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2.
Cytokine ; 74(2): 313-7, 2015 Aug.
Artigo em Inglês | MEDLINE | ID: mdl-25922275

RESUMO

Interleukin (IL)-18 is a pro-inflammatory cytokine that was firstly described as an interferon (IFN)-γ-inducing factor. Similar to IL-1ß, IL-18 is synthesized as an inactive precursor requiring processing by caspase-1 into an active cytokine. The platform for activating caspase-1 is known as the inflammasome, a multiple protein complex. Macrophages and dendritic cells are the primary sources for the release of active IL-18, whereas the inactive precursor remains in the intracellular compartment of mesenchymal cells. Finally, the IL-18 precursor is released from dying cells and processed extracellularly. IL-18 has crucial host defense and antitumor activities, and gene therapy to increase IL-18 levels in tissues protects experimental animals from infection and tumor growth and metastasis. Moreover, multiple studies in experimental animal models have shown that IL-18 over-expression results to emphysematous lesions in mice. The published data prompt to the hypothesis that IL-18 induces a broad spectrum of COPD-like inflammatory and remodeling responses in the murine lung and also induces a mixed type 1, type 2, and type 17 cytokine responses. The majority of studies identify IL-18 as a potential target for future COPD therapeutics to limit both the destructive and remodeling processes occurring in COPD lungs.


Assuntos
Células Dendríticas/imunologia , Interleucina-18/imunologia , Pulmão/imunologia , Macrófagos/imunologia , Doença Pulmonar Obstrutiva Crônica/imunologia , Linfócitos T Auxiliares-Indutores/imunologia , Animais , Caspase 1/imunologia , Células Dendríticas/patologia , Modelos Animais de Doenças , Humanos , Pulmão/patologia , Macrófagos/patologia , Camundongos , Doença Pulmonar Obstrutiva Crônica/patologia , Doença Pulmonar Obstrutiva Crônica/terapia , Linfócitos T Auxiliares-Indutores/patologia
3.
Eur J Case Rep Intern Med ; 6(12): 001340, 2019.
Artigo em Inglês | MEDLINE | ID: mdl-31893206

RESUMO

INTRODUCTION: Carbon monoxide (CO) poisoning may cause severe cellular hypoxia. MATERIALS AND METHODS: A 28-year-old male presented reduced levels of consciousness and dyspnoea after CO exposure. Clinical examination revealed tachypnoea, bilateral rales, dilated jugular veins and confusion. Troponin I, lactate and carboxyhaemoglobin levels were increased. Thoracic X-ray depicted pulmonary oedema and an echocardiogram, severe heart failure (HF; EF<25%). He was intubated due to clinical deterioration. RESULTS: He remained intubated for 5 days with excellent improvement of left ventricular function (EF>55%). He was discharged 1 week later with full recovery. DISCUSSION: Acute HF is a rare serious complication of CO poisoning, even in healthy young individuals. LEARNING POINTS: Acute CO poisoning is an emergent condition necessitating prompt diagnosis and treatment.Neurologic and cardiovascular manifestations are the most worrying complications, which may leave permanent sequelae.Acute heart failure is a rare complication of CO poisoning, characterized by regional or global left ventricular wall hypokinesia.

4.
Tob Prev Cessat ; 3: 5, 2017.
Artigo em Inglês | MEDLINE | ID: mdl-32432180

RESUMO

BACKGROUND: Although the use of e-cigarettes is increasing worldwide, their short and long-term effects remain undefined. We aimed to study the acute effect of short-term use of e-cigarettes containing nicotine on lung function and respiratory symptoms in smokers with airways obstructive disease (COPD, asthma), "healthy" smokers, and healthy never smokers. METHODS: Respiratory symptoms, vital signs, exhaled NO, airway temperature, airway resistance (Raw), specific airway conductance (sGaw) and single nitrogen breath test were assessed before and immediately after short term use of an e-cigarette containing 11mg of nicotine among adults with COPD, asthma, "healthy" smokers, and never-smokers. The effect of the use of nicotine-free e-cigarettes among "healthy" never smokers was also studied. RESULTS: The majority of participants reported acute cough. Short term use of nicotine e-cigarettes was associated: a) with increased heart rate in all subjects except in the COPD group, b) decreased oxygen saturation in "healthy" and COPD smokers, c) increased Raw in asthmatic smokers, "healthy" smokers, and healthy never smokers, d) decreased sGaw in healthy subjects, and e) changed slope of phase III curve in asthmatic smokers. Short-term use of nicotine-free e-cigarettes increased Raw and decreased sGaw among healthy never smokers. CONCLUSIONS: Short-term use of an e-cigarette has acute effects on airways physiology and respiratory symptoms in COPD smokers, asthmatic smokers, "healthy" smokers and healthy never smokers. E-cigarette use was associated with effects in "healthy" never smokers irrespectively of nicotine concentration. More studies are needed to investigate both short and long-term effects of e-cigarette use.

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