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1.
Photobiomodul Photomed Laser Surg ; 38(4): 195-205, 2020 Apr.
Artigo em Inglês | MEDLINE | ID: mdl-32301669

RESUMO

Objective: The objective of this retrospective review was to examine the impact that adding photobiomodulation therapy (PBMt) to rehabilitation therapy had on the pathology of degenerative myelopathy (DM) in canine patients. Background: Canine DM is a progressive, fatal neurodegenerative disease for which there exists a dearth of effective treatments, limiting clinicians to pursue symptom palliation. Methods: Clinical records of dogs referred for presumed DM to a specialty rehabilitation facility were screened for patients meeting study criteria. Qualifying patients were divided into two groups: Protocol A (PTCL-A) and Protocol B (PTCL-B) group, based on the PBMt protocol used. Data related to demographics, diagnostics, rehabilitation protocols, and progression of clinical signs were collected. Data were analyzed to determine differences in outcomes between the two treated groups and historical data expectations, as given by a previously published study. Results: The times between symptom onset and euthanasia of dogs in the PTCL-B group: 38.2 ± 14.67 months (mean ± SD), were significantly longer than those of dogs in the PTCL-A group: 11.09 ± 2.68 months. Similarly, the times between symptom onset and nonambulatory paresis (NAP) or paralysis of dogs in the PTCL-B group: 31.76 ± 12.53 months, were significantly longer than those of dogs in the PTCL-A group: 8.79 ± 1.60 months. Further, Kaplan-Meier survival analysis showed that the times from symptom onset to NAP of dogs in the PTCL-B group were significantly longer than those of dogs in the PTCL-A group (Mantel-Cox Log Rank statistic = 20.434, p < 0.05) or the historical data group (Mantel-Cox Log Rank statistic = 16.334, p < 0.05). Conclusions: The data reviewed show significantly slower disease progression-longer survival times-for patients in the PTCL-B group than those in the PTCL-A group or published historical data. Further studies are warranted.

2.
Front Immunol ; 11: 558, 2020.
Artigo em Inglês | MEDLINE | ID: mdl-32308656

RESUMO

Accumulation of activated neutrophils at the feto-maternal interface is a defining hallmark of intrauterine inflammation (IUI) that might trigger an excessive immune response during pregnancy. Mechanisms responsible of this massive neutrophil recruitment are poorly investigated. We have previously showed that intraamniotic injection of LPS in rhesus macaques induced a neutrophil predominant inflammatory response similar to that seen in human IUI. Here, we demonstrate that anti-TNF antibody (Adalimumab) inhibited ~80% of genes induced by LPS involved in inflammatory signaling and innate immunity in chorio-decidua neutrophils. Consistent with the gene expression data, TNF-blockade decreased LPS-induced neutrophil accumulation and activation at the feto-maternal interface. We also observed a reduction in IL-6 and other pro-inflammatory cytokines but not prostaglandins concentrations in the amniotic fluid. Moreover, TNF-blockade decreased mRNA expression of inflammatory cytokines in the chorio-decidua but not in the uterus, suggesting that inhibition of TNF-signaling decreased the inflammation in a tissue-specific manner within the uterine compartment. Taken together, our results demonstrate a predominant role for TNF-signaling in modulating the neutrophilic infiltration at the feto-maternal interface during IUI and suggest that blockade of TNF-signaling could be considered as a therapeutic approach for IUI, the major leading cause of preterm birth.

