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Article ; Online: Internal Delensing of Cosmic Microwave Background Polarization B-Modes with the POLARBEAR Experiment.

Adachi, S / Aguilar Faúndez, M A O / Akiba, Y / Ali, A / Arnold, K / Baccigalupi, C / Barron, D / Beck, D / Bianchini, F / Borrill, J / Carron, J / Cheung, K / Chinone, Y / Crowley, K / El Bouhargani, H / Elleflot, T / Errard, J / Fabbian, G / Feng, C /

Fujino, T / Goeckner-Wald, N / Hasegawa, M / Hazumi, M / Hill, C A / Howe, L / Katayama, N / Keating, B / Kikuchi, S / Kusaka, A / Lee, A T / Leon, D / Linder, E / Lowry, L N / Matsuda, F / Matsumura, T / Minami, Y / Namikawa, T / Navaroli, M / Nishino, H / Peloton, J / Pham, A T P / Poletti, D / Puglisi, G / Reichardt, C L / Segawa, Y / Sherwin, B D / Silva-Feaver, M / Siritanasak, P / Stompor, R / Tajima, O / Takatori, S / Tanabe, D / Teply, G P / Vergès, C

Physical review letters

2020 Volume 124, Issue 13, Page(s) 131301

Abstract: ... B-mode polarization delensing on subdegree scales at more than 5σ significance. We achieve a 14% B ... paving the way for the optimal analysis of next-generation primordial B-mode experiments. ...

Abstract	Using only cosmic microwave background polarization data from the polarbear experiment, we measure B-mode polarization delensing on subdegree scales at more than 5σ significance. We achieve a 14% B-mode power variance reduction, the highest to date for internal delensing, and improve this result to 22% by applying for the first time an iterative maximum a posteriori delensing method. Our analysis demonstrates the capability of internal delensing as a means of improving constraints on inflationary models, paving the way for the optimal analysis of next-generation primordial B-mode experiments.
Language	English
Publishing date	2020-04-17
Publishing country	United States
Document type	Journal Article
ZDB-ID	208853-8
ISSN	1079-7114 ; 0031-9007
ISSN (online)	1079-7114
ISSN	0031-9007
DOI	10.1103/PhysRevLett.124.131301
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Article ; Online: Diabetes Induced by Immune Checkpoint Inhibitors (ICIs).

Vergès, Bruno

Annales d'endocrinologie

2023 Volume 84, Issue 3, Page(s) 351

MeSH term(s)	Humans ; Immune Checkpoint Inhibitors/adverse effects ; Diabetes Mellitus ; Lung Neoplasms
Chemical Substances	Immune Checkpoint Inhibitors
Language	English
Publishing date	2023-03-24
Publishing country	France
Document type	Journal Article
ZDB-ID	299-9
ISSN	2213-3941 ; 0003-4266
ISSN (online)	2213-3941
ISSN	0003-4266
DOI	10.1016/j.ando.2023.03.012
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Article ; Online: Cardiovascular disease in type 1 diabetes, an underestimated danger: Epidemiological and pathophysiological data.

Vergès, Bruno

Atherosclerosis

2023

Abstract: Cardiovascular disease (CV) is a common complication of type 1 diabetes (T1D) and a leading cause of death. T1D patients are more likely to develop CV disease (CVD) early in life and show a reduction of life expectancy of at least 11 years. Patients with ...

