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Characteristics of Persons Who Report Using Only Nicotine-Containing Products Among Interviewed Patients with E-cigarette, or Vaping, Product Use-Associated Lung Injury - Illinois, August-December 2019.

报告在接受采访的电子烟或 Vaping 患者中仅使用含尼古丁产品的人的特征,产品使用相关肺损伤-Illinois,2019年8月到12月。

  • 影响因子:7.42
  • DOI:10.15585/mmwr.mm6903e1
  • 作者列表:"Ghinai I","Navon L","Gunn JKL","Duca LM","Brister S","Love S","Brink R","Fajardo G","Johnson J","Saathoff-Huber L","King BA","Jones CM","Krishnasamy VP","Layden JE
  • 发表时间:2020-01-24
Abstract

:In 2019, the United States experienced an outbreak of e-cigarette, or vaping, product use-associated lung injury (EVALI) (1). Most EVALI patients have reported using tetrahydrocannabinol (THC)-containing e-cigarette, or vaping, products obtained from informal sources (2,3), and vitamin E acetate in these products has been closely linked with EVALI (4,5). However, some EVALI patients report using only nicotine-containing products. This study compared demographic, product use, and clinical characteristics of EVALI patients in Illinois who reported using only nicotine-containing e-cigarette, or vaping, products with those of patients who reported using any THC-containing products. Among 121 interviewed Illinois EVALI patients, 17 (14%) reported using only nicotine-containing products, including nine (7%) patients who had no indication of any THC use, based on self-report or toxicology testing. Compared with patients who used any THC-containing products, these nine patients were significantly more likely to be older and female and were less likely to experience constitutional symptoms or to have leukocytosis on initial evaluation. Although vitamin E acetate has been strongly linked with EVALI, evidence is not sufficient to rule out the contribution of other chemicals of concern, including chemicals in either THC- or non-THC-containing products, in some reported EVALI cases. The contributing cause or causes of EVALI for patients reporting use of only nicotine-containing products warrants further investigation.

摘要

: 在 2019,美国经历了电子香烟,或 vaping,产品使用相关的肺损伤 (EVALI) (1) 的爆发。大多数 EVALI 患者报告使用含有四氢大麻酚 (THC) 的电子烟或 vaping,从非正式来源获得的产品 (2,3), 这些产品中的维生素e 乙酸酯与 EVALI (4,5) 密切相关。然而,一些 EVALI 患者报告仅使用含尼古丁的产品。本研究比较了伊利诺伊州 EVALI 患者的人口统计学、产品使用和临床特征,他们报告仅使用含尼古丁的电子烟或 vaping, 产品与报告使用任何含 THC 产品的患者的产品。在接受采访的 121 名伊利诺伊州 EVALI 患者中,17 名 (14%) 报告仅使用含尼古丁的产品,包括 9 名 (7%) 没有任何 THC 使用指征的患者, 基于自我报告或毒理学测试。与使用任何含 THC 产品的患者相比,这 9 例患者年龄较大和女性明显更大,初次评估时不太可能出现全身症状或白细胞增多。尽管维生素e 乙酸酯与 EVALI 密切相关,但证据不足以排除其他关注化学品的贡献,包括含 THC 或不含 THC 的产品中的化学品, 在一些报道的 EVALI 病例中。对于报告仅使用含尼古丁产品的患者,EVALI 的促成原因或原因值得进一步研究。

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影响因子:6.12
发表时间:2020-01-01
DOI:10.1111/bph.14861
作者列表:["De Cunto G","Brancaleone V","Riemma MA","Cerqua I","Vellecco V","Spaziano G","Cavarra E","Bartalesi B","D'Agostino B","Lungarella G","Cirino G","Lucattelli M","Roviezzo F"]

