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The differences between studies could be due to studying different populations (younger vs older; experimental vs clinical pain) or using different measurement tools for catastrophizing.
This may be due to disruption of Vhl's Hif-independent roles, or alternatively this may be due to studying the effects of activation of genetically induced hypoxia in a whole organism.
While the failure to detect a treatment effect might be due to studying patients with advanced deficits and substantial preexisting irreversible neuroaxonal tissue loss, it might also relate to limited experience in neuroprotection trial design.
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The evidence summarised in this systematic review needs to be interpreted with caution, the inconsistent study results may be due to study design, exposure assessment, and avoidance measure.
The differences may be due to study design, or may reflect differences in lifestyle, diet or be due to genetic predisposition triggered by environmental factors.
We speculate that this could be due to study effect or to good compliance.
One possible source of disparity may be due to study methodologies.
The differences in rates of measurement may be due to study design.
The reason for this may be due to study group differences.
This mismatch could be due to study period differences and study subject differences in the two researches.
This led us to believe that the difference could be due to study biases in the LC data.
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Justyna Jupowicz-Kozak
CEO of Professional Science Editing for Scientists @ prosciediting.com