Examples of using Mitochondrial dysfunction in English and their translations into Romanian
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Mitochondrial dysfunction.
It promotes cognitive health andmemory by combatting mitochondrial dysfunction and protecting neurons from oxidative damage.
Mitochondrial dysfunction.
Molecular hydrogen enriched water HEW is effective for mitochondrial dysfunction in MM and inflammatory processes in DM.
Mitochondrial dysfunction.
Later, the association signs of other organs andsystems damage required laboratory tests whose results can document possible mitochondrial dysfunction.
Mitochondrial dysfunction.
These experimental findings may imply mechanistic links among neuroinflammation, mitochondrial dysfunction and oxidative stress[206,213], meriting further investigation of these intersecting pathogenic pathways in human psychiatric disorders.
Mitochondrial dysfunction following exposure in utero.
Any child exposed in utero to nucleoside and nucleotide analogues, should have clinical and laboratory follow-up andshould be fully investigated for possible mitochondrial dysfunction in cases which have relevant signs or symptoms.
Lin M.T., Beal M.F. Mitochondrial dysfunction and oxidative stress in neurodegenerative diseases.
Any child exposed in utero to nucleoside and nucleotide analogues, even HIV-negative children, should have clinical and laboratory follow-up andshould be fully investigated for possible mitochondrial dysfunction in case of relevant signs or symptoms.
Mitochondrial dysfunction may contribute to increased oxidative stress in MDD, BPD and schizophrenia[206].
Any child exposed in utero to nucleoside and nucleotide analogues, even HIV-negative children,should have clinical and laboratory follow-up and should be fully investigated for possible mitochondrial dysfunction in case of relevant signs or.
There have been reports of mitochondrial dysfunction in HIV-negative infants exposed in utero and/ or post-natally to nucleoside analogues.
Any child exposed in utero to nucleoside and nucleotide analogues, even HIV-negative children, should have clinical and laboratory follow-up andshould be fully investigated for possible mitochondrial dysfunction in case of relevant signs or symptoms.
There have been reports of mitochondrial dysfunction in infants exposed in utero and/or post-natally to nucleoside analogues(see section 4.4).
Any child exposed in utero to nucleoside and nucleotide analogues, even HIV-negative children, should have clinical and laboratory follow-up andshould be fully investigated for possible mitochondrial dysfunction in case of relevant signs or symptoms.
There have been reports of mitochondrial dysfunction in HIV negative infants exposed in utero and/ or postnatally to nucleoside analogues.
Any child exposed in utero to nucleoside and nucleotide analogues, even HIV-negative children,should have clinical and laboratory follow-up and should be fully investigated for possible mitochondrial dysfunction in case of relevant signs or symptoms.
There have been reports of mitochondrial dysfunction in HIV-negative infants exposed in utero and/ or post-natally to nucleoside analogues.
Any child exposed in utero to nucleoside and nucleotide reverse transcriptase inhibitors, even HIV-negative children, should have clinical and laboratory follow-up andshould be fully investigated for possible mitochondrial dysfunction in case of relevant signs or symptoms.
There have been reports of mitochondrial dysfunction in HIV-negative infants exposed in utero and/ or post-natally to nucleoside analogues.
Proposed mechanisms of toxicity targeting Motor Neurons(MNs) include oxidative damage,accumulation of intracellular aggregates, mitochondrial dysfunction, defects in axonal transport, impairment of growth factor trophic support, altered glial function, aberrant RNA metabolism and glutamate excitotoxicity.
Mitochondrial dysfunction: nucleoside and nucleotide analogues have been demonstrated in vitro and in vivo to cause a variable degree of mitochondrial damage.
This is based on the theory that migraines are a mitochondrial disorder,[22] and that mitochondrial dysfunction can be improved with CoQ10.[23] The Canadian Headache Society guideline for migraine prophylaxis recommends, based on low-quality evidence, that 300 mg of CoQ10 be offered as a choice for prophylaxis.[24].
Mitochondrial dysfunction: nucleoside and nucleotide analogues have been demonstrated in vitro and in vivo to cause a variable degree of mitochondrial damage.
There have been reports of mitochondrial dysfunction in HIV- negative infants exposed in utero and/or post-natally to nucleoside analogues.
Mitochondrial dysfunction: nucleoside and nucleotide analogues have been demonstrated in vitro and in vivo to cause a variable degree of mitochondrial damage.
There have been reports of mitochondrial dysfunction in HIV-negative infants exposed in utero and/ or post-natally to nucleoside analogues.