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1 019 to assess which approaches work best and why.
4 e significant implications for understanding why a hypomorphic loss of BCCIP functions is more releva
5 design and provide mechanistic insights into why a leading INSTI retains efficacy against a broad spe
9 0S generation and offer an explanation as to why a subtle dysfunction of BCCIP can be tumorigenic but
10 igin, have latent skin competence explaining why aberrant hair follicles or sebaceous glands are some
12 tonic inhibition at low glucose, explaining why alpha-cells are electrically active under hypoglycae
13 wth than previously assumed, helping explain why alternative nitrogenase genes persist in diverse dia
15 age is underappreciated as a determinant for why an insulin granule is selected for secretion and may
16 rovide some answers to the question "How and why anchoring metal nanoparticles, clusters, or single a
18 ew the importance of stereology, and propose why and how it should be applied to the study of adult n
25 and misleading-that clearly explain how and why anthropogenic sensory pollutants impact organisms.
26 ng epitopes is crucial for the understanding why antibodies display different therapeutic activities
27 inance contrast in future work investigating why aposematic patterns take the particular forms that t
30 cond, ungulates are large and long-lived, so why are they occasionally intermediate instead of defini
32 sensitive to feedback inhibition, explaining why assembly occurs under physiological conditions that
33 e perirolandic cortex and it remains unknown why atrophy in different locations would cause the same
34 ariables indicate about the speaker-that is, why attention to vocal cues may be favored in intrasexua
37 A repair is poorly understood, it is unclear why BRCA-deficient cells require APE2 for viability.
40 mulate its lipid kinase activity, explaining why catalytically active Fig4 is required for maximal PI
41 nce of RDH expression on CDK11 could explain why CDK11 is essential for the growth of many cancers.
43 time evolution as a way to begin deciphering why certain aspects of flowering are seemingly so conser
46 ralizing Marcus theory framework, we explain why charge-transfer-dynamic modulations can only be unve
48 ides important information for understanding why children of depressed mothers may be more vulnerable
49 in chronic back pain, which helps explaining why chronic pain can be resistant to change, and where c
51 The editorialist discusses the findings and why closing the intention-to-behavior gap for those will
53 tical work has been devoted to understanding why colloidal nanocrystals (NCs) self-assemble into such
54 his work provide a framework for determining why common groundwater constituents affect the E(H)-depe
55 contradicting evidence in cells, focusing on why controversies about the composition, properties, and
57 s with comorbidities may offer insight as to why COVID-19 symptoms are often more severe in these ind
58 o elucidate the role of the CR and determine why CR deletion generates toxicity, we designed PrP(C) c
60 d to voluntary action, but an explanation of why decisions to act emerge at particular points in time
62 taxa, leading to new knowledge about how and why developmental pathways are rewired and elaborated th
68 ty in the fusiform arise in development, and why does it develop so systematically in the same locati
69 ss two unresolved fundamental questions: (i) why does repeat behavior differ between model systems an
71 tor occupation in the striatum, and explains why dopamine ramps are an effective signal to occupy dop
73 Can the Second Law of Thermodynamics explain why ecosystems naturally organize into a complex structu
76 imensional interactions provide insight into why endocardial mapping alone may not fully characterize
79 D risk genes, and explain, at least in part, why every HSV1-infected person is not equally likely to
80 nt a conceptual framework to explain how and why females might evaluate a male's BT before mating.
81 oncerned with understanding whether, how and why genetic differences between human beings are linked
82 eed to be taken to authentically communicate why genomic research is necessary and how data donation,
83 e discuss the optimal group size and explain why, given the highly infectious nature of the disease,
86 nce of most species, this is the main reason why habitat loss has been highlighted as the main threat
87 e perceptual-inference hierarchy may explain why hallucinations and delusions tend to cluster togethe
91 other equally, but he has not yet explained why human morality also allows and enables much inequali
92 into account, we can address the question of why humans seek to learn, teach, and innovate - three pr
93 th unrelated and unfamiliar individuals, and why humans' unprecedented cooperative flexibility is nev
95 e purpose of this Perspective is to consider why identification rates continue to be low in untargete
98 proteins to MCL-1 and vice versa, explaining why in vivo combinations of BCL-2 and MCL-1 antagonists
101 clinical-radiological paradox could explain why individuals with similar injuries can respond differ
105 an and animal minds, it becomes clearer: (1) why it is reasonable to assume that cognitive mechanisms
108 lopments in the postwar period and considers why it took so long to hold up a mirror to the past.
