ライフサイエンスコーパス: AIH

1 AIH also enhances excitatory and reduces inhibitory conn

2 AIH has been associated with autoantibodies against memb

3 AIH has been demonstrated to be a disease of middle-aged

4 AIH occurred in 0.4% of UC patients and in 0.3% of CD pa

5 AIH-induced pLTF requires spinal NADPH oxidase activity

6 AIH-induced respiratory plasticity and stem cell therapy

7 4+CD25- T cells from 24 patients with type 1 AIH and 22 healthy controls were cultured for up to 5 we

8 43 patients with AIH, all of whom had type 1 AIH equating to 1090 cases per 100,000 patient follow-up

9 h autoimmune liver disease (AILD) (33 type 1 AIH, 31 type 2 AIH, and 17 autoimmune sclerosing cholant

10 and immunological changes resembling type 1 AIH, including marked and persistent liver mononuclear c

11 During Trial 1 (AIH) participants were exposed to eight 4 min episodes o

12 A total of 130 AIH, 70 PBC, and 81 PSC patients were included contribut

13 A total of 133 AIH patients were included.

14 reactivity is frequent in type 1 and type 2 AIH and ASC, defining patients with a worse prognosis.

15 We describe a case of type 2 AIH with serological positivity for PBC-specific anti-mi

16 nt in 58% of patients with type 1 and type 2 AIH, 41% with ASC, but in only 3 pathologic controls.

17 rlap with PBC are virtually absent in Type 2 AIH, a pediatric form of AIH which is distinct precisely

18 ver disease (AILD) (33 type 1 AIH, 31 type 2 AIH, and 17 autoimmune sclerosing cholantitis [ASC]), 14

19 Using a murine model of type 2 AIH, we identified susceptibility factors for autoimmune

20 all 3 types of AILD, particularly in type 2 AIH.

21 Autoimmune hepatitis type 2 (AIH-2) is a severe organ-specific disorder characterized

22 autoantigen of autoimmune hepatitis type 2 (AIH-2), are permitted by a numerical and functional impa

23 autoantigen of autoimmune hepatitis type 2 (AIH-2), are permitted by a numerical and functional impa

24 DRB1 allele analyses were performed in 264 AIH and 399 non-AIH patients.

25 Between 2000 and 2014, 354 AIH patients from Hannover Medical School were included.

26 C57BL/6 AIH mice, xenoimmunized with DNA coding for human liver

27 enotype was assessed by flow cytometry in 75 AIH patients.

28 Upon admission, AIH types 1 and 2 were observed in 95 and 17 patients, r

29 shed if synaptic inhibition is blocked after AIH.

30 renders respiratory activity irregular after AIH.

31 onged increase in phrenic motor output after AIH has ended.

32 to sustained increases in motor output after AIH.

33 liver transplantation (grade II, +112%), and AIH (grade III, +105%).

34 he incidence and prevalence of PSC, ASC, and AIH were 0.2 and 1.5 cases, 0.1 and 0.6 cases, and 0.4 a

35 y intrahepatic T cell population changes and AIH development after transfer of liver T cells into imm

36 cted PBC portal tracts compared with CHC and AIH (P < .001).

37 intervals, and compared to time control and AIH-treated rats.

38 C) and 16 cholestatic/mixed injury (CS)] and AIH (n = 28) were evaluated for Ishak scores, prominent

39 ve salvage therapy, even in the elderly, and AIH must be considered in all patients with graft dysfun

40 Both apnoea-induced and AIH-induced LTF were associated with a decreased CO(2) r

41 l proliferation in both healthy subjects and AIH/AISC patients through a mechanism which is dependent

42 hypoxic sensory response was unaffected and AIH was ineffective in eliciting sLTF in CIH-exposed HET

43 versus 95%), and seven patients diagnosed as AIH using the revised original system were nondiagnostic

44 identified all cases of pediatric PSC, ASC, AIH, and inflammatory bowel disease (IBD) in a geographi

45 We also associated AIH with variants of SH2B3 (rs3184504, 12q24; P = 7.7 x

46 cently, drug-induced AIH and IgG4-associated AIH have been proposed as distinct clinicopathological e

47 genome-wide association study, we associated AIH type 1 with variants in the major histocompatibility

48 We associated AIH with a variant in the major histocompatibility compl

49 ver-related outcomes in the population-based AIH cohort from Canterbury, New Zealand.

