ライフサイエンスコーパス: ASH

1 ASH membership has grown from a few hundred curious atte

2 ASH neuronal cell death required ced-3 caspase function,

3 ASH neurons distinguish between these stimuli because ha

4 ASH sensory neurons are required in Caenorhabditis elega

5 ASH was associated with a shorter length of stay, and pa

6 ASH-2 and RBR-2 act in the germline, at least in part, t

7 ASH-mediated aversive responses are increased by activat

8 in the absence of a known provoker in 21.2%, ASH in 33.9%, and poststroke infection in 13.6%.

9 same evidence-based methodology as in 2013, ASH has identified 5 additional tests and treatments tha

10 SC /ESH grade I compared to those graded ACC/ASH stage I hypertension (p = 0.0122).

11 measured in all groups belonging to the ACC/ASH classifications were within the normal values for ag

12 sed as stage 1 hypertension based on the ACC/ASH guidelines (p = 0.00022, p = 0.0179, p = 0.0409 and

13 inositol 5-phosphatase domain followed by an ASH and a RhoGAP-like domain.

14 1 functions in chemosensory neurons (ADL and ASH) independently of its postsynaptic partner NLG-1 to

15 ASCO and ASH convened an Expert Panel to review the evidence and

16 Receptor gene expression in the ASI and ASH sensory neurons appears to be regulated via distinct

17 led previously unknown properties of AVA and ASH neurons.

18 s and show that death cue sensing by AWB and ASH leads to physiological changes that promote reproduc

19 e lysates, activates sensory neurons AWB and ASH, triggering a glutamate- and acetylcholine-dependent

20 induced potentiation of sensory behavior and ASH neuron function.

21 he glutamatergic sensory neurons AWC(ON) and ASH have distinct synaptic dynamics associated with toni

22 ces the "2017 ACC/AHA/AAPA/ABC/ACPM/AGS/APhA/ASH/ASPC/NMA/PCNA Guideline for the Prevention, Detectio

23 and the function of sensory neurons such as ASH.

24 ncology/American Society of Hematology (ASCO/ASH) recommendations for the use of epoetin.

25 The sensory neurons AWC, ASH, and ASER are the major shear stress-sensitive neuro

26 due to the sensation of noxious chemicals by ASH and ADL neurons; it requires the genes ocr-2 and osm

27 Lifespan extension induced by ASH-2 complex deficiency requires the presence of an int

28 ltering and avoidance behaviors initiated by ASH on similar timescales.

29 ending amplitude), which are not mediated by ASH activation.

30 Nose touch sensitivity (mediated by ASH sensory neurons) is defective in mutants lacking GLR

31 ASCO fully endorsed the CAP-ASH guideline on initial diagnostic work-up of AL and in

32 The CAP-ASH guideline on initial diagnostic work-up of AL was re

33 -cells (ADF) and one new class of off-cells (ASH).

34 this new hybrid feeding model shifts chronic ASH with macrophage inflammation and perisinusoidal and

35 Furthermore, in the absence of SPP1, chronic ASH mice without weekly binge begin to develop AH.

36 ans photoreceptor protein LITE-1 in ciliated ASH photosensory neurons, we performed a genetic screen

37 Deficiencies in members of the ASH-2 complex-ASH-2 itself, WDR-5 and the H3K4 methyltransferase SET-2

38 d financial professionals frequently contact ASH members for information and perspective on drugs, de

39 ology (ASH) domains; CoA is bound at the CSH-ASH interface in mutually exclusive productive or unprod

40 rence genomes into a visualization database, ASH ( ).

41 r), functioned in sensory neurons designated ASH and ASI to actively suppress innate immune responses

42 the expression of the SA lineage-determining ASH-1 and Phox2 genes.

43 f infusion, mice developed features of early ASH accompanied by a marked increase in the level of EVs

44 g LD biogenesis, offering hope for effective ASH treatments.

45 C. elegans ASH neurons function as polymodal sensory neurons that g

46 ngths was assessed in Caenorhabditis elegans ASH sensory neurons in young and old animals.

