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 physician relationships could ever survive a frank admission of rationing at the bedside.

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

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

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

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

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 K. Frank Austen describes the work culminating in the ident

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

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

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

20 icate that new focal lesions associated with frank BBB leakage are preceded by subtle, progressive al

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

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

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

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

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

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

27 the malignant conversion of benign tumors to frank cancer.

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

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

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

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

32 can induce urothelial proliferation but not frank carcinoma formation.

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

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

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

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

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

38 nd occasionally dysplasia, without eliciting frank carcinomas.

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

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

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

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

43 cervical intraepithelial neoplasia, but not frank cervical carcinoma.

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

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

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

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

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

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

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

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

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

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

54 CNF1 intoxication, a finding that suggested frank cytotoxicity.

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

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

57 etachromatic leukodystrophy diagnosed before frank degenerative symptoms developed.

58 been associated with cognitive impairment or frank delirium.

59 ebilitation, including motor dysfunction and frank dementia.

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

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

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

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

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

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

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

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

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

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

70 ssociated with either glucose intolerance or frank diabetes.

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

72 female physicians were less likely to favor frank disclosure over pessimistically discrepant disclos

73 were more likely to favor no disclosure over frank disclosure, and that female physicians were less l

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

75 protracted latent period before the onset of frank disease likely reflects the ability of c-Myc to in

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

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

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

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

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

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

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

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

84 ese cluster classes is comparable to that of frank double-strand breaks; among all complex damages in

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

86 Cushing syndrome, which are associated with frank dyslipidemia.

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

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

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

90 Increased neuronal excitability and frank epileptiform discharges were observed after a sign

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

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

93 ted survival estimates, they would provide a frank estimate only 37% of the time and would provide no

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 e accessed from http:/ /www.bioss.sari.ac.uk/frank/Genetics and by anonymous ftp from typ://ftp.bioss

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

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

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

107 , with clinically overt tamponade in 40% and frank hemodynamic collapse (systolic blood pressure <60

108 w a reduced lifespan in vivo but there is no frank hemolysis.

109 Frank holes were present on day 2.

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

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

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

113 After cessation of loading, frank hypophosphatemia occurred.

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

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

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

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

118 tivated microglia were prominent in zones of frank infarction and in adjacent paramedian cortex; the

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

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

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

122 are highly sensitive to shock waves and that frank injury to tubules and vessels may be more closely

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

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

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

126 Frank-Kasper phases are tetrahedrally packed structures

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

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

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

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

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

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

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

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

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

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

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

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

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

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

141 s, while the submaximal tetanus now elicited frank LTD of synaptic EPSPs at perforant path synapses.

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

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

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

145 een in microlymphomas of 2 cases and in both frank lymphomas.

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

147 as mutation alone is insufficient to produce frank malignancy.

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

149 ementary mutations are required to produce a frank malignancy.

150 and immunophenotype prior to the onset of a frank malignancy.

151 this vulnerability and drives the cell into frank malignancy.

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

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

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

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

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

157 of intimal hyperplasia and does not require frank mechanical injury.

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

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

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

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

162 leading to the destruction of incipient and frank neoplasia.

163 lastic changes that ultimately culminated in frank neoplasia.

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

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

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

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

168 Frank neuron loss in the entorhinal cortex is specific f

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

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

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

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

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

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

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

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

177 events within NB cholinergic neurons before frank NFT deposition.

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

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

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

181 iated with fatty liver and abdominal pain or frank pancreatitis (the chylomicronaemia syndrome) is un

182 Furthermore, we show that the frank plasmablastic lymphoma that develops in patients w

183 cell follicles but may form microlymphoma or frank plasmablastic lymphoma.

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

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

194 renia, but is not typically characterized by frank psychosis.

195 ted to the sparing of patients with SPD from frank psychosis.

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

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

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

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

200 ho achieve remission subsequently experience frank relapse of their disease, and their ultimate progn

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

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

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

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

205 pectively, but only about half that level of frank single strand breaks in double strand breaks.

206 andom modification at guanine in the form of frank single-strand break (ssb) and base modifications,

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

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

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

232 nd consequently the mechanism underlying 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 , p < 0.005), confirming the presence of the Frank-Starling mechanism in the LA.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

274 /6J mice, TG accumulated in liver, producing frank steatosis.

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

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

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

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

279 t older patients were more likely to receive frank survival estimates, that the most experienced phys

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

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

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 rowths and not to differential growth of the frank tumors or to decreased middle T gene expression.

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

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

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

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

294 orsum of the right hand, which progressed to frank ulceration following chemotherapy.

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