Tumor necrosis factor (TNF)-A is present in the microenvironment of human tumors, including malignant pleural effusion (MPE). Although the cytokine is produced in the pleural cavity by both tumor and host cells, its effects on MPE formation are unknown. In these studies, we sought to determine the role of TNF-A in the pathogenesis of MPE and to assess the therapeutic effects of its neutralization in a preclinical model. For this, MPEs were generated in immunocompetent mice using intrapleural injection of mouse lung adenocarcinoma cells. The roles of tumor-and host-derived TNF-A were assessed using combined experimentation with TNF-a gene-deficient mice and in vivo TNF-A neutralization.
Cognitive deficits in patients with obstructive sleep apnea syndrome (OSAS) are well demonstrated, but the pathophysiology of these deficits is still controversial, as the relationship between OSA severity and cognitive deficits is usually weak. Our study considers the possible relationship between OSA-related cognitive deficits and the overall intellectual function of OSA patients. Forty-seven OSA patients and 36 normal individuals underwent a neuropsychological battery test assessing attention and alertness. According to the resulting IQ score, patients and controls were divided into a high-intelligence group (IQ > or = 90th percentile) and a normal-intelligence group (50 < or = IQ < 90%ile). Between the two patient groups there were no significant differences noticed, regarding OSA severity or sleepiness. High-intelligence patients showed the same attention/alertness performance compared with the high-intelligence controls. On the contrary, patients with normal-intelligence showed attention/alertness decline compared with the normal-intelligence control group. The two patient groups were re-examined with the same battery test after at least 1 year of CPAP treatment. At re-examination neither patient group showed any differences regarding attention and alertness compared with the control groups. We assume that high-intelligence may have a protective effect against OSA-related cognitive decline, perhaps due to increased cognitive reserve.
Single photon emission computed tomography, a rotating gamma camera, and continuous inhalation or infusion of krypton 81m (half life 13 seconds) were used to measure regional ventilation (V), perfusion (Q), and ventilation-perfusion (V/Q) ratios in five normal subjects in supine, prone, and lateral decubitus postures and in three asthmatic patients (supine posture only) before and after inhalation of 2.5 mg nebulised salbutamol. Vertical and horizontal gradients of V, Q, and V/Q were examined at three levels in each lung in regions of 1.9 cm3 size. In normal subjects V and Q increased along the axis of gravity in all postures and at all levels in the lung except for V in the prone position. Smaller horizontal gradients were found with an increase in V and Q from caudal to cranial-again except in the prone posture, where the gradient was slightly reversed. Constraint to outward motion of the ventral chest and abdominal wall is the most likely explanation for the different behaviour in the prone posture. In chronic asthma the vertical gradients of V and V/( were the reverse of normal, but the Q gradient was normal. Bronchodilator treatment did not affect the vertical or horizontal gradients significantly, but analysis of individual regions showed that, relatively, V/0 worsened in 42% of them; this was associated in two thirds with an increase in fractional Q. After inhalation of agonist local vasodilatation may influence V/Q ratios in some units more than bronchodilatation.Three dimensional reconstruction of function in an organ where gravity plays a prominent role offers definite advantages over two dimensional mapping. With emission computed tomography either with single photons (SPECT)' or with positrons (PET)23 ventilation (V), perfusion ((>), and V/Q ratios can be obtained using appropriate radionuclides. Because of their special properties (monoenergetic y ray emission in coincidence) precise attentuation corrections can be made only with positron emission tomography (PET).4 PET machines, in general, offer a limited survey of the lung (at present a maximum of five transaxial cuts), and an online cyclotron is required. With SPECT and a rotating gamma camera the whole lung can be surveyed but the attenuation corrections are extremely complex and of doubtful accuracy, and have generally been omitted.'
Tumour necrosis factor (TNF) and interleukin-1 (IL-1) are powerful mediators with a key role in inflammation. This study was undertaken to study the presence of TNF and IL-1 in tuberculous effusion where there is marked inflammation and where examination of the pleural fluid may give information about the local inflammatory reaction. Adenosine deaminase activity (ADA, a marker of TB pleurisy) was also tested. Tumour necrosis factor, IL-1 and ADA levels were measured in the pleural fluid and serum of 97 patients; 33 with tuberculous effusion, 33 with malignant effusion, and 31 patients with benign non-tuberculous effusion. Pleural fluid TNF and ADA levels were higher in tuberculous (TB) patients than in patients with benign disorders or cancer (P < 0.01). Serum TNF levels were also higher in TB patients than other benign (P < 0.01) or malignant (P < 0.05) effusions. There was a positive correlation between serum and pleural fluid values (r = 0.998-0.999, P < 0.001) although pleural fluid concentration was higher (P < 0.001), possibly suggesting local production in the pleural cavity. Pleural fluid IL-1 levels were not raised in any patient group but there was a positive correlation between TNF and IL-1. In addition, a positive correlation was found between TNF and ADA levels, probably indicating some common production mechanism. Furthermore, ADA sensitivity in the diagnosis of tuberculous effusion was augmented by the combined use of TNF and ADA. The use of both these markers may prove useful in the differential diagnosis of TBC pleurisy.
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