3.
Br J Pharmacol ; 177(2): 360-371, 2020 Jan.
Artigo em Inglês | MEDLINE | ID: mdl-31655023

RESUMO

BACKGROUND AND PURPOSE: 5-Oxo-6,8,11,14-eicosatetraenoic acid (5-oxo-ETE), acting via the OXE receptor, is unique among 5-lipoxygenase products in its ability to directly induce human eosinophil migration, suggesting its involvement in eosinophilic diseases. To address this hypothesis, we synthesized selective indole-based OXE receptor antagonists. Because rodents lack an OXE receptor orthologue, we sought to determine whether these antagonists could attenuate allergen-induced skin eosinophilia in sensitized monkeys. EXPERIMENTAL APPROACH: In a pilot study, cynomolgus monkeys with environmentally acquired sensitivity to Ascaris suum were treated orally with the "first-generation" OXE antagonist 230 prior to intradermal injection of 5-oxo-ETE or Ascaris extract. Eosinophils were evaluated in punch biopsy samples taken 6 or 24 hr later. We subsequently treated captive-bred rhesus monkeys sensitized to house dust mite (HDM) allergen with a more recently developed OXE antagonist, S-Y048, and evaluated its effects on dermal eosinophilia induced by either 5-oxo-ETE or HDM. KEY RESULTS: In a pilot experiment, both 5-oxo-ETE and Ascaris extract induced dermal eosinophilia in cynomolgus monkeys, which appeared to be reduced by 230. Subsequently, we found that the related OXE antagonist S-Y048 is a highly potent inhibitor of 5-oxo-ETE-induced activation of rhesus monkey eosinophils in vitro and has a half-life in plasma of about 6 hr after oral administration. S-Y048 significantly inhibited eosinophil infiltration into the skin in response to both intradermally administered 5-oxo-ETE and HDM. CONCLUSIONS AND IMPLICATIONS: 5-Oxo-ETE may play an important role in allergen-induced eosinophilia. Blocking its effects with S-Y048 may provide a novel therapeutic approach for eosinophilic diseases.

4.
J Allergy Clin Immunol ; 145(1): 312-323, 2020 Jan.
Artigo em Inglês | MEDLINE | ID: mdl-31627909

RESUMO

BACKGROUND: Ozone (O3) inhalation elicits airway inflammation and impairs treatment responsiveness in asthmatic patients. The underlying immune mechanisms have been difficult to study because of the lack of relevant experimental models. Rhesus macaques spontaneously have asthma and have a similar immune system to human subjects. OBJECTIVES: We sought to investigate mucosal immune changes after O3 inhalation in a clinically relevant nonhuman primate asthma model and to study the effects of an antioxidant synthetic lignan (synthetic secoisolariciresinol diglucoside [LGM2605]). METHODS: A cohort of macaques (n = 17) previously characterized with airway hyperreactivity (AHR) to methacholine was assessed (day 1). Macaques were treated (orally) with LGM2605 (25 mg/kg) or placebo twice per day for 7 days, exposed to 0.3 ppm O3 or air for 6 hours (on day 7), and studied 12 hours later (day 8). Lung function, blood and bronchoalveolar lavage (BAL) fluid immune cell profile, and bronchial brushing and blood cell mRNA expression were assessed. RESULTS: O3 induced significant BAL fluid neutrophilia and eosinophilia and increased AHR and expression of IL6 and IL25 mRNA in the airway epithelium together with increased BAL fluid group 2 innate lymphoid cell (ILC2s), CD1c+ myeloid dendritic cell, and CD4+ T-cell counts and diminished surfactant protein D expression. Although LGM2605 attenuated some of the immune and inflammatory changes, it completely abolished O3-induced AHR. CONCLUSION: ILC2s, CD1c+ myeloid dendritic cells, and CD4+ T cells are selectively involved in O3-induced asthma exacerbation. The inflammatory changes were partially prevented by antioxidant pretreatment with LGM2605, which had an unexpectedly disproportionate protective effect on AHR.