METHODS:BACKGROUND AND PURPOSE:A critical role for sphingosine kinase/sphingosine-1-phosphate (S1P) pathway in the control of airway function has been demonstrated in respiratory diseases. Here, we address S1P contribution in a mouse model of mild chronic obstructive pulmonary disease (COPD). EXPERIMENTAL APPROACH:C57BL/6J mice have been exposed to room air or cigarette smoke up to 11 months and killed at different time points. Functional and molecular studies have been performed. KEY RESULTS:Cigarette smoke caused emphysematous changes throughout the lung parenchyma coupled to a progressive collagen deposition in both peribronchiolar and peribronchial areas. The high and low airways showed an increased reactivity to cholinergic stimulation and α-smooth muscle actin overexpression. Similarly, an increase in airway reactivity and lung resistances following S1P challenge occurred in smoking mice. A high expression of S1P, Sph-K2 , and S1P receptors (S1P2 and S1P3 ) has been detected in the lung of smoking mice. Sphingosine kinases inhibition reversed the increased cholinergic response in airways of smoking mice. CONCLUSIONS AND IMPLICATIONS:S1P signalling up-regulation follows the disease progression in smoking mice and is involved in the development of airway hyperresponsiveness. Our study defines a therapeutic potential for S1P inhibitors in management of airways hyperresponsiveness associated to emphysema in smokers with both asthma and COPD.

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翻译标题与摘要 下载文献
影响因子:3.94
发表时间:2020-01-15
DOI:10.1016/j.taap.2019.114847
作者列表:["Bernstein DM","Toth B","Rogers RA","Kling DE","Kunzendorf P","Phillips JI","Ernst H"]

METHODS::The interim results from this 90-day multi-dose, inhalation toxicology study with life-time post-exposure observation has shown an important fundamental difference in persistence and pathological response in the lung between brake dust derived from brake-pads manufactured with chrysotile, TiO2 or chrysotile alone in comparison to the amphiboles, crocidolite and amosite asbestos. In the brake dust exposure groups no significant pathological response was observed at any time. Slight macrophage accumulation of particles was noted. Wagner-scores, were from 1 to 2 (1 = air-control group) and were similar to the TiO2 group. Chrysotile being biodegradable, shows a weakening of its matrix and breaking into short fibers & particles that can be cleared by alveolar macrophages and continued dissolution. In the chrysotile exposure groups, particle laden macrophage accumulation was noted leading to a slight interstitial inflammatory response (Wagner-score 1-3). There was no peribronchiolar inflammation and occasional very slight interstitial fibrosis. The histopathology and the confocal analyses clearly differentiate the pathological response from amphibole asbestos, crocidolite and amosite, compared to that from the brake dust and chrysotile. Both crocidolite and amosite induced persistent inflammation, microgranulomas, and fibrosis (Wagner-scores 4), which persisted through the post exposure period. The confocal microscopy of the lung and snap-frozen chestwalls quantified the extensive inflammatory response and collagen development in the lung and on the visceral and parietal surfaces. The interim results reported here, provide a clear basis for differentiating the effects from brake dust exposure from those following amphibole asbestos exposure. The subsequent results through life-time post-exposure will follow.

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影响因子:4.04
发表时间:2020-01-10
DOI:10.1042/BST20191010
作者列表:["Zaragosi LE","Deprez M","Barbry P"]

METHODS::The respiratory tract is lined by a pseudo-stratified epithelium from the nose to terminal bronchioles. This first line of defense of the lung against external stress includes five main cell types: basal, suprabasal, club, goblet and multiciliated cells, as well as rare cells such as ionocytes, neuroendocrine and tuft/brush cells. At homeostasis, this epithelium self-renews at low rate but is able of fast regeneration upon damage. Airway epithelial cell lineages during regeneration have been investigated in the mouse by genetic labeling, mainly after injuring the epithelium with noxious agents. From these approaches, basal cells have been identified as progenitors of club, goblet and multiciliated cells, but also of ionocytes and neuroendocrine cells. Single-cell RNA sequencing, coupled to lineage inference algorithms, has independently allowed the establishment of comprehensive pictures of cell lineage relationships in both mouse and human. In line with genetic tracing experiments in mouse trachea, studies using single-cell RNA sequencing (RNAseq) have shown that basal cells first differentiate into club cells, which in turn mature into goblet cells or differentiate into multiciliated cells. In the human airway epithelium, single-cell RNAseq has identified novel intermediate populations such as deuterosomal cells, 'hybrid' mucous-multiciliated cells and progenitors of rare cells. Novel differentiation dynamics, such as a transition from goblet to multiciliated cells have also been discovered. The future of cell lineage relationships in the respiratory tract now resides in the combination of genetic labeling approaches with single-cell RNAseq to establish, in a definitive manner, the hallmarks of cellular lineages in normal and pathological situations.

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