ライフサイエンスコーパス: long latency

1 developed one or more mammary tumors after a long latency.

2 cells of mGluR6-null mice, but they occur at long latency.

3 rs non-lethal invasive prostate cancer after long latency.

4 ltered myelopoiesis with severe anemia after long latency.

5 and induces pre-T-cell tumors in mice after long latency.

6 ch, results in mammary tumor formation after long latency.

7 sistent viral replication and maintains life-long latency.

8 s, including breast cancer, appeared after a long latency.

9 cancer is low and occurs after a relatively long latency.

10 rs in mutant glands at low frequency after a long latency.

11 uently causes epilepsy that develops after a long latency.

12 age and, therefore, often after a relatively long latency.

13 which progressed to secondary leukemia after long latency.

14 ctivity in ITC were weak and occurred with a long latency.

15 K14-Cre led to mammary tumor formation with long latency.

16 ent of invasive IHCC with low penetrance and long latency.

17 development of myeloid leukemia, it is with long latency.

18 EC) mice developed intestinal tumors after a long latency.

19 on their own induce T-cell malignancies with long latency.

20 plasia in vivo that progress to tumors after long latency.

21 induced SCC and develop spontaneous SCC with long latency.

22 us myeloid, T- and B-cell malignancies after long latencies.

23 r cells exhibited the late peak with similar long latencies.

24 ulation evokes electromyograms at abnormally long latencies.

25 .55; 0.33-0.93), particularly persons with a long latency (10+ years) between the 2 conditions.

26 The long latency (234-299 days) and clonal chromosomal abnor

27 After long latency, 30% of the MN1-TEL-positive mice developed

28 Reach adaptation produced an increase in the long-latency (45-100 ms delay) feedback gains with respe

29 The long latency 5-HT-evoked increase in BAT SNA was prevent

30 with features of human APL, but only after a long latency (8.5 months in MRP8 PML-RARA mice).

31 /abl transgenic mice known to develop, after long latency, a myeloproliferative disorder resembling h

32 We conclude that short as well as long latency acoustic transmissions to click change in t

33 tency activation (<25 msec; 55.1% of cells), long latency activation (>65 msec; 56% of cells), and in

34 ectrode significantly reduced both short and long latency activations evoked in DA neurons by vBNST s

35 play a significant role in short as well as long latency, adaptive acoustic transmission that can en

36 The absence of long-latency AEPs should not, therefore, be considered i

37 Short latency afferent inhibition (SAI) and long latency afferent inhibition (LAI) measured with tra

38 ficantly increase survival; however, after a long latency, all tumors subsequently became resistant.

39 culture, and generate a partially penetrant, long-latency AML in bone marrow transplant recipients.

40 riod and were found to develop lymphoma with long latency and at high probability (more than 85% over

41 rcoma-associated herpesvirus, establish life-long latency and can reactivate in immunocompromised ind

42 of the transfected terminals, along with the long latency and complex physiological responses of thal

43 Given the long latency and incomplete penetrance of AD dementia wi

44 Mammary tumour formation occurs after long latency and is associated with genetic instability

45 f Lmo1 and Lmo2 cause T cell leukaemias with long latency and that Lmo2 expression leads to an inhibi

46 At low levels, spikes occurred with long latency and the firing frequency increased througho

47 d that Mcph1(-/-) mice developed tumors with long latency, and that primary lymphoma developed signif

48 terozygous strain also formed tumors after a long latency, and the cells from those tumors lacked p53

49 Older age and short or long latencies are not associated with DILI mortality.

50 ly variable escape responses with relatively long latencies as well as the unilateral recruitment of

51 Mammary (and other) tumors occur at long latency as compared to oncogene-induced mouse tumor

52 The long latency associated with the development of colorect

53 ess higher auditory processing capabilities, long-latency auditory evoked potentials (AEPs) were reco

54 der lines develop mammary tumors, but with a long latency (average age of 18 months).

55 Pten(fl/fl)) develops prostate cancer with a long latency, because disease initiation in this model r

56 of the early M20, as well as the strength of long latency beta oscillations.

57 The high burden of morbidity, coupled with a long latency between BMT and the development of chronic

58 f its ubiquity, treatment-related morbidity, long latency between premalignant lesions and clinically

59 No wind-up of either long latency C-fibre or short latency Adelta responses w

60 for discrimination between short-latency and long-latency C-starts (SLCs vs. LLCs) in larval zebrafis

61 for discrimination between short-latency and long-latency C-starts (SLCs vs. LLCs) in larval zebrafis

62 Longer follow-up for typically long-latency cancers and attention to specific cancer si

63 we used dsTMS to systematically investigate long-latency causal interactions between right-hemispher

64 chimeric mice, and these tumours occur with long latency compared with those found in MLL-Af9 chimer

65 Whereas the long-latency component seemed to occur with the eye move

66 ions supported the hypothesis that short and long latency components of blink responses represented c

67 In these subjects, the long latency components of the reflex response could, in

68 COMT activity specifically alters long-latency components of the event-related response.

69 from non-DS simple cells for both short- and long-latency components, with temporal phase differences

70 se was composed of two movements: short- and long-latency components.