5.
MCN Am J Matern Child Nurs ; 45(2): 74-81, 2020.
Artigo em Inglês | MEDLINE | ID: mdl-31804228

RESUMO

As part of our special topics issue on inpatient maternity care, experts were asked to offer their thoughts about the main issues putting mothers and babies at risk in the maternity inpatient setting and what quality and safety practices may be beneficial in keeping them safe from harm. Each of the experts has a unique perspective. Loraine O'Neill was one of the original perinatal patient safety nurses who were established as part of an effort by a professional liability company to promote patient safety in birthing hospitals that they covered in several states (). She now is the perinatal patient safety officer in a large academic medical center in New York City. Lisa Miller is a well-known expert on fetal assessment during labor, certified nurse midwife, attorney, educator, patient safety expert, and editor of a popular fetal monitoring textbook (). She has taught fetal monitoring to nurses, midwives, and physicians in multidisciplinary groups all over the United States and consulted on numerous patient safety initiatives. Annie Rohan is a dual-certified neonatal and pediatric nurse practitioner with a 30-plus year clinical practice career with infants, children, and families facing critical and chronic illness. She is currently a healthcare researcher, and oversees advanced practice and doctoral nursing programs at SUNY Downstate Health Sciences University.

6.
PLoS One ; 14(9): e0222817, 2019.
Artigo em Inglês | MEDLINE | ID: mdl-31536601

RESUMO

Antenatal corticosteroids (ACS) are standard of care for women at risk of preterm delivery, although choice of drug, dose or route have not been systematically evaluated. Further, ACS are infrequently used in low resource environments where most of the mortality from prematurity occurs. We report proof of principle experiments to test betamethasone-phosphate (Beta-P) or dexamethasone-phosphate (Dex-P) given orally in comparison to the clinical treatment with the intramuscular combination drug beta-phosphate plus beta-acetate in a Rhesus Macaque model. First, we performed pharmacokinetic studies in non-pregnant monkeys to compare blood levels of the steroids using oral dosing with Beta-P, Dex-P and an effective maternal intramuscular dose of the beta-acetate component of the clinical treatment. We then evaluated maternal and fetal blood steroid levels with limited fetal sampling under ultrasound guidance in pregnant macaques. We found that oral Beta is more slowly cleared from plasma than oral Dex. The blood levels of both drugs were lower in maternal plasma of pregnant than in non-pregnant macaques. Using the pharmacokinetic data, we treated groups of 6-8 pregnant monkeys with oral Beta-P, oral Dex-P, or the maternal intramuscular clinical treatment and saline controls and measured pressure-volume curves to assess corticosteroid effects on lung maturation at 5d. Oral Beta-P improved the pressure-volume curves similarly to the clinical treatment. Oral Dex-P gave more variable and nonsignificant responses. We then compared gene expression in the fetal lung, liver and hippocampus between oral Beta-P and the clinical treatment by RNA-sequencing. The transcriptomes were largely similar with small gene expression differences in the lung and liver, and no differences in the hippocampus between the groups. As proof of principle, ACS therapy can be effective using inexpensive and widely available oral drugs. Clinical dosing strategies must carefully consider the pharmacokinetics of oral Beta-P or Dex-P to minimize fetal exposure while achieving the desired treatment responses.


Assuntos
Corticosteroides/administração & dosagem , Betametasona/análogos & derivados , Dexametasona/análogos & derivados , Modelos Animais , Cuidado Pré-Natal/métodos , Administração Oral , Corticosteroides/sangue , Corticosteroides/farmacocinética , Animais , Betametasona/administração & dosagem , Betametasona/sangue , Betametasona/farmacocinética , Dexametasona/administração & dosagem , Dexametasona/sangue , Dexametasona/farmacocinética , Feminino , Maturidade dos Órgãos Fetais/efeitos dos fármacos , Maturidade dos Órgãos Fetais/genética , Perfilação da Expressão Gênica/métodos , Regulação da Expressão Gênica no Desenvolvimento/efeitos dos fármacos , Hipocampo/efeitos dos fármacos , Hipocampo/embriologia , Humanos , Injeções Intramusculares , Fígado/efeitos dos fármacos , Fígado/embriologia , Fígado/metabolismo , Pulmão/efeitos dos fármacos , Pulmão/embriologia , Pulmão/metabolismo , Macaca mulatta , Gravidez , Nascimento Prematuro/genética , Nascimento Prematuro/metabolismo
7.
Sci Rep ; 9(1): 9039, 2019 06 21.
Artigo em Inglês | MEDLINE | ID: mdl-31227752

