Although the results are not supportive of the original hypothesis, the study is well-designed and provides further insight into the role of TRPV4 in vivo in the regulation of cardiovascular function.
In contrast to this original hypothesis, several studies reported lower baseline cortisol levels in PTSD in plasma [ 12- 14], saliva [ 15- 17], and urine [ 18- 21], but some studies have found significantly higher cortisol excretion [e.g., [ 22]] or no differences between groups [e.g., [ 23- 25]].
DYC conceived the study, generated the original hypothesis, designed the study, acquired clinical data, analyzed data, and drafted and revised the manuscript.
CCL generated the original hypothesis, designed the study, analyzed data and drafted the manuscript.
M.P.S. formulated the original hypothesis, drove the study design, and wrote the manuscript with B.Y.
In contrast to our original hypothesis, in our study we observed few differences in serum concentrations of inflammatory markers during AI therapy between cases and controls, suggesting that AIMSS is not due to a systemic inflammatory response.
On the basis of AIHW published data, 3 4 6 and the only previous Australian study to analyse the contribution of CVD risk factor prevalence differences to the rural/regional urban CVD mortality gap, 22 our original hypothesis in this study was that GGT CVD risk factor profiles, and CVD mortality, would be worse than in NWA.
Several of the least causally associated categories are estrogen related, including: delivery without complications; pregnancies that had an abortive outcome; and malignant neoplasm of the cervix uteri and other female genital organs, consistent with the original hypothesis of the study, that conditions associated with estrogen may be associated with decreased risk of PD.
The original hypothesis for this study was that weekly measurement of EQ-5D may not fully capture the disutility associated with a disease which has a highly variable symptom course that varies daily according to meteorological variation and therefore might underestimate the benefit of primary prevention treatment.
Regarding inflammatory gene expression, our original hypothesis prior to the study described below was that monocyte activity might be a diagnostic biomarker for BD and thus a trait factor.
