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1.
Rev Prat ; 74(6): 677-682, 2024 Jun.
Artigo em Francês | MEDLINE | ID: mdl-39011708

RESUMO

SARGASSUM SEAWEED AS SAULTS THE FRENCH WEST INDIES. Since 2011, Martinique and the islands of Guadeloupe have been affected by repeated groundings, culminating in an exceptional wave in 2018. While the sargassum ( Sargassum natans and S. fluitans ) involved in these phenomena are neither toxic nor urticating, indirect toxicity linked to the presence of microorganisms and heavy metals (arsenic, mercury, etc.) in sargassum clusters has been described. Similarly, after a 24 to 48 hours stay on the shore, sargassum algae enter a putrefaction cycle responsible to produce hydrogen sulfide (H2S) and ammonia (NH3). The acute toxicity of these gases is well known. However, very few data are available on the clinical effects of prolonged exposure to low doses of H2S and NH3. Our team has recently described the syndromic features of chronic exposure, supposing for deleterious effects on the cardiovascular, respiratory and neurological systems.


ALGUES SARGASSES À L'ASSAUT DES ANTILLES. Depuis 2011, la Martinique et les îles de la Guadeloupe sont touchées par des échouements à répétition d'algues sargasses qui ont culminé avec une vague exceptionnelle en 2018. Si les sargasses (Sargassum natans et S. fluitans) impliquées dans ces phénomènes ne sont ni toxiques ni urticantes, une toxicité indirecte liée à la présence de micro-organismes et de métaux lourds (arsenic, mercure…) dans les amas de sargasses est décrite. De même, après un séjour de vingt-quatre à quarante-huit heures sur le littoral, les algues sargasses entrent dans un cycle de putréfaction responsable de la production d'hydrogène sulfuré (H2S) et d'ammoniac (NH3). La toxicité aiguë de ces gaz est bien connue. Il existe en revanche très peu de données disponibles sur les effets cliniques d'une exposition prolongée à de faibles doses d'H2S ou NH3. Notre équipe a récemment décrit le tableau syndromique de l'exposition chronique et suppose des effets délétères sur le système cardiovasculaire, respiratoire et neurologique.


Assuntos
Sargassum , Alga Marinha , Humanos , Sulfeto de Hidrogênio/intoxicação , Sulfeto de Hidrogênio/toxicidade , Guadalupe/epidemiologia , Martinica/epidemiologia , Amônia/toxicidade , Índias Ocidentais/epidemiologia , Exposição Ambiental/efeitos adversos
3.
Toxins (Basel) ; 16(3)2024 Mar 13.
Artigo em Inglês | MEDLINE | ID: mdl-38535812

RESUMO

Bothrofav, a monospecific antivenom, was introduced in June 1991 and has shown excellent effectiveness against life-threatening and thrombotic complications of Bothrops lanceolatus envenoming. Because of the reoccurrence of cerebral stroke events despite the timely administration of antivenom, new batches of Bothrofav were produced and introduced into clinical use in January 2011. This study's aim was to evaluate the effectiveness of Bothrofav generations at treating B. lanceolatus envenoming. During the first period of the study (2000-2010), 107 patients were treated with vials of antivenom produced in June 1991, while 282 envenomed patients were treated with vials of antivenom produced in January 2011 in the second study period (2011-2023). Despite timely antivenom administration, thrombotic complications reoccurred after an interval free of thrombotic events, and a timeframe analysis suggested that the clinical efficacy of Bothrofav declined after it reached its 10-year shelf-life. In of the case of an antivenom shortage due to the absence of regular batch production, no adverse effects were identified before the antivenom reached its 10-year shelf-life, which is beyond the accepted shelf-life for a liquid-formulation antivenom. While our study does not support the use of expired antivenom for potent, life-threatening B. lanceolatus envenoming, it can be a scientific message to public entities proving the necessity of new antivenom production for B. lanceolatus envenoming.


