ライフサイエンスコーパス: HAM

1 HAM and WUS share common targets in vivo and their physi

2 HAM specifically inhibits endothelial cell growth and th

3 HAM-A scores decreased by 13.4 points (SD=9.7) (55%; eff

4 HAM-D scores at the end of treatment were significantly

5 HAM/TSP patients had significantly higher Ab responses f

6 ly different from placebo (effect size, 0.03 HAM-D points; 95% CI, -0.7 to 0.8; P = .94).

7 eatment-end difference was (-infinity, 0.07) HAM-D points, indicating a non-inferiority margin of 1.3

8 derators of any deterioration (increase >/=1 HAM-D or BDI point), reliable deterioration (increase >/

9 sis, participants in treatment averaged 2.11 HAM-D points greater improvement than control subjects (

10 n peripheral mononuclear cells (PBMCs) in 14 HAM/TSP patients, 34 MS patients and 20 healthy controls

11 into any mood episode (YMRS score > or =15, HAM-D score > or =15, or hospitalization).

12 inical disability scores were measured in 18 HAM/TSP patients, 4 asymptomatic carriers (ACs) of HTLV-

13 In 2 HAM/TSP patients, spinal cord cross-sectional area was m

14 Remission rates were 28% (HAM-D) and 33% (QIDS-SR).

15 , indicating a non-inferiority margin of 1.3 HAM-D points or greater; this margin is lower than the p

16 ng core emotional symptoms (effect size, 2.3 HAM-D points during 8 weeks, 95% CI, 1.6 to 3.1; P < .00

17 17 asymptomatic carriers of HTLV-1 (AC), 47 HAM/TSP, 74 relapsing-remitting MS [RRMS], 17 secondary

18 Primary outcomes were response rate (>=50% HAM-D-17 score reduction) after the maintenance phase, a

19 oint), reliable deterioration (increase >/=8 HAM-D or >/=9 BDI points), extreme nonresponse (posttrea

20 n partially mediated group effects on week 8 HAM-D.

21 Remission was defined as a HAM-D score of 7 or below for 2 consecutive weeks.

22 eline of more than 50% in the HAM-D score, a HAM-D score of 7 or lower, and a Clinical Global Impress

23 Baseline craving (p < 0.001) and HAM-D assessment (p < 0.01) were also associated with pe

24 points (SD=9.7) (55%; effect size=1.4), and HAM-D scores decreased by 11.2 points (SD=8.8) (54%; eff

25 Y-BOCS, HAM-A, and HAM-D scores all decreased significantly during the firs

26 eneral psychopathology subscales, HAM-A, and HAM-D than for placebo.

27 ntaneous proliferation of PBMCs from ATL and HAM/TSP patients by 67.1% and 86.4%, respectively.

28 s may exert therapeutic benefits for ATL and HAM/TSP patients.

29 HTLV-I-seronegative donors, ACs, and ATL and HAM/TSP patients.

30 LV-I asymptomatic carriers (ACs) and ATL and HAM/TSP patients.

31 lect patients with HTLV-I-associated ATL and HAM/TSP.

32 phoma (ATL), an aggressive blood cancer, and HAM/TSP, a progressive neurological and inflammatory dis

33 day follow-up period and fNIRS, craving, and HAM-D assessments.

34 this study confirms the formation of HAN and HAM dominant species found in disinfected water, dichlor

35 fNIRS results, baseline craving scores, and HAM-D scores created a robust predictive model (DeltaF(3

36 e overlapping expression patterns of WOX and HAM family members underlie the formation of diverse ste

37 a fourth, more distantly related Arabidopsis HAM homolog, AtHAM4, exhibits overlapping function with

38 us for knockout alleles in three Arabidopsis HAM orthologs (Atham1,2,3 mutants) exhibit loss of indet

39 of associated inflammatory diseases such as HAM/TSP.

40 The study assessments (HAM-D-6, MADRS, SDQ, PAS, CGI-S, and CGI-I) were perform

41 or placebo and who had a completed baseline HAM-D assessment and at least one post-baseline HAM-D as

42 were randomly assigned, with a mean baseline HAM-D score of 19.8 (SD=3.8).

43 a mean age of 36.7 years and a mean baseline HAM-D score of 20.7.

44 The mean baseline HAM-D score was 25.2 in the SAGE-217 group and 25.7 in t

45 -D assessment and at least one post-baseline HAM-D assessment.

