ライフサイエンスコーパス: frank

1 iologist Robert Trivers and economist Robert Frank.

2 motion, as predicted by Burton, Cabrera, and Frank.

3 t Robert Trivers (1971) and economist Robert Frank (1988).

4 Surgeons were frank about the potential for serious complications and

5 on of prostatic intraepithelial neoplasia to frank adenocarcinoma.

6 Lack of practice effects is common, but frank adverse cognitive outcomes are observed in a subse

7 r, pronounced BBB permeation was noted, with frank albumin leakage around larger vessels (>10 microm)

8 e, referred to as the sigma (sigma) phase by Frank and Kasper more than 50 years ago, nucleates and g

9 The National Institutes of Health, the B Frank and Kathleen Polk Assistant Professorship in Epide

10 lity in science is a real issue, and without frank and open discussions leading to positive action it

11 Engagement in frank and transparent communication with our patients an

12 A new study by Franks and colleagues (pp. 2222-2234) provides new mecha

13 Findings by Franks and Isaacson in this issue of Neuron suggest that

14 e for Chemistry to Jacques Dubochet, Joachim Frank, and Richard Henderson for "developing cryoelectro

15 f the BLB, there was severe vacuolization or frank apparent necrosis of VECs and loss of subcellular

16 , review its use in the field, and provide a frank assessment of its relative strengths and weaknesse

17 Frank atrophy of the retinal pigment epithelium (RPE) an

18 ly-onset end-stage macular degeneration with frank atrophy of the RPE or neovascularization.

19 K. Frank Austen describes the work culminating in the ident

20 mice harboring the E613R mutation developed frank autoimmunity on a susceptible genetic background.

21 periments the formation of myelin ovoids and frank axonolysis occurred in more than 95% of fibers.

22 ident in spleen and bone marrow, followed by frank B cell malignancy.

23 itatively accounted for by the change of the Frank-Bilby dislocation content in the grain boundary.

24 uction, leading to loss of visual acuity and frank blindness.

25 mportantly, cartilage ECM could not generate frank bone tissue if devitalized by standard "freeze & t

26 amine this issue, the current study examined frank brain damage and changes in cortical activation as

27 Frank Burr Mallory's landmark observation in 1911 on the

28 estrogen uncovered an ability of E5 to cause frank cancer.

29 the malignant conversion of benign tumors to frank cancer.

30 of high-grade intraepithelial lesions and in frank cancer.

31 tion in other organs should explore not only frank cancers but other premalignant lesions.

32 arly treated nontransgenic mice, although no frank cancers were detected.

33 ere grade 1, both features were grade 2, and frank capsular breach were grade 3.

34 s naive adult murine prostatic epithelium to frank carcinoma and override the effect of androgen abla

35 can induce urothelial proliferation but not frank carcinoma formation.

36 auses hyperplasia that neither progresses to frank carcinoma nor regresses to normal urothelium throu

37 active c-Src(Y529F), the tubules progress to frank carcinoma with invasion and display markers of epi

38 iving steatotic-neoplastic transformation to frank carcinoma, through genetic modification of existin

39 sgenics demonstrates that the development of frank carcinomas is accompanied by a failure of multipar

40 ly required in three cell lines derived from frank carcinomas, and each kinase requirement was traced

41 nd occasionally dysplasia, without eliciting frank carcinomas.

42 re in the Editorial by Mattias Bjornmalm and Frank Caruso.

43 tudy suggests that occlusal surfaces without frank cavitation (ICDAS 0-4) that are sealed with a clea

44 on can be quantified at early stages, before frank cavitation, intervention methods can be tested by

45 caused aberrancies of adult skin, but not a frank cEDS-like phenotype, as skin hyperextensibility at

46 cervical intraepithelial neoplasia, but not frank cervical carcinoma.

47 T can demonstrate varices and ascites before frank cirrhosis is evident and can help evaluate the pro

48 -) humans, although unlikely to present with frank classic Ehlers-Danlos syndrome, are likely to have

49 orrelations that parallel those found in the frank clinical disorders of autism (e.g., superior tempo

50 is that less than 1% of homozygotes develop frank clinical haemochromatosis.

