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Thus, the presented data show that neither decreased insulin sensitivity nor significantly decreased β-cell function after stimulation with hyperglycaemia or during challenge with arginine and GLP-1 explain the abnormalities in the glucose homeostasis in TS.
For example, no morphological basis was found in hemolymphatic tissues to explain the abnormalities in the number of various populations of T cells recorded in Spns2 tm1a homozygous mice (Nijnik et al., 2012).
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One possible mechanism discussed by various authors that explains the abnormalities in bone metabolism under medication is the activation of pregnane X rececptor (PXR) by some drugs (Table 1), that may be responsible for the acceleration of vitamin D catabolism through the upregulation of CYP3A4 and CYP24A1, leading to vitamin D deficiency and, eventually, to osteopenia or osteomalacia.
[ 20- 22] Autonomic dysfunction at the level of the lacrimal glands and the pupil presumably explain the abnormalities seen in this condition.
Two mechanisms have been suggested to explain the abnormalities of these interactions in neural tissue: (a) the aggregation of protein mediated by redox-active metal ions; and (b) metal catalyzed oxidation reactions (MCO) [ 10].
This reciprocal connection between brainstem vestibular nuclei and structures involved in modulation of trigeminal nociceptive inputs may explain the VEMP abnormalities in migraineurs.
The results presented here suggest a novel mechanism to explain the behavioral abnormalities found in Cra1/+ mice.
Peripheral and central neural dysregulation or both have been involved in explaining these abnormalities in visceral and somatic sensitivity.
CONCLUSIONS: These histopathologic abnormalities may not only explain the changes in viral distribution observed in the lymphoid tissue in different stages of the disease, but may also reflect different functional states of the immune system during the progression of HIV-1 infection from early- to late-stage disease.
Therefore, absence of accumulated glycogen within brain samples of LAMP-2-deficient mice may explain the lack of gross abnormalities in neuronal autophagy and suggest a distinct function of LAMP-2 within the hippocampus for autophagic clearance of neuronal proteins.
Their definitions of extrasynovial abnormalities are different than ours which could explain the differences in the results.
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