46 pressant responders had significantly better HAM-D scores over time than placebo-treated patients, bu

47 Y-BOCS, HAM-A, and HAM-D scores all decreased significantly duri

48 Both HAM/TSP patients followed longitudinally showed thoracic

49 redictor of drug-placebo separation for both HAM-D(1)(7) continuous score change (beta=2.24, p=0.034)

50 Loss of both HAM-1 and its target, the kinase PIG-1 [PAR-1(I)-like Ge

51 amilton Depression Rating Scale (HAM-D), but HAM-D score independently predicted poorer Trails B and

52 Definite HAM/TSP developed in 5 (1.47%) patients.

53 Of 414 subjects, 76 had definite HAM/TSP, 87 had possible or probable HAM/TSP, and 251 su

54 on the Hamilton Rating Scale for Depression (HAM-D(1)(7)) score as the primary outcome.

55 n-item Hamilton Rating Scale for Depression (HAM-D) and Beck Depression Inventory (BDI).

56 7-item Hamilton Rating Scale for Depression (HAM-D-17).

57 rom the clinician-rated Hamilton Depression (HAM-D) rating scale.

58 ssion (Hamilton Rating Scale for Depression [HAM-D] total score >/=26) in four hospitals in the USA.

59 immunoprecipitation system could distinguish HAM/TSP patients from ACs at a true-positive rate of 85.

60 nal repertoire 'signature' could distinguish HAM/TSP patients from healthy controls, as well as from

61 tion with subject information to distinguish HAM/TSP patients from ACs (odds ratio = 14.12) and from

62 C. elegans HAM-1 is an asymmetrically distributed cortical protein

63 The mixed effects model-estimated HAM-D ratings were not significantly different between t

64 ted a new allele of the transcription factor HAM-1 [HSN (Hermaphrodite-Specific Neurons) Abnormal Mig

65 l measures that are potential biomarkers for HAM/TSP.

66 ted patients who do not fulfill criteria for HAM/TSP present with neurological complaints related to

67 el protein and define residues important for HAM-1 function and distribution to the cell cortex.

68 T cells may be a viable treatment option for HAM/TSP.

69 CD4(+)CD25(+) and CD4(+)CD25(-) T cells from HAM/TSP patients exhibited reduced TGF-betaRII expressio

70 eatment of isolated PBMCs and CNS cells from HAM/TSP patients with an antibody that targets CCR4+ T c

71 PEDF primers amplified a single product from HAM RNA.

72 Soluble proteins from HAM inhibited proliferation of human umbilical vein endo

73 ongitudinal analysis of TCR repertoires from HAM/TSP patients demonstrated a correlation of the TCR c

74 Compared with the placebo group, HAM-A somatic anxiety symptoms were also significantly (

75 her levels of education or income had higher HAM-D remission rates; longer index episodes, more concu

76 trajectory modeling was applied to identify HAM-D response trajectories, and regression techniques w

77 lam group had significantly (P<.01) improved HAM-A psychic anxiety symptoms compared with the placebo

78 1 or BDI score >/=31), superior improvement (HAM-D or BDI decrease >/=95%), and superior response (po

79 In HAM/TSP patients, SCCSA extensively correlated with Ambu

80 The NF-kappaB activation in HAM/TSP PBMCs was reversed by a novel small-molecule inh

81 liferation, a marker of T-cell activation in HAM/TSP, also was reduced.

82 average spinal cord cross-sectional area in HAM/TSP and progressive MS show spinal cord atrophy.

83 T4 to T9 spinal cord cross-sectional area in HAM/TSP.

84 ment failure (<30% decrease from baseline in HAM-D score).

85 the significance of change from baseline in HAM-D scores.

86 was enhanced on surface of CD14(+) cells in HAM/TSP patients.

87 ction and enhanced IL-15 on CD14(+) cells in HAM/TSP patients.

88 greater reductions in depression (change in HAM-D score) than the clinical monitoring group.

89 -CRP concentration (P = .01), with change in HAM-D scores (baseline to week 12) favoring infliximab-t

90 zed treatment effect size (ES) for change in HAM-D-17 from baseline to treatment week 8.

91 provement (defined by the relative change in HAM-D-17 total score from baseline to week 4), lower bas

92 nd visualization of peptide-HLA complexes in HAM/TSP CD4+ CD25+ T cell subsets that are shown to stim

93 The entire spinal cord in HAM/TSP patients was thin compared to HVs, whereas only

94 ong those who remitted, the mean decrease in HAM-D score was 24.7 points (95% CI=23.4, 25.9), with a

95 The mean estimated overall decreases in HAM-D score did not significantly differ between treatme

96 gh' inflammation) had medium ES decreases in HAM-D-17 scores vs subjects 'low' on these biomarkers.

97 of cytokines, are prominently deregulated in HAM/TSP and underlie many of the characteristic immune a

98 ation and inflammatory autoimmune disease in HAM/TSP patients.

99 Despite higher TCR clonal expansions in HAM/TSP patients, no disease-specific TCRs were shared a

100 nd Ab responses for all 3 Ags were higher in HAM/TSP patients than in ATL patients.

