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Thus, it has been speculated that inflammation plays a positive role in the occurrence of autophagy.
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It has been speculated that systemic inflammation related to COPD plays a role in the development of extrapulmonary comorbid conditions (3– 5).
It has been speculated that NTHi-driven inflammation in the context of COPD may be a risk factor for the development of lung cancer [65].
Moreover, on the observation that elevated inflammatory molecules are associated with increased risk of cardiovascular diseases in the general population, it has been speculated that RA-related inflammation might contribute to endothelial dysfunction [ 1].
It has been speculated that onychomadesis occurs secondary to inflammation of the nail matrix or maceration associated finger blisters [ 7].
On the basis of the observation that smokers may present with a lower level of gingival inflammation, it has been speculated that the gingival blood flow in smokers may be less in comparison to nonsmokers [ 8, 10].
While it had been speculated that fish oil or n-3 PUFA would reduce inflammation in IBD, clinical trials have not consistently supported this.
It has been speculated that whole-body DGAT1 deficiency is associated with reduced inflammation due to the absence of DGAT1 in white adipose tissue, whereas DGAT1 deficiency in macrophages increases the disposition to FA-induced inflammation [7].
It has been speculated that RDW is an integrative measure of underlying pathologic conditions leading to increased oxidative stress and subclinical inflammation; however, further studies are needed.
It has been speculated that with more severe asthma, airway closures may occur in larger airways (≥2 mm) due to airway remodeling and inflammation.
It can be speculated, that the ongoing inflammation in patients with chronic pancreatitis is capable to generate PIF.
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