コーパス検索結果 (1語後でソート)
通し番号をクリックするとPubMedの該当ページを表示します
1 SPW-R was more pronounced during waking than sleeping.
2 r in the brain waves that occur while we are sleeping.
3 infants devote the majority of their time to sleeping.
4 e time with screens than any activity except sleeping.
5 allowing (2.1, 1.1-3.9; p=0.017), difficulty sleeping (1.9, 1.3-2.8; p=0.001), arthralgias (2.0, 1.1-
6 ing, 33 (30%); concurrent illness, 13 (12%); sleeping, 10 (9%); drugs/medication, 9 (8%); and emotion
7 DBP ranged from 16.8% to 40.4% for daytime, sleeping, 24-hour and office beat-to-beat measurements.
10 fer alternative to benzodiazepines and other sleeping aids(8,9), and is one of the most popular suppl
14 s with KCN should inquire about breathing or sleeping and, when appropriate, refer patients for evalu
15 ssess sleep patterns - with focus on daytime sleeping - and alertness in a Latin American crew overwi
17 tial (LFP) recordings on flies spontaneously sleeping, and compare their brain activity to flies indu
21 als who sleep >7 hours/night with no trouble sleeping are 40% less likely to have severe periodontal
22 the new design, especially the second-storey sleeping area because of the privacy and security of ups
23 choretic insect that hides within its host's sleeping area manages to travel long distances is not ye
24 t time, how leaving worn clothing exposed in sleeping areas when travelling can be exploited by bed b
27 incidence of botulism in shoreline birds at Sleeping Bear Dunes National Lakeshore (SLBE) in Lake Mi
29 bling times of 5-10 years at Sturgeon Point, Sleeping Bear Dunes, and Eagle Harbor, but these concent
30 ased sequencing and bioinformatics pipeline, Sleeping Beauty (SB) capture hybridization sequencing (S
31 son mutagenesis strategy based on a two-step Sleeping Beauty (SB) forward genetic screen to identify
34 e have advanced DNA vectors derived from the Sleeping Beauty (SB) system to avoid the expense and man
35 -derived CD19 CAR T cells generated with the Sleeping Beauty (SB) transposon and differentiated into
36 a hybrid genetic screening system where the Sleeping Beauty (SB) transposon and single guide RNA cas
37 strate biased genome-wide integration of the Sleeping Beauty (SB) transposon by combining it with com
39 ectal cancer (CRC) progression, we performed Sleeping Beauty (SB) transposon mutagenesis screens in m
41 driving leukemia, we targeted cre-dependent Sleeping Beauty (SB) transposon mutagenesis to the blood
43 sion (GEC(HO-1) rats) were generated using a Sleeping Beauty (SB) transposon system and extent of les
48 a development and metastasis, we performed a Sleeping Beauty (SB) transposon-based forward genetic sc
50 lls that were genetically modified using the Sleeping Beauty (SB) transposon/transposase system to ex
52 ite profiling of the piggyBac (PB), Tol2 and Sleeping Beauty (SB) transposons and the murine leukemia
55 ON) and compare them with the preferences of Sleeping Beauty and piggyBac, showing that each superfam
56 lated when delivered into the genome via the Sleeping Beauty DNA transposon, suggesting that the obse
57 gene for colorectal cancer (CRC) in several Sleeping Beauty DNA transposon-based forward genetic scr
58 tract cancer susceptibility gene in multiple Sleeping Beauty DNA transposon-based forward genetic scr
63 5 (Stat5b-CA) with mice in which a mutagenic Sleeping Beauty transposon (T2/Onc) was mobilized only i
68 an insertional mutagenesis screen using the Sleeping Beauty transposon system in mice with mammary-s
69 Recently in Nature, Sun et al. (2014) used a sleeping beauty transposon system to demonstrate that na
71 d mobilization of a single-copy inactivating Sleeping Beauty transposon to Pten disruption within the
72 in the biliary tract was accomplished by the Sleeping Beauty transposon transfection system with tran
73 ovirus, lentivirus, PiggyBac transposon, and Sleeping Beauty transposon, in aggregate >108,000 vector
74 Exploiting the local hopping activity of the Sleeping Beauty transposon, the lacZ reporter gene was d
76 in cultured human PAX7+ satellite cells with Sleeping Beauty transposon-mediated nonviral gene transf
79 ession of hMet and mutant-beta-catenin using sleeping beauty transposon/transposase leads to hepatoce
80 essing mice and forward genetic screens with Sleeping Beauty transposons implicate additional signali
81 ion elements, which were further deployed by Sleeping Beauty transposons throughout the genome of hum
83 le with two transposon systems, PiggyBac and Sleeping Beauty, and give guidance on the use of differe
87 rons to the presentation of song variants in sleeping birds, and by examining HVC activity in singing
92 Our results suggest a model of the human sleeping brain in which rapid bidirectional interactions
93 However, recent research has shown that the sleeping brain is not completely disconnected from its e
95 definition, but it is still unclear how the sleeping brain responds differently to sensory stimuli.