RESUMO

Antenatal corticosteroids (ANS) are the major intervention to decrease respiratory distress syndrome and mortality from premature birth and are standard of care. The use of ANS is expanding to include new indications and gestational ages, although the recommended dosing was never optimized. The most widely used treatment is two intramuscular doses of a 1:1 mixture of betamethasone-phosphate (Beta-P) and betamethasone-acetate (Beta-Ac) - the clinical drug. We tested in a primate model the efficacy of the slow release Beta-Ac alone for enhancing fetal lung maturation and to reduce fetal corticosteroid exposure and potential toxic effects. Pregnant rhesus macaques at 127 days of gestation (80% of term) were treated with either the clinical drug (0.25 mg/kg) or Beta-Ac (0.125 mg/kg). Beta-Ac alone increased lung compliance and surfactant concentration in the fetal lung equivalently to the clinical drug. By transcriptome analyses the early suppression of genes associated with immune responses and developmental pathways were less affected by Beta-Ac than the clinical drug. Promoter and regulatory analysis prediction identified differentially expressed genes targeted by the glucocorticoid receptor in the lung. At 5 days the clinical drug suppressed genes associated with neuronal development and differentiation in the fetal hippocampus compared to control, while low dose Beta-Ac alone did not. A low dose ANS treatment with Beta-Ac should be assessed for efficacy in human trials.

8.
Bioorg Med Chem ; 27(8): 1456-1478, 2019 04 15.
Artigo em Inglês | MEDLINE | ID: mdl-30858025

RESUMO

With the goal of discovering more selective anti-inflammatory drugs, than COX inhibitors, to attenuate prostaglandin signaling, a fragment-based screen of hematopoietic prostaglandin D synthase was performed. The 76 crystallographic hits were sorted into similar groups, with the 3-cyano-quinoline 1a (FP IC50 = 220,000 nM, LE = 0.43) being a potent member of the 6,6-fused heterocyclic cluster. Employing SAR insights gained from structural comparisons of other H-PGDS fragment binding mode clusters, the initial hit 1a was converted into the 70-fold more potent quinoline 1d (IC50 = 3,100 nM, LE = 0.49). A systematic substitution of the amine moiety of 1d, utilizing structural information and array chemistry, with modifications to improve inhibitor stability, resulted in the identification of the 300-fold more active H-PGDS inhibitor tool compound 1bv (IC50 = 9.9 nM, LE = 0.42). This selective inhibitor exhibited good murine pharmacokinetics, dose-dependently attenuated PGD2 production in a mast cell degranulation assay and should be suitable to further explore H-PGDS biology.


Assuntos
Inibidores Enzimáticos/química , Inibidores Enzimáticos/farmacologia , Oxirredutases Intramoleculares/antagonistas & inibidores , Lipocalinas/antagonistas & inibidores , Quinolinas/química , Quinolinas/farmacologia , Animais , Descoberta de Drogas , Inibidores Enzimáticos/farmacocinética , Humanos , Oxirredutases Intramoleculares/química , Oxirredutases Intramoleculares/metabolismo , Lipocalinas/química , Lipocalinas/metabolismo , Masculino , Camundongos Endogâmicos C57BL , Simulação de Acoplamento Molecular , Quinolinas/farmacocinética
9.
JAMA Intern Med ; 179(4): 479-488, 2019 04 01.
Artigo em Inglês | MEDLINE | ID: mdl-30776079

