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In order to explain these effects (today the causality of the relationship is certain) there are many possible factors, particularly regarding particulate exposures: an increase in cardiovascular risk biomarkers (fibrinogen, white blood cells, and platelets), atherosclerosis, chronic inflammation of lung tissues increased by acute exposure, etc.
In contrast, based on population exposures, an increase of a 5-day average of ultrafine particles was associated with a small decrease in SBP and DBP (Ibald-Mulli et al. 2004).
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At excessive exposures, an increased risk for hemorraghic pneumonia and death among infants has been reported.
Despite strong size fluctuations, which possibly resulted from imperfections of the electron beam exposure, an increase of QD occupation is observed for larger hole diameters.
For an IQR increment in PM10 exposure an increase of 18.3 % (95%% confidence interval (CI): 5.6 to 33.4 %, p = 0.004) in 8-OHdG was observed.
In patients without prior cisplatin exposure, an increase in 2.4 months in the median OS was obtained with vinflunine, reducing the risk of death by 35% (P=0.07).
With the exception of a non-significant O.R. for febrile illness there was no increased reporting of symptoms at intermediate exposure but an increase at high exposure.
Data strongly suggested a decrease in DEHP exposure and an increase in DiNP exposure over time, which is exactly what we observed during the years 1980 1996.
During the first year of 5-ARI exposure, an increasing duration of the restriction period was associated with a decreasing risk of prostate cancer (fig 1).
Using a 72 h drug exposure, an increasing sensitivity against temozolomide within the BTL cell model was detected by the vitality assay.
Acute insulin exposure stimulated an increase in CD98hc mRNA expression, however longer exposure resulted in suppressed gene expression.
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CEO of Professional Science Editing for Scientists @ prosciediting.com