50 ented by blocking synaptic inhibition before AIH.

51 d ventilated male Sprague-Dawley rats before AIH (three 5 min episodes, 11% O(2)).

52 rgide (306 microg kg(-1), 15 microl) blocked AIH-induced pLTF in both MSX-3 and aCSF treated rats, co

53 frequency was found in PBC, compared to both AIH and healthy controls.

54 A subgroup of 24% of mice is affected by AIH, characterized by lymphoplasmacytic and periportal h

55 ilation that is comparable to that evoked by AIH.

56 ties are caused both in vitro and in vivo by AIH, which increases synaptic inhibition within the preB

57 re tested routinely to diagnose and classify AIH, liver-infiltrating lymphocytes are regarded as the

58 of >or=6 (probable AIH) and >or=7 (definite AIH) were calculated.

59 ia was 90% for probable and 61% for definite AIH.

60 erall diagnosis of AIH (probable or definite AIH) among the 70 patients with fulminant liver failure

61 explore potential hallmarks to differentiate AIH versus DILI.

62 o these "pre-phrenic" cells increased during AIH.

63 sient hepatitis there was a chronic evolving AIH, finally leading to portal and lobular fibrosis.

64 s model provides a practical tool to explore AIH pathogenesis and novel therapies.

65 nd emperiopolesis were features that favored AIH (P < 0.02).

66 endent phrenic and hypoglossal LTF following AIH.

67 For AIH, PBC, and PSC cohorts, SMRs for all-cause mortality

68 -70%) for ASC, and 15% (95% CI = 7%-33%) for AIH.

69 73%) and predictability (92% versus 82%) for AIH than the revised original system, and it more common

70 99%) for ASC, and 87% (95% CI = 71%-95%) for AIH.

71 tinct genetic and immunopathogenic basis for AIH and PBC at the MIF locus.

72 findings support a complex genetic basis for AIH pathogenesis and indicate that part of the genetic s

73 peutic effects by enhancing the capacity for AIH-induced respiratory plasticity.

74 an overlap of histologic findings exists for AIH and DILI, sufficient differences exist so that patho

75 erful and tailored form of immunotherapy for AIH-2.

76 erful and tailored form of immunotherapy for AIH-2.

77 rons are a major source of ROS necessary for AIH-induced pLTF.

78 range, 14-69 years) undergoing treatment for AIH underwent unenhanced and gadolinium-enhanced MR imag

79 r PSC, 11.3 years for ASC, and 9.8 years for AIH.

80 The four AIH-favoring features listed above were consistently mor

81 Five subjects had AIH with anti-SLA/LP as the sole markers.

82 splantation (+53), and autoimmune hepatitis (AIH) (+27).

83 C (CHC) (n = 30), and autoimmune hepatitis (AIH) (n = 8).

84 Autoimmune hepatitis (AIH) after liver transplantation has been defined histol

85 ion of liver damage in autoimmune hepatitis (AIH) and autoimmune sclerosing cholangitis (AISC) either

86 CD74, was assessed in autoimmune hepatitis (AIH) and primary biliary cirrhosis (PBC).

87 hoice in patients with autoimmune hepatitis (AIH) and results in remission induction in over 80% of p

88 cholangitis (ASC), and autoimmune hepatitis (AIH) are not well characterized.

89 (DILI) from idiopathic autoimmune hepatitis (AIH) can be challenging.

90 Autoimmune hepatitis (AIH) can lead to cirrhosis, hepatic failure, and death.

91 -old woman with type 1 autoimmune hepatitis (AIH) failed to sustain remission when steroids were with

92 ) hepatitis resembling autoimmune hepatitis (AIH) has been reported after bone marrow transplantation

93 The understanding of autoimmune hepatitis (AIH) has evolved in the past two decades since diagnosti

94 the natural history of autoimmune hepatitis (AIH) has not been well characterized.