51 ney proximal tubule cells, in the absence of frank CNS pathology.

52 to accelerated cognitive impairment or even frank cognitive disorders in later life.

53 PTSD, 36% performed at a level indicative of frank cognitive impairment.

54 the tunneling matrix element as well as the Frank-Condon factor.

55 for electron transfer, we find near optimal Frank-Condon factors for electron transfer from MutY to

56 nd field transitions rather than oscillating Frank-Condon overlap.

57 at tissue dysfunction, in the form of either frank damage or hypoperfusion, to the left inferior pari

58 (OH)D, suggesting vitamin D insufficiency or frank deficiency.

59 on cell (RGC) axon dysfunction that precedes frank degeneration.

60 etachromatic leukodystrophy diagnosed before frank degenerative symptoms developed.

61 been associated with cognitive impairment or frank delirium.

62 ebilitation, including motor dysfunction and frank dementia.

63 ificant islet T-cell accumulation (day 7) or frank diabetes (days 10-14).

64 vated in the serum before the development of frank diabetes and appears to identify insulin resistanc

65 was already diminished before development of frank diabetes and only increased minimally during growt

66 als with impaired glucose tolerance (IGT) or frank diabetes based on the rarely utilized oral glucose

67 ansition from clinically silent insulitis to frank diabetes by cross-presenting autoantigen to self-r

68 evented the development of hyperglycemia and frank diabetes in NOD mice.

69 Thirty subjects with frank diabetes mellitus who received medications also ha

70 lucose levels rise relatively rapidly to the frank diabetes of stage 4, which is characterized as sta

71 with prediabetes are at risk for developing frank diabetes worldwide.

72 male hProC(A7)Y-CpepGFP mice do not develop frank diabetes, yet the misfolded proinsulin perturbs in

73 d alphaL (ItgaL) in developing insulitis and frank diabetes.

74 ssociated with either glucose intolerance or frank diabetes.

75 pan-colitis, and the infected mice developed frank diarrhea with a doubling of the fecal water conten

76 loss of hope, cause some physicians to avoid frank disclosure.

77 he importance and challenge of having clear, frank discussions during clinic visits about treatment c

78 forming to alpha-SiC, with radiation-induced Frank dislocation loops serving as the apparent nucleati

79 riences (PLEs) in nonclinical populations to frank disorder.

80 Ps may be linked to genetic predispositions, frank disorders or adverse drug responses, or they may s

81 Patients with areas of frank dissemination had a 5-year EFS of 36% +/- 15%.

82 en John Enders at Harvard, who pointed me to Frank Dixon at Scripps in La Jolla, California, for post

83 Under Frank Dixon, my work examined how antibodies to the glom

84 ent that might result from the misjoining of frank double strand breaks.

85 ning pathway, which predominantly deals with frank double-strand breaks (DSB), is not involved in the

86 Ionizing radiation-induced frank double-strand breaks can thus be quantified by sin

87 began in 1960 with Project OZMA conducted by Frank Drake.

88 Cushing syndrome, which are associated with frank dyslipidemia.

89 ggest that pathological eating behaviors and frank eating disorders are surprisingly common in older

90 ection by a repulsive force generated by the Frank elasticity.Disclination lines are topological defe

91 d COPD, including in regions of lung without frank emphysema, and may represent a distinct pathologic

92 e dorsal skin was very thin and fragile with frank erosions.

93 nt syndrome, Barrett's esophagus, as well as frank esophageal cancer, we utilized cDNA microarray tec

94 In this issue of Neuron, Frank et al. overturn the notion that synaptic homeostas

95 Franks et al. now show that mRNP remodeling is required

96 Accordingly, we uncover frank exchange of Ca(2+)-calmodulin to interfaces beyond

97 tion, which may occur even in the absence of frank extrusion.

98 continuum of head movements generated during frank eye-head saccades.

99 ts developed impaired (110 to 125 mg/dl) and frank fasting hyperglycemia (>125 mg/dl) 2 weeks earlier

100 bowel function ranging from fecal urgency to frank fecal incontinence.