Abstract	Cardiovascular disease (CV) is a common complication of type 1 diabetes (T1D) and a leading cause of death. T1D patients are more likely to develop CV disease (CVD) early in life and show a reduction of life expectancy of at least 11 years. Patients with a young age of T1D onset have a substantially higher CV risk. The reasons for increased atherosclerosis in T1D patients are not entirely explained. In addition to the typical CV risk factors, long-term hyperglycemia has a significant impact by inducing oxidative stress, vascular inflammation, monocyte adhesion, arterial wall thickening and endothelial dysfunction. Additionally, CVD in T1D is also associated with nephropathy. However, CVD risk is still significantly increased in T1D patients, in good glycemic control without additional CV risk factors, indicating the involvement of supplementary potential factors. By increasing oxidative stress, vascular inflammation, and endothelial dysfunction, hypoglycemia and glucose variability may exacerbate CVD. Moreover, significant qualitative and functional abnormalities of lipoproteins are present in even well-controlled T1D patients and are likely to play a role in the development of atherosclerosis and the promotion of CVD. According to recent research, immune system dysfunction, which is typical of auto-immune T1D, may also promote CVD, likely via inflammatory pathways. In addition, T1D patients who are overweight or obese exhibit an additional CV risk due to pathophysiological mechanisms that are similar to those seen in T2D.
Language	English
Publishing date	2023-06-20
Publishing country	Ireland
Document type	Journal Article ; Review
ZDB-ID	80061-2
ISSN	1879-1484 ; 0021-9150
ISSN (online)	1879-1484
ISSN	0021-9150
DOI	10.1016/j.atherosclerosis.2023.06.005
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Article ; Online: Systems biology and artificial intelligence analysis highlights the pleiotropic effect of IVIg therapy in autoimmune diseases with a predominant role on B cells and complement system.

Segú-Vergés, Cristina / Caño, Silvia / Calderón-Gómez, Elisabeth / Bartra, Helena / Sardon, Teresa / Kaveri, Srini / Terencio, José

Frontiers in immunology

2022 Volume 13, Page(s) 901872

Abstract: ... from IVIg treatment were mainly characterized by deregulated processes in B cells and the complement system ... Indeed, our results show that proteins related to B-cell and complement system pathways, which are ... through several mechanisms. Although B-cell responses and complement system have a key role in diseases benefiting from IVIg ...

Abstract	Intravenous immunoglobulin (IVIg) is used as treatment for several autoimmune and inflammatory conditions, but its specific mechanisms are not fully understood. Herein, we aimed to evaluate, using systems biology and artificial intelligence techniques, the differences in the pathophysiological pathways of autoimmune and inflammatory conditions that show diverse responses to IVIg treatment. We also intended to determine the targets of IVIg involved in the best treatment response of the evaluated diseases. Our selection and classification of diseases was based on a previously published systematic review, and we performed the disease characterization through manual curation of the literature. Furthermore, we undertook the mechanistic evaluation with artificial neural networks and pathway enrichment analyses. A set of 26 diseases was selected, classified, and compared. Our results indicated that diseases clearly benefiting from IVIg treatment were mainly characterized by deregulated processes in B cells and the complement system. Indeed, our results show that proteins related to B-cell and complement system pathways, which are targeted by IVIg, are involved in the clinical response. In addition, targets related to other immune processes may also play an important role in the IVIg response, supporting its wide range of actions through several mechanisms. Although B-cell responses and complement system have a key role in diseases benefiting from IVIg, protein targets involved in such processes are not necessarily the same in those diseases. Therefore, IVIg appeared to have a pleiotropic effect that may involve the collaborative participation of several proteins. This broad spectrum of targets and 'non-specificity' of IVIg could be key to its efficacy in very different diseases.
MeSH term(s)	Artificial Intelligence ; Autoimmune Diseases/drug therapy ; Complement System Proteins ; Humans ; Immunoglobulins, Intravenous ; Systems Biology
Chemical Substances	Immunoglobulins, Intravenous ; Complement System Proteins (9007-36-7)
Language	English
Publishing date	2022-09-30
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2606827-8
ISSN	1664-3224 ; 1664-3224
ISSN (online)	1664-3224
ISSN	1664-3224
DOI	10.3389/fimmu.2022.901872
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Article ; Online: Intestinal lipid absorption and transport in type 2 diabetes.

