Anthropogenic CO2 in the Azores region

The AZORES-I cruise was conducted in August 1998, spanning the length of three latitudinal large-scale sections at 22, 28 and 32ºW. The oceanic carbon system was oversampled by measuring total alkalinity, total inorganic carbon and pH. It is thus possible to estimate anthropogenic CO2 (CANT) and to investigate its relationship with the main water masses that are present. CANT is calculated using the latest back-calculation techniques: jCTº and TrOCA methods. Although the two approaches produce similar vertical distributions, the results of the TrOCA method show higher CANT variability and produce higher inventories than those of the jCTº method. The large proportion of Mediterranean Water found in the northern part of the study area is the main cause of the observed increase northwards of CANT inventories. Changes in CANT inventories between 1981 and 2004 are evaluated using data from the TTO-NAS, OACES-93 and METEOR-60/5 cruises. According to the jCTº and TrOCA approaches, the average long-term rates of CANT inventory change are 1.32±0.11 mol C m-2 y-1 (P=0.008) and 1.18±0.16 mol C m-2 y-1 (P=0.018), respectively. During the 1993-1998 a significant increase in the CANT storage rate was detected by the jCTº method. It is thought that this stems directly from the enhanced Labrador Seawater formation after the increased advection observed at the time.

Prediction of clinical toxicity in localized cervical carcinoma by radio-induced apoptosis study in peripheral blood lymphocytes (PBLs)

[EN] Background: Cervical cancer is treated mainly by surgery and radiotherapy. Toxicity due to radiation is a limiting factor for treatment success. Determination of lymphocyte radiosensitivity by radio-induced apoptosis arises as a possible method for predictive test development. The aim of this study was to analyze radio-induced apoptosis of peripheral blood lymphocytes. Methods: Ninety four consecutive patients suffering from cervical carcinoma, diagnosed and treated in our institution, and four healthy controls were included in the study. Toxicity was evaluated using the Lent-Soma scale. Peripheral blood lymphocytes were isolated and irradiated at 0, 1, 2 and 8 Gy during 24, 48 and 72 hours. Apoptosis was measured by flow cytometry using annexin V/propidium iodide to determine early and late apoptosis. Lymphocytes were marked with CD45 APC-conjugated monoclonal antibody. Results: Radiation-induced apoptosis (RIA) increased with radiation dose and time of incubation. Data strongly fitted to a semi logarithmic model as follows: RIA = βln(Gy) + α. This mathematical model was defined by two constants: α, is the origin of the curve in the Y axis and determines the percentage of spontaneous cell death and β, is the slope of the curve and determines the percentage of cell death induced at a determined radiation dose (β = ΔRIA/Δln(Gy)). Higher β values (increased rate of RIA at given radiation doses) were observed in patients with low sexual toxicity (Exp(B) = 0.83, C.I. 95% (0.73-0.95), p = 0.007; Exp(B) = 0.88, C.I. 95% (0.82-0.94), p = 0.001; Exp(B) = 0.93, C.I. 95% (0.88-0.99), p = 0.026 for 24, 48 and 72 hours respectively). This relation was also found with rectal (Exp(B) = 0.89, C.I. 95% (0.81-0.98), p = 0.026; Exp(B) = 0.95, C.I. 95% (0.91-0.98), p = 0.013 for 48 and 72 hours respectively) and urinary (Exp(B) = 0.83, C.I. 95% (0.71-0.97), p = 0.021 for 24 hours) toxicity. Conclusion: Radiation induced apoptosis at different time points and radiation doses fitted to a semi logarithmic model defined by a mathematical equation that gives an individual value of radiosensitivity and could predict late toxicity due to radiotherapy. Other prospective studies with higher number of patients are needed to validate these results.