ライフサイエンスコーパス: HVA

1 HVA functions as a repressor and interacts with TOPLESS

2 HVA levels increased with treatment in some affected ind

3 HVA peak current densities in tg and stg were increased

4 levels of DA metabolites homovanillic acid (HVA) and 3,4-dihydroxyphenylacetic acid (DOPAC) reflecte

5 BP) with plasma levels of homovanillic acid (HVA) and clinical symptoms.

6 the dopamine metabolites homovanillic acid (HVA) and dihydroxyphenylacetic acid (DOPAC), in five bra

7 ylacetic acid (DOPAC) and homovanillic acid (HVA) and in the DOPAC/dopamine ratio in the putamen, cau

8 as the model analyte and Homovanillic acid (HVA) as the target bioanalyte within both phosphate-buff

9 lacetic acid (DOPAC), and homovanillic acid (HVA) by 76%, 53% and 40%, respectively, in the striatum

10 ylacetic acid (DOPAC) and homovanillic acid (HVA) in caudate nucleus resulting from the METH treatmen

11 age percentage of labeled homovanillic acid (HVA) in lumbar cerebrospinal fluid (CSF) was 54% (SD, 9%

12 or to sacrifice increased homovanillic acid (HVA) levels in the left medial prefrontal cortex (mPFC)

13 points and an increase in homovanillic acid (HVA) or 5-hydroxyindoleacetic acid (5-HIAA) concentratio

14 CSF concentration of homovanillic acid (HVA) was significantly lower in the Lewy body variant pa

15 f the dopamine metabolite homovanillic acid (HVA) were decreased in severely affected patients and in

16 f the dopamine metabolite homovanillic acid (HVA) were determined in 30 recently abstinent cocaine-de

17 CSF homovanillic acid (HVA), 5-hydroxyindoleacetic acid (5-HIAA), and 3-methoxy

18 henylacetic acid (DOPAC), homovanillic acid (HVA), 5-hydroxyindoleacetic acid (5-HIAA), and serotonin

19 hes were analyzed for DA, homovanillic acid (HVA), and DA activity (HVA/DA) using HPLC.

20 uramine, norfenfluramine, homovanillic acid (HVA), cortisol, and prolactin were determined.

21 f the dopamine metabolite homovanillic acid (HVA), in an extended inbred vervet monkey (Chlorocebus a

22 doleacetic acid (5-HIAA), homovanillic acid (HVA), or 3-methoxy-4-hydroxyphenylgycol (MHPG).

23 ylacetic acid (DOPAC) and homovanillic acid (HVA), were elevated over the same time period.

24 ylacetic acid (DOPAC) and homovanillic acid (HVA), were found to be decreased by >95% in the right pu

25 ylacetic acid (DOPAC) and homovanillic acid (HVA).

26 es, followed by DOPAC and homovanillic acid (HVA).

27 ylacetic acid (DOPAC) and homovanillic acid (HVA).

28 phenylalanine (DOPAC) and homovanillic acid (HVA); norepinephrine (NE) and its metabolite 3-methoxy-4

29 ylacetic acid (DOPAC) and homovanillic acid (HVA)] levels and tyrosine hydroxylase (TH) expression in

30 Plasma homovanillic acid (HVA, a dopamine metabolite), adrenocorticotropic hormone

31 ), and 4-hydroxy-3-methoxyphenylacetic acid (HVA) were significantly diminished in the striata of the

32 acid [5-HIAA]), dopamine (homovanillic acid [HVA]), and norepinephrine (3-methoxy-4-hydroxyphenylglyc

33 High voltage activated (HVA) Ca2+ channels are composed of a pore-forming alpha

34 High voltage activated (HVA) Ca2+ channels are composed of a pore-forming alpha1

35 ip characteristic of high-voltage activated (HVA) Ca2+ channels.

36 patients displayed a high-voltage activated (HVA) Ca2+ conductance with a pronounced Ca2+-dependent i

37 ategorized as either high-voltage activated (HVA) or low-voltage activated (LVA), and a subtype (or s

38 o calcium influx via high-voltage-activated (HVA) (N- and P/Q-type) calcium channels and calcium-acti

39 of two components: a high voltage-activated (HVA) and a low voltage-activated (LVA) calcium current.

