ライフサイエンスコーパス: AHP

1 AHP current did not have time to decay between action po

2 AHP dUTP is a versatile clickable nucleotide with potent

3 AHP expression appears unaffected by Mn(II), yet the lar

4 AHP is blocked by 6-cyano-7-nitroquinoxaline-2,3-dione (

5 AHP is blocked by Li+o substitution for Na+o and by ouab

6 AHP is seen in dissociated horizontal cells (HCs) and hy

7 AHP never occurs in depolarizing, or ON type, bipolar ce

8 AHP occurs only in neurons that are depolarized by gluta

9 AHP was asymptomatic in 2 patients; 2 reported sporadic

10 AHPs triggered with theta-burst firing every 30 s were p

11 osteric 4-(aminomethyl)-1-hydroxypyrazole (4-AHP) analogues of muscimol, a GABA(A) receptor agonist,

12 The unsubstituted 4-AHP analogue (2a) (EC(50) 19 muM, R(max) 69%) was a mode

13 A slowly accumulating AHP current, also insensitive to apamin, was extremely s

14 examined how changes in PIP2 levels affected AHPs, somatic [Ca(2+) ]i , and whole cell Ca(2+) current

15 is terminated by an afterhyperpolarization (AHP) that displays two main components; the medium AHP (

16 ce and absence of an afterhyperpolarization (AHP).

17 Medians of AP and afterhyperpolarization (AHP) durations and AP overshoots were significantly grea

18 es in the post-burst afterhyperpolarization (AHP) and spike-frequency accommodation, is altered durin

19 enhanced post-burst afterhyperpolarization (AHP), in CA1 hippocampal pyramidal neurons.

20 ng, sodium-dependent afterhyperpolarization (AHP) following bursts of action potentials that was medi

21 the Ca2+ -dependent afterhyperpolarization (AHP) following spike trains is significantly larger duri

22 to the long lasting afterhyperpolarization (AHP) that follows an action potential in many central ne

23 of the long-lasting afterhyperpolarization (AHP) that follows individual theta bursts.

24 ad larger and longer afterhyperpolarization (AHP) as well as slower frequency-responses to depolarizi

25 pendent, K+-mediated afterhyperpolarization (AHP) is related to cognitive decline.

26 BK channel mediated afterhyperpolarization (AHP), repetitive spiking is maintained, through the incr

27 the slow and medium afterhyperpolarization (AHP) currents (I(sAHP), I(mAHP)).

28 owed by a monophasic afterhyperpolarization (AHP).

29 on, the amplitude of afterhyperpolarization (AHP) and the pattern of AP firing; SLO-2 is also importa

30 ion of the postburst afterhyperpolarization (AHP) have been repeatedly demonstrated in multiple brain

31 ons of the postburst afterhyperpolarization (AHP) in hippocampal pyramidal neurons have been shown ex

32 ion in the postburst afterhyperpolarization (AHP).

33 del with a postspike afterhyperpolarization (AHP), but absent from those calculated from the discharg

34 Action potential afterhyperpolarization (AHP) enhances precision of firing by ensuring that the i

35 lowed by a prolonged afterhyperpolarization (AHP) that influences firing frequency and affects neuron

36 possess a prominent afterhyperpolarization (AHP) that contributes to spike patterning.

37 a slowly recovering afterhyperpolarization (AHP), but, unlike in cortical cells, this AHP is not pri

38 ute to a medium-slow afterhyperpolarization (AHP) after spike bursts, regulating membrane excitabilit

39 with increased slow afterhyperpolarization (AHP) potential, whereas vulnerability was associated wit

40 a depression of the afterhyperpolarization (AHP) and an increase in frequency of evoked and spontane

41 ngs, we examined the afterhyperpolarization (AHP) in CA1 pyramidal cells in hippocampal slices from y

42 The afterhyperpolarization (AHP) that follows each spike, however, decays relatively

43 currents that cause afterhyperpolarizations (AHPs) and afterdepolarizations (ADPs).

44 y calcium-dependent afterhyperpolarizations (AHPs) following a train of action potentials that are cr

45 KEY POINTS: Afterhyperpolarizations (AHPs) generated by repetitive action potentials in supra

46 e rise to prominent afterhyperpolarizations (AHPs).

47 approximately 20 s) afterhyperpolarizations (AHPs) that were insensitive to blockade of voltage-gated

48 s underwent strabismus surgery to correct an AHP and/or improve ocular alignment.

