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1 or patients with childhood-onset SLE without neurocognitive deficit.
2 e of the disease, characterized by pervasive neurocognitive deficit.
3 calvarial deformation and possible long-term neurocognitive deficits.
4 alleviated gut microbiota depletion-mediated neurocognitive deficits.
5 f an HSCT are at risk for severe, persistent neurocognitive deficits.
6 e, notably stunting, immune dysfunction, and neurocognitive deficits.
7 th CNS-directed chemotherapy are at risk for neurocognitive deficits.
8 ral and CNS inflammation, neuronal death and neurocognitive deficits.
9 n certain growth disorders may contribute to neurocognitive deficits.
10 ic leukemia (ALL) exhibit increased rates of neurocognitive deficits.
11 nd neuropsychiatric manifestations including neurocognitive deficits.
12 iation between early anesthetic exposure and neurocognitive deficits.
13 ructural brain anomalies as well as multiple neurocognitive deficits.
14 t of human female carriers have seizures and neurocognitive deficits.
15 elia burgdorferi, often manifests by causing neurocognitive deficits.
16 s a valid model for studying ADHD-associated neurocognitive deficits.
17 ications developed to target ADHD-associated neurocognitive deficits.
18 als with FASDs and related these findings to neurocognitive deficits.
19 difiers and the management and prevention of neurocognitive deficits.
20  of patients with bipolar disorder (BD) have neurocognitive deficits.
21 preterm (<33 weeks) are at increased risk of neurocognitive deficits.
22  an impact on aspects of disability, such as neurocognitive deficits.
23 ls which may explain space radiation-induced neurocognitive deficits.
24 erges as a promising preventive strategy for neurocognitive deficits.
25            Microglial depletion reversed the neurocognitive deficits.
26 ith schizophrenia, including the presence of neurocognitive deficits; abnormalities in brain structur
27                    Although intellectual and neurocognitive deficits accompany schizophrenia, there a
28 nosis was the most prominent risk factor for neurocognitive deficits among survivors of MB despite re
29                                          The neurocognitive deficits among survivors of primary centr
30  cerebellum volume, which is associated with neurocognitive deficits and a lower estimated glomerular
31 lammation, which may accelerate the onset of neurocognitive deficits and cardiovascular dysfunction.
32 pse and long-term complications that include neurocognitive deficits and cardiovascular events that o
33 xamined whether the combination of patients' neurocognitive deficits and criticism by others would pr
34 neurodevelopmental disorder characterized by neurocognitive deficits and obesity.
35                                 The study of neurocognitive deficits and psychosocial functioning in
36 ssociated with long-term sequelae, including neurocognitive deficits and secondary neoplasms.
37 brovascular impairment, it did contribute to neurocognitive deficits and the severity of neuronal dam
38 ient at deciphering post-concussion residual neurocognitive deficits and thus has a potential clinica
39 4 counts were linked both to the severity of neurocognitive deficits and to discordant resistance pat
40                      Secondary malignancies, neurocognitive deficits and treatment failure continue t
41 ed in patients with childhood-onset SLE with neurocognitive deficit, and the reduction was positively
42 ropriate screening for these mood disorders, neurocognitive deficits, and cardiovascular complication
43 eral consistent findings emerge on symptoms, neurocognitive deficits, and neuroimaging parameters and
44                  Both psychotic symptoms and neurocognitive deficits appear to contribute independent
45                                              Neurocognitive deficits are among the most promising ind
46                               Neuropathy and neurocognitive deficits are common among chronic alcohol
47                 This study demonstrates that neurocognitive deficits are common even in recently diag
48 ct transition to psychosis, and determine if neurocognitive deficits are robust or explained by poten
49 e positive effects on neurophysiological and neurocognitive deficits associated with schizophrenia, w
50  gene is thought to have a major role in the neurocognitive deficits associated with Trisomy 21.
51 established that schizophrenic patients have neurocognitive deficits, but it is not known how these d
52 ) exposure is associated with neuromotor and neurocognitive deficits, but the exact mechanism of Mn n
53 tcomes including microcephaly, epilepsy, and neurocognitive deficits, collectively known as Congenita
54                 In this study, we calculated neurocognitive deficits combining EEG analysis with thre
55 th schizophrenia have taken into account the neurocognitive deficits common to this illness.
56 are at increased risk for language and other neurocognitive deficits compared to term controls (TC).
57  with OSAS that may help explain some of the neurocognitive deficits described in these children.