40 Both high voltage-activated (HVA) and low voltage-activated (LVA) calcium currents we

41 ns express prominent high-voltage-activated (HVA) and small low-voltage-activated (LVA) macroscopic (

42 nd OFF cells express high-voltage-activated (HVA) Ca(2+) channels, only OFF RGCs also express low-vol

43 ns potently inhibits high voltage-activated (HVA) Ca(2+) channels, providing a powerful means of modu

44 iated exclusively by high-voltage-activated (HVA) Ca(2+) channels.

45 =20 ms) that evoked high-voltage-activated (HVA) Ca(2+) currents (I(Ca)) and elevations in intracell

46 in several genes for high-voltage-activated (HVA) Ca2+ channel subunits are linked to spike-wave seiz

47 High voltage-activated (HVA) Ca2+ current (ICa) was recorded from neonatal rat h

48 nt inhibition of the high voltage-activated (HVA) Ca2+ current, with little or no effect on the low v

49 endent inhibition of high voltage-activated (HVA) Ca2+ currents in Xenopus laevis embryo spinal neuro

50 of inhibition of the high voltage-activated (HVA) Ca2+ currents were produced by 5-HT.

51 density of high threshold voltage-activated (HVA) calcium (Ca(2+)) channels was markedly enhanced in

52 fects of riluzole on high voltage-activated (HVA) calcium channels of rat dorsal root ganglion neuron

53 High-voltage-activated (HVA) calcium channels represent an important class of co

54 -activated (LVA) and high-voltage-activated (HVA) calcium current (I(Ca)).

55 ude of the high-threshold voltage-activated (HVA) calcium current.

56 High-voltage-activated (HVA) calcium currents were recorded from acutely dissoci

57 annel subunits alter high-voltage-activated (HVA) calcium currents, impair neurotransmitter release,

58 -activated (LVA) and high-voltage-activated (HVA) calcium currents.

59 -activated (LVA) and high voltage-activated (HVA) components of calcium current were decreased, demon

60 nd -70 mV as well as high voltage-activated (HVA) current with an activation voltage around -30 mV.

61 n reversibly reduced high-voltage-activated (HVA) currents to 33 +/- 5 % (n = 40) of the control leve

62 T currents), but not high-voltage-activated (HVA) currents.

63 ecific components of high voltage-activated (HVA) IBa, pharmacologically isolated by use of Ca2+ chan

64 predominantly of the high-voltage-activated (HVA) type, which could be carried by Ba2+ and inhibited

65 pressing PP2B, total high-voltage-activated (HVA) VOCCs were suppressed by about 60% at a test potent

66 Ca(2)(+)) influx via high-voltage-activated (HVA), Ca(v)2, channels ("N-, P/Q-, or R-types") that are

67 A, homovanillic acid (HVA), and DA activity (HVA/DA) using HPLC.

68 embrane lipids, via homeoviscous adaptation (HVA), counteracts membrane dysfunction due to temperatur

69 using PPG to predict healthy vascular aging (HVA) based on two approaches: machine learning (ML) and

70 Diagnosis of Hymenoptera venom allergy (HVA) is straightforward in the majority of patients, but

71 individuals with Hymenoptera venom allergy (HVA) who needed VIT from referral centers in Slovenia, A

72 stic precision in Hymenoptera venom allergy (HVA), in particular in patients with double sensitizatio

73 dopamine and DOPAC levels but did not alter HVA, 5-HT, or 5-HIAA.

74 ere Hymenoptera venom-triggered anaphylaxis (HVA).

75 sk factor for Hymenoptera venom anaphylaxis (HVA).

76 ased risk for Hymenoptera venom anaphylaxis (HVA).

77 median of 62 points (IQR 39-93; p=0.005) and HVA concentrations by a median of 25 nmol/L (IQR 11-48;

78 Concentrations of CSF 5-HIAA (P = 0.01) and HVA (P < 0.001) were lower in the aggressive group (medi

79 Lower levels of 5-HIAA (P = 0.02) and HVA (P = 0.04) were found in the subgroup of aggressive

80 antly increased anxiety, ACTH, cortisol, and HVA.

81 nduced increases in neostriatal DOPAC/DA and HVA/DA ratios were normalized by age/food-deprivation wh

82 n of dopamine and its metabolites, DOPAC and HVA and the formation of 3-NT in PC12 cells.

