolled in the International NTBC [2-(2-nitro-4-trifluoromethyl benzoyl)-1,3-cyclohexanedione] Trial. Previously, almost all patients died in infancy and early childhood, and only isolated case reports described affected adults. In the 50 years since the description of tyrosinemia [3], the course of the disease has been improved successively by the introduction of diet therapy, neonatal screening, and hepatic transplantation. The advent of liver and kidney transplantation as a definitive treatment [7–11] revolutionized the outcome. Recently, the availability of NTBC, a chemical now designated as nitisinone and commercialized as Orfadin (Swedish Orphan International AB), has provided hope for a nonsurgical solution for some patients. On a fundamental level, tyrosinemia raises questions in hepatology, biochemical and population genetics, cell biology, oncology, and public health.
PATHOPHYSIOLOGY
Tyrosinemia is caused by a deficiency of fumarylacetoacetate hydrolase (FAH; enzyme [EC] 3.7.1.2), the last enzyme of tyrosine degradation (Figure 29.1A). The site of the primary metabolic block in tyrosinemia was elegantly deduced by Lindblad et al. in 1977 [12] and subsequently confirmed enzymatically by several investigators [13–15].