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1 failure or shock in whom medical therapy is failing.
2 se findings may not mean that peer review is failing.
3 munity, although fundamental, is fragile and failing.
5 moderate to severe hidradenitis suppurativa failing adalimumab therapy, or those ineligible to recei
6 Immune aging manifests with a combination of failing adaptive immunity and insufficiently restrained
9 n cardiac progenitor cell [FhCPC]) and adult failing (adult human cardiac progenitor cell [AhCPC]) he
10 linical Trials Group 5230 evaluated patients failing an initial nonnucleoside reverse-transcriptase i
13 ector control field studies, highlight major failings and strengths of published studies, and provide
15 s not associated with risk of their children failing any developmental domain (aOR, 1.33; 95% CI, 0.9
16 ology was associated with increased risk for failing any developmental domain but only when singleton
17 t also was not significantly associated with failing any developmental domain for ovulation induction
20 phoma for whom treatment was at high risk of failing appear to benefit from early treatment intensifi
24 ive in 53(88% [95% CI, 78%-94%]) of 60 cases failing azithromycin; all failures had gyrA and parC mut
26 ere we isolate and functionally characterize failing beta cells from various experimental models of d
27 e mid-infrared and long-wavelength infrared, failing beyond, roughly 2.5 mum, our generalization of t
28 human health and well-being, increasingly, a failing brain is the arbiter of a death preceded by a gr
30 e NaV1.5 proteins purified from adult WT and failing CaMKIIdeltac-overexpressing (CaMKIIdeltac-Tg) mo
31 atively modified and desensitized by GRK2 in failing cardiomyocytes, contributing to post-MI remodeli
32 sion patterns are pivotal characteristics of failing cardiomyocytes, with several excitation-transcri
36 A strains lacking STK1 become susceptible to failing cephalosporins, such as Ceftriaxone and Cefotaxi
43 T failures; (2) second-line LA-ART for those failing first-line therapy; and (3) first-line LA-ART fo
44 of NAD(+) biosynthetic enzymes in the human failing heart and in the heart of a mouse model of dilat
46 er abnormal calcium-handling proteins in the failing heart are candidates for gene therapy; many shor
47 rial dysfunction and energy depletion in the failing heart are innovative therapeutic targets in hear
50 derstand why MyBP-C dephosphorylation in the failing heart contributes to contractile dysfunction and
51 cycle length decreases, both the normal and failing heart develop T-wave alternans, but only the fai
54 ocaine autoradiography to determine that the failing heart has 30% lower SCN5A levels - the first ev
59 a 30% loss in levels of NAD(+) in the murine failing heart of both DCM and transverse aorta constrict
60 results indicate that the hypertrophied and failing heart shifts to ketone bodies as a significant f
61 trometry revealed that the hypertrophied and failing heart shifts to oxidizing ketone bodies as a fue
62 heart develop T-wave alternans, but only the failing heart shows QRS alternans (although moderate) at
65 the cell and tissue level have increased the failing heart's susceptibility to dynamic instabilities
66 amage and DDR activation are observed in the failing heart, however, the type of DNA damage and its r
67 (GRKs), some of which are upregulated in the failing heart, making them desirable therapeutic targets
69 ble alterations of NAD(+) homeostasis in the failing heart, we quantified the expression of NAD(+) bi
94 ence in regional work between nonfailing and failing hearts after MI and offer novel insight into the
95 P2 in cardiomyocytes facilitated recovery of failing hearts after reversible transverse aortic constr
96 hondrial function, also are present in human failing hearts as well as in mouse hearts with pathologi
97 2 cm/s (95% CI, 27-37; P=0.001) in 12 native failing hearts at 1000 ms pacing cycle length (PCL).
98 reased conduction velocity in both donor and failing hearts but shortened action potential duration o
99 t studies also identified amylin deposits in failing hearts from patients with obesity or type 2 diab
101 achidonic acid (AA) in mitochondria from non-failing hearts was calcium-dependent phospholipase A2zet
103 Th1) and Th17 (versus Treg) predominance in failing hearts, and with expansion of memory T cells in
106 ransients duration (CaD) in donor but not in failing hearts, because of desensitization of beta1-adre
109 nnels arachidonic acid into EETs, whereas in failing hearts, increased iPLA2gamma activity channels A
110 idates are often differentially expressed in failing hearts, with an inverse correlation between 3'UT
127 tly attenuated activation characteristics of failing human cardiac fibroblasts isolated from end-stag
128 hondrial oxidation and ultrastructure in the failing human heart by using respirometry, transmission
129 increased ketone utilization in the severely failing human heart independent of diabetes mellitus, an
135 re, FYN expression was markedly decreased in failing human hearts, corroborating its role as a regula
136 Stable isotope kinetics revealed that in non-failing human hearts, cPLA2zeta metabolically channels a
143 yocyte stiffness contributed to stiffness of failing human myocardium because of reduced titin disten
144 ed the Ca(2+)-induced opening of the mPTP in failing human myocardium, and the highly selective pharm
148 Multiple approaches to ablate biofilms on failing implants have been proposed and include use of l
151 etects malignancy about 80-90% of the times, failing in places when (1) the tumor is small at early s
154 obstructive pulmonary disease, cancer, weak/failing kidneys, diabetes, hepatitis, depression, and he
155 nary disease: OR 1.65; cancer: OR 1.23; weak/failing kidneys: OR 2.29; diabetes: OR 1.56; hepatitis:
156 Surprisingly, respiratory capacities for failing LV isolated mitochondria (n = 9) were not signif
157 processing gene expression between donor and failing LVs revealed 0.64-fold reduced transcript levels
159 tension/inner unrest (37 [69%] vs 50 [88%]), failing memory (41 [76%] vs 44 [77%]), and weight gain (
162 Mycoplasma genitalium samples from cases failing moxifloxacin were sequenced for fluoroquinolone
163 in were treated with moxifloxacin, and those failing moxifloxacin were treated with pristinamycin.