47 The Caenorhabditis elegans ASH sensory neurons mediate responses to nose touch, hyp

48 to untreated ones, suggesting that elevated ASH Ca(2+) transients result in enhanced ASH-mediated be

49 Genes encoding ASH domains thus represent good candidates for primary c

50 ted ASH Ca(2+) transients result in enhanced ASH-mediated behavior.

51 LA0716 identified another trichome-expressed ASH gene on chromosome 9 (M82, Solyc09g075710; LA0716, S

52 There were 3 clusters for ASH, the largest of which was in the left hemisphere.

53 er EVs as a potentially novel diagnostic for ASH.

54 specific miRNA cargo, which are specific for ASH-related liver injury.

55 nd miR-340, were increased in blood EVs from ASH mice (P < 0.05), but not in blood EVs from three oth

56 The transcriptome analysis of HC-EVs from ASH mice detected differentially expressed miRNAs, inclu

57 Damaged hepatocytes from ASH mice are a key EV source with a specific miRNA cargo

58 the olfactory chip to record responses from ASH sensory neurons exposed to high-osmotic-strength sti

59 Action on Smoking and Health (ASH), Alcohol Health Alliance, and Obesity Health Allian

60 The American Society of Hematology (ASH) and British Committee for Standards in Haematology

61 The American Society of Hematology (ASH) and the ASH Research Collaborative have instituted

62 that of the American Society of Hematology (ASH) by more than 11 years and Stratton and Dameshek hel

63 CAP) and the American Society of Hematology (ASH) developed an evidence-based guideline on the initia

64 le of the US American Society of Hematology (ASH) membership was surveyed.

65 In 2011, the American Society of Hematology (ASH) published updated guidelines for the management of

66 The American Society of Hematology (ASH) released its first Choosing Wisely((R)) list in 201

67 The American Society of Hematology (ASH) turns 50 years old in 2008, and we have much to cel

68 eting of the American Society of Hematology (ASH), and financial professionals frequently contact ASH

69 ittee of the American Society of Hematology (ASH).(1) The purpose of this initiative is to create a n

70 (304 of 1373) for active splenic hemorrhage (ASH) and 20% (276 of 1373) for contained vascular injury

71 scular injury and active splenic hemorrhage (ASH) were frequently reported, and rates of intervention

72 ule flanked by acyl-CoA synthetase homology (ASH) domains, with ATP and citrate binding the ASH domai

73 our flexible acetyl-CoA synthetase homology (ASH) domains; CoA is bound at the CSH-ASH interface in m

74 ices such as the Anesthetic Scavenging Hood (ASH), SiBI tube connector and mask stopper.

75 th the shallow aragonite saturation horizon (ASH) and high carbonate dissolution rates there, fueled

76 prising two closely spaced AspM-Spd-2-Hydin (ASH) domains, play a critical role in centrosome assembl

77 An abdominoscrotal hydrocele (ASH) is a rare lesion and should be considered in the di

78 al hydrocele - an abdominoscrotal hydrocele (ASH).

79 l infection, and acute stress hyperglycemia (ASH) in 1,208 acute ischemic stroke patients prospective

80 s, like the archetype similarity hypothesis (ASH).

81 rain susceptibility to acute severe hypoxia (ASH), and could underlie the unfavorable prognosis of ce

82 nine nucleotide exchange factor RIC-8 act in ASH in a mutually dependent fashion to activate Galpha(o

83 timately the signaling molecule that acts in ASH to delay octanol response.

84 otein fragments formed protein aggregates in ASH neurons, and the number of ASH neurons containing ag

85 ine receptor DOP-4 acts cell autonomously in ASH to mediate effects on response magnitude.

86 ed the calcium indicator protein cameleon in ASH and analyzed intracellular Ca(2+) responses followin

87 I also propose changes in ASH policy that may help safeguard public trust as well

88 the TRPV channel OSM-9, a sensory channel in ASH neurons.

89 ressing the mammalian TRPV1 (VR1) channel in ASH nociceptor neurons avoid the TRPV1 ligand capsaicin,

90 as the major mechanotransduction channel in ASH, a polymodal nociceptor in Caenorhabditis elegans.

91 not the only mechanotransduction channel in ASH: loss of deg-1 revealed a minor current whose proper

92 Exocytosis in ASH and AWC(ON) is differentially affected by SNARE-comp

93 10 is a novel cytosolic protein expressed in ASH and three other classes of sensory neurons.