Vergès, Bruno

Diabetologia

2022 Volume 65, Issue 10, Page(s) 1587–1600

Abstract: ... in chylomicron synthesis; (2) higher stability and availability of apolipoprotein B-48; and (3) increased de novo ...

Abstract	Postprandial hyperlipidaemia is an important feature of diabetic dyslipidaemia and plays an important role in the development of cardiovascular disease in individuals with type 2 diabetes. Postprandial hyperlipidaemia in type 2 diabetes is secondary to increased chylomicron production by the enterocytes and delayed catabolism of chylomicrons and chylomicron remnants. Insulin and some intestinal hormones (e.g. glucagon-like peptide-1 [GLP-1]) influence intestinal lipid metabolism. In individuals with type 2 diabetes, insulin resistance and possibly reduced GLP-1 secretion are involved in the pathophysiology of postprandial hyperlipidaemia. Several factors are involved in the overproduction of chylomicrons: (1) increased expression of microsomal triglyceride transfer protein, which is a key enzyme in chylomicron synthesis; (2) higher stability and availability of apolipoprotein B-48; and (3) increased de novo lipogenesis. Individuals with type 2 diabetes present with disorders of cholesterol metabolism in the enterocytes with reduced absorption and increased synthesis. The increased production of chylomicrons in type 2 diabetes is also associated with a reduction in their catabolism, mostly because of a reduction in activity of lipoprotein lipase. Modification of the microbiota, which is observed in type 2 diabetes, may also generate disorders of intestinal lipid metabolism, but human data remain limited. Some glucose-lowering treatments significantly influence intestinal lipid absorption and transport. Postprandial hyperlipidaemia is reduced by metformin, pioglitazone, alpha-glucosidase inhibitors, dipeptidyl peptidase 4 inhibitors and GLP-1 agonists. The most pronounced effect is observed with GLP-1 agonists, which reduce chylomicron production significantly in individuals with type 2 diabetes and have a direct effect on the intestine by reducing the expression of genes involved in intestinal lipoprotein metabolism. The effect of sodium-glucose cotransporter 2 inhibitors on intestinal lipid metabolism needs to be clarified.
MeSH term(s)	Apolipoprotein B-48/metabolism ; Apolipoprotein B-48/pharmacology ; Cholesterol ; Chylomicron Remnants/metabolism ; Chylomicron Remnants/pharmacology ; Chylomicrons/metabolism ; Diabetes Mellitus, Type 2/metabolism ; Dipeptidyl-Peptidase IV Inhibitors/pharmacology ; Glucagon-Like Peptide 1/metabolism ; Glucose/pharmacology ; Glycoside Hydrolase Inhibitors ; Humans ; Hyperlipidemias ; Insulin/metabolism ; Intestinal Absorption ; Lipid Metabolism ; Lipoprotein Lipase/metabolism ; Lipoproteins ; Metformin/pharmacology ; Pioglitazone ; Postprandial Period ; Sodium ; Triglycerides/metabolism
Chemical Substances	Apolipoprotein B-48 ; Chylomicron Remnants ; Chylomicrons ; Dipeptidyl-Peptidase IV Inhibitors ; Glycoside Hydrolase Inhibitors ; Insulin ; Lipoproteins ; Triglycerides ; Glucagon-Like Peptide 1 (89750-14-1) ; Metformin (9100L32L2N) ; Cholesterol (97C5T2UQ7J) ; Sodium (9NEZ333N27) ; Lipoprotein Lipase (EC 3.1.1.34) ; Glucose (IY9XDZ35W2) ; Pioglitazone (X4OV71U42S)
Language	English
Publishing date	2022-07-30
Publishing country	Germany
Document type	Journal Article ; Review
ZDB-ID	1694-9
ISSN	1432-0428 ; 0012-186X
ISSN (online)	1432-0428
ISSN	0012-186X
DOI	10.1007/s00125-022-05765-8
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Article ; Online: Abnormal hepatic apolipoprotein B metabolism in type 2 diabetes.

