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1 DNA methyltransferase (DNMT) gene expression is ill defined.
2 nomenclature for minimally invasive surgery is ill defined.
3 the virulence of gastrointestinal pathogens is ill defined.
4 functions, its role in cell differentiation is ill defined.
5 nment to regulate circulating glucose levels is ill defined.
6 prostate cancer dissemination and lethality is ill defined.
7 including high-mobility group box 1 (HMGB1), is ill defined.
8 l activity leads to transporter inactivation is ill defined.
9 rial dysfunction and inflammasome activation is ill defined.
10 lar function of these receptors in cognition is ill defined.
11 ell's proliferative and apoptotic mechanisms is ill defined.
12 polarization in skeletal muscle regeneration is ill defined.
13 e activating complexes of the lectin pathway is ill defined.
14 from traditional measures to novel therapies is ill defined.
15 machinery regulating exit from pluripotency is ill defined.
16 rticipate in innate defense against bacteria is ill defined.
17 The underlying molecular mechanism, however, is ill defined.
18 iac death for asymptomatic mutation carriers is ill defined.
19 poietic lineage differentiation in the adult is ill defined.
20 20% of bacterial genomes; however, its role is ill defined.
21 responses, the benefit for T cell responses is ill defined.
22 various nutrients, but their clinical impact is ill defined.
23 ction (H-function) in potential heart donors is ill defined.
24 cular basis for AC-induced inhibition of DCs is ill defined.
25 NA interaction by the acidic C-terminal tail is ill defined.
26 onse, however, the mechanism for this uptake is ill-defined.
27 cardiac imaging in ethnic minority patients is ill-defined.
28 although their role in Fas-induced apoptosis is ill-defined.
29 although their role in Fas-induced apoptosis is ill-defined.
30 l to clinical and stress testing evaluation, is ill-defined.
31 The genetic basis of Gilbert's syndrome is ill-defined.
32 impact of its absence on biological systems is ill-defined.
33 as octamers and the cause of their pathology is ill-defined.
34 length of stay (LOS), but their performance is ill-defined.
35 lated by external signals, but the mechanism is ill-defined.
36 ounds such as perfluorooctanoic acid (PFOA), is ill-defined.
37 rgy expenditure, but exactly how this occurs is ill-defined.
38 M (IgM) in the first trimester of pregnancy is ill-defined.
39 tribution of these variants to tumorigenesis is ill-defined.
40 eting to either mitochondria or chloroplasts is ill-defined.
41 the relative importance of each interaction is ill-defined.
42 e appropriate amount of biventricular pacing is ill-defined.
43 mitochondria, but regulation of this process is ill-defined.
44 conformations, particularly if the receptor is ill-defined.
45 or perturb the cooperative activation events are ill defined.
46 rapy (ALA-PDT), but its nature and mediation are ill defined.
47 nociceptors, but the details of this process are ill defined.
48 the limitations of RNAi antiviral strategies are ill defined.
49 ors that promote tumor growth, their origins are ill defined.
50 Mechanisms mediating this enhanced risk are ill defined.
51 smission of pathogens during epidemic spread are ill defined.
52 ges associated with cellular differentiation are ill defined.
53 ate graft failure in acute cardiac rejection are ill defined.
54 atrix-degrading proteases during lung injury are ill defined.
55 infection, but the cellular sources of iNOS are ill defined.
56 al mechanisms responsible for this, however, are ill defined.
57 ing pathways that regulate their development are ill defined.
58 tures justifying longer or shorter durations are ill defined.
59 mation, but the cellular mechanisms involved are ill defined.
60 induce hepatic character within the endoderm are ill defined.
61 eurons and oligodendrocytes after CNS injury are ill defined.
62 development and progression, but mechanisms are ill defined.
63 ion in shear-resistant cell arrest on VCAM-1 are ill defined.
64 t govern neutrophil migration across the BBB are ill defined.
65 y Ranbp2 in tissue homeostasis, such as RPE, are ill defined.
66 nhibition play in the pathophysiology of FXS are ill defined.
67 ise mechanisms governing this susceptibility are ill defined.
68 he underlying causative molecular mechanisms are ill defined.
69 , although the precise contributions of each are ill defined.
70 in PDAC pathogenesis, epigenetic alterations are ill defined.
