No abstract

Forecasting pollination can help the allergist to establish the appropriate treatment and advice for patients. Based on previous studies, we have related the climate variables with the grass pollen counts in the search for pollination predictors. By relating the meteorological data of the temperature recorded every 6 h and of the rainfall in hourly periods, together with the daily pollen counts obtained by the Hirst volumetric system, over a period of 3 years, we have tried to predict the start, duration and severity of the grass pollination, as well as the days of peak pollination. We have established a relationship by means of a polynomic regression originating from the mean cumulated temperature higher than 9 degrees C [R2 = 0.927 (P = 0.0001)], with the pollination season starting from 300 degrees C and the maximum peak at 356 degrees C, in the 3 years of the study. During the days of pollination, peaks higher than 50 grains/m3 coincide with average daily temperatures of 18.7 +/- 3 and lower than 50 grains/m3 with temperatures of 16.8 +/- 3 (significant to 95%). The duration of the pollination is influenced by the cumulated average temperatures (from 800 to 900 degrees C) and especially by precipitation at the start of and during pollination. In order to forecast grass pollination, the cumulated average temperatures are useful, starting from a basal (9 degrees C), pollination begins when this sum is greater than 300 degrees C, whereas when 800 degrees C is reached and depending on the rainfall during the season, pollination will end.(ABSTRACT TRUNCATED AT 250 WORDS)

No abstract

Parathyroid hormone (PTH)-related protein (PTHrP) is the main factor responsible for humoral hypercalcemia of malignancy. Both PTH and PTHrP bind to the common type I PTH/PTHrP receptor (PTHR), thereby activating phospholipase C and adenylate cyclase through various G proteins, in bone and renal cells. However, various normal and transformed cell types, including hypercalcemic Walker 256 (W256) tumor cells, do not produce cAMP after PTHrP stimulation. We characterized the PTHrP receptor and the signaling mechanism upon its activation in the latter cells. Scatchard analysis of PTHrP-binding data in W256 tumor cells revealed the presence of high affinity binding sites with an apparent K d of 17 nM, and a density of 90 000 sites/cell. In addition, W256 tumor cells immunostained with an anti-PTHR antibody, recognizing its extracellular domain. Furthermore, reverse transcription followed by PCR, using primers amplifying two different regions in the PTHR cDNA corresponding to the N-and C-terminal domains, yielded products from W256 tumor cell RNA which were identical to the corresponding products obtained from rat kidney RNA. Consistent with our previous findings on cAMP production, 1 µM PTHrP(1-34), in contrast to 10 µg/ml cholera toxin or 1 µM isoproterenol, failed to affect protein kinase A activity in W256 tumor cells. However, in these cells we found a functional PTHR coupling to G q/11 , whose presence was demonstrated in these tumor cell membranes by Western blot analysis. Our findings indicate that W256 tumor cells express the PTHR, which seems to be coupled to G q/11 . Taken together with previous data, these results support the hypothesis that a switch from the cAMP pathway to the phospholipase C-intracellular calcium pathway, associated with PTHR activation, occurs in malignant cells.

No abstract