Vergès, Bruno

Atherosclerosis

2010 Volume 211, Issue 2, Page(s) 353–360

Abstract: Increased Very Low Density Lipoprotein (VLDL) production is a major feature of diabetic dyslipidemia with consequences on the metabolism of other lipoproteins such as Low Density Lipoproteins (LDL) and High Density Lipoproteins (HDL). More precisely, we ... ...

Abstract	Increased Very Low Density Lipoprotein (VLDL) production is a major feature of diabetic dyslipidemia with consequences on the metabolism of other lipoproteins such as Low Density Lipoproteins (LDL) and High Density Lipoproteins (HDL). More precisely, we observe, in patients with type 2 diabetes, an increased production of VLDL(1) particles that is potentially detrimental by generating atherogenic remnants, small dense LDL particles and triglyceride-rich HDL particles. Several pathophysiological factors are responsible for increased VLDL production, in type 2 diabetes. Among those, insulin resistance plays an important role. Indeed, defective activation of PI3-kinase, secondary to insulin resistance, is associated with a reduction of apoB degradation in the hepatocytes, a rise in MTP expression (by increasing nuclear transcription factors Fox01 and Foxa2) and an increased activity of phospholipase D1 and ARF-1, which are involved in VLDL(1) formation. Moreover, peripheral insulin resistance is responsible for increased lipolysis of adipose tissue leading to augmented portal flux of FFA to the liver and, as a consequence, activation of VLDL production. In addition, increased de novo lipogenesis is observed in type 2 diabetes. This is secondary to increased activation of SREBP-1c (Sterol Regulatory Element-Binding Protein-1c), mainly by Endoplasmic Reticulum stress, and of ChREBP (Carbohydrate Responsive Element Binding Protein), mainly by hyperglycemia. Furthermore, decreased plasma adiponectin observed in type 2 diabetes, may also play a role in increased VLDL production by decreasing liver AMP-kinase activation and by increasing plasma FFA levels as a consequence of reduced muscle FFA oxidation.
MeSH term(s)	Adiponectin/metabolism ; Animals ; Apolipoproteins B/metabolism ; Atherosclerosis ; Diabetes Mellitus, Type 2/blood ; Diabetes Mellitus, Type 2/metabolism ; Gene Expression Regulation ; Hepatocytes/metabolism ; Humans ; Insulin/metabolism ; Insulin Resistance ; Lipogenesis ; Lipoproteins, LDL/metabolism ; Lipoproteins, VLDL/metabolism ; Liver/metabolism ; Models, Biological ; Triglycerides/metabolism
Chemical Substances	Adiponectin ; Apolipoproteins B ; Insulin ; Lipoproteins, LDL ; Lipoproteins, VLDL ; Triglycerides
Language	English
Publishing date	2010-08
Publishing country	Ireland
Document type	Journal Article ; Review
ZDB-ID	80061-2
ISSN	1879-1484 ; 0021-9150
ISSN (online)	1879-1484
ISSN	0021-9150
DOI	10.1016/j.atherosclerosis.2010.01.028
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Article ; Online: Genetic variability of human respiratory syncytial virus group B in Panama reveals a novel genotype BA14.

Ábrego, Leyda E / Delfraro, Adriana / Franco, Danilo / Castillo, Juan / Castillo, Marlene / Moreno, Brechla / López-Vergès, Sandra / Pascale, Juan M / Arbiza, Juan

Journal of medical virology

2017 Volume 89, Issue 10, Page(s) 1734–1742

Abstract: ... on HRSV-B in Panama have been described yet. In this study, 24 sequences of Panamanian HRSV-B ... amino acid substitutions in the Panamanian HRSV-B strains were observed, some previously described and others found only ...