49 These cells commonly respond with only an AHP component.

50 ted from the discharge of a model without an AHP.

51 orrelated with BLA neuronal excitability and AHP.

52 AP overshoots and AHP durations were similar in nociceptors of all CV grou

53 associated with a reduction in rheobase and AHP.

54 ability were related to the altered ADPs and AHPs.

55 P current (I(AHP)) was insufficient to block AHP plasticity, suggesting that plasticity is manifested

56 Inhibition of both AHP components by L-type Ca(2+) channel antagonists was

57 amplicon with all 335 thymidines replaced by AHP dU was shown to be a perfect copy of the template fr

58 hat adult hippocampal stem/progenitor cells (AHPs) express receptors and signalling components for Wn

59 result in accumulation of calcium-dependent AHP current.

60 ach produce acceptable collapse of chin-down AHP, the former frequently induces a V-pattern esotropia

61 erically undemanding azide analogue of dTTP (AHP dUTP) with an alkyl chain and ethynyl attachment to

62 ned that an apamin-sensitive medium-duration AHP (mAHP) and an apamin-insensitive slow AHP (sAHP) wer

63 ications for the potential use of endogenous AHPs in neurological disease.

64 Because enhanced AHP in aging neurons has been hypothesized to be seconda

65 enhanced sI(AHP) contributes to the enhanced AHP in aging.

66 onses/no. of stimuli) by using the estimated AHP to create a fixed threshold 'daughter' model MN to m

67 Cells with exclusively AHP responses are tonically depolarized.

68 AHP became faster and shallower, and a fast AHP emerged.

69 We therefore suggest that the large, fast AHP is a key feature of BD and a main contributor to the

70 er a burst of action potentials and the fast AHP (fAHP) after individual action potentials.

71 through BK channels, contributes to the fast AHP and appears to offset the DAP; this current is sensi

72 ng, we isolated T-DNA insertions in the five AHP genes that are predicted to encode functional HPts a

73 ew of 150 patients who underwent surgery for AHP associated with nystagmus.

74 Thirty-one patients had surgery for AHP in the pitch (chin up/down) position, whereas 119 ha

75 assays, indicating both a positive role for AHPs in cytokinin signaling and functional overlap among

76 In contrast with the other four AHPs, AHP4 may play a negative role in some cytokinin re

77 of Wnt signalling reduces neurogenesis from AHPs in vitro and abolishes neurogenesis almost complete

78 is sufficient to increase neurogenesis from AHPs in vitro and in vivo.

79 decay times (24.67 vs. 11.02 ms) and greater AHP amplitudes (3.27 vs. 1.56 mV) than MNs lacking SK3-i

80 Fewer patients in the FRMD7 group had AHPs, their amplitude of nystagmus being lower in primar

81 The syndrome of Anosognosia for Hemiplegia (AHP) can provide unique insights into the neurocognitive

82 ies propose that anosognosia for hemiplegia (AHP) results from specific impairments in motor planning

83 ium (SK2) channels, also reduced hippocampal AHPs and closely reproduced the effects of BDNF on theta

84 on, whereas 119 had surgery for a horizontal AHP.

85 However AHP is not blocked by nifedipine and is insensitive to [

86 rst, the model MN's after-hyperpolarisation (AHP) was deduced from its interval histogram for tonic f

87 nels mediate medium after-hyperpolarization (AHP) conductances in neurons throughout the central nerv

88 nd amplitude of the after-hyperpolarization (AHP), without affecting the pre- and postsynaptic membra

89 e potential, termed after-hyperpolarization (AHP).

90 share a large, fast after-hyperpolarization (AHP).

91 s and long-lasting after-hyperpolarizations (AHPs), mediated by calcium-activated, cyclic AMP-sensiti

92 Two prominent after-hyperpolarizations (AHPs), one of medium duration that was apamin-sensitive

93 ed fast and medium after-hyperpolarizations (AHPs); (iv) strongly enhanced burst firing and increased

94 hannels that underlie after hyperpolarizing (AHP) currents and contribute to the shaping of the firin

95 onditions, calcium-activated K(+) current (I(AHP)) improved efficient spike-rate coding at the expens

96 ckade of the apamin-sensitive AHP current (I(AHP)) was insufficient to block AHP plasticity, suggesti

97 o the distinct activation requirements for I(AHP) and I(M), which in turn dictate whether those curre

98 mical systems analysis, we demonstrate how I(AHP) minimizes perturbation of the interspike interval c

99 The reduction of I(AHP) was occluded by previous blockade of calcium-activa

100 d on their distinct activation properties, I(AHP) implements noise shaping that improves spike-rate c

101 polarization amplitudes (ADP), and reduced I(AHP) and enhanced I(ADP).