95 iagnostic criteria for autoimmune hepatitis (AIH) have been codified by an international panel, and a

96 iagnostic criteria for autoimmune hepatitis (AIH) have been created and revised by the International

97 tRNP((Ser)Sec)/SLA) in autoimmune hepatitis (AIH) have been investigated using partially purified or

98 Patients with autoimmune hepatitis (AIH) have reduced numbers and function of CD4+CD25(high)

99 h a prior diagnosis of autoimmune hepatitis (AIH) in remission, presented with bilateral lower limb u

100 Autoimmune hepatitis (AIH) is a chronic inflammatory disease characterized by

101 Autoimmune hepatitis (AIH) is a chronic inflammatory liver disease associated

102 Autoimmune hepatitis (AIH) is a chronic, progressive hepatitis of uncertain ca

103 Autoimmune hepatitis (AIH) is an important cause of severe liver disease and i

104 Autoimmune hepatitis (AIH) is an uncommon autoimmune liver disease of unknown

105 Autoimmune hepatitis (AIH) is characterized by a loss of immunological toleran

106 Autoimmune hepatitis (AIH) is characterized by chronic inflammation of the liv

107 Autoimmune hepatitis (AIH) is defined as a chronic liver disease with loss of

108 hildhood, while type 2 autoimmune hepatitis (AIH) is eminently a paediatric disease.

109 Autoimmune hepatitis (AIH) is known as a T cell-mediated disease.

110 he etiopathogenesis of autoimmune hepatitis (AIH) remains poorly understood.

111 Autoimmune hepatitis (AIH) typically responds to treatment in 90% of patients.

112 ervention candidate in autoimmune hepatitis (AIH), a condition characterized by impaired T-reg number

113 y during the course of autoimmune hepatitis (AIH), and some autoantibodies have been associated with

114 maintain remission in autoimmune hepatitis (AIH), but up to 18% of patients are unresponsive.

115 iver diseases, such as autoimmune hepatitis (AIH), has been hampered by a lack of autochthonous chron

116 ical lesion typical of autoimmune hepatitis (AIH), is composed of CD4 and CD8 T lymphocytes and of in

117 In autoimmune hepatitis (AIH), liver-damaging CD4 T cell responses are associated

118 nd cancer incidence of autoimmune hepatitis (AIH), primary biliary cirrhosis (PBC), and primary scler

119 cirrhosis secondary to autoimmune hepatitis (AIH), yet the true incidence remains unknown due to a la

120 aracteristics of human autoimmune hepatitis (AIH).

121 ly and functionally in autoimmune hepatitis (AIH).

122 c criteria for de novo autoimmune hepatitis (AIH).

123 une diseases including autoimmune hepatitis (AIH).

124 of patients develop an autoimmune hepatitis (AIH).

125 However, AIH patients refractory to conventional treatment have b

126 APS-1, we generated a murine model of human AIH on a BALB/c mouse background, in which Aire is trunc

127 e sought to develop an animal model of human AIH to gain insight into the immunological mechanisms dr

128 eading to chronic hepatitis resembling human AIH type 1.

129 acterize autoantigenic peptides within human AIH-specific soluble liver antigen/liver pancreas antige

130 t, or exposed to acute intermittent hypoxia (AIH) at disease end stage.

131 ICANCE STATEMENT Acute intermittent hypoxia (AIH) can trigger spinal plasticity associated with susta

132 s augmented, and acute intermittent hypoxia (AIH) induced sensory long-term facilitation (sLTF) of th

133 Acute intermittent hypoxia (AIH) induces a form of spinal motor plasticity known as

134 Acute intermittent hypoxia (AIH) induces phrenic long-term facilitation (pLTF), a fo

135 (pLTF) following acute intermittent hypoxia (AIH) is a form of spinal, serotonin-dependent synaptic p

136 (vLTF) following acute intermittent hypoxia (AIH) is only expressed if CO2 is maintained above normoc

137 that exposure to acute intermittent hypoxia (AIH) leads to fundamental changes in the neuromodulatory

138 l (SOD1(G93A) ), acute intermittent hypoxia (AIH) restores phrenic nerve activity to normal levels vi

139 n contributes to acute intermittent hypoxia (AIH)-induced pLTF.

140 utput induced by acute intermittent hypoxia (AIH).

141 ygen reductions [acute intermittent hypoxia (AIH)] evokes spinal plasticity.

142 ced by acute intermittent isocapnic hypoxia (AIH, three 5 min isocapnic hypoxic episodes).