71 ere that shape-from-shading stimuli evoked a long-latency contextual pop-out response in V1 and V2 ne

72 These results indicate that long-latency contributions to reciprocal inhibition of s

73 se of the study was to assess whether or not long-latency contributions to reciprocal inhibition of s

74 Findings indicate that long-latency contributions to reciprocal inhibition of t

75 n the left eye, whereas the long CS produced long-latency CRs in the right eye.

76 Within this variation, we found robust long-latency decreases (300 and 2000 ms after stimulus p

77 uced leukemias in irradiated recipients with long latencies, demonstrating both a requirement for sup

78 A long-latency depolarization interrupts the IPSP with a p

79 hyperpolarization and before the peak of the long-latency depolarization yields an augmenting respons

80 Long-latency DRPs were also present and superimposed on

81 vocal performance and that HVo neurons show long latency electrophysiologic auditory responses.

82 r stimulation triggers synaptically mediated long-latency epileptiform burst discharges.

83 in <60 ms after perturbation, during the R2 long-latency epoch (~45-75 ms).

84 rved ~75 ms after perturbation during the R3 long-latency epoch (~75-105 ms).

85 ce of a nonpathogenic helper virus developed long-latency erythroblastosis, and subsequent viral pass

86 Prion infections can have long latencies even though there is no protective immune

87 ibition (61.8% of cells, usually followed by long latency excitation).

88 rate that mPFC stimulation evokes short- and long-latency excitation and inhibition in DA neurons.

89 cervical interneurons tested also exhibited long latency excitatory responses to lumbar dorsal root

90 o interneurons was strong enough to generate long-latency feedforward GABAergic input onto pyramidal

91 ishabituation of the electrically stimulated long-latency giant fiber pathway response were shown in

92 A subset responded to taste with long latencies (>1.0 s), suggesting the activation of ex

93 These connections were weak, had long latencies (>4 msec), and therefore were probably po

94 Long-latency (> 10 ms) EPSPs were seen in both cell type

95 Both short-latency (< 50 ms) and long-latency (> 50 ms) excitatory responses were seen.

96 rus that infects humans and establishes life-long latency, has evolved numerous mechanisms to evade h

97 l frequency, and speed, whereas neurons with long latencies have high spatial acuity, low sensitiviti

98 ice develop lung tumours at high rates after long latencies, implicating defects in the mitotic check

99 ro and induces acute myeloid leukemias after long latencies in syngeneic recipient mice.

100 nduces acute myelogenous leukemia (AML) with long latency in bone marrow transplantation assays.

101 uman alpha-herpesviruses that establish life-long latency in neural ganglia after initial primary inf

102 roinvasive dsDNA viruses that establish life-long latency in peripheral nervous system (PNS) neurons

103 Later evolution of long latency in Plasmodium vivax was a necessary adaptat

104 Human herpesviruses establish life-long latency in the host, and it is plausible that a lat

105 ll lymphotrophic viruses that establish life-long latency in the host.

106 e other herpesviruses, KSHV establishes life-long latency in the human host with intermittent periods

107 embles the APL-like disease that occurs with long latency in the PML/RARalpha transgenics, suggesting

108 othalamic terminals induced small-amplitude, long-latency increases and/or decreases of activity in t

109 o2 in T cells results in clonal tumours with long latency indicating that mutations in other genes ar

110 rs appear stochastically and with relatively long latency, indicating an additional requirement for o

111 althcare providers unfamiliar with acute and long latency infections and diseases common in this popu

112 rotrophic factor (BDNF), have both rapid and long-latency influences on synaptic strength.

113 Subjects (n=14) had long-latency inhibition at rest (x = -35.0 +/- 18.7%).

114 n, the latter suggesting that N2 may reflect long-latency inhibition of irrelevant stimuli.

115 l electrical stimulation produced bilateral, long latency inhibitory postsynaptic potentials (IPSPs).

116 correspond to the properties of the second, long-latency inhibitory component of type IV responses.

117 ese excitatory inputs were often followed by long-latency inhibitory postsynaptic potentials.

118 The long-latency inputs could potentially arise from lagged

119 Thus, long-latency interhemispheric interactions, likely refle

120 These pathways are likely to convey long-latency jaw-muscle stretch reflexes and may contrib

121 ons responded weakly to sensory stimuli, had long latencies, large receptive fields, and poorly devel

122 dent modulation of monosynaptic (middle) and long-latency (late) stimulation-evoked EMG responses was

123 inct MLL fusion proteins to promote short or long latency leukemogenesis.