RESUMO

Importance: Group B Streptococcus (GBS) is an important cause of invasive bacterial disease. Previous studies have shown a substantial and increasing burden of GBS infections among nonpregnant adults, particularly older adults and those with underlying medical conditions. Objective: To update trends of invasive GBS disease among US adults using population-based surveillance data. Design, Setting, and Participants: In this population-based surveillance study, a case was defined as isolation of GBS from a sterile site between January 1, 2008, and December 31, 2016. Demographic and clinical data were abstracted from medical records. Rates were calculated using US Census data. Antimicrobial susceptibility testing and serotyping were performed on a subset of isolates. Case patients were residents of 1 of 10 catchment areas of the Active Bacterial Core surveillance (ABCs) network, representing approximately 11.5% of the US adult population. Patients were included in the study if they were nonpregnant, were 18 years or older, were residents of an ABCs catchment site, and had a positive GBS culture from a normally sterile body site. Main Outcomes and Measures: Trends in GBS cases overall and by demographic characteristics (sex, age, and race), underlying clinical conditions of patients, and isolate characteristics are described. Results: The ABCs network detected 21 250 patients with invasive GBS among nonpregnant adults from 2008 through 2016. The GBS incidence in this population increased from 8.1 cases per 100 000 population in 2008 to 10.9 in 2016 (P = .002 for trend). There were 3146 cases reported in 2016 (59% male; median age, 64 years; age range, 18-103 years). The GBS incidence was higher among men than women and among blacks than whites and increased with age. Projected to the US population, an estimated 27 729 cases of invasive disease and 1541 deaths occurred in the United States in 2016. Ninety-five percent of cases in 2016 occurred in someone with at least 1 underlying condition, most commonly obesity (53.9%) and diabetes (53.4%). Resistance to clindamycin increased from 37.0% of isolates in 2011 to 43.2% in 2016 (P = .02). Serotypes Ia, Ib, II, III, and V accounted for 86.4% of isolates in 2016; serotype IV increased from 4.7% in 2008 to 11.3% in 2016 (P < .001 for trend). Conclusions and Relevance: The public health burden of invasive GBS disease among nonpregnant adults is substantial and continues to increase. Chronic diseases, such as obesity and diabetes, may contribute.


Assuntos
Vigilância da População , Saúde Pública , Infecções Estreptocócicas/epidemiologia , Streptococcus agalactiae/isolamento & purificação , Adolescente , Adulto , Distribuição por Idade , Idoso , Idoso de 80 Anos ou mais , Feminino , Humanos , Incidência , Masculino , Pessoa de Meia-Idade , Estudos Retrospectivos , Distribuição por Sexo , Infecções Estreptocócicas/microbiologia , Estados Unidos/epidemiologia , Adulto Jovem
10.
Am J Respir Cell Mol Biol ; 60(6): 687-694, 2019 06.
Artigo em Inglês | MEDLINE | ID: mdl-30571139

RESUMO

Mucus overproduction is a major contributor to morbidity and mortality in asthma. Mucus overproduction is induced by orchestrated actions of multiple factors that include inflammatory cytokines and γ-aminobutyric acid (GABA). GABA is produced only by pulmonary neuroendocrine cells (PNECs) in the mouse lung. Recent studies in a neonatal mouse model of allergic inflammation have shown that PNECs play an essential role in mucus overproduction by GABA hypersecretion. Whether PNECs mediate dysregulated GABA signaling for mucus overproduction in asthma is unknown. In this study, we characterized the cellular source of GABA in the lungs of nonhuman primates and humans and assessed GABA secretion and signaling in primate disease models. We found that like in mice, PNECs were the major source of GABA in primate lungs. In addition, an infant nonhuman primate model of asthma exhibited an increase in GABA secretion. Furthermore, subjects with asthma had elevated levels of expression of a subset of GABA type α (GABAα) and type ß (GABAß) receptors in airway epithelium compared with those of healthy control subjects. Last, employing a normal human bronchial epithelial cell model of preinduced mucus overproduction, we showed pharmaceutical blockade of GABAα and GABAß receptor signaling reversed the effect of IL-13 on MUC5AC gene expression and goblet cell proliferation. Together, our data demonstrate an evolutionarily conserved intraepithelial GABA signaling that, in concert with IL-13, plays an essential role in mucus overproduction. Our findings may offer new strategies to ameliorate mucus overproduction in patients with asthma by targeting PNEC secretion and GABA signaling.