Assuntos
Antivenenos , Bothrops , Serpentes Peçonhentas , Humanos , Animais , Martinica , Resultado do Tratamento
5.
Artigo em Inglês | PAHO-IRIS | ID: phr-59158

RESUMO

The prevalence of snakebite envenoming and its understated impact on health and socioeconomic well-being in the Caribbean demand urgent attention. As a One Health challenge, this issue intersects human, animal, and environmental health, necessitating a multifaceted approach for comprehensive management. Despite the Caribbean’s rich biodiversity and cultural mosaic, there is a scarcity of data on the epidemiology and impact of snakebites in the region. This gap in knowledge, coupled with the absence of systematic records or survey-based studies, hampers the development of effective interventions. In countries such as Belize, Saint Lucia, and Trinidad and Tobago, among others, venomous snakes pose a significant threat, particularly to those in rural agricultural settings. Snakebite envenoming not only inflicts a direct health burden, evidenced by high rates of mortality and morbidity among humans, but also precipitates profound financial repercussions. The cost of clinical management for those affected and the loss of productivity due to long-term sequelae are considerable. Moreover, the impact on domestic animals, primarily livestock, translates into tangible economic losses for rural households, who rely on these animals for sustenance and income.


Assuntos
Mordeduras de Serpentes , Saúde Ambiental , Região do Caribe
6.
Sci Total Environ ; 912: 168886, 2024 Feb 20.
Artigo em Inglês | MEDLINE | ID: mdl-38016560

RESUMO

BACKGROUND: Sargassum invasion of Caribbean and American shorelines is a recurring environmental hazard. Potential health effects of long-term chronic exposure to sargassum gaseous emissions, notably hydrogen sulfide (H2S), are overlooked. H2S plays an important role in neurotransmission and is involved in generating and transmitting respiratory rhythm. Central sleep apnea (CSA) has been attributed to the depression of respiratory centers. OBJECTIVE: Evaluate the effects of exposure to sargassum-H2S on CSA. METHODS: This study, set in the Caribbean, describes the clinical and polysomnographic characteristics of individuals living and/or working in areas impacted by sargassum strandings, in comparison with non-exposed subjects. Environmental exposure was estimated by the closest ground H2S sensor. Multivariate linear regression was applied to analyze CSA changes according to cumulative H2S exposure over time. Effects of air pollution and other sargassum toxic compounds (NH3) on CSA were also controlled. RESULTS: Among the 685 study patients, 27 % were living and/or working in sargassum impacted areas. Compared with non-exposed patients, exposed ones had similar sleep apnea syndrome risk factors, but had increased levels of CSA events (expressed as absolute number or % of total sleep apnea). Multivariate regression retained only male gender and mean H2S concentration over a 6-month exposure period as independent predictors of an increase in CSA events. A minimal exposure length of 1 month generated a significant rise in CSA events, with the latter increasing proportionally with a cumulative increase in H2S concentration over time. CONCLUSION: This pioneer work highlights a potential effect of sargassum-H2S on the central nervous system, notably on the modulation of the activity of the brain's respiratory control center. These observations, jointly with previous studies from our group, constitute a body of evidence strongly supporting a deleterious effect of sargassum-H2S on the health of individuals chronically exposed to low to moderate concentration levels over time.


Assuntos
Sulfeto de Hidrogênio , Sargassum , Síndromes da Apneia do Sono , Apneia do Sono Tipo Central , Humanos , Masculino , Apneia do Sono Tipo Central/complicações , Sulfeto de Hidrogênio/toxicidade , Síndromes da Apneia do Sono/etiologia , Região do Caribe
8.
J Immunol ; 210(9): 1363-1371, 2023 05 01.
Artigo em Inglês | MEDLINE | ID: mdl-36946774

RESUMO

Insulin resistance is a compromised response to insulin in target tissues such as liver. Emerging evidence shows that vascular endothelial cells (ECs) are critical in mediating glucose metabolism. However, how liver ECs can regulate inflammation in the setting of insulin resistance is still unknown. Using genome-wide transcriptome analysis of ECs isolated from diabetic mice, we found enrichment of the genes involved in epidermal growth factor receptor (Egfr) signaling. In line with this, hepatic sinusoidal ECs in diabetic mice had elevated levels of Egfr expression. Interestingly, we found an increased number of hepatic myeloid cells, especially macrophages, and systemic glucose intolerance in Cdh5Cre/+Egfrfl/fl mice lacking Egfr in ECs compared with littermate control mice with type II diabetes. Egfr deficiency upregulated the expression of MCP-1 in hepatic sinusoidal ECs. This resulted in augmented monocyte recruitment and macrophage differentiation in Cdh5Cre/+Egfrfl/fl mice compared with littermate control mice as determined by a mouse model of parabiosis. Finally, MCP-1 neutralization and hepatic macrophage depletion in Cdh5Cre/+Egfrfl/fl mice resulted in a reduced number of hepatic macrophages and ameliorated glucose intolerance compared with the control groups. Collectively, these results demonstrate a protective endothelial Egfr signaling in reducing monocyte-mediated hepatic inflammation and glucose intolerance in type II diabetic mice.


