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1 selective neural vulnerability in DNA repair deficiency disease.
2  MyD88 offered partial protection from Foxp3 deficiency disease.
3 ) in organ culture and animal models of bone-deficiency disease.
4 ated disorder but is not a respiratory chain-deficiency disease.
5 ty the enzyme may be used to treat ADS lyase deficiency disease.
6 hich may advance our understanding of immune-deficiency diseases.
7 ted a variety of vitamin D insufficiency and deficiency diseases.
8 ardiovascular, neurodegenerative, and immune deficiency diseases.
9 n the treatment for obesity-related vascular deficiency diseases.
10 orm for many endocrine disorders and hormone deficiency diseases.
11 hepcidin, causing frequent iron overload and deficiency diseases.
12  mutations in the ECD can result in the zinc-deficiency disease Acrodermatitis enteropathica.
13 utritional requirement in humans is the zinc deficiency disease, acrodermatitis enteropathica.
14 ve therapeutic relevance for the human SSADH deficiency disease and GHB overdose and toxicity.
15 an innovative therapy for correcting genetic deficiency diseases and augmenting immune function.
16  provide mechanistic insight into telomerase-deficiency diseases and encourage the development of gen
17 s, prevention and treatment of micronutrient deficiency diseases, and nutritional support for at-risk
18                                     Nutrient deficiency diseases are giving way to energy imbalances,
19                               Primary immune deficiency diseases arise due to heritable defects that
20 rrelate with increased propensity for energy deficiency diseases as well as longevity.
21 crobial signals in the pathogenesis of Foxp3 deficiency disease by studying Foxp3 mutant mice that ha
22 in activity observed in a child with a CPTII deficiency disease, establishes that Glu(487) is crucial
23 reviously unidentified family of ganglioside deficiency diseases exist.
24 disrupt this regulatory mechanism cause Moco deficiency disease in humans.
25 od allergy, drug allergy, and primary immune deficiency disease in racial and ethnic underserved popu
26                           Here we describe a deficiency disease in two human siblings that presented
27 r subunit-alpha syndrome (COPA) and DNASE1L3 deficiency, diseases in which IFN-I apparently promotes
28 enefit patients suffering from other hormone deficiency diseases including liver disease and Parkinso
29 mmune responses to the pathogenesis of Foxp3 deficiency disease is unknown.
30       The etiology of most pediatric hormone deficiency diseases is poorly understood.
31  results suggest a link between primary MMUT deficiency, diseased mitochondria, mitophagy dysfunction
32 titrypsin (AAT) variants responsible for AAT deficiency disease: null Hong Kong (NHK) and Z allele.
33           Imbalances in our food can lead to deficiency diseases or obesity and associated metabolic
34 f antibodies to patients with primary immune deficiency diseases (PIDD) and for prophylaxis against i
35               The most severe primary immune deficiency diseases (PIDs) have been successfully treate
36 ers studying therapy for rare primary immune deficiency diseases (PIDs), including severe combined im
37                                    Monogenic deficiency diseases provide unique opportunities to defi
38  new, cell type-selective leukocyte adhesion deficiency disease, providing new insights into CF patho
39 a mean requirement of 46 mg/d to prevent the deficiency disease scurvy.
40  are potential drug targets for thioesterase deficiency diseases such as INCL.
41 ces in time course of murine and human RPE65-deficiency diseases suggests that preclinical efficacy t
42          The shift from acute infectious and deficiency diseases to chronic noncommunicable diseases
43 to cold climates and contributing to "energy deficiency" diseases today.
44       For many years, severe combined immune deficiency diseases, which are characterized by virtual
45 ton's tyrosine kinase (btk) cause the B cell deficiency diseases X-linked agammaglobulinemia (XLA) in
46      Moreover, DDB2 is mutated in the repair-deficiency disease xeroderma pigmentosum (Group E).
47 tected in patients suffering from the repair deficiency disease xeroderma pigmentosum (group E).
48 ng protein DDB has been linked to the repair deficiency disease xeroderma pigmentosum group E (XP-E),
49 repair, and it has been linked to the repair deficiency disease xeroderma pigmentosum.
50 e proved to be good models for the human NER deficiency disease, xeroderma pigmentosum, leading to sp
51  E2F1-activated transcription and the repair deficiency disease XP-E.