102 stration that altered awareness of action in AHP reflects a dominance of motor intention prior to act

103 bserved non-veridical awareness of action in AHP.

104 HCC in AHP occurred in the absence of cirrhosis, which contrast

105 The pathogenesis of hepatocarcinogenesis in AHP is unknown and needs further investigation.

106 KGluc, repetitive theta-burst firing induced AHP plasticity that mimics learning-related reduction in

107 Place-cell-train-induced AHPs were blocked by ouabain or removal of extracellular

108 PIP2 appears to influence AHPs in OT neurons by reducing Ca(2+) influx during spik

109 ng was governed by a fast apamin-insensitive AHP current that did not accumulate, but rather showed d

110 uced findings, we propose that the intrinsic AHP level might determine the degree of synaptic plastic

111 re hyperpolarized potentials and have larger AHPs than young neurons.

112 ce cell train" generated small, long-lasting AHPs capable of reducing neuronal excitability for many

113 mmunoreactivity exhibit significantly longer AHP half-decay times (24.67 vs. 11.02 ms) and greater AH

114 mechanism (reduction in SK channel-mediated AHP) that led to the learning-induced increased intrinsi

115 ationships between SK3 expression and medium AHP properties.

116 ability was associated with decreased medium AHP.

117 influenced by the SK channel-mediated medium AHP (mAHP), because the SK blocker apamin reduced the sh

118 l cord may contribute to the range of medium AHP durations across specific MN functional types and ma

119 currents generate an apamin-sensitive medium AHP (mAHP) after each AP; and bursts of APs generate lon

120 hat displays two main components; the medium AHP (I(mAHP)), lasting a few hundred milliseconds and th

121 threshold hyperpolarized 6.7 mV, the medium AHP became faster and shallower, and a fast AHP emerged.

122 distinguishable currents known as the medium AHP current (I(mAHP)) and the slow AHP current (I(sAHP))

123 erformance-related differences in the medium AHP.

124 ccessful, while ET in a patient with a minor AHP was corrected by performing a bimedial recession.

125 anipulations of PIP2 levels did not modulate AHPs by influencing Ca(2+) release from IP3 -triggered C

126 ctivation of GluR6-containing KARs modulates AHP amplitude, and influences the firing frequency of py

127 However, no AHP plasticity was observed using KMeth.

128 hannels results in the generation of a novel AHP not seen in wild-type Purkinje neurons that also acc

129 ) and adaptive hierarchically penalized NSC (AHP-NSC), with two different penalty functions for micro

130 these to the time course and accumulation of AHP currents using whole-cell and perforated patch recor

131 Outcome measures included amount of AHP and deviation at last follow-up.

132 thalmological papers, as a possible cause of AHP.

133 Successful collapse of AHP was defined as being <=10 degrees .

134 The primary outcome was collapse of AHP.

135 n = 131), 125 patients (95%) had collapse of AHP.

136 ismus, in addition to failure of collapse of AHP.

137 Collapse of AHP: At the 1-3-week follow-up (n = 131), 125 patients (

138 membrane properties, and on the induction of AHP plasticity in CA1 pyramidal neurons from rat hippoca

139 On average, a reduction of AHP of 1.3 degrees /mm was achieved by predominantly per

140 current models indicating relocalization of AHP protein into the nucleus in response to cytokinin ar

141 Studies of AHP plasticity require stable long-term recordings, whic

142 HCC in a multicenter, longitudinal study of AHP.

143 regulates differentiation and maturation of AHPs non-cell-autonomously via SCG2.

144 or IP3 availability, i.e. PIP2 modulation of AHPs is not likely to involve downstream Ca(2+) release

145 To assess the role of AHPs in cytokinin signaling, we isolated T-DNA insertion

146 We examined the effects of cytokinin on AHP subcellular localization in Arabidopsis and, contrar

147 e trains in OT neurons, but had no effect on AHPs evoked by uncaging intracellular Ca(2+) .

