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Although there is no global consensus on the biochemical definition of vitamin D deficiency, a cut-off point of ≤ 37.5 nmol/L (≤ 15 ng/mL) 25(OH D is typically used to determine deficiency [ 13].
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Further, a risk-based framework is used to determine deficiencies in the safety management systems.
Blood tests can determine deficiencies.
Most common of these is lactose intolerance, which is a genetically determined deficiency of the enzyme lactase that is needed to digest the milk sugar, lactose.
We wanted to know, if a genetically determined deficiency in sensing meningococcal LPS increases risk of disease.
Dogs with a genetically determined deficiency of complement C3 more often develop renal and infectious diseases [ 18].
As with selenium, there is a lack of published information on choline status in dogs and, in particular, methods of determining deficiency.
Although C3 and C4 (Table 1, proteins 19 and 20 and Table 2, proteins 1 and 23) play a significant role in the innate immune system [ 15] a mouse model demonstrated that deficiency in C3 can be compensated by thrombin [ 41] and a genetically determined deficiency of C4 increases the risk for developing systemic lupus erythematosus [ 42].
A genetically or epigenetically determined deficiency of GGFs is compatible with the limited regeneration of motor neurons observed in schizophrenia [ 104, 105] and with the incomplete remission of the disorder, which is the foundation of Kraepelin's schizophrenia (dementia praecox) concept.
Such a gene-environmental exposure interaction was recently demonstrated for passive smoking and asthma in children: a genetically determined deficiency of glutathione S transferase (GST) enzymes involved in the detoxification of environmental tobacco smoke (ETS) accounted for a massive increase in the risk for current asthma and asthma symptoms such as wheeze and shortness of breath [ 29].
To begin to explore the biological roles of periostin in the airway in asthma, we took advantage of a periostin deficient mouse previously described 8 to determine how deficiency of periostin modulates airway responses to allergic airway inflammation.
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