Assuntos
Diabetes Mellitus Experimental , Diabetes Mellitus Tipo 2 , Intolerância à Glucose , Resistência à Insulina , Camundongos , Animais , Monócitos/metabolismo , Intolerância à Glucose/metabolismo , Células Endoteliais/metabolismo , Diabetes Mellitus Experimental/metabolismo , Fígado/metabolismo , Inflamação/metabolismo , Receptores ErbB/metabolismo , Camundongos Endogâmicos C57BL
11.
PLoS Negl Trop Dis ; 17(2): e0011083, 2023 02.
Artigo em Inglês | MEDLINE | ID: mdl-36854042

RESUMO

Snakebite envenomation is a relevant medical hazard in French Guiana and Martinique, two French territories in the Americas. All snakebite envenomations in Martinique are inflicted by the endemic viperid species Bothrops lanceolatus, whereas Bothrops atrox is responsible for the majority of snakebites in French Guiana, although other venomous snake species also occur in this South American territory. This review summarizes some of the key aspects of the natural history of these species, as well as of their venom composition, the main clinical manifestations of envenomations, and their treatment by antivenoms. B. atrox venom induces the typical set of clinical manifestations characteristic of Bothrops sp. venoms, i.e., local tissue damage and systemic alterations associated with coagulopathies, hemorrhage, hemodynamic alterations, and acute kidney injury. In the case of B. lanceolatus venom, in addition to some typical features of bothropic envenomation, a unique and severe thrombotic effect occurs in some patients. The pathogenesis of this effect remains unknown but may be related to the action of venom components and inflammatory mediators on endothelial cells in the vasculature. A monospecific antivenom has been successfully used in Martinique to treat envenomations by B. lanceolatus. In the case of French Guiana, a polyvalent antivenom has been used for some years, but it is necessary to assess the preclinical and clinical efficacy against viperid venoms in this country of other antivenoms manufactured in the Americas.


Assuntos
Bothrops , Venenos de Crotalídeos , Mordeduras de Serpentes , Animais , Mordeduras de Serpentes/tratamento farmacológico , Mordeduras de Serpentes/epidemiologia , Antivenenos/uso terapêutico , Guiana , Martinica , Células Endoteliais , Imunoterapia
12.
J Physiol ; 601(11): 2099-2120, 2023 06.
Artigo em Inglês | MEDLINE | ID: mdl-35661362

RESUMO

Visceral adipose tissue (VAT) is a metabolic organ known to regulate fat mass, and glucose and nutrient homeostasis. VAT is an active endocrine gland that synthesizes and secretes numerous bioactive mediators called 'adipocytokines/adipokines' into systemic circulation. These adipocytokines act on organs of metabolic importance like the liver and skeletal muscle. Multiple preclinical and in vitro studies showed strong evidence of the roles of adipocytokines in the regulation of metabolic disorders like diabetes, obesity and insulin resistance. Adipocytokines, such as adiponectin and omentin, are anti-inflammatory and have been shown to prevent atherogenesis by increasing nitric oxide (NO) production by the endothelium, suppressing endothelium-derived inflammation and decreasing foam cell formation. By inhibiting differentiation of vascular smooth muscle cells (VSMC) into osteoblasts, adiponectin and omentin prevent vascular calcification. On the other hand, adipocytokines like leptin and resistin induce inflammation and endothelial dysfunction that leads to vasoconstriction. By promoting VSMC migration and proliferation, extracellular matrix degradation and inflammatory polarization of macrophages, leptin and resistin increase the risk of atherosclerotic plaque vulnerability and rupture. Additionally, the plasma concentrations of these adipocytokines alter in ageing, rendering older humans vulnerable to cardiovascular disease. The disturbances in the normal physiological concentrations of these adipocytokines secreted by VAT under pathological conditions impede the normal functions of various organs and affect cardiovascular health. These adipokines could be used for both diagnostic and therapeutic purposes in cardiovascular disease.