148 HW: 3.9 +/- 0.7 ms) spike AHPs with only one AHP minimum (TTP: 0.9 +/- 0.1 ms).

149 associated to a new onset of sudden, painful AHP with normal ocular exam).

150 We show that animal haem peroxidases (AHPs) located on the outer membrane and within the secre

151 e and that of histidine phosphotransferases (AHPs) in guard cell signalling remain to be fully elucid

152 C) is increased in acute hepatic porphyrias (AHP).

153 rection of chin-down abnormal head position (AHP) associated with infantile nystagmus syndrome (INS).

154 n maintaining the learning-related postburst AHP reduction observed in CA1 pyramidal neurons.

155 Anomalous head posture (AHP) or torticollis is a relatively common condition in

156 adopt a significant anomalous head posture (AHP) towards the fixing eye in order to dampen the nysta

157 The presence of anomalous head posture (AHP) was significantly higher in the non-FRMD7 group (P

158 ing, reduced afterhyperpolarizing potential (AHP) and increased slow afterdepolarization amplitudes (

159 tude of the after-hyperpolarizing potential (AHP) following a train of spikes and the underlying apam

160 uction of afterhyperpolarization potentials (AHPs) in hippocampal CA1 cells, suggesting a direct role

161 hereafter, the analytical hierarchy process (AHP) and Dempster-Shafer (DS) methods are independently

162 e compared the analytical hierarchy process (AHP) based and logistic regression (LR) based approaches

163 al, Nursing and Allied Health Professionals (AHP) through the entirety of training to senior consulta

164 iferating adult hippocampal stem/progenitor (AHP) progeny and lead to the exclusive generation of cel

165 maturation of adult hippocampal progenitors (AHPs).

166 thaliana histidine phosphotransfer proteins (AHPs) are similar to bacterial and yeast histidine phosp

167 bidopsis histidine phosphotransfer proteins (AHPs), which have been suggested to translocate to the n

168 entiation and affected the maturation of rat AHPs.

169 Rather, AHPs actively maintain a consistent nuclear/cytosolic di

170 roup, and required correction of a recurrent AHP (P = .06).

171 nating esotropia, and 1 to correct recurrent AHP.

172 onditioned mice show a significantly reduced AHP after trains of parallel fiber stimuli and after cli

173 reover, our results suggest that the reduced AHP is related to a down-regulation of SK2/SK3 channel s

174 alcium-activated potassium channels regulate AHP and excitability in neurons.

175 Pyramidal cells of layer V exhibit robust AHP currents composed of two kinetically and pharmacolog

176 hat the longest component of the GP neuron's AHP is blocked by apamin, a selective antagonist of calc

177 Apamin-sensitive AHP (SK) current was measured by subtraction of tail cur

178 Blockade of the apamin-sensitive AHP current (I(AHP)) was insufficient to block AHP plast

179 nant SK2 channels, neuronal apamin-sensitive AHP currents, and the excitability of CA1 neurons.

180 ion in SK channel-mediated, apamin-sensitive AHP is a critical contributing mechanism.

181 ward calcium-activated potassium current (sI(AHP)), a major constituent of the AHP, also facilitate l

182 the apamin-insensitive slow AHP current (sI(AHP)).

183 Thus, an enhanced sI(AHP) contributes to the enhanced AHP in aging.

184 ng neurons were found to have an enhanced sI(AHP,) the amplitude of which was significantly correlate

185 n in young neurons; however, the residual sI(AHP) was still significantly larger in aging neurons tha

186 ning, suggest that the enhancement of the sI(AHP) in aging is a mechanism that contributes to age-rel

187 quantitatively greater reductions in the sI(AHP) in aging neurons than in young neurons; however, th

188 pe Ca2+ channels, we further examined the sI(AHP) in the presence of an L-type Ca2+ channel blocker,

189 facilitate learning in aging animals, the sI(AHP) was pharmacologically isolated and characterized.

190 c and voltage-dependent properties of the sI(AHP).

191 In typical patients who adopt a significant AHP accompanied by a large ET, we suggest an initial com

192 ppocampal pyramidal cells reveal that a slow AHP is reduced by blocking different components of the C

193 afterdepolarizing potential (ADP), and slow AHP (sAHP) that was attributable to calcium influx via h

194 in robustly blocked both the medium and slow AHP currents (ImAHP and IsAHP ) of OT, but not VP neuron

195 of PIP2 levels affected both medium and slow AHP currents in oxytocin (OT) neurons of the supraoptic

196 the modulation of a potassium current (slow AHP current, I(sAHP)) known to be targeted by multiple t

197 on AHP (mAHP) and an apamin-insensitive slow AHP (sAHP) were specifically increased in OT neurons.