101 Frank finds no mistakes in our analyses.

102 ug synergy where cells were destroyed not by frank G2-M phase abrogation but rather by initiating a c

103 cal changes to the small vessels) instead of frank haemorrhages on histology.

104 Conversion of AKT/CAT tumor cells to frank HCC during passage was associated with induction o

105 s primary MET/CAT tumors emerged directly as frank HCC.

106 nt or delay diabetes, reverse diabetes after frank hyperglycemia, and lead to the development of cell

107 and trans-QTLs at an age before the onset of frank hypertension suggests that these heritable changes

108 is still within the normal range and before frank hypokalemia ensues, in addition to the classic fee

109 After cessation of loading, frank hypophosphatemia occurred.

110 classic presentation is of florid shock with frank hypotension, fever, and elevated white blood cell

111 it is altered prior to the first episode of frank illness.

112 ice are unable to nurse their litters due to frank impairment of mammary gland development.

113 iewed as quantitative traits that range from frank impairment to normal variation, as found in the ge

114 essment of psychotic symptoms (attenuated or frank) in mental health services and better understandin

115 Brief periods of ischemia, without frank infarction, cause low-level cTnT release, and smal

116 -APP immunoreaction was observed in zones of frank infarction.

117 the barrier alone is not sufficient to cause frank inflammatory bowel disease.

118 arcinoma from an indolent in situ state to a frank invasive carcinoma.

119 "One-component" soft material Frank-Kasper (FK) phases are an intriguing structural fo

120 provide access to non-canonical soft matter Frank-Kasper A15 and sigma phases.

121 to various ordered structures, including the Frank-Kasper A15 phase and dodecagonal quasicrystal.

122 ordered supramolecular lattices including a Frank-Kasper A15 phase, which resembles the essential st

123 hases also triggers formation of the related Frank-Kasper A15 sphere packing as well as a common body

124 like dendrimers self-organize a Pm3 n cubic (Frank-Kasper A15) phase which exhibits chirality on the

125 n of chirality in micellar-like spheres of a Frank-Kasper phase raises the fundamental question wheth

126 cc) close-packed micelles to a succession of Frank-Kasper phases (sigma to C14 to C15) upon the addit

127 Frank-Kasper phases and liquid quasicrystals self-organi

128 Frank-Kasper phases are tetrahedrally packed structures

129 All the experimentally observed Frank-Kasper phases can be constructed from the basic un

130 the emergence of tetragonally close-packed, Frank-Kasper phases in soft matter.

131 nsufficient conformational asymmetry to form Frank-Kasper phases in the neat-melt state undergo an in

132 Frank-Kasper phases, a family of ordered structures form

133 ations show that these, and other associated Frank-Kasper phases, have nearly degenerate free energie

134 igh-symmetry bcc phase to the lower-symmetry Frank-Kasper phases, wherein the reconfiguration of the

135 ce unconventional phase formation, including Frank-Kasper phases.

136 BCC) structure forms, whereas below TOOT the Frank-Kasper sigma phase is the stable morphology.

137 n, low-symmetry lyotropic liquid crystalline Frank-Kasper sigma phase.

138 The recent discovery of the Frank-Kasper sigma-phase in diblock and tetrablock polym

139 DES-exposed non-tumor kidney tissue, and in frank kidney tumors indicate that these genetic aberrati

140 The 2016 Frank Lautenberg Chemical Safety for the 21st Century Ac

141 llowed to 24-26 mo of age, 4 (20%) developed frank leukemia and died of the disease.

142 nt to erythroderma often in association with frank leukemia, as in Sezary syndrome.

143 onic twin pair, one preleukemic and one with frank leukemia, we establish the lineal relationship bet

144 gh frequency of LICs (<1:6900) and permitted frank leukemic engraftment from a remission sample conta

145 romycin-associated hepatotoxicity, including frank liver failure, were received.

146 phase is related to the existence of sessile Frank loops.