143 Approximately 20% of icteric AIH presentations fail corticosteroid therapy.

144 In AIH and HS, Tim-3(pos) cells proliferated less vigorousl

145 In AIH, CD39(pos) Tregs are decreased in frequency, exhibit

146 In AIH, CD39(pos) Tregs are decreased in number, fail to ad

147 In AIH, Gal9(pos) T-regs were fewer and contained less FOXP

148 In AIH, Tim-3(pos) cells within CD4(pos) CD25(neg) cells an

149 In AIH, Treg FOXP3 expression is lower than in normal subje

150 In AIH/AISC we noted a substantial increase in peripheral b

151 ory and high-expression -794 CATT7 allele in AIH, compared to PBC, whereas lower frequency was found

152 f action of Tregs in healthy subjects and in AIH patients using Transwell experiments, where Tregs ar

153 ies of T regulatory 1 cells in health and in AIH/AISC, though suppressive function is lost in patient

154 eripheral tolerance to liver autoantigens in AIH is paramount.

155 y was to assess the autoantibody behavior in AIH and its significance as predictors of biochemical an

156 not influence target cell apoptosis, but in AIH, spontaneous apoptosis of CD4(+)CD25(-) T cells is r

157 The role of T cells in AIH establishment was supported by intrahepatic T cell p

158 generated de novo from CD4+CD25- T cells in AIH patients and healthy controls.

159 to directly monitor autoreactive T cells in AIH patients in clinical studies.

160 1-restricted autoantigen-specific T cells in AIH patients were analyzed with tetramer and interferon-

161 Cirrhosis in AIH is the sine qua non for HCC development, which subse

162 atisfactory and similar to that described in AIH.

163 ed by the possession of DR3 and A1-B8-DR3 in AIH type 1 and ASC, and prevented by the possession of A

164 healthy controls and, to a lesser extent, in AIH patients.

165 Although fibrosis is a common feature in AIH and is often moderate to severe, no significant corr

166 er disease with several pathologies found in AIH, including elevated serum aminotransferases in the c

167 nction in liver disease pathologies found in AIH.

168 s contribute to impaired immunoregulation in AIH by rendering effector cells less prone to T-reg cont

169 uggesting that defective immunoregulation in AIH might result not only from reduced Treg number and f

170 tigated whether impaired immunoregulation in AIH results from reduced expression of Gal9 in T-regs an

171 compare the survival and cancer incidence in AIH, PBC, and PSC in the same population.

172 ic malignancy was significantly increased in AIH and PSC patients.

173 be the focus of novel immune intervention in AIH-2.

174 ory challenge in healthy subjects but not in AIH/AISC.

175 ed above were consistently more prevalent in AIH, whereas portal neutrophils and intracellular (hepat

176 gs display a more proinflammatory profile in AIH, which is characterized by elevated CD127 positivity

177 25(neg) and Tim-3(pos) cell proliferation in AIH and HS.

178 yte antigen (HLA)-A2 restricted responses in AIH-2 (20 patients, 11 HLA-A2+).

179 all evaluated cases, but were more severe in AIH (P < 0.05) than DILI (HC).

180 shak inflammation scores were more severe in AIH than DILI (CS) (P </= 0.05).

181 Studies in AIH have focused on autoreactive CD4 and CD8 T cells and

182 -regs were higher in normal controls than in AIH patients.

183 fusion of ex vivo expanded CXCR3(+) Tregs in AIH patients could be an effective therapeutic approach

184 Recently, drug-induced AIH and IgG4-associated AIH have been proposed as distin

185 Moderate AIH-induced pLTF is normally elicited via cellular mecha

186 zed, paralyzed and ventilated rats, moderate AIH-induced pLTF was abolished by siBDNF and UO126, but

187 of pMF, we sought to illustrate why moderate AIH (mAIH) elicits pMF but mASH does not.

188 developed a new model of experimental murine AIH (emAIH) by a self-limited adenoviral infection with

189 We developed a new murine AIH model closely resembling AIH in patients that explai

190 alyses were performed in 264 AIH and 399 non-AIH patients.

191 Patients with AIH and non-AIH etiologies of liver disease were identified from ded

192 toimmune-like hepatitis transplanted for non-AIH in two centers (n=35 and 20) were reviewed.

193 26 with variant syndromes, and 302 with non-AIH).

194 90s could be described as the 'Dark Ages' of AIH treatment research.

195 ses of PSC, 12 cases of ASC, and 44 cases of AIH.

196 d immunoregulation that is characteristic of AIH.