94 ndependent of two TRPV channels expressed in ASH.

95 TRPV4 function in ASH required the endogenous C. elegans osmotic and nose

96 ctivity of the corresponding interneurons in ASH's motor circuit becomes asynchronous.

97 n and for regulation of cyclic AMP levels in ASH neurons.

98 enhanced neurodegeneration were observed in ASH neurons that coexpressed Htn-Q150 and a subthreshold

99 view underlines LDs as pivotal organelles in ASH progression and therapeutic innovation.

100 ion occur via distinct signaling pathways in ASH and that OSM-10 is required for osmosensory signalin

101 f noxious stimuli evoked strong responses in ASH including quinine, denatonium, detergents, heavy met

102 terplay between Ca(2+) and cAMP signaling in ASH neurons to control the sensitivity of the worm's nos

103 that ARR-1 is required for GPCR signaling in ASH, ASI, AQR, PQR, and URX neurons, which control the u

104 elease and more presynaptic release sites in ASH neurons, with only the latter requiring nrx-1.

105 Y604F also abolishes Ca(2+) transients in ASH, while sustaining avoidance behaviour, yet it disrup

106 Expression of mammalian TRPV4 in ASH neurons of osm-9 worms restored avoidance responses

107 The combination of SCD-focused initiatives, ASH Research Collaborative, CONSA, and Sickle Cell Clini

108 odegeneration but not in OSM10::GFP-mediated ASH neurodegeneration.

109 rative process and an evidence-based method, ASH has identified 5 tests and treatments that in some c

110 The modern ASH promotes cutting-edge science, sponsors research by

111 iciencies in the H3K4me3 chromatin modifiers ASH-2, WDR-5 or SET-2 in the parental generation extend

112 OCTR-1 and SER-3 antagonistically modulate ASH signalling directly, with OCTR-1 signalling mediated

113 tide release from interneurons that modulate ASH activity indirectly.

114 tyra-2 expression in the nociceptive neuron, ASH, is necessary and sufficient to induce osas#9 avoida

115 M-9 expressed in the head nociceptor neuron, ASH, we study nocifensive behaviour and Ca(2+) influx.

116 Ablation of the nociceptive neurons ASH and ADL transforms social animals into solitary feed

117 ein ODR-4, acting in the nociceptive neurons ASH and ADL.

118 d receptor, functions in the sensory neurons ASH and ASI to suppress innate immune responses in non-n

119 ed by the Caenorhabditis elegans nociceptive ASH sensory neurons.

120 ive behavior mediated by the two nociceptive ASH sensory neurons and requires the expression of the a

121 ediated by a pair of polymodal, nociceptive, ASH sensory neurons.

122 ing that TRPV4 is integrated into the normal ASH sensory apparatus.

123 lumina-silica-water (Al(2)O(3)-SiO(2)-H(2)O, ASH) system, breakdowns to contain further hydrated mine

124 A key component of ASH adaptation is GPC-1, a G-protein gamma-subunit expre

125 rimethylation (H3K4me3) complex, composed of ASH-2, WDR-5 and the histone methyltransferase SET-2, re

126 helped galvanize support for the creation of ASH.

127 he age-dependent functional deterioration of ASH.

128 The prolonged expression of ASH in D. magna furthermore suggests that it is involved

129 identified as a member of a novel family of ASH (ASPM, SPD-2, Hydin) domains.

130 (-) flux needed for glial GABA inhibition of ASH sensory neuron function and for regulation of cyclic

131 essential for the serotonergic modulation of ASH-mediated aversive responses.

132 aggregates in ASH neurons, and the number of ASH neurons containing aggregates increased as animals a

133 5% CI: 0.6, 0.86; P < .001), and presence of ASH at CT (OR, 0.74; 95% CI: 0.62, 0.88; P < .001).

134 Spontaneous resolution of ASH is rare, but asymptomatic patients can be followed u

135 By varying the severity of ASH and targeting competing mechanisms of pMF, we sought

136 Stimulation of ASH or RIM neurons using channelrhodopsin-2 (ChR2) resul

137 The next 50 years of ASH are likely to see many profound changes, but one thi

138 OS effect on ASH was partially abolished in vitamin C-treated worms.

139 dance tests, to investigate the OS effect on ASH-dependent behaviors.