147 l-to-mesenchymal transition (EMT), including frank loss of E-cadherin expression and up-regulation of

148 nts showed a decreased NHEJ/SSA ratio due to frank loss of NHEJ, which corresponded to all known stru

149 Prior to frank lymphoma development, unexpectedly low levels of E

150 nerated from SOT recipients, even those with frank lymphoma, or who are receiving immunosuppressive d

151 uding 8 cases with microlymphomas and 2 with frank lymphomas, were studied.

152 d the bloodstream unexpectedly early, before frank malignancy could be detected by rigorous histologi

153 as mutation alone is insufficient to produce frank malignancy.

154 uring the transition of carcinoma in situ to frank malignancy.

155 ementary mutations are required to produce a frank malignancy.

156 this vulnerability and drives the cell into frank malignancy.

157 ntially from low-grade dysplastic nodules to frank malignant HCC.

158 cy levels of E can induce protection against frank mammary cancer.

159 oneering experimental work by Alexis Carrel, Frank Mann, Norman Shumway, and Richard Lower.

160 One-third of the mice develop frank masses comprised of neural progenitors, and in 20%

161 on from asymptomatic clonal hematopoiesis to frank MDS, and, ultimately, to secondary AML.

162 The bone marrow showed frank megaloblastic morphology, and the Schilling test i

163 yc mice developed highly aggressive HCC with frank metastasis to the lungs.

164 Critically, no frank misclassification (activated B-cell-like DLBCL to

165 on of androgen receptor in the stroma drives frank murine prostate adenocarcinoma in the adjacent epi

166 leading to the destruction of incipient and frank neoplasia.

167 evolution of many cancers and often precedes frank neoplastic conversion.

168 Perineural involvement without frank neuritis was present in advanced rejection.

169 tions leading to synaptic deficits, prior to frank neurodegeneration in AD brains.

170 Frank neuron loss in the entorhinal cortex is specific f

171 ical phenotype in HD, even in the absence of frank neuronal cell loss.

172 ns of hippocampal synaptic efficacy prior to frank neuronal degeneration, and that the synaptic dysfu

173 suggest specific phenotypic changes, but not frank neuronal degeneration, early in the disease proces

174 the concept that phenotypic changes, but not frank neuronal degeneration, occur early in cognitive de

175 flect phenotypic age-related changes and not frank neuronal degeneration.

176 that precedes progression of the disease to frank neuronal disruption.

177 late-onset brain volume loss associated with frank neuronal loss and FTD-like changes in social behav

178 shing but no multimer-neutral mutants caused frank neurotoxicity akin to the proapoptotic protein Bax

179 events within NB cholinergic neurons before frank NFT deposition.

180 entorhinal cortex and dentate gyrus, with no frank noradrenergic cell body loss.

181 The authors, like Trivers and Frank, offer an implausible explanation of the fact that

182 (IR)-induced DSBs, blocks the resolution of frank or microhomologous DNA ends, and abrogates IR-indu

183 l attachment loss in older age; presence of "frank" periodontitis affecting a single tooth; and asses

184 crolymphomas to monoclonal microlymphoma and frank plasmablastic lymphomas in MCD patients.

185 Frank presents an alternative interpretation of our data

186 esions, but distinct from CSCs obtained from frank prostate tumors.

187 ient to activate the protective HSR prior to frank proteotoxic damage.

188 functional brain abnormalities, similarly to frank psychiatric disorders, may account for the atypica

189 findings provide evidence that the onset of frank psychosis is preceded by presynaptic dopaminergic

190 The onset of frank psychosis is usually preceded by a prodromal phase

191 nst the severe cognitive/social deficits and frank psychosis of chronic schizophrenia.

192 linical high risk who subsequently developed frank psychosis.

193 n subjects, was associated with the onset of frank psychosis.

194 utcomes, such as non-remission/transition to frank psychosis.

195 high-risk (UHR) for psychosis do not develop frank psychosis.

196 dels of the progression from being at CHR to frank psychosis.

197 at clinical risk for psychosis and 22 with a frank psychotic disorder.

198 ism that is distinct from that implicated in frank psychotic illness.

199 Additional study and frank public discourse are needed to understand the impl

200 ces Control Act (TSCA) was revised under the Frank R.

