1 na, including motivational conflict, that it
sets out to.
2 In this study, we
set out to 1) investigate striatal development in autism
3 uestion, the MAL-ED network of investigators
set out to achieve 3 goals: (1) develop harmonized proto
4 Here, we
set out to address the motor network activity and synchr
5 Therefore, we
set out to address the role of a specific GSL (gangliosi
6 We
set out to address this issue by studying how various mR
7 We
set out to address this problem by generating multiple g
8 We
set out to address whether neglect presentation could be
9 We
set out to analyze (1) our experience in diagnosing gian
10 This study
set out to analyze such factors produced or induced by I
11 This study
set out to analyze the brains of selected arthropods wit
12 We
set out to analyze the development of this connectivity
13 We
set out to analyze the role of two major non-HLA gene po
14 We
set out to analyze the very early phenotypic expression
15 We therefore
set out to assess the association between preoperative C
16 We
set out to assess the contribution of ER stress, oxidati
17 We
set out to assess the dynamics of retinal injury after a
18 We
set out to assess the mechanisms underlying a previous r
19 Here we
set out to assess this hypothesis, and find an unexpecte
20 We therefore
set out to assess whether children diagnosed after the a
21 ecognize microbial or endogenous signals, we
set out to assess whether their functions are locally in
22 Here we
set out to better understand how miR-122 inhibition infl
23 Here, we
set out to better understand the regulation of MMPs by i
24 We
set out to bridge this gap.
25 l Nucleotide Sequence Database Collaboration
set out to capture, preserve and present globally compre
26 We
set out to characterise the changes in macroscopic muscl
27 Therefore, we
set out to characterize a distinct human NK cell populat
28 Therefore, we
set out to characterize alterations in miRNA expression
29 We thus
set out to characterize BAP1 in CM and discovered an une
30 Using fMRI we
set out to characterize both the task and stimulus depen
31 In this study, we
set out to characterize changes in DNA methylation and g
32 Herein we
set out to characterize the carbohydrate minimal binding
33 We
set out to characterize the cell types of the amphioxus
34 We therefore
set out to characterize the cellular and molecular immun
35 We
set out to characterize the effects of exogenous methane
36 We
set out to characterize the evolutionary co-variation su
37 Here, we
set out to characterize the physical interaction between
38 We
set out to characterize the retention of acquired tolera
39 In this investigation, we
set out to characterize the roles of the WDR5 subunit in
40 Here we
set out to characterize transcriptional heterogeneity in
41 erstand its apparent biological activity, we
set out to chemically synthesize d-allo-ShK and determin
42 Therefore, we
set out to clarify the functional relevance of C3b bindi
43 We
set out to clarify these relationships using polarized h
44 We
set out to clone and characterize a novel dog allergen,
45 d the Mdr2:CCR1 double knockouts (DKOs), and
set out to compare inflammation and tumorigenesis among
46 Here we
set out to compare protein synthesis in haematopoietic s
47 We
set out to compare several measures of community viral l
48 We
set out to compare the incidence of bowel repair and/or
49 Therefore, we
set out to compare three experimental protocols using mi
50 We
set out to comprehensively study the role of genetic var
51 We
set out to conduct the first review study of adult intus
52 rities in regeneration among vertebrates, we
set out to define at high resolution the changes in gene
53 We
set out to define precisely the morphological events of
54 We
set out to define the role of 1alpha,25-dihydroxy vitami
55 We
set out to define the role of UL31 in CMV replication.
56 f pathology development remained unclear, we
set out to delineate in detail the underlying pathogenes
57 Here, we
set out to delineate the protein degradation mechanism o
58 We
set out to deorphanize a subset of putative Drosophila o
59 We therefore
set out to describe cellularization in the beetle Tribol
60 The study
set out to describe the involvement of the nursing team
61 accreditation to international standards, we
set out to design and assess an accreditation procedure
62 We
set out to design, synthesize and optimize a DNA-minimal
63 The present study
set out to determine consistent, specific regional brain
64 We
set out to determine how nutrients diffuse during extrac
65 We
set out to determine if adhesive ligand tether length is
66 In this study, we
set out to determine if chronically activated microglia
67 closely related Drosophila melanogaster, we
set out to determine if integrative analysis of daily ac
68 In this study, we
set out to determine if the same is true for B cells usi
69 genes in cases of uncomplicated malaria, we
set out to determine if there was any evidence of a sele
70 In the current study, we
set out to determine its assembly in aqueous solution.
