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1 ma-free days (i.e., fewer days without acute brain dysfunction).
2 d of mechanisms by which infection can cause brain dysfunction.
3 lular and molecular mechanisms that underlie brain dysfunction.
4 s well as processes that lead to age-related brain dysfunction.
5 sses the blood-brain barrier (BBB) to induce brain dysfunction.
6 vels may contribute to neurodegeneration and brain dysfunction.
7 y present a sensitive measure of HIV-related brain dysfunction.
8 otential therapeutic targets for age-related brain dysfunction.
9 ily a neurological disorder with progressive brain dysfunction.
10 he degenerative diseases of aging, including brain dysfunction.
11  do not understand the mechanisms underlying brain dysfunction.
12 elopmental-onset model of myotonic dystrophy brain dysfunction.
13 standing and potentially treating poststroke brain dysfunction.
14 ally high phenylalanine concentrations cause brain dysfunction.
15 adherence to delirium guidelines and reduced brain dysfunction.
16 a pathway from neuroinflammation to systemic brain dysfunction.
17 ly extracellular histones, in sepsis-related brain dysfunction.
18 MAPK signaling after TBI and prevent lasting brain dysfunction.
19 evels of somatic mosaicism can contribute to brain dysfunction.
20 tially also rendered the brain vulnerable to brain dysfunction.
21 arly iron treatment in preventing ID-induced brain dysfunction.
22 rocytic consequences of cirrhosis-associated brain dysfunction.
23 lying synaptic and nonsynaptic mechanisms of brain dysfunction.
24 d reverses neurofibrillary tangle-associated brain dysfunction.
25 ay help prevent and modulate the severity of brain dysfunction.
26 urbs inhibitory synapse formation and causes brain dysfunction.
27 acement, debility, neurologic disorders, and brain dysfunction.
28 ed by H2O2, might contribute to H2O2-induced brain dysfunction.
29 l neurodegenerative diseases and age-related brain dysfunction.
30 whereas recessive mutations lead to skin and brain dysfunction.
31 n and cell death do not play a major role in brain dysfunction.
32 ently influence the anatomic localization of brain dysfunction.
33 treatment are recommended to prevent ongoing brain dysfunction.
34  care unit survivors at high risk of ongoing brain dysfunction.
35 onnecting DNA sequence to disease-associated brain dysfunction.
36 lth problem in the form of acute and chronic brain dysfunction.
37 tient is not necessarily free of significant brain dysfunction.
38 zepine drugs and may lower the risk of acute brain dysfunction.
39 on of pain in migraine is due to lateralized brain dysfunction.
40 her factors in shaping the risk of postnatal brain dysfunctions.
41 consistent with the concept of developmental brain dysfunction, a term we use to describe the abnorma
42 rium is a highly prevalent syndrome of acute brain dysfunction among critically ill patients that has
43 ignals as potent drivers of both age-related brain dysfunction and brain rejuvenation.
44 dosage imbalance for Synj1 may contribute to brain dysfunction and cognitive disabilities in DS.
45  (SAE) is characterized by acute and diffuse brain dysfunction and correlates with long-term cognitiv
46 asoprotective role of PGRN may contribute to brain dysfunction and damage in conditions associated wi
47 ognized contribution of peripheral organs to brain dysfunction and damage.
48 a, including concussion, can lead to chronic brain dysfunction and degeneration but the underlying me
49 mmune homeostasis and counteract age-related brain dysfunction and diseases.
50 precision medicine to mitigate immune-driven brain dysfunction and improve mental health outcomes.
51  known about the effect of biological sex on brain dysfunction and injury mechanisms.
52 rch furthers our understanding of AD-related brain dysfunction and motivates refining existing framew
53 ufficient cerebral blood flow contributes to brain dysfunction and neurodegeneration.
54 on that may underlie molecular mechanisms of brain dysfunction and neurodegeneration.
55 diovascular disease, which converge to cause brain dysfunction and neurodegeneration.
56                                Stroke causes brain dysfunction and neuron death, and the lack of effe
57 estations of TBI (including a combination of brain dysfunction and psychological trauma and interrela
58  cerebral compliance, potentially preventing brain dysfunction and reducing stroke risk in hypertensi
59 crete population of neurons can cause global brain dysfunction and that phenotype severity depends on
60 sorders was to establish the most consistent brain dysfunctions and to address task- and subtype-rela
61 tandard iron indicators to detect ID-induced brain dysfunction, and evaluate the efficacy of early ir
62    However, uric acid is not responsible for brain dysfunction, and it has been suggested that purine
63  of brain cells, mechanisms of virus-induced brain dysfunction, and treatment strategies.
64 e disease with clear pathological hallmarks, brain dysfunction, and unknown etiology.