124 , short latency sustained (SLS, n = 12), and long-latency (LL, n = 6) to CRD.

125 Both short-latency (SL; 3-5 ms) and long-latency (LL; >/=9 ms) responses were observed after

126 latency for a switch from the short- to the long-latency location.

127 short-duration activation of neurons and (2) long-latency, long-duration activation of neurons.

128 ked in Golgi cells by the same stimuli was a long-latency, long-lasting depression of firing, found i

129 The most common response was a modest, long-latency, long-lasting increase in simple spike outp

130 rtical neurons interposed in a transcortical long-latency loop leading to pre-programmed reactions to

131 ce expressing PML-RAR alpha develop APL with long latency, low penetrance, and acquired cytogenetic a

132 e retinal ganglion cells (ipRGCs), including long latencies, marked poststimulus persistence, and a p

133 The long latency (mean = 157 days), reduced penetrance, and

134 reased BAT SNA (peak: +342% of control) at a long latency (mean onset: 23 min).

135 Om neurons responded to whisker stimuli with long-latency (median, 27 msec) and low-magnitude respons

136 late responses as likely mediated by either long-latency monosynaptic (n = 108) or non-monosynaptic

137 Both old and new M1 generated putative long-latency monosynaptic and non-monosynaptic effects;

138 Long-latency muscle responses paralleled changes in the

139 The long-latency neurons had a mean onset latency of 36.0 +/

140 ma oscillations, infants display a distinct, long latency, noxious evoked 18-fold energy increase in

141 Given the relatively long latency of conditioned responses we observed in PL

142 rences in outcomes of patients with short vs long latency of DILI.

143 The long latency of HD after transplant and lack of associat

144 The long latency of mammary tumors in WAP-h-Int3sh mice coul

145 eriods of cancer cell dormancy can result in long latency of metastasis development.

146 The long latency of prostate cancer development provides an

147 its answer remains controversial due to the long latency of the auditory feedback pathway and techni

148 However, owing to the long latency of tumor formation and the sporadic occurre

149 clonal Ikaros-mutant pre-B cells resulted in long-latency oligoclonal pre-B-ALL, which demonstrates t

150 The long-latency ON responses are not blocked by metabotropi

151 In mGluR6-null mice, long-latency ON responses are observed in the visual cor

152 y tumors escaped immune surveillance after a long latency or equilibrium period.

153 l pancreas, with tumors forming only after a long latency or pancreatitis induction.

154 f the animals develop acute leukemia after a long latency period (6-13 months).

155 The long latency period and incomplete penetrance suggest th

156 However, the long latency period between infection and development of

157 w causes a myeloproliferative disease with a long latency period but with high penetrance.

158 d with caution given the short follow-up and long latency period for most cancers, the intensive medi

159 even decades, which may explain the observed long latency period for neurological disease onset among

160 n infected with HPV clear their lesions, the long latency period from infection to resolution indicat

161 ive cancer progression after a comparatively long latency period is primarily driven by the mobilizat

162 The molecular mechanisms underlying the long latency period of mesothelioma and driving carcinog

163 ular changes drive carcinogenesis during the long latency period of mesothelioma development and show

164 jury, inflammation, and proliferation in the long latency period of MM development that may be perpet

165 Given the long latency period of pancreatic cancer, exploring the

166 potentially contributes to the indolence and long latency period of this disease.

167 The long latency period suggests that additional genetic alt

168 of leukemia and neurological disease after a long latency period, and the mechanism by which the viru

169 imals develop B and T cell lymphomas after a long latency period, but the incidence is dramatically e

170 After a long latency period, we find epithelial-specific PTEN de

171 t (ANV) of MMC (tumor evasion model) after a long latency period.

172 nal noise exposure even after allowing for a long latency period.

173 focal hepatocellular carcinoma (HCC) after a long latency period.

174 duce colorectal cancer risk but only after a long latency period.

175 ce developed mature T cell leukemias after a long latency period.

176 Thus, in spite of long latency periods during which secondary alterations

177 ouse ltk(-) cells confirm a channel that has long latency periods to opening (1.67 +/- 0.073 s at +60

178 Many cancers have long latency periods, and dietary factors in adolescence

179 nesis, by reduced penetrance or by extremely long latency periods.

180 t effect on prostate cancer risk except with long latency periods.

181 ynaptic (n=2), di-or tri-synaptic (n=18) and long-latency polysynaptic (n=16) responses were recorded

182 C5-C7) suggest that much of the delay in the long-latency polysynaptic responses require a bilaterall

183 appears during response preparation, as in a long-latency positive SOA.

184 Selective attention strongly modulated long-latency potentials evoked by words.

185 nsplant (BMT) model, whereas T/T(F) causes a long-latency, pre-B-cell lymphoblastic lymphoma.