111 he present interglaciation(7), understanding why LIG global mean sea level may have been six to nine
112 eedles may be the missing link in explaining why lightning flickers with multiple discharges, but thi
114 which provides a mechanistic explanation for why Lis1 is required for efficient transport of many dyn
116 urther metabolic stress, which could explain why local neurodegeneration does not remain confined, bu
117 and alterations in this map may help explain why lonely individuals endorse statements such as "peopl
118 affinities for the mu and KOR could explain why lower doses of naltrexone can have greater clinical
119 red in arcs with thick crust, which explains why magmatism and differentiation in continental arcs, l
120 ation, and this stress tolerance may explain why many cancers aberrantly express MAGEs Here, we prese
123 lin T1 than primary cells, which may explain why many LRAs are functional in model systems but relati
124 tline will deliver new insights into how and why masting patterns might respond to a changing environ
125 d then we consider possible explanations for why MCU-deficient mice are spared from energy crises und
127 ration, providing a potential suggestion for why metformin increases acid secretion and reduces gastr
131 that we can better understand how, when, and why moonlighting proteins may take on multiple roles.
133 For example, one would like to understand why mu-OR is more selective to G(i) than a stimulatory G
134 of specific DNA-bridging proteins like LacI, why multiple bridges are required to create stable indep
136 incing theories are still lacking to explain why natural evolution and human design have failed to op
137 le is selected for secretion and may explain why newly synthesized insulin is preferentially secreted
138 levels at median exposure levels may explain why no relationship between exposure to TTR-binding comp
139 this provides a theoretical explanation for why noninteger dimensions are useful in many branches of
141 -cell level(13) means that precisely how and why nuclei reorganize remains an area of intense investi
142 e concept of empathy within nursing, explain why nurses are sometimes warry of adapting concepts from
144 OMVs with host cell membranes to understand why OMV uptake depends on the length of constituent lipo
145 further investigation is needed to determine why only a minority of those trained have begun treating
146 stinct AD phenotypes here could help explain why only a subset of AD patients typically respond to an
153 of NLRP3 inflammasome activation and explain why patients with XLA are prone to develop Crohn's disea
156 ovides a computational and neural account of why people learn less from observing outgroups.SIGNIFICA
157 re widely used to investigate when, how, and why people make judgments that are consistent with utili
158 troversy over two competing hypotheses about why people object to randomized experiments: 1) People u
159 lation to energetics, but it remains unclear why people reduce asymmetry in step lengths, but prefer
161 tly, thus revealing the structural basis for why peptidiscs can stabilize such a large variety of mem
163 common double mutations are likely to be and why PI3Kalpha with double mutations responds effectively
164 xosome-deficient mutants, perhaps explaining why plants have evolved mechanisms to suppress PROMPTs.
165 ocal mechanism for CP regulation can explain why plasticity induced by the odorant geranyl acetate (w
166 r experimental testing but also help explain why polarization in beliefs about human-caused climate c
168 f new X-ray structures of Thal also explains why premixing of FDHs with reduced flavin adenine dinucl
169 binding and catalysis and clearly elucidate why previous structures of mammalian dCTPase were cataly
170 electrostatic potential to establish how and why protons intercalate in V(2) O(5) in aqueous media.
171 This advance provides an understanding of why psilocybin is showing considerable promise as a ther
172 erefore, to understand not only how but also why psychology varies, we need to grapple with cross-tem
173 Images of large areas provided insight into why published values of ENS density vary up to 150-fold-
176 to understand where corals bleach, when and why-resulting in a large-yet still somewhat patchy-knowl
177 e we propose that Gestalt theory may explain why rodent islet architecture has historically been seen
178 S-RNase activity by NaTrxh helps to explain why S-RNase alone could be insufficient for pollen rejec
179 thrombotic strategies, this article explains why safer anticoagulants are needed, provides the ration
182 the lack of stereoselectivity, and evaluates why selectivity may not occur and when it will likely oc
183 cell reduces its contractibility and explain why SERCA gene therapy, a change in calcium handling to
184 ference in OCN regulation, which may explain why serum concentrations of OCN are higher in mouse than
185 s in promoting multimerization and explained why several C-terminal domain mutations are remarkably r
187 ulus to cause insulin resistance, explaining why short-term, insulin-dependent glucose utilization do
188 e size of the window region elicits EADs and why shrinking the window region can eliminate them.