Assuntos
Doenças Cardiovasculares , Leptina , Humanos , Resistina/metabolismo , Adiponectina/metabolismo , Doenças Cardiovasculares/metabolismo , Gordura Intra-Abdominal/metabolismo , Adipocinas/metabolismo , Inflamação/metabolismo , Tecido Adiposo/metabolismo
13.
Toxics ; 10(8)2022 Aug 05.
Artigo em Inglês | MEDLINE | ID: mdl-36006132

RESUMO

Rubigine® is an anti-rust stain remover containing fluorides which is believed to have been the cause of many deaths in Martinique. However, after the modification of its composition in 2006, serious poisoning from old formulas containing fluorides persisted. Our main objective was to determine the clinical characteristics and prognostic factors of these intoxications. Methods: Any patient admitted to the Martinique University Hospital for acute Rubigine® poisoning was included from 1 January 2000 to 31 December 2016. Usual demographic and clinical data were collected and comparisons between surviving and deceased patients made using a univariate analysis and logistic regression. Results: Fifty-five patients were included (mean age: 43 years; sex ratio M/F: 1.1), and the main clinical characteristics were: changes in electrocardiogram (ECG) (80%), digestive system disorders (75%), and neurological disorders (12%). The main features linked to death were the presence of hydrofluoric acid (p < 0.0001), age over 55 years (p = 0.01), hypocalcemia after the initial intravenous calcium supplementation (p = 0.0003), diarrhea (p < 0.0001), hypersialorrhea (p < 0.0001), myocardial excitability (p < 0.0001), and state of shock (p < 0.0001). Three patients required circulatory support by venous-arterial ECMO. Mortality was 10.9%. Conclusions: Rubigine® poisoning is responsible for significant morbidity and mortality. Fortunately, its incidence as well as mortality has sharply decreased in Martinique thanks to the measures taken by the French state. This retrospective work nevertheless shows that acute intoxication by the old formula of Rubigine® remains the main factor of poor prognosis.

14.
Toxins (Basel) ; 14(8)2022 08 03.
Artigo em Inglês | MEDLINE | ID: mdl-36006197

RESUMO

Ciguatera poisoning (CP) is one of the most common causes worldwide of marine poisoning associated with fish consumption from tropical areas. Its incidence is underreported. CP cases seem to increase with grouped cases reported during summer. Exposure to ciguatoxins, toxins responsible for CP with sodium-channel agonistic, voltage-gated potassium channel blocking, cholinergic, and adrenergic activities, may result in a large spectrum of manifestations. We aimed to describe the clinical characteristics, management, and outcome of CP in Martinique, French West Indies. We conducted an observational retrospective single-center study during six years (October 2012 to September 2018) including all CP patients managed by the prehospital medical services, admitted to the university hospital emergency department, or declared to the regional health agency. A total of 149 CP patients (81 females/63 males; median age, 46 years (interquartile range, 34-61)) were included. Acute features consisted in general (91%; mainly, myalgia pruritus, and asthenia), gastrointestinal (90%; mainly diarrhea, abdominal pain, and nausea), neurological (72%; mainly, paresthesia, dysgeusia, and impairment of hot/cold feeling), and cardiovascular manifestations (22%; bradycardia, hypotension, and heart conduction disorders). Management was supportive. No patient died but symptoms persisted in 40% of the 77 patients with follow-up at day 15. CP was mainly attributed to the ingestion of trevallies (59%), snappers (13%), and king mackerels (8%) with collective contaminations (71%). Unusual fish (tuna, salmon, and spider conchs) were suspected in rare cases. Ingestion of trevallies was associated with significantly higher persistent symptoms (odds ratio, 3.00; 95% confidence interval, (1.20-8.00); p = 0.03). CP incidence was 0.67 cases per 10,000 patient-years in Martinique over the study period. To conclude, CP represents an increasing public health issue in Martinique, as is the case in other Caribbean islands. Patients present usual but possibly life-threatening features. Outcome is excellent despite frequently prolonged manifestations.