65  when disorders encompassed by developmental brain dysfunction are considered as a group, the penetra
66           Neuronal cell death and subsequent brain dysfunction are hallmarks of aging and neurodegene
67       The mechanisms by which sepsis induces brain dysfunction are likely to include vascular and neu
68 , the mechanisms contributing to SCI-induced brain dysfunction are poorly understood.
69 he CNV to a mechanistic understanding of how brain dysfunction arises.
70 is on micronutrient deficiency, and explores brain dysfunction as a possible mechanism.
71 zheimer transgenic mouse studies demonstrate brain dysfunction, as beta-amyloid levels rise, months b
72 e of vitamin D supplementation in mitigating brain dysfunction associated with sepsis which needs for
73 in which TAU has to be reduced to counteract brain dysfunctions associated with Dravet syndrome and t
74 his work opens perspectives to explore human brain dysfunction at early phases of development.
75                                     Studying brain dysfunction at this stage is difficult, and human
76 ewborns have a prominently increased risk of brain dysfunctions attributed to white-matter damage, wh
77 s, and has no effect on kidney, germ cell or brain dysfunction, but exacerbates liver pathology and p
78 vascular reactivity predicts prolonged acute brain dysfunction, but relationships between endothelial
79  to induce progressive neurodegeneration and brain dysfunction by causing axonopathy and conserved tr
80 e findings imply that regional variations in brain dysfunction can occur in Alzheimer's disease, with
81  information is useful for understanding how brain dysfunctions contribute to movement disorders such
82 phan ratios and presence or absence of acute brain dysfunction (defined as delirium/coma-free days) i
83 nine pathway activity in intensive care unit brain dysfunction (delirium and coma) remains unknown.
84                 The occurrence rate of acute brain dysfunction (delirium and coma) was 68.4% in the d
85                      Secondary outcomes were brain dysfunction (delirium or coma), length of ICU stay
86               We assessed patients daily for brain dysfunction (delirium, using Confusion Assessment
87 nvestigated cellular and molecular causes of brain dysfunctions derived from altered K-ATP channel fu
88 nuates the development of neuropathology and brain dysfunction during acute and chronic phases includ
89                     The consequence of acute brain dysfunction during crucial neurocognitive developm
90 oscale spatiotemporal activity with emergent brain dysfunction during seizures.
91 ry to understand the mechanisms that lead to brain dysfunction during seizures.
92 ed delirium, a common manifestation of acute brain dysfunction during sepsis.
93 lay an important role in the pathogenesis of brain dysfunction during sepsis.
94 nalysis provides more detailed estimation of brain dysfunction for the comparison of the 2 interventi
95             Delirium is a condition of acute brain dysfunction for which a pre-existing diagnosis of
96 ye movement disorders in patients with focal brain dysfunction have added to our understanding of hum
97    Additionally, possible mechanisms for gut-brain dysfunction have been identified, suggesting prima
98 benzodiazepine drugs may contribute to acute brain dysfunction, ie, delirium and coma, associated wit
99                                              Brain dysfunction improved: the mean delirium duration d
100 heral inflammation as potential mediators of brain dysfunction in AD may lead to the development of e
101 nd the underlying mechanisms associated with brain dysfunction in aged C57BL/6 male mice using a cont
102 yloid plaques and neurofibrillary tangles to brain dysfunction in Alzheimer disease is critical for t
103 ts in synaptic homeostasis may contribute to brain dysfunction in Alzheimer's disease.
104 us but are not bioindicators of brain ID and brain dysfunction in children.
105 etic therapies could address both muscle and brain dysfunction in DMD patients.
106 bryonic brain development are a component of brain dysfunction in DS.
107     To determine the metabolic substrates of brain dysfunction in DYT1 dystonia, we scanned 7 nonmani
108 stence of different mechanisms of underlying brain dysfunction in familial and sporadic schizophrenia
109  Tat may thus be an important participant in brain dysfunction in HIV dementia.
110 n defect of amino acid metabolism in humans, brain dysfunction in individuals with PKU is still not w
111 ated with fewer days alive and without acute brain dysfunction in intensive care unit patients.
112 al oscillations, is critical for elucidating brain dysfunction in neuropsychiatric disorders.
113 igodendrocyte defects account for aspects of brain dysfunction in NF1 that can be identified by neuro
114 s in which maternal IgG may cause persistent brain dysfunction in offspring.
115 at all 3 biochemical disturbances underlying brain dysfunction in phenylketonuria can be targeted by
116 to all 3 biochemical disturbances underlying brain dysfunction in phenylketonuria.
117 dies have suggested links between kidney and brain dysfunction in Plasmodium falciparum infection.
118 abuse and abstinence may underlie persistent brain dysfunction in primates and be a target for therap
119  form of plasticity that could contribute to brain dysfunction in psychiatric disease.