71 Here we
set out to determine the differential contributions and
72 Here, we
set out to determine the disease mechanism of 7 de novo
73 ing a new model of mild contusion injury, we
set out to determine the effect of contusion on iGAS bac
74 Hence we
set out to determine the effects of TIGAR expression on
75 We
set out to determine the etiology of the craniofacial ph
76 Here, we
set out to determine the extent to which dynamic changes
77 We
set out to determine the frequency of TH17 cells in pati
78 e factors and effective vaccine antigens, we
set out to determine the genetic determinants of K. king
79 Here we
set out to determine the genetic reasons for the differe
80 We
set out to determine the independent association of diff
81 nctions of HuD in a variety of processes, we
set out to determine the mechanisms that promote HuD mRN
82 Here we
set out to determine the mechanisms underpinning variant
83 We
set out to determine the molecular mechanisms underlying
84 We
set out to determine the physiological relevance and cel
85 We therefore
set out to determine the precise contributions of Esco1
86 We
set out to determine the specific AMPAR subunit required
87 nteract and affect the function of TRPV1, we
set out to determine the structural features of these li
88 We
set out to determine the structural properties of membra
89 In this report, we
set out to determine what viral components are responsib
90 In this study, we
set out to determine whether 5-AzaCdR treatment can repr
91 On the basis of these results, we next
set out to determine whether AMG655 possibly interferes
92 We
set out to determine whether an enteral supply of argini
93 ly demonstrated to enhance HIV infection, we
set out to determine whether any of the liquefaction-gen
94 We
set out to determine whether any of these genes are invo
95 We
set out to determine whether attenuated total reflection
96 We
set out to determine whether B-cell tolerance to A/B-inc
97 Here, we
set out to determine whether changes in rate constants r
98 ion genetic analysis of wild populations, we
set out to determine whether evidence supports a role fo
99 To address this challenge, we
set out to determine whether follow up for surgical site
100 rtant to glomerular permselectivity, we next
set out to determine whether IP receptor agonism similar
101 We
set out to determine whether movements during REM sleep
102 We therefore
set out to determine whether NS3 from the replicatively
103 Here we
set out to determine whether oscillatory activity in the
104 ses iron absorption in infants is unclear.We
set out to determine whether prebiotic consumption affec
105 We
set out to determine whether the 1858T allele of PTPN22
106 or threonine, my group at the Salk Institute
set out to determine whether the polyomavirus middle T-t
107 We
set out to determine whether this important mechanical c
108 lular protein kinases, and in this study, we
set out to determine whether this modification is requir
109 fter establishing this reward modulation, we
set out to determine whether we could correctly classify
110 We
set out to determine whether, similarly, common cancer s
111 This study
sets out to determine whether the products of advanced o
112 We
set out to develop a method to overcome this obstacle by
113 nt animal models do not meet these needs, we
set out to develop a nonhuman primate model of pertussis
114 Thus, we
set out to develop a NSCLC model to further characterize
115 We
set out to develop a simple, low-cost odour-baited trap
116 We
set out to develop an inhibitor compound targeting the b
117 Therefore, we
set out to develop dCK inhibitors with favorable pharmac
118 s of affecting disease progression, our team
set out to develop LRRK2 inhibitors to test this hypothe
119 Therefore, we
set out to develop the first, to our knowledge, robust a
120 and functions in the dendritic endosome, we
set out to discover how Nsg1 and Nsg2 localization to en
121 The present review
sets out to discuss recent developments and prospects of
122 This review
sets out to discuss the strengths and limitations of pre
123 This study
set out to elucidate the functional consequences of OPN
124 Next, we
set out to elucidate the genetic network that results in
125 Here, we
set out to elucidate the mechanism underlying cAMP-depen
126 We
set out to elucidate the role of Hh signaling in CP-CML
127 We
set out to elucidate the role of NADPH oxidase-generated
128 We therefore