186 The long latency raises the possibility that Golgi cells rec

187 is essentially ipsilateral, and in whom the long-latency reflex components following digital nerve s

188 for the perturbation but also increases the long-latency reflex gain associated with leftward displa

189 avior is mediated by volitional and possibly long-latency reflex pathways with delays of at least 120

190 ondly, that such responses do not use those 'long-latency' reflex pathways probed by cutaneomuscular

191 1 Hz reduced the amplitude of both MEPs and long latency reflexes by 20-30 % for about 10 min after

192 Long latency reflexes were facilitated with the same tim

193 Cardiac T2* changes have a long latency relative to liver iron accumulation.

194 esulted in a significant wind-up response of long latency response in six of ten cells studied.

195 Furthermore, failures of the long-latency response during habituation, which normally

196 in the interior of the fly brain and (ii) a long-latency response in which electrical stimulation tr

197 The long-latency response is obliterated at concentrations s

198 sponse to whisker deflection, those having a long-latency response, and neurons whose firing is suppr

199 ring learning correlated with changes in the long-latency response, showing subjects who adapted more

200 The TTM muscles of cpo mutants exhibit long latency responses coupled with decreased following

201 ere unresponsive and twenty-eight (24%) gave long latency responses following SCN stimulation.

202 Long-latency responses (>25 msec delay; "weakly coupled"

203 Furthermore, long-latency responses at the edge of the receptive fiel

204 Adapted long-latency responses expressed (de-) adaptation simila

205 y that maintained consistent activity of the long-latency responses ranged from 40 to 60 Hz, whereas

206 The long-latency responses to epidural stimulation are corre

207 expectedly, many V1 neurons gave significant long-latency responses to texture stimuli located entire

208 At higher intensities, long-latency responses were recruited in a highly nonlin

209 of the quadrature model because of a lack of long-latency responses.

210 es, although middle (monosynaptic) and late (long latency) responses were more prominent on the non-d

211 value information is taken into account for long-latency saccades.

212 No long-latency spike responses were evoked in response to

213 al level difference sensitivity contained in long-latency spikes.

214 tion between primary SLCs and less frequent, long-latency startle responses (LLCs).

215 The long-latency stretch reflex (LLSR) in human elbow muscle

216 s report is the first demonstration that the long-latency stretch reflex can be modified by repeated,

217 The amplitude of the long-latency stretch reflex of the contralesional hand d

218 ouse model; however, tumors developed with a long latency, suggesting a second event is needed to tri

219 nd a low percentage of mammary tumors with a long latency, suggesting that the resulting tumors were

220 Such long-latency suppressions also included monotonically in

221 est frequency (BF) of a neuron, we uncovered long-latency suppressions caused by single-tone stimulat

222 Most cells showed long-latency sustained responses.

223 horns of normal spinal cord slices revealed long-latency synaptic responses in lamina II and short-l

224 HSV-1 establishes life-long latency that can result in clinical relapses or in

225 n the intestine can been observed only after long latencies, they result in rapid carcinogenesis in t

226 le and developed in one or more glands after long latency (time for median tumor-free survival of app

227 second cancers involves modeling: because of long latency times, available data is usually for older,

228 Reflexes occurred unreliably and at long latency to 44.0 or 0.3 degrees C and were not appro

229 Responding with an unusually long latency to light stimulation, OND RGCs respond earl

230 ped in Mll-AF4 mice after prolonged latency; long latency to malignancy indicates that Mll-AF4-induce

231 The switch to long latency-to-onset occurred abruptly as a function of

232 western Pacific suggests the possibility of long-latency toxins, but pinning down a specific causati

233 hese cerebral events reflect components of a long-latency transcerebral reflex pathway that is affect

234 oneurons and/or interneurons, rather than by long-latency transcortical reflex responses.

235 the increase in force is similar to that of 'long-latency' transcortical reflexes recorded from muscl

236 or cells expressing JAK3 mutants developed a long-latency transplantable T-ALL-like disease, characte

237 ammary tumors from double transgenic mice to long latency tumors from single transgenic mice and obse

238 tumors is changing with increasing latency, long latency tumors in other organs could occur in the f

239 After a long latency, tumors also develop in animals never expos

240 l short-latency units (< 12 ms) but never in long-latency units (> or = 12 ms).

241 The long-latency units were recorded at an average depth of

242 as NMDAR blockade was much more effective in long-latency units.

243 ade reduced onset spikes more effectively in long-latency units.

244 its but reduced spikes substantially for all long-latency units.

245 that the amygdala enables the development of long-latency (US anticipatory) responses and prevents th

246 models, leukemia developed after a variably long latency, with variable penetrance.

247 M1 with complex dynamics, as well as evoking long-latency, wM1-dependent whisking.