Abstract	In Panama, human respiratory syncytial virus (HRSV) is responsible of 20-40% of acute respiratory infections in children under 5 years old. Currently, little is known about the genetic variability of HRSV in Central America and the Caribbean. Recently, we reported the genetic variability of HRSV-A, however; no studies on HRSV-B in Panama have been described yet. In this study, 24 sequences of Panamanian HRSV-B, from children (<5 years) with acute respiratory infections (ARI), collected from July 2008 to November 2012 were analyzed. All sequences share the characteristic 60-nt duplication of the BA strains. Six Panamanian strains grouped with the BA10 genotype and 12 samples clustered together in a separate monophyletic clade with an aLRT support value of 0.92 and an intra-group p-distance less than 0.07. This fulfills the criteria to consider a new genotype in HRSV, which we named BA14 genotype. Another six strains remain unclassified, but closely related to BA9, BA11, or the new BA14 genotypes, according to their genetic p-distance. Different amino acid substitutions in the Panamanian HRSV-B strains were observed, some previously described and others found only on Panamanian strains. This study contributes to the knowledge of the genetic variability and evolution of HRSV in Central America.
MeSH term(s)	Child, Preschool ; Female ; Genetic Variation ; Genotype ; High-Throughput Nucleotide Sequencing ; Humans ; Infant ; Panama/epidemiology ; Phylogeny ; RNA, Viral/genetics ; Real-Time Polymerase Chain Reaction ; Respiratory Syncytial Virus Infections/epidemiology ; Respiratory Syncytial Virus Infections/virology ; Respiratory Syncytial Virus, Human/genetics ; Respiratory Tract Infections/virology ; Sequence Analysis, DNA
Chemical Substances	RNA, Viral
Language	English
Publishing date	2017-05-23
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	752392-0
ISSN	1096-9071 ; 0146-6615
ISSN (online)	1096-9071
ISSN	0146-6615
DOI	10.1002/jmv.24838
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Article ; Online: Cardiovascular disease in type 1 diabetes: A review of epidemiological data and underlying mechanisms.

Vergès, Bruno

Diabetes & metabolism

2020 Volume 46, Issue 6, Page(s) 442–449

Abstract: Cardiovascular disease (CVD) is highly prevalent in patients with type 1 diabetes (T1D) and a major cause of mortality. CVD arises earlier in life in T1D patients and is responsible for a significant reduction of at least 11 years' life expectancy. Also, ...

Abstract	Cardiovascular disease (CVD) is highly prevalent in patients with type 1 diabetes (T1D) and a major cause of mortality. CVD arises earlier in life in T1D patients and is responsible for a significant reduction of at least 11 years' life expectancy. Also, the incidence of CVD is much more pronounced in patients with T1D onset at an earlier age. However, the factors responsible for increased atherosclerosis and CVD in T1D are not yet totally clarified. In addition to the usual cardiovascular (CV) risk factors, chronic hyperglycaemia plays an important role by promoting oxidative stress, vascular inflammation, monocyte adhesion, arterial wall thickening and endothelial dysfunction. Diabetic nephropathy and cardiac autonomic neuropathy are also associated with increased CVD in T1D. In fact, the CVD risk remains significantly increased even in well-controlled T1D patients who have no additional CV risk factors, indicating that other potential factors are likely to be involved. Hypoglycemia and glucose variability could enhance CV disease by promoting oxidative stress, vascular inflammation and endothelial dysfunction. Furthermore, even well-controlled T1D patients show significant qualitative and functional abnormalities of lipoproteins that are likely to be implicated in the development of atherosclerosis and premature CVD. In addition, recent data suggest that a dysfunctional immune system, which is typical of autoimmune T1D, might also promote CVD possibly through inflammatory pathways. Moreover, overweight and obese T1D patients can manifest additional CV risk through pathophysiological mechanisms resembling those observed in type 2 diabetes (T2D).
MeSH term(s)	Age of Onset ; Autonomic Nervous System Diseases/epidemiology ; Autonomic Nervous System Diseases/metabolism ; Autonomic Nervous System Diseases/physiopathology ; Cardiovascular Diseases/epidemiology ; Cardiovascular Diseases/metabolism ; Cardiovascular Diseases/physiopathology ; Cell Adhesion/physiology ; Diabetes Complications/epidemiology ; Diabetes Complications/metabolism ; Diabetes Complications/physiopathology ; Diabetes Mellitus, Type 1/epidemiology ; Diabetes Mellitus, Type 1/metabolism ; Diabetes Mellitus, Type 1/physiopathology ; Diabetic Nephropathies/epidemiology ; Diabetic Nephropathies/metabolism ; Diabetic Nephropathies/physiopathology ; Diabetic Neuropathies/epidemiology ; Diabetic Neuropathies/metabolism ; Diabetic Neuropathies/physiopathology ; Endothelium, Vascular/physiopathology ; Humans ; Inflammation/metabolism ; Inflammation/physiopathology ; Lipoproteins/metabolism ; Monocytes ; Overweight/epidemiology ; Overweight/metabolism ; Overweight/physiopathology ; Oxidative Stress/physiology
Chemical Substances	Lipoproteins
Language	English
Publishing date	2020-09-28
Publishing country	France
Document type	Journal Article ; Review
ZDB-ID	1315751-6
ISSN	1878-1780 ; 1262-3636 ; 0338-1684
ISSN (online)	1878-1780
ISSN	1262-3636 ; 0338-1684
DOI	10.1016/j.diabet.2020.09.001
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Article ; Online: Dyslipidemia in Type 1 Diabetes: AMaskedDanger.