Assuntos
Células Caliciformes/patologia , Pulmão/patologia , Células Neuroendócrinas/metabolismo , Ácido gama-Aminobutírico/metabolismo , Lesão Pulmonar Aguda/patologia , Animais , Asma/patologia , Brônquios/patologia , Modelos Animais de Doenças , Células Epiteliais/metabolismo , Humanos , Hiperplasia , Interleucina-13/metabolismo , Macaca mulatta , Muco/metabolismo , Receptores de GABA/metabolismo , Transdução de Sinais
14.
JCI Insight ; 3(6)2018 03 22.
Artigo em Inglês | MEDLINE | ID: mdl-29563340

RESUMO

Neutrophil infiltration of the chorioamnion-decidua tissue at the maternal-fetal interface (chorioamnionitis) is a leading cause of prematurity, fetal inflammation, and perinatal mortality. We induced chorioamnionitis in preterm rhesus macaques by intraamniotic injection of LPS. Here, we show that, during chorioamnionitis, the amnion upregulated phospho-IRAK1-expressed neutrophil chemoattractants CXCL8 and CSF3 in an IL-1-dependent manner. IL-1R blockade decreased chorio-decidua neutrophil accumulation, neutrophil activation, and IL-6 and prostaglandin E2 concentrations in the amniotic fluid. Neutrophils accumulating in the chorio-decidua had increased survival mediated by BCL2A1, and IL-1R blockade also decreased BCL2A1+ chorio-decidua neutrophils. Readouts for inflammation in a cohort of women with preterm delivery and chorioamnionitis were similar to findings in the rhesus macaques. IL-1 is a potential therapeutic target for chorioamnionitis and associated morbidities.


Assuntos
Corioamnionite/imunologia , Corioamnionite/metabolismo , Decídua/imunologia , Inflamação/imunologia , Interleucina-1/metabolismo , Infiltração de Neutrófilos/imunologia , Transdução de Sinais , Âmnio/metabolismo , Animais , Apoptose , Corioamnionite/genética , Corioamnionite/patologia , Córion , Citocinas/metabolismo , Decídua/efeitos dos fármacos , Decídua/patologia , Feminino , Humanos , Recém-Nascido , Quinases Associadas a Receptores de Interleucina-1/metabolismo , Interleucina-8/metabolismo , Lipopolissacarídeos/efeitos adversos , Macaca mulatta , Antígenos de Histocompatibilidade Menor/metabolismo , Neutrófilos/imunologia , Gravidez , Proteínas Proto-Oncogênicas c-bcl-2/metabolismo , Receptores de Interleucina-1/metabolismo
15.
ACS Med Chem Lett ; 9(2): 120-124, 2018 Feb 08.
Artigo em Inglês | MEDLINE | ID: mdl-29456799

RESUMO

Biaryl amides as new RORγt modulators were discovered. The crystal structure of biaryl amide agonist 6 in complex with RORγt ligand binding domain (LBD) was resolved, and both "short" and "long" inverse agonists were obtained by removing from 6 or adding to 6 a proper structural moiety. While "short" inverse agonist (8) recruits a corepressor peptide and dispels a coactivator peptide, "long" inverse agonist (9) dispels both. The two types of inverse agonists can be utilized as potential tools to study mechanisms of Th17 transcriptional network inhibition and related disease biology.

16.
J Perinat Neonatal Nurs ; 32(1): 53-58, 2018.
Artigo em Inglês | MEDLINE | ID: mdl-29373418

RESUMO

Litigation in perinatal nursing represents a disproportionate share of indemnity payouts and results in excessive psychological stress. Testimony at deposition or trial can be challenging for clinicians; little is taught in training or postgraduate education regarding litigation. Nurses, midwives, and physicians can effectively navigate the deposition process and prepare for trial testimony by understanding the plaintiff's goals, recognizing the role of documentation, and becoming familiar with various plaintiff's strategies including reptile theory. Knowledge of psychological concepts such as confirmation bias and cognitive dissonance may assist clinicians in responding to plaintiff's lines of questioning. Deposition preparation is crucial to the defense and requires active participation on the part of clinicians; it may include mock deposition or use of simulation laboratories. Common mistakes in deposition may be avoided with foresight and anticipatory planning by clinicians working closely with risk managers and defense attorneys. This article provides an overview of the deposition process, including the plaintiff's goals and common approaches, as well as the role of documentation and common errors of deponents.