Assuntos
Ciguatera , Ciguatoxinas , Animais , Ciguatera/epidemiologia , Ciguatoxinas/toxicidade , Feminino , Peixes , Humanos , Masculino , Martinica/epidemiologia , Estudos Retrospectivos , Índias Ocidentais
15.
Life Sci Alliance ; 5(11)2022 11.
Artigo em Inglês | MEDLINE | ID: mdl-35732465

RESUMO

Pulmonary hypertension (PH) is a vascular disease characterized by elevated pulmonary arterial pressure, leading to right ventricular failure and death. Pathogenic features of PH include endothelial apoptosis and vascular inflammation, which drive vascular remodeling and increased pulmonary arterial pressure. Re-analysis of the whole transcriptome sequencing comparing human pulmonary arterial endothelial cells (PAECs) isolated from PH and control patients identified AREG, which encodes Amphiregulin, as a key endothelial survival factor. PAECs from PH patients and mice exhibited down-regulation of AREG and its receptor epidermal growth factor receptor (EGFR). Moreover, the deficiency of AREG and EGFR in ECs in vivo and in vitro heightened inflammatory leukocyte recruitment, cytokine production, and endothelial apoptosis, as well as diminished angiogenesis. Correspondingly, hypoxic mice lacking Egfr in ECs (cdh5 cre/+ Egfr fl/fl) displayed elevated RVSP and pulmonary remodeling. Computational analysis identified NCOA6, PHB2, and RRP1B as putative genes regulating AREG in endothelial cells. The master transcription factor of hypoxia HIF-1⍺ binds to the promoter regions of these genes and up-regulates their expression in hypoxia. Silencing of these genes in cultured PAECs decreased inflammation and apoptosis, and increased angiogenesis in hypoxic conditions. Our pathway analysis and gene silencing experiments revealed that BCL2-associated agonist of cell death (BAD) is a downstream mediator of AREG BAD silencing in ECs lacking AREG mitigated inflammation and apoptosis, and suppressed tube formation. In conclusion, loss of Amphiregulin and its receptor EGFR in PH is a crucial step in the pathogenesis of PH, promoting pulmonary endothelial cell death, influx of inflammatory myeloid cells, and vascular remodeling.


Assuntos
Anfirregulina , Hipertensão Pulmonar , Anfirregulina/genética , Anfirregulina/metabolismo , Animais , Apoptose/genética , Células Endoteliais/metabolismo , Receptores ErbB/genética , Humanos , Hipertensão Pulmonar/genética , Hipertensão Pulmonar/patologia , Hipóxia/genética , Hipóxia/metabolismo , Inflamação/genética , Inflamação/metabolismo , Camundongos , Remodelação Vascular
16.
Front Immunol ; 13: 882484, 2022.
Artigo em Inglês | MEDLINE | ID: mdl-35634304

RESUMO

Although it is well known that hypoxia incites unleashed cellular inflammation, the mechanisms of exaggerated cellular inflammation in hypoxic conditions are not known. We observed augmented proliferation of hematopoietic stem and progenitor cells (HSPC), precursors of inflammatory leukocytes, in mice under hypoxia. Consistently, a transcriptomic analysis of human HSPC exposed to hypoxic conditions revealed elevated expression of genes involved in progenitor proliferation and differentiation. Additionally, bone marrow cells in mice expressed high amount of vascular endothelial growth factor (VEGF), and HSPC elevated VEGF receptor 1 (VEGFr1) and its target genes in hypoxic conditions. In line with this, VEGFr1 blockade in vivo and in vitro decreased HSPC proliferation and attenuated inflammation. In silico and ChIP experiments demonstrated that HIF-1α binds to the promoter region of VEGFR1. Correspondingly, HIF1a silencing decreased VEGFr1 expression in HSPC and diminished their proliferation. These results indicate that VEGF signaling in HSPC is an important mediator of their proliferation and differentiation in hypoxia-induced inflammation and represents a potential therapeutic target to prevent aberrant inflammation in hypoxia-associated diseases.


