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

6 ASH-mediated aversive responses are increased by activat

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

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

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

10 led previously unknown properties of AVA and ASH neurons.

11 induced potentiation of sensory behavior and ASH neuron function.

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

13 and the function of sensory neurons such as ASH.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

35 er EVs as a potentially novel diagnostic for ASH.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

52 al hydrocele - an abdominoscrotal hydrocele (ASH).

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

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

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

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

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

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

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

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

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

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

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

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

65 10 is a novel cytosolic protein expressed in ASH and three other classes of sensory neurons.

66 ndependent of two TRPV channels expressed in ASH.

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

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

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

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

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

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

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

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

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

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

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

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

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

80 tide release from interneurons that modulate ASH activity indirectly.

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

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

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

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

85 ed by the Caenorhabditis elegans nociceptive ASH sensory neurons.

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

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

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

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

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

91 helped galvanize support for the creation of ASH.

92 he age-dependent functional deterioration of ASH.

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

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

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

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

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

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

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

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

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

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

103 Other ASH candidates for APT activity were functionally charac

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

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

106 o soluble repellents sensed by the polymodal ASH neurons.

107 o soluble repellents sensed by the polymodal ASH nociceptors.

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

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

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

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

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

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

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

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

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

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

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

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

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

121 The ASH guidelines indicate that for severe thrombocytopenia

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

123 The ASH neurons are therefore hypothesized to be polymodal n

124 The ASH sensory neuron displays reduced sensitivity to stimu

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

140 5-HT receptors appear to be expressed in the ASH sensory neurons mediating octanol sensitivity, we id

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

159 indicating that adaptation occurs within the ASH sensory neuron.

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

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

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

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

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

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

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

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

168 modulates the octanol responsiveness of the ASHs directly.

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

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

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

172 recovery of hippocampal slices subjected to ASH.

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