201 ity is mediated by dislocation emission from Frank-Read sources and multiplication, partial dislocati

202 decrease in spatial tuning, while Cheng and Frank report that the exploration of novel space leads t

203 In contrast, an Ent(+) Ybt(+) strain was a frank respiratory pathogen, causing pneumonia despite Lc

204 essation of antegrade contrast-dye motion or frank reversal of contrast-dye motion during systole) at

205 Under plausible conditions, frank reversal of exposure-outcome associations can occu

206 ecame hypotensive and was admitted to ICU in frank septic shock requiring inotropes, and with demonst

207 d abasic sites, alone or in combination with frank single-strand breaks, can be quantified by convert

208 ed T-cells) translocation to the nucleus and frank spine loss.

209 e vast majority of such patients do not have frank ST-segment elevation myocardial infarction.

210 The Frank-Starling 'law of the heart' is implicated in certa

211 activation (LDA), the cellular basis of the Frank-Starling cardiac regulatory mechanism.

212 ues were located on the flatter portion of a Frank-Starling curve because of attenuated decreases in

213 ues were located on the steeper portion of a Frank-Starling curve because of augmented decreases in S

214 oint to a flatter portion of the heat stress Frank-Starling curve thereby attenuating the reduction i

215 compared over a range of loading conditions (Frank-Starling curve).

216 heart is operating on a steeper portion of a Frank-Starling curve.

217 oint to a flatter portion of the heat stress Frank-Starling curve.

218 SV) via altering the operating position on a Frank-Starling curve.

219 define LV pressure-volume relationships and Frank-Starling curves.

220 We demonstrate the Frank-Starling effect at the single cardiomyocyte level

221 ps maintain a high ejection fraction via the Frank-Starling effect.

222 rrestin 2, or AT1R were unable to generate a Frank-Starling force in response to changes in cardiac v

223 We demonstrate that Frank-Starling is evident at maximal [Ca(2+) ] activatio

224 sistent contractile forces that followed the Frank-Starling law and accepted physiological pacing.

225 The Frank-Starling law and the Anrep effect describe exquisi

226 andling will deepen our understanding of the Frank-Starling law and the Anrep effect, and also provid

227 ng RLC phosphorylation as a modulator of the Frank-Starling law in the heart.

228 The Frank-Starling law of the heart is a physiological pheno

229 ther cardiac regulatory mechanisms, like the Frank-Starling law of the heart.

230 nd consequently the mechanism underlying the Frank-Starling law of the heart.

231 main cellular mechanism responsible for the Frank-Starling law of the heart.

232 ggests that these effects play a role in the Frank-Starling law of the heart.

233 uscle but also because it contributes to the Frank-Starling law, a mechanism by which the heart incre

234 The Frank-Starling mechanism allows the amount of blood ente

235 structural unit of the cardiac myocytes, the Frank-Starling mechanism consists of the increase in act

236 These data support the hypothesis that a Frank-Starling mechanism contributes to compromised bloo

237 Reconstitution of the Frank-Starling mechanism is an important milestone for p

238 These data suggest that a Frank-Starling mechanism may contribute to improvements

239 le of the giant elastic protein titin in the Frank-Starling mechanism of the heart by measuring the s

240 s that titin may be a factor involved in the Frank-Starling mechanism of the heart by promoting actom

241 The Frank-Starling mechanism of the heart is due, in part, t

242 that these two proteins are involved in the Frank-Starling mechanism of the heart.

243 he fine-tuning of cardiac performance by the Frank-Starling mechanism that relates the pressure exert

244 The Frank-Starling Mechanism was reduced in a graded fashion

245 all stress, thereby obscuring the use of the Frank-Starling mechanism, a fundamental mechanism by whi

246 According to the Frank-Starling mechanism, as the heart is stretched, it

247 hECTs reconstituted the Frank-Starling mechanism, generating an average maximum

248 y strong-binding cross-bridges underlies the Frank-Starling mechanism, we inhibited force and strong

249 and AT1R as key regulatory molecules in the Frank-Starling mechanism, which potentially can be targe

250 thin-filament activation contributes to the Frank-Starling mechanism.

251 on by neural and hormonal factors and by the Frank-Starling mechanism.