96 a flexible and task-dependent manner by the sleeping brain, all the way up to the preparation of rel
97 hatic function is primarily a feature of the sleeping brain, rather than the waking brain, and is slo
104 Here we used bioinformatics to identify a "sleeping carboxylase function" in the superfamily of med
105 aging in close-to-perfect conditions, these sleeping champagne bottles awoke to tell us a chapter of
109 CSR) is believed to only occur in supine and sleeping conditions, and thus, CSR treatment is applied
113 mance measures compared to sleeping on LR or sleeping directly on spring mattresses without a topper.
114 as modafinil, are used for the treatment of sleeping disorders and investigated as potential therape
116 of specific tryptamines for the treatment of sleeping disorders, bupropion for substance abuse disord
122 alance between maintaining the wake state or sleeping during the day has important health implication
127 stions addressing perception of light in the sleeping environment may provide a crude yet affordable
133 rt system administered questions on life and sleeping habits; health; and sleep, mental, and organic
134 igh frequency distal body temperature (DBT), sleeping heart rate (HR), sleeping heart rate variabilit
135 esting (P = 0.001), stressed (P = 0.037) and sleeping heart rate (P = 0.038) were increased compared
136 temperature (DBT), sleeping heart rate (HR), sleeping heart rate variability (HRV), and sleep timing,
137 rt devices were fitted for 7 days to measure sleeping heart rate, activity levels, and resting, activ
138 eviant external stimuli detected by the less-sleeping hemisphere caused more arousals and faster beha
140 me in bed during weekdays, and later weekend sleeping hours correlate with smaller brain grey matter
141 ttachment locations for 24 hours, waking and sleeping hours, and to test comparability of PA cut poin
151 in one hundred sixty-two 2- to 25-month-old sleeping infants (60 epsilon4 carriers and 102 noncarrie
153 uction of solid foods), and early childhood (sleeping <12 h/d, presence of a television set in the
154 recordings along the dorsal CA1-DG axis from sleeping male mice, we detected and classified two types
155 egulation and control found in bihemispheric sleeping mammals and the harbor porpoise were present in
156 egulation and control found in bihemispheric sleeping mammals were present in the harbor porpoise, wi
159 conditions, we analyzed changes in 24 EE and sleeping metabolic rate (SLEEP) in a whole-room indirect
160 r baseline energy requirements for 8 wk, and sleeping metabolic rate (SMR) and 24-h sedentary energy
161 stage for the whole night and separately for sleeping metabolic rate (SMR; ie, 3-h period during the
165 cooling of lightly anesthetized or naturally sleeping mice disrupts thalamocortical slow oscillation
167 as protein levels are up-regulated in short-sleeping mutants and also in wild type animals following
168 emically mutagenized flies to identify short-sleeping mutants and found one, redeye (rye) that shows
169 uth irritation (n = 4 and n = 0), difficulty sleeping (n = 3 and n = 2), and vivid dreams (n = 3 and
172 ng data were obtained on a 3T scanner in 138 sleeping nonsedated neonates: 55 full-term neonates (ges
175 or only 0.69 h d(-1) (7.4% of the time spent sleeping on land), indicating that ecological demands fo
176 me athletic performance measures compared to sleeping on LR or sleeping directly on spring mattresses
177 ation sessions did not prevent patients from sleeping; on the contrary, they seem to aid sleep when c
178 ce an exogenous stressor, such as prone/side sleeping or soft bedding, during a critical developmenta
181 and ambient temperature on human resting or sleeping patterns using mobile phone data of a large num
183 by sleep deprivation or caffeine during the sleeping period potentiates light resetting of the maste
184 study demonstrates the strong dependency of sleeping person exposure on air exchange rate between hi
185 , a kinase partner of CycA, rescue the short-sleeping phenotype of tara and CycA mutants, while incre
187 idem (Ambien) is the most widely prescribed "sleeping pill." It makes the inhibitory neurotransmitter
190 es, addition of hydrocortisone reduced total sleeping problems and disorders of initiating and mainta
192 e SCORAD), symptoms (POEM, VAS pruritus, VAS sleeping problems) and previous treatment of AD were ass
194 vity from the primary motor cortex of 4 male sleeping rats to investigate how SO and spindles interac
195 aring experimental observations of naturally-sleeping rats with a mean field model of an adapting, re
199 Trypanosoma brucei, the causative agent of sleeping sickness (Human African Trypanosomiasis, HAT),
201 cei, which is the parasite that causes human sleeping sickness and is also partially responsible for
202 oma brucei is the causative agent of African sleeping sickness and is known for its unique RNA proces
204 anosoma brucei is a protist parasite causing sleeping sickness and nagana in sub-Saharan Africa.