189 ellular hemoglobin composition also explains why sickle trait, the heterozygous condition, and the co
191 uration and survival, which may help explain why Slc7a5 mutations prevent normal brain development an
192 more, these results shed additional light on why sleep is important during early childhood, a period
199 Consequently, the reader will understand why some crystals break during polymerization, while oth
204 g studies could advance our understanding of why some individuals develop mental health disorders.
205 counts continue to rise, it remains unclear why some individuals recover from infection, whereas oth
208 mportant questions have remained unanswered: why some patients develop severe disease, while others d
209 isease (CVD) is different for every patient, why some patients with type 2 diabetes mellitus (T2DM) d
211 xclusive competing interactions, may explain why some proteins are dynamic while others are rigid.
215 Our findings highlight possible reasons why some underrepresented minority and female postdocs c
216 esolved questions remain, such as the reason why SOST binds to LRP6 E1E2 with higher affinity than to
218 amylose revives a long-standing question of why starch granules contain amylose, rather than amylope
220 They also provide a possible explanation why such connectivity and activity patterns have been pr
222 emerge and persist throughout nature(1), and why such structures often exhibit similar scale-invarian
224 resent in the CO-poisoned layer that explain why, surprisingly, CO desorbs at stepped and flat Pt cry
225 Fe(III) species over several hours explains why SznF was previously purified and crystallographicall
227 studies provide a structural explanation of why TAT-SF1 must be displaced before the stable addition
228 stallography and NMR, providing insight into why tetramer stabilization inhibits amyloid assembly.
230 plant-pathogen response, which could explain why the 20rDNA line is hyper-resistant to both bacterial
234 ings provide a mechanistic explanation as to why the deletion of CFHR3 and CFHR1 is protective in AMD
236 countered by the NS1 protein, and establish why the dsRNA-binding activity of NS1 is required for it
237 tive effect of Dantu, and fresh insight into why the efficiency of P. falciparum invasion might vary
238 swer to this vexing problem, while exploring why the Elp1 gene that is mutated in familial dysautonom
241 nt difficult to make and has been the reason why the influence of lens growth on visual function rema
244 ated intervention to improve patient safety, why the intervention did or did not lead to safety impro
247 r study advances an adaptive explanation for why the placenta evolves by arguing that an increased de
248 Our data provide a mechanistic explanation why the same proteins can act either as tolerogens or as
250 esponse, we reply to these concerns, discuss why the technical-reasoning hypothesis does not minimize
253 sis, we begin to illustrate how, and explore why, the developmental decision of metamorphosis relies
257 beta-adrenergic sensitivity may help explain why therapies that work in HFrEF are ineffective in HFpE
258 , and less so Ca(V)3 channels, it is unclear why there have not been major shifts toward dependence o
260 properties that led to such widespread use, why there is now an increasing drive to minimize usage,
261 -down MALDI-ISD FT-ICR mass spectra and show why these distributions can deviate from theoretical pro
262 es in synapsis, providing an explanation for why these genes have evaded previous genetic screens.
264 these pfk13 variants, potentially explaining why these resistance alleles have not increased in frequ
268 survive in changing environments can explain why they encode multiple eIF4E (LeishIF4Es) and eIF4G (L
269 w descriptions of RHV-specific responses and why they fail to prevent persistent infection in this mo
274 ice lacking muscle-derived IL-6 (mIL-6), and why this deficit is correctable by osteocalcin but not b
280 as the "bamboo ceiling." It remains unclear why this problem exists and whether it applies to all As
282 R9 and low levels of TLR7, which may explain why TLR9 dysregulation is particularly consequential ear
284 alling pathways in the cell, and this may be why TP53 is the most commonly mutated gene in human canc
285 me community practitioners as evidence as to why transplants should not be performed at this time, co
286 e cerebellum in SCA17 raises the question of why ubiquitously expressed polyQ proteins can cause neur
287 babilities do not capture the varied reasons why vaccines fail to advance to regulatory approval.
288 A long-standing mystery in the field is why vertebrates have two non-visual arrestins, arrestin-
291 goal of this research has been to determine why VZV, when grown in cultured cells, invariably is mor
293 grafts for corneal transplantation, which is why we are working toward on expanding cooperation with
294 over human evolutionary history may explain why we cooperate readily with unrelated and unfamiliar i
296 s review, we present a brief overview of (a) why we should be interested in stress in the context of
297 and insightful theory of obligation explains why we sometimes sense an obligation to treat each other
299 onavirus disease 2019 (COVID-19) and discuss why we think that a clinical trial of a drug in this cla