Assuntos
Células-Tronco Hematopoéticas , Hipóxia , Fator A de Crescimento do Endotélio Vascular , Receptor 1 de Fatores de Crescimento do Endotélio Vascular , Animais , Diferenciação Celular/genética , Proliferação de Células/genética , Células-Tronco Hematopoéticas/citologia , Humanos , Hipóxia/genética , Subunidade alfa do Fator 1 Induzível por Hipóxia/genética , Subunidade alfa do Fator 1 Induzível por Hipóxia/metabolismo , Inflamação , Camundongos , Fator A de Crescimento do Endotélio Vascular/genética , Fator A de Crescimento do Endotélio Vascular/metabolismo , Receptor 1 de Fatores de Crescimento do Endotélio Vascular/genética , Receptor 1 de Fatores de Crescimento do Endotélio Vascular/metabolismo
17.
Nat Aging ; 2(2): 140-154, 2022 02.
Artigo em Inglês | MEDLINE | ID: mdl-37117763

RESUMO

Accumulation of senescent cells with age is an important driver of aging and age-related diseases. However, the mechanisms and signaling pathways that regulate senescence remain elusive. In this report, we performed post-genome-wide association studies (GWAS) functional studies on the CDKN2A/B locus, a locus known to be associated with multiple age-related diseases and overall human lifespan. We demonstrate that transcription factor CUX1 (Cut-Like Homeobox 1) specifically binds to an atherosclerosis-associated functional single-nucleotide polymorphism (fSNP) (rs1537371) within the locus and regulates the CDKN2A/B-encoded proteins p14ARF, p15INK4b and p16INK4a and the antisense noncoding RNA in the CDK4 (INK4) locus (ANRIL) in endothelial cells (ECs). Endothelial CUX1 expression correlates with telomeric length and is induced by both DNA-damaging agents and oxidative stress. Moreover, induction of CUX1 expression triggers both replicative and stress-induced senescence via activation of p16INK4a expression. Thus, our studies identify CUX1 as a regulator of p16INK4a-dependent endothelial senescence and a potential therapeutic target for atherosclerosis and other age-related diseases.


Assuntos
Aterosclerose , Inibidor p16 de Quinase Dependente de Ciclina , Humanos , Aterosclerose/genética , Senescência Celular/genética , Inibidor de Quinase Dependente de Ciclina p15/genética , Inibidor p16 de Quinase Dependente de Ciclina/genética , Células Endoteliais/metabolismo , Estudo de Associação Genômica Ampla , Proteínas de Homeodomínio/genética , Proteínas Repressoras/genética , Fatores de Transcrição/genética
18.
Cell Mol Immunol ; 18(2): 374-384, 2021 02.
Artigo em Inglês | MEDLINE | ID: mdl-33420357

RESUMO

Myeloid cells, such as neutrophils, are produced in the bone marrow in high quantities and are important in the pathogenesis of vascular diseases such as pulmonary hypertension (PH). Although neutrophil recruitment into sites of inflammation has been well studied, the mechanisms of neutrophil egress from the bone marrow are not well understood. Using computational flow cytometry, we observed increased neutrophils in the lungs of patients and mice with PH. Moreover, we found elevated levels of IL-6 in the blood and lungs of patients and mice with PH. We observed that transgenic mice overexpressing Il-6 in the lungs displayed elevated neutrophil egress from the bone marrow and exaggerated neutrophil recruitment to the lungs, resulting in exacerbated pulmonary vascular remodeling, and dysfunctional hemodynamics. Mechanistically, we found that IL-6-induced neutrophil egress from the bone marrow was dependent on interferon regulatory factor 4 (IRF-4)-mediated CX3CR1 expression in neutrophils. Consequently, Cx3cr1 genetic deficiency in hematopoietic cells in Il-6-transgenic mice significantly reduced neutrophil egress from bone marrow and decreased neutrophil counts in the lungs, thus ameliorating pulmonary remodeling and hemodynamics. In summary, these findings define a novel mechanism of IL-6-induced neutrophil egress from the bone marrow and reveal a new therapeutic target to curtail neutrophil-mediated inflammation in pulmonary vascular disease.


