The diagnostic challenge of pulmonary tumour thrombotic microangiopathy as a presentation for metastatic gastric cancer: a case report and review of the literature.

Background: Pulmonary tumour thrombotic microangiopathy (PTTM) is a rare complication of metastatic cancer with a distinct histological appearance which presents with dyspnoea and pulmonary arterial hypertension and leads to death in hours to days. It is a challenging diagnosis to make ante mortem, in part due to the rapid clinical decline. Herein, we report a case of a young woman initially felt to have pulmonary sarcoidosis but who then died eight days later from what was found at post mortem to be PTTM.

[Pathogenesis of chronic obstructive pulmonary disease. Molecular mechanisms (part II)].

Chronic obstructive pulmonary disease (COPD) is a major cause of morbidity and mortality worldwide. Smoking is considered the major cause of the disease. Relatively little is known about the molecular mechanisms underlying inflammatory response in smokers' lungs and how this relates to the susceptibility to the disease, particularly why only 10-15% of smokers develop COPD.

[Pathogenesis of chronic obstructive pulmonary disease. Cellular mechanisms (part I)].

Chronic obstructive pulmonary disease (COPD) is a major cause of morbidity and mortality worldwide. Smoking is considered the major cause of the disease. All smokers develop airway inflammation through oxidative stress with macrophages, neutrophiles, lymphocytes, eosinophils, NK-cells and mediators involved.

The effect of smoking on the transcriptional regulation of lung inflammation in patients with chronic obstructive pulmonary disease.

Rationale: Chronic obstructive pulmonary disease (COPD) is believed to result from an abnormal inflammatory response in the lungs to noxious particles and gases usually found in cigarette smoke.

Objectives: In this study, the molecular mechanisms for the enhanced proinflammatory cytokine gene transcription in COPD were investigated.

Methods: Lung tissue was examined from 56 subjects undergoing resection for peripheral lung tumors as follows: current smokers with (n = 14) and without COPD (n = 17), ex-smokers with COPD (n = 13), and nonsmokers (n = 12).

Oxidative stress and cigarette smoke alter chromatin remodeling but differentially regulate NF-kappaB activation and proinflammatory cytokine release in alveolar epithelial cells.

Oxidative stress is implicated in lung inflammation due to its effect on proinflammatory gene transcription. Changes in gene transcription depend on chromatin remodeling and the relative activities of histone acetyltransferases (HATs) and histone deacetylases (HDACs). Alterations in the nuclear histone acetylation:deacetylation balance may result in uncontrolled transcription of specific proinflammatory genes.

[Influence of orthopnoea position on spirometric and plethysmographic parameters in patients with chronic obstructive pulmonary disease ].

Chronic obstructive pulmonary disease (COPD) is characterized by the lack or only slight reversibility of obstruction which can be assessed by spirometry after inhalation of short-acting beta 2-mimetic (e.g. Salbutamol).

[Antibodies seroprevalence for mycoplasma pneumoniae antigens in patients with bronchial asthma].

Microorganisms causing respiratory system infections, mainly viruses but also bacteria, among which there are atypical such as Chlamydophila pneumoniae, play a role in etiopathogenesis of bronchial asthma. Mycoplasma pneumoniae is suggested to take part in the initiation and the bronchial asthma exacerbation. The aim of the paper was to determine the frequency of occurrence of anti-Mycoplasma pneumoniae antibodies in serum of patients suffering from bronchial asthma in comparison with the control group of healthy persons.

[Incidence of selected bacterial pathogens of the respiratory tract in patients with bronchial asthma].

Chronic bacterial infections intensify the reactivity of bronchi and aggravate the course and the control of asthma. They cause the disorders of both function and the structure of respiratory epithelium. Not only structural elements of bacteria but also their toxins intensify the release of mediators of the inflammatory reaction (leucotriens, histamine, IL1, IL4, IL6, IL8, TNF alpha).