101 EGCG (20 micromol/L) for 0.5 to 24 hours in HAM's F12 and RPMI 1640 mixed medium at 37 degrees C, be

102 We further hypothesize in HAM/TSP that is possible that neuroglial loss from a tho

103 s a potential target for immunomodulation in HAM/TSP.

104 compared with 20.5%) and mean improvement in HAM-D total scores (-6.4 [SD=6.4] compared with -3.3 [SD

105 T cells was demonstrated to be increased in HAM/TSP and correlated with HTLV-I proviral DNA load, HT

106 e changes predicted IFN-induced increases in HAM-D 4 weeks later (R(2) = 0.17, p = 0.022) and anti-TN

107 portion of patients in remission, but not in HAM-D improvement among drug injectors.

108 t under recognized reservoir particularly in HAM/TSP patients.

109 pper cervical cord, most of the pathology in HAM/TSP is seen in the thoracolumbar cord, which in turn

110 PEDF in HAM has a major role in eliciting this antiangiogenic ac

111 The expression of PEDF in HAM was confirmed at the RNA level by RT-PCR and DNA seq

112 pigment epithelium-derived factor (PEDF) in HAM was demonstrated at the protein level by Western blo

113 ically significant improvement vs placebo in HAM-D17 total score (p=0.032) and nearly significant imp

114 ed a treatment response (>/=50% reduction in HAM-D score at any point during treatment) of 62% (8 of

115 t was associated with a greater reduction in HAM-D score, higher response and remission rates, shorte

116 At 60 h, mean reduction in HAM-D total score from baseline was 21.0 points (SE 2.9)

117 icant and clinically meaningful reduction in HAM-D total score, compared with placebo.

118 spinal cord cross-sectional area (SCCSA) in HAM/TSP and MS patients to that of healthy volunteers (H

119 for the more extensive cord atrophy seen in HAM/TSP.

120 nd resulted in reduced cytokine signaling in HAM/TSP PBMCs.

121 uency and function of CD4(+)CD25(+) Tregs in HAM/TSP patients might be affected.

122 nflammatory neurological disorders including HAM/TSP, associated with human T-cell lymphotropic virus

123 e 17-question Hamilton Depression Inventory (HAM-d), and the Beck Anxiety Index (BAI).

124 was the change from baseline in the 17-item HAM-D total score at 60 h, assessed in all randomised pa

125 rior to bitemporal ECT regarding the 24-item HAM-D scores after the ECT course (mean difference=1.08

126 group had statistically significantly lower HAM-D scores than the medication only group.

127 d quality of life were associated with lower HAM-D remission rates.

128 zing vimentin and human alveolar macrophage (HAM)-56, markers of glial cells and macrophages, respect

129 Mean HAM-D scores dropped from 25.9 to 17.7 in NRs and from 1

130 Mean HAM-D-17 scores decreased from 22.2 (95% CI, 20.3-24.1)

131 The difference in adjusted mean HAM-D scores at study end was 4.2 (95% CI=1.6, 6.9).

132 At week 10, the mean HAM-D score change was 7.35 for CBT relative to 0.05 for

133 cross the three depression outcome measures (HAM-D: -2.8, 95% CI=-5.1, -0.6; MADRS: -4.9, 95% CI=-8.2

134 Human amniotic membrane (HAM) transplantation is commonly used in corneal surface

135 nstrate that the Arabidopsis HAIRY MERISTEM (HAM) family of transcription regulators act as conserved

136 hat in Arabidopsis SAMs, the HAIRY MERISTEM (HAM) family transcription factors form a concentration g

137 The Petunia hybrida HAIRY MERISTEM (HAM) gene, a member of the GRAS family of transcriptiona

138 halamus in patients with severe and moderate HAM was higher than that in the healthy volunteers, sugg

139 Hypercholesterolemia-associated monocytosis (HAM) developed from increased survival, continued cell p

140 virus type 1 (HTLV-1)-associated myelopathy (HAM) is an inflammatory condition characterized by sever

141 homa (ATL) and HTLV-I associated myelopathy (HAM).

142 HTLV-1-associated myelopathy (HAM; HTLV-1 is human T-lymphotropic virus type 1) is a c

143 al upstream role in the immune activation of HAM/TSP, and identify the NF-kappaB pathway as a potenti

144 basis underlying antiangiogenic activity of HAM.

145 us CD14(+) cells, but not CD4(+) T cells, of HAM/TSP patients, which correlated with proviral DNA loa

146 No overall difference in change of HAM-D scores between treatment groups across time was fo

147 with HTLV-1 infection and the development of HAM/TSP.

148 The effects of HAM protein on proliferation of vascular endothelial cel

149 ion and monocyte aggregation are features of HAM, reflecting widespread inflammatory change, which ma

150 x was detected in the cerebrospinal fluid of HAM/TSP patients, implying that extracellular Tax may be

151 omolog, define the concentration gradient of HAM in the SAM through activating a group of microRNAs.