71 statin and immune cells from the bovine host are ill defined.
72 terms of molecular processes and cell fates are ill defined.
73 ms that regulate obesity-driven inflammation are ill defined.
74 ated, but the cell-specific roles in the StV are ill defined.
75 ers where the functions of pSTAT1 and uSTAT1 are ill defined.
76 llular mechanisms responsible for this event are ill defined.
77 fferent IFN-I sources and signaling pathways are ill defined.
78 isms by which CENP-Bs effect their functions are ill defined.
79 r mechanisms of action in pulmonary diseases are ill defined.
80 s in this ecosystem and to clinical outcomes are ill defined.
81 n recognized in the adult and its management are ill defined.
82 ar mechanisms that underlie these properties are ill defined.
83 s that drive neurogenesis within these zones are ill defined.
84 immune protection in this patient population are ill defined.
85 fector activities in vivo at infection sites are ill defined.
86 nd 2 (M2; crisis) of human replicative aging are ill defined.
87 usceptibility to contact allergic dermatitis are ill defined.
88 rder, brain regions affected in the disorder are ill defined.
89 r complications, and associated risk factors are ill defined.
90 athways controlled by the actin cytoskeleton are ill defined.
91 ricuspid valve replacement in young children are ill defined.
92 g SAg-associated immunosuppression in humans are ill-defined.
93 m cell maintenance, but the ligands involved are ill-defined.
94 nal consequences of takotsubo cardiomyopathy are ill-defined.
95 rgent evolution of "new" enzymatic functions are ill-defined.
96 et the roles for the toxins during infection are ill-defined.
97 mechanistic links between Idic15 and autism are ill-defined.
98 oglial cells in vivo during CNS autoimmunity are ill-defined.
99 However, the substrates for these enzymes are ill-defined.
100 ated kinase pathway, although the mechanisms are ill-defined.
101 after, yet the underlying neural mechanisms are ill-defined.
102 d, the molecular functions of the polyamines are ill-defined.
103 s underlying enhanced somatic susceptibility are ill-defined.
104 ry mechanisms and neuronal circuit functions are ill-defined.
105 that contribute to a protumorigenic ecology are ill-defined.
106 P dynamics in these subcellular compartments are ill-defined.
107 r, biological predictors of response to CIRT are ill-defined.
108 ma, but its pathogenesis and natural history are ill-defined.
109 as being important, but their specific roles are ill-defined.
110 -OPA1 in mitochondrial fusion and energetics are ill-defined.
111 rs; however, the mechanisms for this process are ill-defined.
112 any of the parameters, such as force fields, are ill-defined.
113 er their roles in astrocytic physiology have been ill defined.
114 ronic infections such as active tuberculosis is ill defined, although several case reports and small
116 tion to RSV genetic and antigenic diversity, is ill defined and has implications for persistence and
117 inflammation, such as rheumatoid arthritis, is ill defined and probably requires tight regulation.
118 olved in cell cycle regulation, but its role is ill defined and the mechanisms have not been explored
122 in B cell and T cell maturation or function are ill defined, and few transcriptional targets are kno
123 intains its plasmid-encoded resistance genes is ill-defined, and novel targets for the treatment of V
125 role of human CAFs in cancer progression has been ill-defined because human CAFs lack a unique marker
126 ical consequences of this replicative stress are ill defined, but any "ageing" effect would carry the
127 2 in the pathogenesis of human breast cancer are ill-defined, but our analysis of publically availabl
128 sms of bladder granulomogenesis and fibrosis are ill defined due to the prior lack of tractable anima
131 ingly, the transgenic cartilaginous elements were ill defined, intermingled with surrounding connecti
132 anisms underlying antigen cross-presentation are ill-defined, most notably in human dendritic cells (
134 Without smoothing, imputation is likely to be ill-defined or jump erratically from one strain to an
135 the precise mechanisms of MeHg neurotoxicity are ill-defined, oxidative stress and altered mitochondr
136 ution of the East Antarctic Ice Sheet (EAIS) is ill defined, restricting our appreciation of potentia
138 by which these improvements occur, however, are ill-defined; thus, the therapeutic potential of exer
139 rbed on GC, for which the voltammetric peaks were ill-defined, too small for coulometric analyses to
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