set out to employ a battery of behavior tests, including
129 We
set out to establish a new human challenge model and asc
130 We
set out to establish a novel model for RPGR disease to t
131 This study
set out to establish if TAG levels persist as a metaboli
132 present a global Porifera microbiome survey,
set out to establish the ecological and evolutionary dri
133 We
set out to estimate the annual number and costs of new P
134 CD8(+) T-LGL leukemia as a model disease, we
set out to evaluate and compare the TCR deep-sequencing
135 ere combined immunodeficiency (ADA-SCID) and
set out to evaluate the association of these 2 clinical
136 Thus we
set out to evaluate the best tools that can be used loca
137 We
set out to evaluate the kinetics of (64)Cu-ATSM distribu
138 Therefore, we
set out to evaluate whether NONO could be involved in th
139 We
set out to examine age-related seroprevalence in a commu
140 Here, we
set out to examine if the direct interaction between two
141 We
set out to examine the prevalence of this mutation in in
142 lly diverse and widely used CB2 agonists, we
set out to examine whether CB2 modulates primary murine
143 As both are heritable, we
set out to examine whether there is a genetic correlatio
144 This paper
sets out to examine key issues associated with biorefini
145 In this study we
set out to explain the differing effects of parabiosis w
146 We
set out to explain the full set of measurements by model
147 Here, we
set out to explore dynamic aspects of twister RNA foldin
148 vity of peptides frequently overlap, we here
set out to explore possible antibacterial effects of int
149 We
set out to explore the role of IL-17 in the host respons
150 the variance in brain microstructure, so we
set out to explore their combined effect on the white ma
151 Here, we
set out to explore what role FFA2 may play in regulation
152 In the current study, we
set out to explore whether adipose tissue infiltration b
153 Here, we first
set out to express and purify the full length Reelin pro
154 The present work
set out to fabricate an engineered muscle flap bearing i
155 Herein, we
set out to functionally characterize a novel HCM-associa
156 We then
set out to further explore and validate our hypothesis i
157 In this study, we
set out to further investigate the role of PilC1 and Pil
158 In this study, we
set out to further understand CD27 as an immunomodulator
159 Here, we
set out to gain further insights into the function of SM
160 Here, we
set out to generate a model in which to decipher signali
161 This synopsis
sets out to highlight recent advances in the field of am
162 We
set out to identify and functionally characterize geneti
163 We
set out to identify and phenotype allergen-responsive ce
164 Hence, this study
set out to identify and validate a small, clinically app
165 We also
set out to identify characteristics of responders.
166 We
set out to identify factors that bind these amyloids and
167 We
set out to identify factors that promote arterial endoth
168 We
set out to identify GCC inhibitors that may be of benefi
169 tory processes that link these responses, we
set out to identify genes that govern early responses to
170 Here, we
set out to identify genes whose products may be involved
171 We
set out to identify genetic alterations that underlie re
172 In this study, we
set out to identify genetic modifiers of collagen deposi
173 We
set out to identify geographical characteristics that co
174 To investigate this, we
set out to identify large chromosomal domains of epigene
175 We
set out to identify mechanisms of dying cardiomyocyte en
176 Here we
set out to identify mechanisms of specificity in protein
177 on of up to several hundred target genes, we
set out to identify microRNAs that target genes in all p
178 We
set out to identify muscles whose stimulation produced a
179 Using this knowledge, we
set out to identify new candidates for context genes whi
180 Here we
set out to identify new high-penetrance susceptibility g
181 We
set out to identify novel and functionally important end
182 In this study, we
set out to identify novel components involved in the sec
183 pounds currently in clinical development, we
set out to identify novel effective treatments for T-PLL
184 In individuals of African ancestry, we
set out to identify null and damaging missense variants,
185 Prospective Evaluation and Risk Assessment)
set out to identify risk factors for development of pain
186 We therefore