Assuntos
Prova Pericial/métodos , Enfermagem Neonatal/legislação & jurisprudência , Assistência Perinatal/legislação & jurisprudência , Humanos , Má Conduta Profissional/legislação & jurisprudência , Psicologia
17.
ILAR J ; 58(2): 269-280, 2017 12 01.
Artigo em Inglês | MEDLINE | ID: mdl-29216343

RESUMO

The respiratory system consists of an integrated network of organs and structures that primarily function for gas exchange. In mammals, oxygen and carbon dioxide are transmitted through a complex respiratory tract, consisting of the nasal passages, pharynx, larynx, and lung. Exposure to ambient air throughout the lifespan imposes vulnerability of the respiratory system to environmental challenges that can contribute toward development of disease. The importance of the respiratory system to human health is supported by statistics from the Centers for Disease Control and Prevention; in 2015, chronic lower respiratory diseases were the third leading cause of death in the United States. In light of the significant mortality associated with respiratory conditions that afflict all ages of the human population, this review will focus on basic and preclinical research conducted in nonhuman primate models of respiratory disease. In comparison with other laboratory animals, the nonhuman primate lung most closely resembles the human lung in structure, physiology, and mucosal immune mechanisms. Studies defining the influence of inhaled microbes, pollutants, or allergens on the nonhuman primate lung have provided insight on disease pathogenesis, with the potential for elucidation of molecular targets leading to new treatment modalities. Vaccine trials in nonhuman primates have been crucial for confirmation of safety and protective efficacy against infectious diseases of the lung in a laboratory animal model that recapitulates pathology observed in humans. In looking to the future, nonhuman primate models of respiratory diseases will continue to be instrumental for translating biomedical research for improvement of human health.


Assuntos
Modelos Animais de Doenças , Doenças Respiratórias/metabolismo , Doenças Respiratórias/patologia , Animais , Asma/metabolismo , Asma/patologia , Doenças Transmissíveis/metabolismo , Doenças Transmissíveis/patologia , Humanos , Primatas , Doença Pulmonar Obstrutiva Crônica/metabolismo , Doença Pulmonar Obstrutiva Crônica/patologia
20.
Environ Toxicol Pharmacol ; 55: 186-195, 2017 Oct.
Artigo em Inglês | MEDLINE | ID: mdl-28892756

RESUMO

Understanding the effect of wildfire smoke exposure on human health represents a unique interdisciplinary challenge to the scientific community. Population health studies indicate that wildfire smoke is a risk to human health and increases the healthcare burden of smoke-impacted areas. However, wildfire smoke composition is complex and dynamic, making characterization and modeling difficult. Furthermore, current efforts to study the effect of wildfire smoke are limited by availability of air quality measures and inconsistent air quality reporting among researchers. To help address these issues, we conducted a substantive review of wildfire smoke effects on population health, wildfire smoke exposure in occupational health, and experimental wood smoke exposure. Our goal was to evaluate the current literature on wildfire smoke and highlight important gaps in research. In particular we emphasize long-term health effects of wildfire smoke, recovery following wildfire smoke exposure, and health consequences of exposure in children.


Assuntos
Poluentes Atmosféricos/efeitos adversos , Saúde Pública , Fumaça/efeitos adversos , Incêndios Florestais , Adulto , Poluentes Atmosféricos/análise , Animais , Pesquisa Biomédica , Criança , Exposição Ambiental , Feminino , Humanos , Masculino , Fumaça/análise
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