207 cei causes African trypanosomiasis, known as sleeping sickness in humans and nagana in domestic anima
211 oms, in this study, we used a mouse model of sleeping sickness in which the acute infection was treat
213 c adenosine signaling.SIGNIFICANCE STATEMENT Sleeping sickness is a fatal disease that disrupts the c
214 d, our findings suggest that the symptoms of sleeping sickness may be because of alterations in homeo
216 this model, we evaluated the effects of the sleeping sickness parasite, Trypanosoma brucei, on sleep
219 ction of rare cell types in blood (including sleeping sickness parasites), and has the potential to e
223 biense human African trypanosomiasis ([gHAT] sleeping sickness) is a vector-borne disease that is typ
224 ambiense Human African Trypanosomiasis (HAT, sleeping sickness), a disease that has often been consid
225 en argued that the risk for trypanosomiasis (sleeping sickness), carried by tsetse flies in bushy env
226 copeia for human African trypanosomiasis (or sleeping sickness), orally dosed fexinidazole stands poi
227 tive agent of Human African Trypanosomiasis (sleeping sickness), yet little is known about which PKs
230 oma brucei is the causative agent of African sleeping sickness, a devastating disease endemic to sub-
231 ing target to develop new treatments against sleeping sickness, a fatal disease caused by this protoz
232 t and Southern Africa are foci for Rhodesian sleeping sickness, a fatal zoonotic disease caused by tr
233 animal trypanosomiases, including Rhodesian sleeping sickness, a zoonosis associated with wilderness
235 ovide different levels of protection against sleeping sickness, but this comes with an increased risk
238 anosoma brucei, a causative agent of African Sleeping Sickness, constantly changes its dense variant
239 e Trypanosoma brucei, the causative agent of sleeping sickness, cycles between an insect and a mammal
240 osoma brucei, the etiologic agent of African Sleeping Sickness, deploys an RNA pol II that contains a
241 osoma brucei, the causative agent of African sleeping sickness, differs from its human host in severa
242 anosoma brucei, the causative agent of human sleeping sickness, has an intrinsic circadian clock that
243 an African trypanosomiasis (HAT), or African sleeping sickness, is a fatal disease found throughout s
245 Human African trypanosomiasis (HAT), or sleeping sickness, is caused by the protozoan parasite T
246 osoma brucei, the causative agent of African sleeping sickness, is transmitted to its mammalian host
247 Trypanosoma brucei, the etiological agent of sleeping sickness, localized its replication origins to
248 he parasitic trypanosomes that cause African sleeping sickness, mating occurs during transmission by
249 ite Trypanosoma brucei, which causes African sleeping sickness, TbISWI down-regulates RNA polymerase
250 s typified by the causative agent of African sleeping sickness, Trypanosoma brucei In mitochondria of
251 energy metabolism in the causative agent of sleeping sickness, Trypanosoma brucei, with that of huma
252 e the causative agents of Chagas disease and sleeping sickness, two neglected tropical diseases where
253 can trypanosomes, parasites that cause human sleeping sickness, undergo a density-dependent different
272 osoma brucei, the causative agent of African sleeping sickness; and Plasmodium spp., the causative ag
273 ge attraction and repulsion from the troop's sleeping site, to relatively local influences including
274 k factors for infants include prone and side sleeping, soft bedding, bed sharing, inappropriate sleep
276 cond (recovery) night of sleep revealed that sleeping the first half of the night, which is dominated
278 glycemia associated with different levels of sleeping time (<11.0, 11.0-11.9, and >/=12.0 hours/day)
279 (SWS), rapid eye movement (REM)-sleep, total sleeping time (TST), sleep stage 2 (S2), and QS [(SWS +
280 based on arbitrary threshold parameters for sleeping time and number of citations, applied to small
281 rse association of either indoor activity or sleeping time with the risk of hyperglycemia among offsp
282 tion of physical activity, TV watching time, sleeping time with the risks of obesity and hyperglycemi
285 ld that owned a bed net, only 36.6% reported sleeping under a long-lasting insecticide-treated net (L
286 difference 0.02, 95% CI - 0.02 to 0.05) and sleeping under an LLIN (0.01; - 0.02 to 0.04) were not p
287 of 1371; 1.10, 1.04-1.16; p=0.001), and baby sleeping under bednet for 8-56 days (4548 [79%] of 5756
288 ill at high altitude and whether training or sleeping under normobaric hypoxic conditions in the week
289 ) and (2) protective efficacy for volunteers sleeping under the LLINs (bite reduction and mosquitoes
291 an array of fundamental behaviors, including sleeping, waking, feeding, stress and motivated behavior
293 cellular recording and labeling in naturally sleeping-waking, head-fixed rats, we investigated the di
296 r orthokeratology (OR, undefined; P = 0.02), sleeping while wearing lenses (OR, 8.00; P = 0.04), stor
297 5% CI, 1.2-10.3) compared to 5-14 years, and sleeping with index case (OR 2.7; 95% CI, 1.3-5.5).
298 nmental awareness and aerodynamic control by sleeping with only one eye closed and one cerebral hemis
299 ever, the benefit of conserving energy while sleeping with the head tucked was countered by reduced a