set out to identify specific target antigens in PAH lung
187 ing plasmodial proteins in host invasion, we
set out to identify such proteins as targets of small gl
188 Here we
set out to identify the biological mechanism affected by
189 In this study we
set out to identify the chemotactic signals that orchest
190 Thus, we
set out to identify the core promoter region and the tra
191 o the regulation of Glut4 palmitoylation, we
set out to identify the palmitoyl acyltransferase (PAT)
192 ing the responsible molecular mechanisms, we
set out to identify the relevant cellular source of thes
193 f a single cyclopean image (cyclopotopy), we
set out to identify the stage in visual processing at wh
194 We
set out to identify whether maternal copy number variant
195 ucidate the regulatory mechanism of Wor1, we
set out to identify Wor1-interacting proteins using a ye
196 In 1990, we
set out to improve the methods used to make genetic mosa
197 ging offers challenges and opportunities, we
set out to investigate and optimize image processing tec
198 We
set out to investigate DMS as a means for separating ato
199 Here, we
set out to investigate effects of UV-A and solar-simulat
200 Therefore, we
set out to investigate how neuronal gp130 regulates mech
201 We
set out to investigate how PGE2 regulates human ILC2 fun
202 We
set out to investigate if the failure of cultured mesenc
203 ociated with these ER abnormalities, we next
set out to investigate if the pattern of Ca(2+) oscillat
204 We, therefore,
set out to investigate in vivo changes in presynaptic do
205 Nearly 50 years ago, I
set out to investigate the clinical problem of hypoglyce
206 We
set out to investigate the emerging intratumoral heterog
207 benefit and ultimately survival outcomes, we
set out to investigate the fate of MDSCs after transfer
208 Here we
set out to investigate the genome-wide localization patt
209 In this study, we
set out to investigate the long-term repeatilibity and r
210 To this end, we
set out to investigate the metabolic effects of NO in cu
211 We
set out to investigate the molecular basis of the aberra
212 We
set out to investigate the molecular mechanisms for FXR-
213 We
set out to investigate the possibility of reducing gastr
214 We
set out to investigate the possible role of microRNAs in
215 We
set out to investigate the potential role of the 9p21.3
216 We
set out to investigate the role in immunity of innate re
217 n contributors to Parkinson disease (PD), we
set out to investigate the role mitochondrial JNK plays
218 In this study, we
set out to investigate the role of humoral versus cellul
219 We
set out to investigate the role of miR-127 in lung injur
220 We
set out to investigate the role that cytokine signaling
221 In the current study, we
set out to investigate this possibility utilizing recomb
222 In this work, we
set out to investigate under what conditions a broadly u
223 Therefore, we
set out to investigate whether DJ-1 plays a role in HD.
224 Here, we
set out to investigate whether Galphai-GIV is a druggabl
225 We
set out to investigate whether mildly basic 2-aminopyrim
226 We
set out to investigate whether Pten is required for hema
227 Here, we
set out to investigate whether strain-specific variabili
228 Here we
set out to investigate whether such type of patterned ne
229 This study
set out to investigate whether these chemokines could se
230 are often generated in immune responses, we
set out to investigate whether these factors are relevan
231 In this study, we
set out to investigate which receptor can best be deploy
232 lamostriatal projection is heterogeneous, we
set out to isolate and study the thalamic afferent input
233 Here we
set out to learn more about the underlying mechanism by
234 Therefore, we
set out to map H2-IA(b)-restricted epitopes along the PV
235 the small protein GB1 as a model system and
set out to map its mechanical unfolding transition-state
236 important determinants of viral tropism, we
set out to map the CV-A24 receptor repertoire and establ
237 Herein, we
set out to maximize the discriminating power of HRM + SV
238 This study
set out to measure cardiac metabolites in non-failing he
239 We
set out to measure changes in HDL in sepsis-mediated ARD
240 In this study, we
set out to probe the function of residues Phe(114) and M
241 ductive and transforming viral infection, we
set out to provide the first robust estimate of the prev
242 standardize the (13)C-MFA modeling work, we