83 DOPAC and HVA changes were measured at 1 day and were reversed wit

84 of adult rats, basal levels of DA, DOPAC and HVA did not differ across prenatal treatments; however,

85 o counteracted the increase in the DOPAC and HVA levels and DOPAC/dopamine ratio induced by L-DOPA in

86 e was increased while the striatal DOPAC and HVA levels and DOPAC/dopamine ratio were significantly r

87 e not significantly decreased, and DOPAC and HVA levels were decreased by only 65% and 30%, respectiv

88 sm (as assessed by the decrease in DOPAC and HVA levels) in the striatum and substantia nigra was sim

89 analyses of DA and its metabolites DOPAC and HVA show that exercise also functionally protects neuron

90 s of dopamine and its metabolites, DOPAC and HVA were analyzed by HPLC equipped with electrochemical

91 atal dopamine and its metabolites (DOPAC and HVA) following MPTP treatment as determined by HPLC meth

92 of dopamine, dopamine metabolites DOPAC and HVA, and the major 5-HT metabolite 5-HIAA, in rat medial

93 n of dopamine, and its metabolites DOPAC and HVA, as well as the significant formation of 3-nitrotyro

94 hyperthermia and depletion of DA, DOPAC and HVA.

95 3,4-dihydroxyphenylacetic acid (DOPAC), and HVA levels in rats that exhibited low levels of locomoto

96 ed a significant depletion of DA, DOPAC, and HVA at all time points.

97 One striatum was examined for DA, DOPAC, and HVA levels using HPLC-EC and the contralateral striatum,

98 e no significant differences in dopamine and HVA concentrations in either suicide group compared to c

99 pamine/metabolite ratios (DOPAC/dopamine and HVA+DOPAC/dopamine) changed with E2 plasma levels, excep

100 nide, DOPAC-glucuronide, HVA-glucuronide and HVA-sulphate were also detected.

101 ly rejected infants had lower CSF 5-HIAA and HVA than low-rejection infants.

102 concentrations and ratios of HVA/5-HIAA and HVA/MHPG did not significantly change with 6 weeks of ei

103 ur patients reduced both the maximal LVA and HVA Ca2+ conductances in murine dorsal root ganglion neu

104 mined biophysical properties of both LVA and HVA Ca2+ currents in thalamic cells of tottering (tg; Ca

105 d the biophysical properties of both LVA and HVA currents in Cm/+ and wild-type thalamic neurons and

106 DmalphaG is required for regulating LVA and HVA derived from Dmca1A in vivo.

107 Post-mortem CSF 5-HIAA, MHPG and HVA were measured by high-performance liquid chromatogra

108 er IBO, DOPAC concentrations in striatum and HVA levels in the frontal cortex were below control valu

109 al meridian (horizontal-vertical anisotropy, HVA) and along the lower than upper vertical meridian (v

110 al meridian (horizontal-vertical anisotropy, HVA) and the lower than upper vertical meridian (vertica

111 anic sites within the Hellenic Volcanic Arc (HVA).

112 cal meridian (horizontal-vertical asymmetry [HVA]) and along the lower than the upper vertical meridi

113 zinc finger transcription factor, AT5G27880/HVA, is responsible for the hva-d phenotype.

114 o a drop in median number of flights between HVA-OPs from 112 flights/wk in April 2019 to 34 in April

115 work, there were 65.1% fewer flights between HVA-OPs, with considerable OPO-level variation (interqua

116 r controlling for breed and age of dogs, but HVA differences may have been breed-dependent.

117 increase suppressed by mibefradil but not by HVA Ca2+ channel antagonists.

118 nism is not dependent on, or accompanied by, HVA channel Ca(2)(+) influx, and is insensitive to agoni

119 e high-voltage-activated Ca(2+) channels (Ca(HVA)) conductance is increased.

120 are almost exclusively controlled by the Ca(HVA) inward current and the I(m) outward K(+) current.

121 ealed during acid exposure as the whole-cell HVA current was depressed.

122 hronic stimulation was related to concurrent HVA plasma elevations, implying DBS-induced dopamine rel

123 CSF HVA is an index of CNS dopamine activity, which is hypot

124 by the genome scan, we mapped a QTL for CSF HVA at a genome-wide level of significance (peak logarit

125 In a similar manner, labeled CSF HVA concentrations were not influenced by duration of di

126 Labeled CSF HVA levels did not significantly correlate with either q

127 +/- 15 pmol/mL; P< or =.001) but normal CSF HVA and MHPG concentrations.

