A palaeoecological perspective on the transformation of the tropical Andes by early human activity.

Palaeoecological records suggest that humans have been in the Andes since at least 14 000 years ago. Early human impacts on Andean ecosystems included an increase in fire activity and the extinction of the Pleistocene megafauna. These changes in Andean ecosystems coincided with rapid climate change as species were migrating upslope in response to deglacial warming. Microrefugia probably played a vital role in the speed and genetic composition of that migration. The period from ca 14 500 to 12 500 years ago was when novel combinations of plant species appeared to form no-analogue assemblages in the Andes. By 12 000 years ago most areas in what are today the Andean grasslands were being burned and modified by human activity. As the vegetation of these highland settings has been modified by human activity for the entirety of the Holocene, they should be regarded as long-term manufactutred landscapes. The sharp tree lines separating Andean forests from grasslands that we see today were probably also created by repeated burning and owe their position more to human-induced fire than climatic constraints. In areas that were readly penetrated by humans on the forested slopes of the Andes, substantial modification and settlement had occurred by the mid-Holocene. In hard-to-reach areas, however, the amount of human modification may always have been minimal, and these slopes can be considered as being close to natural in their vegetation. This article is part of the theme issue 'Tropical forests in the deep human past'.

Pleural fluid tumour markers in malignant pleural effusion with inconclusive cytologic results.

BACKGROUND: The presence of tumour cells in pleural fluid or tissue defines an effusion as malignant. Cytology analysis of the pleural fluid has about 60% diagnostic sensitivity. Several tests have been proposed to improve diagnosis-among them, the concentrations of tumour markers in pleural fluid. We evaluated whether the concentrations of tumour markers in pleural fluid could improve the diagnosis of malignant pleural effusion (mpe) when cytology is doubtful. METHODS: Lymphocytic pleural fluids secondary to tuberculosis or malignancy from 156 outpatients were submitted for cytology and tumour marker quantification [carcinoembryonic antigen (cea), cancer antigen 15-3 (ca15-3), carbohydrate antigen 19-9 (ca19-9), cancer antigen 72-4 (ca72-4), cancer antigen 125 (ca125), and cyfra 21-1). Oneway analysis of variance, the Student t-test or Mann-Whitney test, and receiver operating characteristic curves were used in the statistical analysis. RESULTS: Concentrations of the tumour markers cea, ca15-3, ca125, and cyfra 21-1 were higher in mpes than they were in the benign effusions (p < 0.001), regardless of cytology results. The markers ca19-9 and ca72-4 did not discriminate malignant from benign effusions. When comparing the concentrations of tumour markers in mpes having positive, suspicious, or negative cytology with concentrations in benign effusions, we observed higher levels of cea, ca15-3, cyfra 21-1, and ca125 in malignant effusions with positive cytology (p = 0.003, p = 0.001, p = 0.002, and p = 0.001 respectively). In pleural fluid, only ca125 was higher in mpes with suspicious or negative cytology (p = 0.001) than in benign effusions. CONCLUSIONS: Given high specificity and a sensitivity of about 60%, the concentrations of tumour markers in pleural effusions could be evaluated in cases of inconclusive cytology in patients with a high pre-test chance of malignancy or a history of cancer.

Effect of temperature and storage time on cellular analysis of fresh pleural fluid samples.

OBJECTIVE: Despite the methodological variability in preparation techniques for pleural fluid cytology, it is fundamental that the cells should be preserved, permitting adequate morphological classification. We evaluated numerical and morphological changes in pleural fluid specimens processed after storage at room temperature or under refrigeration. METHODS: Aliquots of pleural fluid from 30 patients, collected in ethylenediaminetetraacetic acid-coated tubes and maintained at room temperature (21 °C) or refrigeration (4 °C) were evaluated after 2 and 6 hours and 1, 2, 3, 4, 7 and 14 days. Evaluation of cytomorphology and global and percentage counts of leucocytes, macrophages and mesothelial cells were included. RESULTS: The samples had quantitative cellular variations from day 3 or 4 onwards, depending on the storage conditions. Morphological alterations occurred earlier in samples maintained at room temperature (day 2) than in those under refrigeration (day 4). CONCLUSIONS: This study confirms that storage time and temperature are potential pre-analytical causes of error in pleural fluid cytology.

Pleural fluid cytokines correlate with tissue inflammatory expression in tuberculosis.

SETTING: A tertiary care research centre in São Paolo, Brazil. OBJECTIVE: To quantify interleukin (IL) 8, tumour necrosis factor alpha (TNF-alpha), vascular endothelial growth factor (VEGF) and transforming growth factor beta(1) (TGF-beta(1)) in pleural fluid from tuberculous patients, correlating its values with the histopathological patterns in pleural biopsies. DESIGN: Cytokines were quantified in patients with transudates secondary to congestive heart failure (n = 8) and exudates secondary to tuberculosis (TB; n = 39). In parietal pleural biopsies from TB patients, the histological patterns of the inflammatory response were quantified by morphometric analysis (stereological point-counting method). RESULTS: IL-8, TNF-alpha, VEGF and TGF-beta(1) levels were higher in TB than in transudates. A positive correlation existed between components of the fibrinoid exudative phase with pleural fluid IL-8 (R = 0.52, P = 0.004) and VEGF (R = 0.42, P = 0.0021) levels. A negative correlation existed between pleural fluid IL-8 (R = -0.37, P = 0.048) and VEGF (R = -0.44, P = 0.0015) levels with tissue components of fibroproliferation. CONCLUSION: The high pleural levels of TNF-alpha, IL-8, VEGF and TGF-beta(1) suggest the involvement of these cytokines in the TB immunological response. The positive correlation between pleural fluid IL-8 and VEGF with the components of the acute exudative phase and the negative correlation between these cytokines with the fibroproliferative components suggest a temporary inflammatory response in the pleural space.