120  increasingly popular technique for studying brain dysfunction in psychiatric patients, and is widely
121 data are compatible with the hypothesis that brain dysfunction in RTT is caused by a loss of the MeCP
122 e measures, supporting distributed models of brain dysfunction in schizophrenia.
123 a need to generate serum measures that index brain dysfunction in the preanemic stage of ID, assess t
124 erstanding of the impact of hyperglycemia on brain dysfunction in the zebrafish model.
125 complex but more realistic representation of brain dysfunction in this illness.
126 brain barrier/neurological injury, and acute brain dysfunction, including delirium, remain unexamined
127 cephalopathy (SAE) is an acutely progressing brain dysfunction induced by systemic inflammation.
128  cortical pyramidal cells, which perpetuates brain dysfunction into adulthood.
129 cal entity, the pathophysiology resulting in brain dysfunction is not fully understood, although it i
130 improved outcomes for people with HIV (PWH), brain dysfunction is still evident.
131 e threshold for somatic mosaicism leading to brain dysfunction is unknown.
132                    Delirium, a form of acute brain dysfunction, is very common in the critically ill
133                 Cirrhosis is associated with brain dysfunction known as hepatic encephalopathy (HE).
134                  Stroke was defined as focal brain dysfunction lasting >/=24 hours from a vascular ca
135  disease risk, particularly those related to brain dysfunctions like learning disorders.
136                                              Brain dysfunction may be the most important and least st
137                                      Frontal brain dysfunction may underlie depression both in cerebr
138 prenatally and is Altman's model of "minimal brain dysfunction", may be a factor in at least some for
139 lycemia as a putative contributor to several brain dysfunctions observed in diabetes patients, such a
140 rst-episode schizophrenia indicates that the brain dysfunction occurred before clinical presentation.
141 ficantly more neuropsychological evidence of brain dysfunction on the Halstead Impairment Index (P=.0
142 s variably called acute brain failure, acute brain dysfunction, or altered mental status.
143 ociation between lowest daily hemoglobin and brain dysfunction (p = 0.69 for delirium), renal dysfunc
144                                  Relevant to brain dysfunction, post-COVID-19 syndromes and pathologi
145  understanding these disorders indicate that brain dysfunction precedes neurodegeneration, but the ro
146                           Diaschisis denotes brain dysfunction remote from a focal brain lesion.
147              Prevention of acute and chronic brain dysfunction requires implementation of a core mode
148  movement disorders, the mechanisms by which brain dysfunction results in dystonia are not understood
149                           If untreated, this brain dysfunction results in severe intellectual disabil
150 on, it is argued that evidence of underlying brain dysfunction revealed by these pictures often rests
151  levels correspond to direct measurements of brain dysfunction, shedding new light on the underlying
152 nt records from 5 impairment groups (stroke, brain dysfunction, spinal cord dysfunction, other neurol
153  development and infancy could contribute to brain dysfunction such as that seen in ASD and other dev
154 s, including learning and memory, as well as brain dysfunctions such as drug addiction and psychologi
155 mprinting in a number of syndromes involving brain dysfunction, such as Prader-Willi syndrome, Angelm
156 atients and to evaluate associations between brain dysfunction, systemic multiple organ dysfunction,
157 ut the potential role of white matter in the brain dysfunction that characterizes HD and the pertinen
158 ancing our understanding of the mechanism of brain dysfunction that occurs in this complex brain diso
159 s suggest that altered sleep triggers severe brain dysfunctions that could precipitate respiratory fa
160  continue to enrich our understanding of the brain dysfunctions that occur in neuropsychiatric diseas
161 epsis is emerging as a key driver of chronic brain dysfunction, the immunological consequence of seve
162 ing on the site of the lesion, the resultant brain dysfunction, the presentation of depression and ti
163 ese results underline the potential of focal brain dysfunction to produce behavioral improvement and
164 ns unknown about how the disease gene causes brain dysfunction ultimately leading to cell death.
165 t cerebrovascular effects that contribute to brain dysfunction underlying dementia by limiting the de
166          A few studies tried to identify the brain dysfunction underlying developmental dyscalculia b
167 europathology, and character and severity of brain dysfunction varied substantially among cases.
168        In 10 of these 47 the primary site of brain dysfunction was anterior temporal and orbital-fron
169 ase classification system and the underlying brain dysfunctions, we applied a fully data-driven appro
170  production during cancer progression causes brain dysfunctions, which ultimately result in cachexia.
171 oward understanding cognition, learning, and brain dysfunction will be identification of the underlyi
172 d, have recently been shown to contribute to brain dysfunction with age.
173 raumatic brain injury (TBI) leads to lasting brain dysfunction with chronic neuroinflammation typifie
174 nd how can molecular mechanisms that lead to brain dysfunction with numerous potential candidate gene
175            Traumatic brain injury (TBI) is a brain dysfunction without present treatment.

 
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