128 gnificantly higher mean concentration of CSF HVA than did the healthy comparison group.

129 idal side effects and have low levels of CSF HVA.

130 Their CSF HVA concentrations averaged only 54% of the concentratio

131 er, both dopamine turnover ratios (DOPAC/DA, HVA/DA) and the serotonin turnover ratio (5-HIAA/5-HT) w

132 igh-dose amoxicillin (1 g three times a day; HVA therapy) for 14 days.

133 A-mediated currents varied with time of day; HVA currents in cells from OVX+E mice were lower than th

134 e acidosis (pH 6.9-6.0) reversibly depressed HVA Ca2+ current amplitude and caused a positive shift i

135 ctivity exhibited by (+)-ACN among different HVA current components suggests that manipulations of st

136 reperfusion increase in DA turnover (DOPAC + HVA/DA) at 5 min after reperfusion.

137 DA turnover, as indicated by a higher (DOPAC+HVA)/DA ratio, seems to be associated to rotenone-induce

138 In the adult, basal levels of DA, DOPAC, HVA and 5-HIAA in n. accumbens did not differ across pre

139 on ex vivo tissue levels of dopamine, DOPAC, HVA, 5-HT and 5-HIAA in multiple brain regions.

140 es were characterized by increases in DOPAC, HVA, MHPG and 5-HIAA coupled with decreases in DA, NE an

141 owever, the levels of DA metabolites, DOPAC, HVA, and the serotonin metabolite, 5-HIAA, were markedly

142 s.c.) also increased tissue levels of DOPAC, HVA and 5-HIAA by 169, 221 and 134% of basal levels in n

143 on of LY379268, mPFC tissue levels of DOPAC, HVA and 5-HIAA were increased in a dose-dependent manner

144 the amygdala and hippocampus, and dopamine (HVA/DA, DOPAC/DA) in prefrontal cortex.

145 ious studies in primates, we find that every HVA receives disynaptic input from the superior collicul

146 esignation of L-type channels as exclusively HVA and reveal a possible role in subthreshold Ca2+ sign

147 ntageous in finding potential biomarkers for HVA prediction.

148 ga-Conotoxin-MVIIC, a nonselective toxin for HVA channels, had no effect on either of the LVA current

149 to controls, although there was a trend for HVA concentrations to be lower in suicides.

150 Further, HVA directly regulates the expression of the auxin trans

151 In both genotypes, HVA currents were predominantly of the omega-agatoxin-IV

152 HT-glucuronide, DOPAC-glucuronide, HVA-glucuronide and HVA-sulphate were also detected.

153 c signal imaging and targeted five pulvinar->HVA pathways for projection-specific rabies tracing.

154 and cell types projecting to each pulvinar->HVA population.

155 ession, function and responsiveness of high (HVA)- and low-voltage-activated (LVA) Ca2+ channels to I

156 via high-voltage-activated Ca2+ channels (I(HVA)).

157 high-voltage-activated barium currents (IBa, HVA) in tiger salamander retinal ganglion cells.

158 This research identifies HVA as a positive regulator of vascular initiation throu

159 very from inactivation of LVA currents or in HVA current densities and kinetics.

160 o evaluate the efficacy and safety of VIT in HVA patients with cMCD.

161 OVX+E mice with estradiol rapidly increased HVA currents primarily through L- and R-type VGCCs by ac

162 release, which was associated with increased HVA plasma levels and improved clinical symptoms, sugges

163 te altered the ability of (+)-ACN to inhibit HVA current in dorsal root ganglion neurons, indicating

164 ates K+ channels and simultaneously inhibits HVA Ca2+ channels via different receptor subtypes.

165 The mean CSF labeled HVA concentration was 34.7 ng/ml (SD, 20.2 ng/ml; range,

166 beled serum LD closely predicted CSF labeled HVA concentrations (r = 0.747, p = 0.033).

167 Third, mRNA levels of lamprey HVA calcium and SKKCa channels in axotomized RS neurons

168 examination for KIT p.D816V in PBL in large HVA populations, we have demonstrated a high burden of c

169 We suggest that a low HVA level is a biological marker with modest association

170 In contrast, in OVX+E mice, HVA-mediated currents varied with time of day; HVA curre

171 iting without warning (5-HIAA 196.0 pmol/ml; HVA 302.0 pmol/ml) compared to dogs that warned (5-HIAA

172 group (median values: 5-HIAA 202.0 pmol/ml; HVA 318.0 pmol/ml) than in controls (5-HIAA 298.0 pmol/m

173 d to dogs that warned (5-HIAA 244.0 pmol/ml; HVA 400.0 pmol/ml).