197 of malignancy on population-based cohorts of AIH, PBC, and PSC in Canterbury, New Zealand.

198 file does not markedly vary in the course of AIH.

199 Development of AIH in APS-1 is dependent on specific Aire mutations and

200 lls was sufficient to prevent development of AIH in mice.

201 Seven false positive diagnoses of AIH occurred, all with simplified scores of 6.

202 y discriminating for a clinical diagnosis of AIH (P=0.04 and 0.05, respectively).

203 The frequency of an overall diagnosis of AIH (probable or definite AIH) among the 70 patients wit

204 re correlated with the clinical diagnosis of AIH based on a retrospective review of clinical and sero

205 scoring system also ascribed a diagnosis of AIH to 20 of 21 patients with cryptogenic chronic hepati

206 The diagnosis of AIH was defined by the criteria established by the Inter

207 A clinical diagnosis of AIH was retrospectively assigned to 24 of 35 (68%) and 1

208 ing system for the pretreatment diagnosis of AIH were determined.

209 fic but lack sensitivity in the diagnosis of AIH, particularly when presenting atypically.

210 r limb ulcers 4 years after the diagnosis of AIH.

211 in patients with few or atypical features of AIH, and the simplified system is better at excluding th

212 ly absent in Type 2 AIH, a pediatric form of AIH which is distinct precisely because it is characteri

213 s study was to assess the natural history of AIH in blacks in comparison with others (nonblacks).

214 The impact of AIH on cervical spinal interneuron (C-IN) discharge and

215 s the first case report in the literature of AIH type 2 with an unexpected PBC-specific AMA positivit

216 in patients that explains the mechanisms of AIH pathophysiology.

217 B-cell depletion in an experimental model of AIH.

218 Models of AIH-induced neuroplasticity have focused on motoneurons;

219 nd fibrosis have been developed as models of AIH.

220 s play an active role in the pathogenesis of AIH in antigen presentation processes and the modulation

221 l with which to study the pathophysiology of AIH, as well as autoantigen-specific T cell responses an

222 PBC from the more inflammatory phenotype of AIH and may play a role in pathogenesis and as biomarker

223 In our case, the presence of AIH-2-specific anti-LKM-1 and PBC-specific AMA was confi

224 variceal bleed as the index presentation of AIH, 20% versus 5.3%, P = 0.003.

225 siently restored by a single presentation of AIH; and (2) preserved ipsilateral to hNPC transplants m

226 success of B-cell depletion for remission of AIH despite its classification as a T cell-mediated auto

227 tolerance to FTCD, and induced remission of AIH.

228 peripheral tolerance and induce remission of AIH.

229 immunosorbent assay in 165 serum samples of AIH, PBC, and controls.

230 ion with histological features suggestive of AIH.

231 ately, clinical research in the treatment of AIH has experienced a renaissance in the 21st century.

232 ights into the pathogenesis and treatment of AIH.

233 t, double-blind, placebo-controlled trial of AIH treatment to date, comparing budesonide to prednison

234 5%; p = 0.0160), but was reduced 15 min post-AIH (0.5%; p = 0.0439).

235 , connectivity remained elevated 15 min post-AIH (30%; p = 0.0002).

236 rats (97 +/- 6% vs. 49 +/- 4% at 60 min post-AIH, respectively; P < 0.05).

237 Sixty minutes post-AIH (three 5-min episodes of 11% O(2), 5 min intervals),

238 Despite its rare prevalence, AIH is one of the most common indications for transplant

239 er-specific autoreactive T cells and prevent AIH.

240 dictive values for scores of >or=6 (probable AIH) and >or=7 (definite AIH) were calculated.

241 ed a new murine AIH model closely resembling AIH in patients that explains the mechanisms of AIH path

242 Development of a severe AIH stemmed from reduced numbers of functional regulator

243 In contrast, severe AIH (sAIH) elicits pLTF through adenosine-dependent mech

244 In contrast, severe AIH elicits pLTF via a distinct mechanism that requires

245 us, PKCtheta plays a critical role in spinal AIH-induced respiratory motor plasticity, and the releva

246 with those of CHC (P < .001) and early-stage AIH (P < .001).

247 To study AIH in APS-1, we generated a murine model of human AIH o

248 We conclude that AIH alters connectivity of the midcervical spinal networ

249 Our results demonstrate that AIH recruits excitatory C-INs into the spinal respirator

250 wledge, this is the first demonstration that AIH induces plasticity within the propriospinal network.