58 -term complications such as hypertension and neurocognitive deficits despite early initiation of ther
59 drome (SLOS) is a malformation syndrome with neurocognitive deficits due to mutations of DHCR7 that i
60 uch complications include secondary tumours, neurocognitive deficits, endocrine disorders and growth
61  and late complications (eg, second cancers, neurocognitive deficits, endocrine disorders, and growth
62 ectrum disorders (FASDs) are associated with neurocognitive deficits for which there are no biologica
63 M impairments which are thought to be a core neurocognitive deficit found in disorders such as autism
64 onal process formation may contribute to the neurocognitive deficits found in SLOS and may represent
65                        Complications include neurocognitive deficits, growth failure, and pulmonary h
66 chological testing confirmed the presence of neurocognitive deficit in 8 patients with childhood-onse
67                                              Neurocognitive deficit in patients with childhood-onset
68 creased the susceptibility to HIV-associated neurocognitive deficits in both species.
69 e to MeHg has been associated with long-term neurocognitive deficits in children that persist into ad
70 her antiglucocorticoid treatments may reduce neurocognitive deficits in major depression.
71                   These results suggest that neurocognitive deficits in mental perspective taking may
72    Functionally, anti-PD-1 treatment induced neurocognitive deficits in mice, independent of T cells,
73                                              Neurocognitive deficits in patients with hepatitis C vir
74 tic drugs have shown promise in ameliorating neurocognitive deficits in patients with schizophrenia,
75 unologic and genetic factors associated with neurocognitive deficits in SM including 551 SM children,
76 microglia via the TLR4/p38 MAPK pathway, and neurocognitive deficits in SPF aGVHD mice.
77 erapy and early detection or amelioration of neurocognitive deficits in survivors of sepsis.
78 ics were used to explore GMV alterations and neurocognitive deficits in these subgroups.
79                               HIV-associated neurocognitive deficits include impaired speed-of-inform
80  STATEMENT Even with antiretroviral therapy, neurocognitive deficits, including impairments in attent
81 alies, neurodevelopmental abnormalities, and neurocognitive deficits, including intellectual, executi
82        However, CSI often leads to long-term neurocognitive deficits, including learning disabilities
83 uals and are likely linked to HIV-associated neurocognitive deficits, including those in learning and
84                                              Neurocognitive deficits manifest across multiple cogniti
85 overall population demonstrated considerable neurocognitive deficits (mean values for all 4 subtests
86 ke, and may have genetic vulnerabilities for neurocognitive deficits (NCDs).
87 term HIV-1 viral protein exposure on chronic neurocognitive deficits observed in pediatric HIV-1 (PHI
88                                    Long-term neurocognitive deficits occur in 15-40% of patients, whe
89                                              Neurocognitive deficits of the impaired subgroup persist
90 charge, excluding patients with a history of neurocognitive deficits or who were readmitted and under
91 c health conditions, impaired health status, neurocognitive deficits, or poorer socioeconomic outcome
92  5 of the V3 loop was highly correlated with neurocognitive deficit (P < 0.0025, Fisher's exact test)
93 ormal brain imaging scans (P = .04) and with neurocognitive deficits (P = .04).
94 f resistance was associated with severity of neurocognitive deficits (P = 0.07), while low nadir CD4
95              Clinicians should be aware that neurocognitive deficits persist and have an adverse effe
96 ssociated with childhood comorbid disorders, neurocognitive deficits, polygenic risk, and residual ad
97 ing is linked to poor glucose metabolism and neurocognitive deficits, pregnant Sprague-Dawley rats we
98 chemic stroke, tachyarrhythmias, malignancy, neurocognitive deficits, psychosis, other neuropsychiatr
99 oning survivors suffer long-term cardiac and neurocognitive deficits related to slow CO clearance, hi
100  this review was to determine which, if any, neurocognitive deficits restrict the functioning of schi
101 st that some of the neuronal dysfunction and neurocognitive deficits seen in TSC patients may be attr
102 logy of the illness, and a potential link to neurocognitive deficits shaping the disorder.
103 ymphoblastic leukaemia (ALL) are at risk for neurocognitive deficits that affect development in adole
104 lymphoblastic leukemia (ALL) are at risk for neurocognitive deficits that are associated with treatme
105 vous system (CNS) macrophages contributes to neurocognitive deficits that develop despite antiretrovi
106 unction, may combine with symptoms and other neurocognitive deficits to influence illness presentatio
107 ollowing cardiac surgery range from discrete neurocognitive deficits to severe neurologic injury such
108  the patients with childhood- onset SLE with neurocognitive deficit versus controls or patients with
109 te the pathological processes underlying the neurocognitive deficits, we compared protein expression
110 ts indicate that malnutrition predisposes to neurocognitive deficits, which in turn predispose to per
111 letions and duplications are associated with neurocognitive deficits, yet few studies compared these

 
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