252 thus resulting in better utilization of the Frank-Starling mechanism.

253 esting an exercise-induced modulation of the Frank-Starling mechanism.

254 anical task, revealing a prime aspect of the Frank-Starling mechanism.

255 l a correlation between titin strain and the Frank-Starling mechanism.

256 hat beta-adrenergic stimulation enhances the Frank-Starling regulatory mechanism predominantly via cM

257 The Frank-Starling relation is a fundamental auto-regulatory

258 ts allowed us to identify two aspects of the Frank-Starling relation.

259 The Frank-Starling relationship is based, in part, on the le

260 Identified more than a century ago, the Frank-Starling relationship is currently known to involv

261 According to the Frank-Starling relationship, greater end-diastolic volum

262 According to the Frank-Starling relationship, increased ventricular volum

263 tivate beta-arrestin signaling preserved the Frank-Starling relationship.

264 ich implicates a novel means for controlling Frank-Starling relationships.

265 rce measurement apparatus exhibited a robust Frank-Starling response to external stretch, and a dose-

266 ardiac index as well as reinstitution of the Frank-Starling response to the native ventricle.

267 for diastolic relaxation and fine-tunes the Frank-Starling response.

268 gth (SL) is, in part, the cellular basis for Frank-Starling's law of the heart.

269 ion of cMyBP-C can influence the SL-tension (Frank-Starling) relationship in cardiac muscle.

270 ainst neoaortic stroke volume demonstrated a Frank-Starling-like curve that shifted upward after HF.

271 The engineered human myocardium exhibits Frank-Starling-type force-length relationships.

272 essively reduced GI motility, culminating in frank stasis that was primarily responsible for decreasi

273 /6J mice, TG accumulated in liver, producing frank steatosis.

274 Frank stone formation was observed in 13% of Cav1-/- mal

275 inct DNA interactions exhibited by AZB002: a frank strand scission leading to the relaxation of super

276 ly, in a side reaction that does not lead to frank strand scission, all four bases of DNA are methyla

277 chordate plan, giving rise in some cases to frank structural homologies with the vertebrate brain.

278 Remarkably, even after emergence of frank symptoms including weight loss, a single treatment

279 pressures may fall, and some may experience frank syncope.

280 ever, Tim-1(Deltamucin) mice did not develop frank systemic autoimmune disease unless they were cross

281 s in an accumulation of fusions, breaks, and frank telomere loss.

282 Tks4 carrying a reported point mutation in a Frank-ter Haar syndrome patient showed aberrant intracel

283 Mutations in SH3PXD2B cause Frank-Ter Haar syndrome, a rare condition characterized

284 are responsible for the autosomal recessive Frank-ter Haar syndrome.

285 oss anatomic defects, loss of lamination, or frank tuber formation.

286 essors showed delayed tumor growth or lacked frank tumor development (20% of animals); tumor capillar

287 )In-cCPE.GST targets claudin-4 expression in frank tumors and preneoplastic tissue, and cCPE imaging

288 ary lymphoma; 45% of infected mice developed frank tumors between 5 and 12 months postinfection, with

289 Individuals with metabolic syndrome and frank type 2 diabetes are at increased risk of atheroscl

290 Insulin resistance with or without frank type 2 diabetes has emerged as a major determinant

291 hat drives impaired glucose tolerance toward frank type 2 diabetes.

292 in an insulin-resistant stage that precedes frank type 2 diabetes.

293 trasmooth templating interface that promotes Frank-van der Merwe regime growth, while allowing facile

294 t rGO underlayer promotes 2D layer-by-layer (Frank-van der Merwe) metal film growth at early stages o

295 ining Ach-induced vasodilation, resulting in frank vasoconstriction (-54% +/- 9%, n = 6).

296 he biomarkers currently available shows that frank vitamin D deficiency is a major public health prob

297 No frank WBCs extravasation in the brain parenchyma was obs

298 ception of a sabbatical year at Harvard with Frank Westheimer, my entire career has been spent at Duk

299 hepatocellular damage, and in severe cases, frank whole-body edema and death.

300 Frank with having proposed defective platelet production