251 We hypothesized that AIH would alter the functional connectivity between C-IN

252 reasing evidence has mounted to suggest that AIH is a disease that often requires long-term treatment

253 The AIH could be treated with prednisolone or adoptive trans

254 Since both the AIH and the PG can present serious diagnostic challenges

255 es for further study and introduced into the AIH scoring systems when applied in the context of liver

256 and the immunological changes underlying the AIH remission caused by B-cell depletion in an experimen

257 atic onset of pyoderma gangrenosum, with the AIH in remission, strengthening the association between

258 etic variants that predispose individuals to AIH.

259 atory, somatic, and/or autonomic response to AIH, and that propriospinal plasticity may contribute to

260 derstanding of the mechanisms giving rise to AIH-induced pLTF and 5-HT induced pMF may inspire novel

261 Similar to AIH-induced LTF, apnoea-induced LTF is serotonin depende

262 enic and XII LTF with a magnitude similar to AIH.

263 phenolate mofeteil, show promise in treating AIH.

264 n AUC of 0.91 in predicting DILI (CS) versus AIH.

265 UROC) of 0.90 in predicting DILI (HC) versus AIH.

266 CD74 were found in patients with PBC versus AIH and controls.

267 onic liver disease were evaluated, (221 with AIH, 26 with variant syndromes, and 302 with non-AIH).

268 onfirmed in tetramer and ELISpot assays with AIH patients' peripheral blood mononuclear cells.

269 ting common mechanisms of ROS formation with AIH-induced pLTF.

270 ver diseases, including 153 individuals with AIH by codified clinical criteria.

271 onclusion: Blacks, especially black men with AIH, have more aggressive disease at the initial present

272 ex vivo expanded CXCR3(+) Tregs in mice with AIH efficiently targeted the inflamed liver, restored pe

273 study of 649 adults in The Netherlands with AIH type 1 and 13,436 controls.

274 A total of 117 patients with AIH (mean age 18.6 [4-69] years) were evaluated and test

275 ctivated subset of Teff, in 32 patients with AIH and 20 with AISC and in 36 healthy subjects.

276 ngTregs were generated from 36 patients with AIH and 23 healthy subjects (controls).

277 Patients with AIH and non-AIH etiologies of liver disease were identif

278 MIF expression was elevated in patients with AIH and PBC versus healthy controls.

279 ospectively obtained cohort of patients with AIH at a single center.

280 ngTregs from patients with AIH contained greater proportions of IL-17+ and RORC+ ce

281 006) retrospective analysis of patients with AIH from a single tertiary care center.

282 h titers of ASMA and/or AAA in patients with AIH is associated with disease activity.

283 ebate exists as to whether all patients with AIH need treatment.

284 esponse, and toxicity in adult patients with AIH prescribed a stable dose of AZA for the maintenance

285 plication panel comprising 451 patients with AIH type 1 in Germany and 4103 controls.

286 One hundred one patients with AIH were eligible for the study.

287 CC was discovered in 15 of 243 patients with AIH, all of whom had type 1 AIH equating to 1090 cases p

288 els are found in the sera from patients with AIH, hepatitis B virus, hepatitis C virus, and nonalcoho

289 d in DNA samples from over 500 patients with AIH, PBC, and controls.

290 R molecule can be generated in patients with AIH-2 and can control CD4 and CD8 T cell effectors targe

291 R molecule can be generated in patients with AIH-2 and can control CD4 and CD8 T cell effectors targe

292 blood mononuclear cells of 17 patients with AIH-2, who were positive for the predisposing HLA-DR7 an

293 blood mononuclear cells of 17 patients with AIH-2, who were positive for the predisposing HLA-DR7 an

294 ht be developed for therapy of patients with AIH.

295 veryday clinical management of patients with AIH.

296 anded and generated de novo in patients with AIH.

297 able new treatment options for patients with AIH.

298 ected de novo in six and three subjects with AIH types 1 and 2, respectively.

299 dic spinal 5-HT receptor activation (without AIH) is sufficient to elicit an NADPH oxidase-dependent

300 ed rats did not exhibit facilitation without AIH (time controls; 7 +/- 5% and 9 +/- 9%, respectively;