140 n, targets the OCTR-1 octopamine receptor on ASH nociceptive neurons to modulate an aversive olfactor

141 Other ASH candidates for APT activity were functionally charac

142 ors that are present in both neurons: phasic ASH release is strongly dependent on UNC-13, whereas ton

143 The C. elegans polymodal ASH sensory neurons detect mechanical, osmotic, and chem

144 o soluble repellents sensed by the polymodal ASH neurons.

145 o soluble repellents sensed by the polymodal ASH nociceptors.

146 f 150 residues (Htn-Q150) led to progressive ASH neurodegeneration but did not cause cell death.

147 By calcium (Ca(2+)) imaging, we quantified ASH activation upon stimulus delivery.

148 entify an unexpected role for the sex-shared ASH sensory neurons in male attraction to ascaroside sex

149 0.99; P = .003) and were more likely to show ASH (OR, 8.05; 95% CI: 5.35, 12.26; P < .001) or CVI (OR

150 that during early alcoholic steatohepatitis (ASH) development, hepatocytes (HCs) release EVs with an

151 alth burden, with alcoholic steatohepatitis (ASH) representing a severe subtype driven by chronic alc

152 eptides encoded by nlp-3 appear to stimulate ASH-mediated aversive behavior through the neuropeptide

153 lium ac/sc genes - achaete-scute homolog (Tc-ASH) a proneural gene and asense (Tc-ase) a neural precu

154 yonic central nervous system we find that Tc-ASH is expressed in all neural precursors and the proneu

155 Ai and misexpression studies we show that Tc-ASH is necessary for neural precursor formation in Tribo

156 Snail rather than ASH is the first gene to be expressed in the nascent neu

157 Finally, behavioral assays indicated that ASH neurons, coexpressing Htn-Q150 and OSM10::GFP, were

158 We propose that ASH nociceptors rely on two genetically distinct mechano

159 d in the nascent neuroblasts suggesting that ASH is not required for the selection of neuroblasts as

160 The ASH 2014 Choosing Wisely((R)) recommendations include: (

161 The ASH Choosing Wisely(R) recommendations focus on avoiding

162 The ASH guidelines indicate that for severe thrombocytopenia

163 The ASH is an active participant in the Choosing Wisely(R) p

164 The ASH neurons are therefore hypothesized to be polymodal n

165 The ASH sensory neuron displays reduced sensitivity to stimu

166 Ablating the ASH, ADL, or ASK sensory neurons connected to RMG by gap

167 Although the ASH becomes deeper moving northwest along the chains, th

168 , the ASJ and ASK gustatory neurons, and the ASH and ADL nociceptors, respond to a rise in CO2 with a

169 American Society of Hematology (ASH) and the ASH Research Collaborative have instituted a multipronge

170 In mutant animals, the ASH sensory neurons fail to express SRA-6 and SRB-6, put

171 Though outdated in some aspects, the ASH and BCSH guidelines still provide a useful framework

172 H) domains, with ATP and citrate binding the ASH domain and CoA binding the ASH-CSH interface to prod

173 e binding the ASH domain and CoA binding the ASH-CSH interface to produce acetyl-CoA and oxaloacetate

174 on responses to other stimuli sensed by the ASH neurons including high osmolarity and chemical repel

175 ns, eliminates osmosensation mediated by the ASH neurons, but does not affect the response to the odo

176 raction with APPL1, which is mediated by the ASH-RhoGAP-like domains of OCRL and is abolished by dise

177 We analyzed the connections from the ASH sensory neurons and RIM interneurons to the command

178 Public opinion data from the ASH YouGov Smokefree Survey 2022 on a nationally represe

179 Here we identify the ASH-2 trithorax complex, which trimethylates histone H3

180 r in depth; AGS-3 activates Galpha(o) in the ASH chemosensory neurons to allow food-deprived animals

181 traps a (3S)-citryl-CoA intermediate in the ASH domain in a configuration that is incompatible with

182 acetyl-CoA and OAA to (3S)-citryl-CoA in the ASH domain, and can load CoA and unload acetyl-CoA in th

183 ate products shows the products bound in the ASH domain, with an additional oxaloacetate in the CSH d

184 als a phospho-citryl-CoA intermediate in the ASH domain.