198 rough changes in the apamin-insensitive slow AHP current (sI(AHP)).

199 ting a few hundred milliseconds and the slow AHP (I(sAHP)), that has a duration of several seconds.

200 The slow AHP (sAHP) recorded from learning-impaired aged rats (AI

201 ol 4,5-bisphosphate (PIP2 ) enabled the slow AHP component (sAHP) in cortical pyramidal neurons.

202 he medium AHP current (I(mAHP)) and the slow AHP current (I(sAHP)).

203 resence of apamin and tetrodotoxin, the slow AHP was strongly reduced by 5-HT, and fully abolished by

204 and bursts of APs generate long-lasting slow AHPs (sAHPs) attributable to apamin-insensitive currents

205 t, we show that in this Roseobacter species, AHPs mediate Mn(II) oxidation not through a direct react

206 Spike AHP currents were measured in voltage clamp as tail curr

207 ion potential afterhyperpolarisations (spike AHPs) of CA1 interneurones were investigated in 25 baske

208 nged with GABA(A) receptor modulators, spike AHPs in basket and bistratified cells were enhanced by z

209 ety showed narrow (HW: 3.9 +/- 0.7 ms) spike AHPs with only one AHP minimum (TTP: 0.9 +/- 0.1 ms).

210 The spike AHPs of three axo-axonic cells tested showed no sensitiv

211 The spike AHPs showed two minima in all regular-spiking (5), burst

212 d time courses resembling those of the spike AHPs.

213 pus autaptic connections contribute to spike AHPs in many interneurones.

214 Interneurones with spike AHPs affected by the GABA(A) receptor ligands exhibited

215 ghlighting two consistent findings: (i) that AHP and accommodation are reduced in pyramidal neurons f

216 mals that have learned a task; and (ii) that AHP and accommodation are enhanced in pyramidal neurons

217 pense of newborn neurons, demonstrating that AHPs in the adult mouse brain are not irrevocably specif

218 These data indicate that AHPs have substantial plasticity, which might have impor

219 Finally, we present data indicating that AHPs maintain a nuclear/cytosolic distribution by balanc

220 The AHP is also reduced by many neuromodulators, such as nor

221 The AHP is supported by at least three subtypes of K(Ca) cha

222 The AHP measured immediately after establishing whole-cell r

223 The AHP width at half-amplitude (HW) was 12.5 +/- 5.7 ms in

224 R code for the ALP-NSC and the AHP-NSC algorithms are available from authors upon reque

225 However, because the AHP is measured following completion of training, it is

226 us studies showing a correlation between the AHP and learning, suggest that the enhancement of the sI

227 influence of prior discharge mediated by the AHP, and it increases in amplitude when AHP amplitude is

228 Correspondingly, the AHP time course was similar to the decay of activity-ind

229 In general, the AHP in KMeth was comparable to the AHP measured in the p

230 restores membrane potential, generating the AHP response.

231 However, the AHP based model detected sinkhole presence by allocating

232 In the AHP method, the proper weight for each input parameter i

233 Furthermore, it seems that reductions in the AHP must occur before learning if young and aging subjec

234 imarily due to a significant decrease in the AHP that in turn resulted in a reduction in the fraction

235 hat mimics learning-related reduction in the AHP.

236 activity is not involved in maintaining the AHP reduction at this point after learning.

237 PKA activity is involved in maintaining the AHP reduction measured ex vivo after successful learning

238 ificantly correlated to the amplitude of the AHP (r = 0.63; p < 0.001).

239 ntracellular solutions on measurement of the AHP and basic membrane properties, and on the induction

240 Examination of the AHP demonstrated that the amplitude was significantly re

241 g from sharp electrodes that the size of the AHP following spike trains increased in OT, but not VP n

242 The Ca2+-dependent components of the AHP have been attributed to the activity of small conduc

243 e results indicate that the amplitude of the AHP in hippocampal pyramidal cells from aged animals is

244 e sought to determine which component of the AHP is enhanced, and whether the enhancement could be re

245 te that activity-dependent plasticity of the AHP occurs with physiologically relevant stimuli in KGlu

246 t affect the subcellular localization of the AHP proteins.