Vergès, Bruno

Trends in endocrinology and metabolism: TEM

2020 Volume 31, Issue 6, Page(s) 422–434

Abstract: Type 1 diabetes (T1D) patients show lipid disorders which are likely to play a role in their increased cardiovascular (CV) disease risk. Quantitative abnormalities of lipoproteins are noted in T1D with poor glycemic control. In T1D with optimal glycemic ... ...

Abstract	Type 1 diabetes (T1D) patients show lipid disorders which are likely to play a role in their increased cardiovascular (CV) disease risk. Quantitative abnormalities of lipoproteins are noted in T1D with poor glycemic control. In T1D with optimal glycemic control, triglycerides and LDL-cholesterol are normal or slightly decreased whereas HDL-cholesterol is normal or slightly increased. T1D patients, even with good glycemic control, show several qualitative and functional abnormalities of lipoproteins that are potentially atherogenic. An association between these abnormalities and CV disease risk has been reported in recent studies. Although the mechanisms underlying T1D dyslipidemia remain unclear, the subcutaneous route of insulin administration, that is responsible for peripheral hyperinsulinemia, is likely to be an important factor.
MeSH term(s)	Cardiovascular Diseases/etiology ; Cardiovascular Diseases/metabolism ; Diabetes Mellitus, Type 1/complications ; Diabetes Mellitus, Type 1/drug therapy ; Diabetes Mellitus, Type 1/metabolism ; Diabetic Ketoacidosis ; Dyslipidemias/etiology ; Dyslipidemias/metabolism ; Humans ; Insulin/administration & dosage ; Insulin/metabolism
Chemical Substances	Insulin
Language	English
Publishing date	2020-03-02
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	1042384-9
ISSN	1879-3061 ; 1043-2760
ISSN (online)	1879-3061
ISSN	1043-2760
DOI	10.1016/j.tem.2020.01.015
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Article ; Online: [No title information]

Louiset, Estelle / Vergès, Bruno

Annales d'endocrinologie

2023 Volume 84, Issue 5, Page(s) 499

Title translation	Éditorial.
Language	French
Publishing date	2023-08-02
Publishing country	France
Document type	Editorial
ZDB-ID	299-9
ISSN	2213-3941 ; 0003-4266
ISSN (online)	2213-3941
ISSN	0003-4266
DOI	10.1016/j.ando.2023.08.001
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