185 ects, and odr-3 function is essential in the ASH neurons that sense noxious chemical and mechanical s

186 and NPR-2 function cell autonomously in the ASH neurons to increase adaptation off food, whereas the

187 e and duration of gustatory responses in the ASH neurons.

188 s necessary for a subset of responses in the ASH nociceptive neurons.

189 tmc-1 is expressed in the ASH polymodal avoidance neurons, where it is required fo

190 5-HT receptors appear to be expressed in the ASH sensory neurons mediating octanol sensitivity, we id

191 rupted by the same missense mutations in the ASH-RhoGAP-like domain that also disrupt APPL1 binding.

192 We show that unlike in the ASH/ASI cilia, the OSM-3 kinesin moves independently of

193 y through distinct receptors to modulate the ASH-mediated locomotory circuit and that C. elegans is a

194 cal avoidance response in the context of the ASH 'nociceptive' neurone.

195 se results align with the predictions of the ASH but not the BIH, and mirror observed patterns of pop

196 After the next 4 months, the size of the ASH decreased remarkably.

197 The identification of the ASH domain family instead indicates possible roles for A

198 he United States surrounding revision of the ASH management guidelines for childhood ITP.

199 e truncated rod-like unbranched cilia of the ASH nociceptive neurons in animals carrying a microtubul

200 OS on wild type worms on the function of the ASH polymodal neuron.

201 cal factors in the calcium transients of the ASH sensory neuron.

202 ance of lifespan extension by members of the ASH-2 complex is dependent on the H3K4me3 demethylase RB

203 Deficiencies in members of the ASH-2 complex-ASH-2 itself, WDR-5 and the H3K4 methyltra

204 rystallographic studies reveal a role of the ASH-RhoGAP-like domains in positioning the phosphatase d

205 FT in the structurally distinct cilia of the ASH/ASI and the AWB chemosensory neurons in Caenorhabdit

206 sential to extend the distal segments of the ASH/ASI cilia, it is not required to build the AWB dista

207 PQ had a similar effect on the ASH neuron response time (rising slope of the Ca(2+) tra

208 the reefs becomes shallower, suggesting the ASH is having little influence on their distribution.

209 e Caenorhabditis elegans nervous system: the ASH polymodal sensory neurons, the AVA, AVD and AVE inte

210 eins, Ses1 and Ses2, which interact with the ASH-RhoGAP-like (ASPM-SPD-2-Hydin homology and Rho-GTPas

211 indicating that adaptation occurs within the ASH sensory neuron.

212 ease of nlp-3-encoded neuropeptides from the ASHs.

213 ra-6-dependent expression of F14D12.6 in the ASHs is sufficient to rescue OA sensitivity in f14d12.6(

214 he RNAi knockdown of ser-5 expression in the ASHs of wild-type animals also abolished 5-HT-dependent

215 ion by activating Galpha(o) signaling in the ASHs that, in turn, inhibits both Galpha(s) and Galpha(q

216 ra-3::gfp appears not to be expressed in the ASHs, but instead in other neurons, including the dopami

217 f14d12.6::gfp is expressed in the ASHs, the neurons responsible for sensitivity to dilute

218 ivating either Galpha(q) or Galpha(s) in the ASHs, with Galpha(s) signaling specifically stimulating

219 ld be restored by expression of SER-5 in the ASHs.

220 modulates the octanol responsiveness of the ASHs directly.

221 mine reversibly modulate the activity of the ASHs, and highlight the utility of the C. elegans model

222 Food or serotonin sensitize the ASHs and stimulate aversive responses through a pathway

223 Here, we describe 2 components of this ASH initiative, the Consortium on Newborn Screening in A

224 Central to ASH pathogenesis is the dysregulation of lipid droplet (

225 mice and of hippocampal slices subjected to ASH was assessed, as well as the effects of MCT blocker

226 recovery of hippocampal slices subjected to ASH.

227 served interaction interface between the two ASH domains.

228 d precision required for chemotaxis, whereas ASH nociceptive neurons integrate noxious cues over seve

229 a shorter length of stay, and patients with ASH had eight times the odds of undergoing invasive trea