174 /ml) than in controls (5-HIAA 298.0 pmol/ml; HVA 552.0 pmol/ml).

175 herefore operate in parallel with the normal HVA-dependent processes.

176 that N(2)O selectively blocks T-type but not HVA Ca(2+) currents in small sensory neurons and Ca(v)3.

177 ere were no diurnal changes in any aspect of HVA-mediated I(Ca) in OVX mice.

178 and beta 2a induce a sustained component of HVA current, and alpha 2-delta also influences the volta

179 a and beta2a induce a sustained component of HVA current, and alpha2-delta also influences the voltag

180 Smokers' low CSF concentrations of HVA may be associated either with chronic inhalation of

181 no significant changes in concentrations of HVA.

182 The depression of HVA Ca2+ currents by low pHo was unaffected by raising t

183 ) subunit captures the functional essence of HVA calcium channels, and introduce alpha(1)-Ca(V)beta f

184 ctivity does not influence the expression of HVA Ca2+ channels, but modulates their function by Ca(2+

185 with a CRISPR-Cas9 approach or expression of HVA fused with an activation domain VP16 (HVA-VP16) resu

186 The finding of HVA calcium channels distributed throughout the whole de

187 alyses were used to dissect the functions of HVA.

188 ed cells induced an up to 5-fold increase of HVA VOCCs.

189 rast to the HVA activation line, knockout of HVA function with a CRISPR-Cas9 approach or expression o

190 ated during the second scan, while levels of HVA and cortisol were not altered significantly during t

191 y examines whether subunit protein levels of HVA Ca(2+) channels are altered in IC neurons that exhib

192 we examined the subcellular localization of HVA calcium channels by using immunocytochemistry at the

193 these results suggest that the modulation of HVA by the JMD could be mediated by changes in the statu

194 We sought to determine the prevalence of HVA and mastocytosis in the United States using an insur

195 n the IBM Watson Database, the prevalence of HVA was 167 per 100,000 (0.167%) and the prevalence of m

196 single-center studies, and the prevalence of HVA with and without mastocytosis in the United States i

197 , CSF monoamine concentrations and ratios of HVA/5-HIAA and HVA/MHPG did not significantly change wit

198 ribute to the overall feedback regulation of HVA-mediated I(Ca) by estradiol.

199 ivated (LVA), and a subtype (or subtypes) of HVA Ca2+ channels link the presynaptic depolarization to

200 enhanced current density of L- and R-type of HVA Ca(2+) channels in IC neurons of the GEPR, and may c

201 Available data on HVA and mastocytosis largely derive from European single

202 The effects of 5-HT on HVA Ca2+ currents were mediated by 5-HT1A and 5-HT1D rec

203 3]) were randomly assigned to LVA therapy or HVA therapy (n=252 in each group).

204 gh Volume by direct Air transport OPO Pairs, HVA-OPs).

205 Inactivation time constants and peak HVA Ca2+ current (ICa) amplitudes did not differ between

206 kers had markedly lower CSF, but not plasma, HVA levels.

207 The conductance ratio of the presynaptic HVA current was 0.9, significantly lower that that of th

208 s of DA and DOPAC, while it slightly reduced HVA concentration.

209 onsiderably more negative than the remaining HVA current.

210 At this membrane voltage, a second HVA current was revealed during acid exposure as the who

211 Half-blockade of (+)-ACN-sensitive HVA current occurred in the range of 3-25 microM, with N

212 ula venom allergy who had experienced severe HVA, 32 cMCD (22 with SM and 10 with MMAS) and 14 contro

213 associated with the highest risk for severe HVA, even higher than having either HalphaT or KIT p.D81

214 HalphaT was also associated with severe HVA and symptoms (p < .01), and remarkably, 31.0% (n = 3

215 the major risk factor associated with severe HVA.

216 Ba2+/Ca2+ conductance ratios of the somatic HVA and LVA channels were 1.4 and 0.7, respectively.

217 significantly lower that that of the somatic HVA current.