set out to publish a user-friendly and programming-free
243 We
set out to quantify and understand how WGS compares with
244 Here, we
set out to quantify Mcp5 organization and identify the b
245 Therefore, we
set out to quantify the contributions from polar and non
246 We
set out to reveal the mechanisms by which embryos are pr
247 We thus
set out to review both published and unpublished informa
248 Given these unexpected findings, we
set out to revisit the role of Hif-1alpha in cell-autono
249 ative and Gavi, the Vaccine Alliance, UNICEF
set out to secure access to IPV supply for around 100 co
250 We
set out to sequence the 9p21.3 region followed by a comp
251 In this work, we
set out to specifically test this hypothesis in the plan
252 Here, we
set out to study native SEPP1 synthesis in vitro to iden
253 We therefore
set out to study outcomes of LDKT with SBN, compared wit
254 Here we
set out to study systematically the neuroadaptive change
255 We
set out to study the associations of longitudinal food c
256 ressed on a broad spectrum of cell types, we
set out to study the expression of CD200 and CD200R on C
257 Here, we
set out to study the functional interaction of 18 relate
258 Therefore, we
set out to study the incidence and sequelae of HEV as a
259 We
set out to study the role of MOF in general hematopoiesi
260 important roles in cell fate transitions, we
set out to study their function during the glial progeni
261 sis for studies of antimalarial efficacy, we
set out to survey parasite carriage in 3 communities in
262 inversely linked to unit cell complexity, we
set out to synthesize a highly complex crystalline mater
263 ents in desirable solid-state properties, we
set out to systematically alter the molecular framework
264 either of these variants acts alone, we have
set out to systematically analyze in a large cohort of h
265 We
set out to systematically identify these subsets in huma
266 We therefore
set out to systematically interrogate epigenetic cancer
267 This review
set out to systematically investigate whether sex ratios
268 Here we
set out to tackle this issue in intact cells by an estab
269 We
set out to take a different approach and mimic the synth
270 In the present work, we
set out to test the generality of this concept by studyi
271 We
set out to test the hypothesis that forkhead box O1 (FOX
272 Using an in vivo model, we
set out to test the hypothesis that formaldehyde inhalat
273 We
set out to test the hypothesis that OGs are generated in
274 We
set out to test the role of adjuvant-mediated cell death
275 In this paper, we
set out to test these ideas within a framework of atomic
276 Here we
set out to test this vaccination strategy in the ferret
277 We
set out to test whether maternal voluntary exercise duri
278 We
set out to test whether mercury concentrations in the ur
279 Here, we
set out to test whether RNAi triggers targeting ATXN1 co
280 We
set out to test whether these complex group behaviours c
281 We
set out to test whether these two accounts of learning p
282 We
set out to turn pyridoxine (1a) into a catalytic chain-b
283 We
set out to uncover a role for IRE1alpha kinase activity
284 We
set out to uncover additional targeting proteins using u
285 We
set out to uncover the mechanism of APOBEC3C (A3C)-media
286 equisite for ExPEC-mediated pathogenesis, we
set out to understand how ExPEC colonizes this niche.
287 Here, we
set out to understand the extent to which shifts in geno
288 We
set out to understand the functions of the ATXN1-CIC com
289 In this study we
set out to understand the manner and extent to which int
290 Here, we
set out to understand the molecular basis for these diff
291 In this study, we
set out to understand the structural basis and impact of
292 The current study
set out to understand the structure-activity relationshi
293 We
set out to understand the underlying mechanisms of these
294 We
set out to understand why some consensus mutations fail
295 ssue of the Journal, Isanaka et al.:861-869)
set out to update an incidence correction factor used fo
296 ents diagnosed between 1985 and 2005, and we
set out to update it by incorporating more recently repo
297 We
set out to use objective outcomes data to determine the
298 This study
set out to validate a map book system for use in urban s
299 We
set out to validate these observations using a model of
300 molecular structure and bulk properties, we
set out to vary the electron affinity of the molecular b