168 nd locally sourced macrophages isolated from failing myocardium expressed different genes in a patter
172 nt expansion of CD8(+) and CD4(+) T cells in failing myocardium, with increased Th1, Th2, Th17, and T
179 Entire SAN complexes were isolated from failing (n=5) and nonfailing (n=9) human hearts cardiopl
180 left ventricular wedge preparations from 12 failing native hearts and 2 rejected cardiac allografts
186 r clearance compared with 10 mg/L, and three failing organs were associated with a 35% lower clearanc
189 buting to focal arrhythmia in the intact non-failing rabbit heart using optical mapping and pharmacol
197 se were shown to be false-positive findings, failing replication with polymerase chain reaction.
199 of Cardiology risk score was higher in those failing screening (risk score 5.5% [interquartile range,
200 munodeficiency virus (HIV)-infected children failing second-line antiretroviral therapy (ART) have no
201 etectable drug levels were at higher risk of failing second-line ART and thus should be closely monit
209 lasty may lead to greater wound healing, but failing this, any straight-line flow into the foot is pu
210 rweight risk paradox may result in part from failing to account for central adiposity, rather than re
215 omprehensive Epilepsy Programme, the odds of failing to achieve 1-year seizure freedom were significa
216 85; P < .001) were independent predictors of failing to achieve complete dosing; private insurance st
217 mance index highlighted countries at risk of failing to achieve the GVAP target of 90% coverage by 20
220 s suggest that large numbers of patients are failing to be assessed properly with a risk of patient h
221 mall data sets, which have led to many genes failing to be consistently associated with transplant ou
224 climate due to reduced chilling, with trees failing to capture favorable conditions in the earlier p
225 sing the resulting analyses, and in general, failing to capture sequences novel to a given genome.
226 alyzed one trait and one SNP at a time, thus failing to capture the underlying complexity of the data
229 utations Y370C and E395C within EL5, whereas failing to confer sensitivity to MTS, nevertheless, redu
232 azzled mutants, resulting in many more axons failing to cross the midline, although mutations in mud
233 ce between published data and a recent study failing to detect a common strain in infants with NEC, m
235 although in slightly different ways, thereby failing to direct full-length APP into the retromer-recy
238 Despite being poorly cytolytic in vivo and failing to expand after encountering Ag, airway CD8 TRM
240 ulation with pre-existing particles, thereby failing to form new cloud condensation nuclei that are t
243 ed blastocysts no longer retain totipotency, failing to form TE and generating PE on their surface.
244 ificant health- and pain-related risks while failing to fulfill smokers' expectations of affect regul
245 proved vision post implantation, with 7 eyes failing to gain vision as a result of pre-existing glauc
246 layed profound defects upon differentiation, failing to generate chimeric embryos and preferentially
249 hat the current certification process may be failing to identify individuals who have demonstrated te
252 ion fully rescued locomotor deficits despite failing to improve cerebellar learning in AS mice, sugge
256 e time frame and show that these efforts are failing to keep pace with the rate of wilderness loss, w
258 nia demonstrate altered effort allocation by failing to make high-effort response choices to maximize
262 ith higher pleurodesis failure (30% vs 24%), failing to meet noninferiority criteria (difference, -6%
265 rations in BAP1 outside the UCH domain, each failing to productively recruit ASXH to the wild-type BA
268 ctivity is weak, with a recent meta-analysis failing to provide strong evidence for either HER2 or TO
269 nts of controversial receptor localizations, failing to provide support for CRF1 expression in centra
274 signal-regulated kinase 1/2 signaling while failing to recruit arrestin, activate inositol phosphate
275 and biological assumptions are misinformed, failing to refute the previously existing hypothesis tha
277 t global approaches have been criticized for failing to render global biodiversity value at a scale s
281 often just that, with genome data routinely failing to reveal useful insights about disease in gener
282 be linked to its regulatory role mean that, failing to scale the data prior to the network analysis,
284 e, all species had similar microbiotas, thus failing to support predictions of the phylosymbiosis hyp
285 g truncation of actin microfilament, thereby failing to support the Sertoli cell morphology and adhes
286 -) nTreg displayed instability in the graft, failing to suppress Ag-specific CD4(+) T cells and preve
287 fection resulting in only local shedding and failing to transmit fully through the gastro-intestinal-
288 g internalized and initiating hemifusion but failing to uncoat the viral nucleocapsid and to replicat
289 nd defect in lung development with lung buds failing to undergo branching morphogenesis and progressi
290 at the 1-2 cell stage, with arrested embryos failing to undergo the maternal-to-zygotic transition.
292 coma that had failed or were at high risk of failing trabeculectomy were randomized to receive an Ahm
295 nflammation are at particularly high risk of failing treatment, and understanding the pathogenesis co
298 The expression of six Navs was observed in failing VCMs as follows: Nav1.5 (57.3%) > Nav1.2 (15.3%)
300 lso showed no ultrastructural remodeling for failing vs. donor mitochondria; however, the fraction of
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