218 annels accounted for only 6 % of the somatic HVA, while L-, N- and R-type Ca2+ channels each accounte

219 nce of SWDs and that altered somatodendritic HVA currents are not required for abnormal thalamocortic

220 eceptor selective agonist, DAMGO, suppressed HVA IBa (in 64/71 neurones) in a naloxone-reversible and

221 , while lowering extracellular pH suppressed HVA Ca2+ currents, Zn2+ current amplitude was affected o

222 s in the pulvinar thus depend on both target HVA and input cell type, such that driving and modulatin

223 Telencephalic HVA as well as the HVA/DA ratio were also significantly

224 The HVA current remaining in LES-treated motoneurons was lit

225 The HVA current was inactivated completely at a holding pote

226 The HVA is geologically and ecologically unique, with report

227 Telencephalic HVA as well as the HVA/DA ratio were also significantly greater in dominant

228 In the nonadapted conditions, the HVA was more pronounced for horizontal than vertical sti

229 1A, alpha 1B and alpha 1E genes encoding the HVA Ca2+ channels P/Q, N and R, respectively, but not al

230 in performance around the visual field: the HVA is less pronounced and the VMA is not present for ch

231 and 86.5% (218 of 252; 81.7 to 90.2) in the HVA group in the intention-to-treat analysis (p=0.70) an

232 n the LVA group and 43 (17%) patients in the HVA group reported adverse events.

233 rapy was 97% in the LVA group and 96% in the HVA group.

234 nature and origin of these compounds in the HVA.

235 Riluzole at 30 microM inhibited the HVA currents.

236 reveal that visual adaptation mitigates the HVA in contrast sensitivity, fostering perceptual unifor

237 l at week 8-10 for the LVA group but not the HVA group.

238 rsibly reduced 34 +/- 1.6 % (n = 102) of the HVA Ca2+ currents.

239 All of the HVA current subtypes are expressed in bushy cells, but t

240 The activation threshold of the HVA current was at -40 mV.

241 Riluzole inhibition of the HVA currents was abolished and partially reduced by addi

242 Riluzole inhibition of the HVA currents was also blocked by internal application of

243 nd shifting of the voltage dependence of the HVA currents.

244 ay be involved in riluzole inhibition of the HVA currents.

245 t affect riluzole's inhibitory effect on the HVA currents.

246 In contrast to the HVA activation line, knockout of HVA function with a CRI

247 addition, we show that Dmca1A underlies the HVA somatodendritic calcium currents in vivo.

248 ctive organic antagonists of high-threshold (HVA) Ca2+ channels, nimodipine, omega-Conotoxin GVIA, an

249 Thus HVA VOCCs, in a phosphorylated state under control condi

250 lysis demonstrated that PIN1 is epistatic to HVA in controlling bundle number.

251 al therapy was effective and non-inferior to HVA dual therapy as first-line treatment of H pylori inf

252 The efficacy of LVA was non-inferior to HVA in the intention-to-treat analysis (risk difference

253 somewhat less effective at inhibiting total HVA current than (+)-ACN, whereas several steroid analog

254 e relatively ineffective at inhibiting total HVA current.

255 with antibodies against P/Q-, N-, and R-type HVA calcium channels demonstrated the presence of these

256 Drosophila Ca(v)2 homolog, Dmca1A, underlies HVA and LVA somatodendritic calcium currents in the same

257 2+ current as well as a further unidentified HVA current that was insensitive to dihydropyridines, om

258 We observed a lower US HVA prevalence than previously reported.

259 of HVA fused with an activation domain VP16 (HVA-VP16) resulted in fewer vascular bundles.

260 lective, more potent, small-molecular-weight HVA channel blockers.

261 composition patterns are not consistent with HVA expectations and suggest a stress response.

262 ociated protein (SNAP25) that interacts with HVA channels, reveals abnormal spike-wave discharges (SW

263 ecommend measuring tryptase in patients with HVA and that those with mastocytosis pursue lifelong ven

264 2018, was queried to identify patients with HVA and/or mastocytosis.

265 pact of mastocytosis on VIT in patients with HVA in a US cohort.

266 owed a 9.7-fold increase among patients with HVA versus the general population.

267 es clonal disease in high-risk patients with HVA who are regularly missed when BST level is used alon

268 23]) of elevated BST level in patients with HVA, and together with KIT p.D816V, it accounted for 90%

269 ocytosis was more common in US patients with HVA, though at lower rates than previously reported.

270 level elevations (20 of 23) in patients with HVA.

271 and 97 per 100,000 (0.097%) among those with HVA.