247 of them underlie the medium component of the AHP that regulates interspike interval and plays an impo

248 Ca(2+) rises showed that mGluR block of the AHP was not mediated by alterations of action potential-

249 , thereby providing the time constant of the AHP's decay of conductance.

250 urrent (sI(AHP)), a major constituent of the AHP, also facilitate learning in aging animals, the sI(A

251 ved phosphoacceptor histidine residue of the AHP, as well as disruption of multiple cytokinin signali

252 ufficient depolarization, enhancement of the AHP, or sustained Na+ channel inactivation.

253 obscures activity-dependent reduction of the AHP.

254 ent, and possibly other constituents, of the AHP.

255 involved in rate-dependent regulation of the AHP.

256 consistent with circadian modulation of the AHP.

257 in a marked reduction or elimination of the AHP.

258 he effect of environmental enrichment on the AHP amplitude.

259 inhibited transmission, and also reduced the AHP amplitude.

260 actam V (0.2 muM), significantly reduced the AHP in CA1 neurons from both control and trained rats, i

261 hat activates PKA, significantly reduced the AHP in CA1 neurons from control animals, but not from ra

262 in slice preparation, we have found that the AHP has a shorter duration in cells firing at higher fre

263 ramidal neurons, the current ascribed to the AHP (IAHP) has three kinetic components.

264 by flumazenil (-31 +/- 13 %, relative to the AHP HW during exposure to zolpidem, 3:4).

265 eral, the AHP in KMeth was comparable to the AHP measured in the perforated-patch configuration.

266 nally, we found calcium contributions to the AHP to be temperature dependent: prominent at room tempe

267 ominantly L- and R-type currents trigger the AHP.

268 red almost 43.4% of the total area under the AHP based approach, whereas the LR based approach alloca

269 -threshold' measure which underestimated the AHP's absolute size but had the same time course, thereb

270 To identify the current(s) underlying the AHP altered in aging neurons, whole-cell voltage-clamp r

271 to the time in question rather than upon the AHP per se; the survivors' mean is more hyperpolarised b

272 etion of training, it is unclear whether the AHP amplitude is strictly dependent on biological aging

273 (ROC) curve of 0.8 compared to 0.73 with the AHP based model.

274 n signaling and functional overlap among the AHPs.

275 urrents underlying AP repolarization and the AHPs.

276 abidopsis and, contrary to expectations, the AHPs maintained a constant nuclear/cytosolic distributio

277 These data indicate that most of the AHPs are redundant, positive regulators of cytokinin sig

278 ones via 5-HT2 receptors, by suppressing the AHPs associated with two distinct calcium-activated pota

279 -dependent potassium currents underlying the AHPs, thereby creating mechanisms for control of the spo

280 These AHPs, rather than a depletion of neurotransmitters (as w

281 dative-peroxidative enzymatic cycle by these AHPs that leads to Mn oxide formation by this organism.

282 ttle is known about PIP2 's control of these AHPs.

283 This AHP is probably underlain by a small-conductance, CA2+-d

284 This AHP persisted for multiple seconds following volleys of

285 n (AHP), but, unlike in cortical cells, this AHP is not primarily driven by an intrinsic cellular pro

286 The estimated 'distance-to-threshold' AHP did not, however, give an accurate measure of the re

287 tify three neural systems that contribute to AHP, when disconnected or directly damaged: the (i) prem

288 the differentiation of neighboring wild-type AHPs, suggesting that REST may play a non-cell-autonomou

289 nt surgical correction of chin-down vertical AHP associated with INS at an academic institution.

290 the AHP, and it increases in amplitude when AHP amplitude is increased by pharmacological manipulati

291 ery 30 s were progressively reduced, whereas AHPs elicited every 150 s were stable.

292 Cells with AHP expressed greater density of sodium currents.

293 In this U.S. study, 1.5% of patients with AHP had HCC.

294 comes, and frequency of HCC in patients with AHP in the United States.

295 Among 327 patients with AHP, 5 (1.5%) were diagnosed with HCC.

296 Patients with AHP, regardless of clinical attacks, should be screened

297 motor planning in awareness in patients with AHP: Four hemiplegic patients with and four without anos

298 tion had a selective effect on patients with AHP; they were more likely than controls (U = 16, P < 0.

299 Replacement of thymidine with AHP dU increases duplex stability, accounting in part fo

300 By contrast, patients without AHP were not influenced by these manipulations, and did