Assuntos
Células da Medula Óssea/patologia , Hipertensão Pulmonar/patologia , Inflamação/complicações , Interleucina-6/metabolismo , Pulmão/patologia , Infiltração de Neutrófilos , Neutrófilos/imunologia , Animais , Células da Medula Óssea/imunologia , Células da Medula Óssea/metabolismo , Feminino , Hipertensão Pulmonar/imunologia , Hipertensão Pulmonar/metabolismo , Inflamação/imunologia , Inflamação/patologia , Interleucina-6/genética , Pulmão/imunologia , Pulmão/metabolismo , Masculino , Camundongos , Camundongos Endogâmicos C57BL , Camundongos Knockout , Camundongos Transgênicos
19.
Clin Toxicol (Phila) ; 59(3): 215-223, 2021 Mar.
Artigo em Inglês | MEDLINE | ID: mdl-32633580

RESUMO

BACKGROUND: Since 2011, there have been ongoing massive unexplained increases of sargassum seaweed strandings along the coastlines of Caribbean countries. The objective of our study was to describe the clinical characteristics of patients exposed to noxious emissions of decomposing sargassum seaweed. METHODS: This observational study included patients from January 2018 to December 2018 for complaints attributed to decomposing sargassum seaweed. History and geographical characteristics of sargassum seaweed strandings as well as detection of ambient air hydrogen sulfide (H2S) levels were documented during the inclusion period. FINDINGS: A total of 154 patients were included. Mean exposure period was 3 months. Neurological (80%), digestive (77%) and respiratory (69%) disorders were the most frequent reasons for medical visit. Temporal distribution of medical visits was related to history of strandings. Geographical origins of patients were consistent with the most impacted areas of strandings as well as the most elevated ambient air H2S levels. INTERPRETATION: The toxicological syndrome induced by sargassum seaweed exposure is close to the toxidrome associated with acute H2S exposure in the range of 0-10 ppm. Our study suggests that patients living in massive stranding areas may be exposed to H2S > 5 ppm for 50 days per year.


Assuntos
Exposição Ambiental/efeitos adversos , Proliferação Nociva de Algas , Sulfeto de Hidrogênio/efeitos adversos , Sargassum , Alga Marinha , Adolescente , Adulto , Idoso , Idoso de 80 Anos ou mais , Região do Caribe , Criança , Pré-Escolar , Exposição Ambiental/estatística & dados numéricos , Feminino , Humanos , Masculino , Martinica/epidemiologia , Pessoa de Meia-Idade , Tempo (Meteorologia) , Adulto Jovem
20.
Sci Transl Med ; 12(553)2020 07 22.
Artigo em Inglês | MEDLINE | ID: mdl-32718989

RESUMO

Patients with insulin resistance have high risk of cardiovascular disease such as myocardial infarction (MI). However, it is not known whether MI can initiate or aggravate insulin resistance. We observed that patients with ST-elevation MI and mice with MI had de novo hyperglycemia and features of insulin resistance, respectively. In mouse models of both myocardial and skeletal muscle injury, we observed that the number of visceral adipose tissue (VAT)-resident macrophages decreased because of apoptosis after these distant organ injuries. Patients displayed a similar decrease in VAT-resident macrophage numbers and developed systemic insulin resistance after ST-elevation MI. Loss of VAT-resident macrophages after MI injury led to systemic insulin resistance in non-diabetic mice. Danger signaling-associated protein high mobility group box 1 was released by the dead myocardium after MI in rodents and triggered macrophage apoptosis via Toll-like receptor 4. The VAT-resident macrophage population in the steady state in mice was transcriptomically distinct from macrophages in the brain, skin, kidney, bone marrow, lungs, and liver and was derived from hematopoietic progenitor cells just after birth. Mechanistically, VAT-resident macrophage apoptosis and de novo insulin resistance in mouse models of MI were linked to diminished concentrations of macrophage colony-stimulating factor and adiponectin. Collectively, these findings demonstrate a previously unappreciated role of adipose tissue-resident macrophages in sensing remote organ injury and promoting MI pathogenesis.


Assuntos
Transplante de Células-Tronco Hematopoéticas , Resistência à Insulina , Infarto do Miocárdio , Tecido Adiposo , Animais , Apoptose , Humanos , Macrófagos , Camundongos , Camundongos Endogâmicos C57BL
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