152 The incidence of HAM/TSP and new signs and neurologic symptoms were compu

153 Evaluation of CSF and spinal cord lesions of HAM/TSP patients revealed the presence of abundant CD4+C

154 pes are unlikely to reflect complete loss of HAM function, as a fourth, more distantly related Arabid

155 nantly localized in the basement membrane of HAM.

156 Although the pathogenesis of HAM/TSP remains to be fully elucidated, previous evidenc

157 the NF-kappaB pathway to the pathogenesis of HAM/TSP, however, has not been fully defined.

158 ells plays a key role in the pathogenesis of HAM/TSP.

159 r T cells contributes to the pathogenesis of HAM/TSP.

160 -I, appears important in the pathogenesis of HAM/TSP.

161 ne mechanisms central to the pathogenesis of HAM/TSP.

162 e treatment showed a more rapid reduction of HAM-D score and a lower incidence of side effects in a p

163 Both treatments led to reduction of HAM-D scores over 9 weeks.

164 minant, of the proviral load and the risk of HAM/TSP.

165 %), and nonresponse (62.5%) or in changes on HAM-D scores.

166 rI -4.83 to -2.39) had the largest effect on HAM-A but it was poorly tolerated (odds ratio 1.44, 95%

167 ient expectancy mediated the group effect on HAM-D scores.

168 showed significantly greater improvement on HAM-A score but not on Visual Analog Scale for Pain scor

169 I, -4.5 to 2.0; t(116) = -0.77; P = .44), or HAM-D scores (placebo, 9.4 vs omega-3, 9.3; 95% differen

170 ted myelopathy/tropical spastic paraparesis (HAM/TSP) and adult T cell leukemia/lymphoma.

171 ted myelopathy/tropical spastic paraparesis (HAM/TSP) and multiple sclerosis (MS).

172 ted myelopathy/tropical spastic paraparesis (HAM/TSP) and multiple sclerosis (MS).

173 ted myelopathy/tropical spastic paraparesis (HAM/TSP) are known to be caused by HTLV-I infection.

174 ted myelopathy/tropical spastic paraparesis (HAM/TSP) exhibit reduced Foxp3 expression and Treg suppr

175 ed) myelopathy/tropical spastic paraparesis (HAM/TSP) has been shown to be a major reservoir for this

176 ted myelopathy/tropical spastic paraparesis (HAM/TSP) is a progressive inflammatory myelopathy occurr

177 ted myelopathy/tropical spastic paraparesis (HAM/TSP) is an immune-mediated inflammatory disorder of

178 ted myelopathy/tropical spastic paraparesis (HAM/TSP) results in a decrease in FOXP3 mRNA and protein

179 ted myelopathy/tropical spastic paraparesis (HAM/TSP), a chronic inflammatory disease of the central

180 ted myelopathy/tropical spastic paraparesis (HAM/TSP), observed in up to 5% of infected individuals.

181 ted myelopathy/tropical spastic paraparesis (HAM/TSP), or adult T cell leukemia/lymphoma (ATL).

182 ted myelopathy/tropical spastic paraparesis (HAM/TSP).

183 ted myelopathy/tropical spastic paraparesis (HAM/TSP).

184 ted myelopathy/tropical spastic paraparesis (HAM/TSP).

185 ted myelopathy/tropical spastic paraparesis (HAM/TSP).

186 ted myelopathy/tropical spastic paraparesis (HAM/TSP).

187 ted myelopathy/tropical spastic paraparesis (HAM/TSP).

188 ted myelopathy/tropical spastic paraparesis (HAM/TSP).

189 ted myelopathy/tropical spastic paraparesis [HAM/TSP]) is suggested to be an immunopathologically med

190 Severely depressed patients (HAM-D score >24) also received antidepressant medication

191 nd was correlated to depression scores (peak HAM-D17 voxel: MNI coordinates (0, 60, 34), p = 0.008).

192 During the maintenance phase, HAM-D-17 and MADRS scores did not change, but the mean I

193 Noninferiority was shown for posttreatment HAM-D and patient-rated depression scores but could not

194 outcome measures included mean posttreatment HAM-D score and patient-rated depression score and 1-yea

195 points), extreme nonresponse (posttreatment HAM-D score >/=21 or BDI score >/=31), superior improvem

196 /=95%), and superior response (posttreatment HAM-D or BDI score of 0) using multilevel models.

197 efinite HAM/TSP, 87 had possible or probable HAM/TSP, and 251 subjects had no neurologic manifestatio

198 As the most prominent HAM species, it is commonly acknowledged that 2,2-dichlo

199 have previously shown that the novel protein HAM-1 controls the asymmetric neuroblast division in thi

200 RC-1, MEK-2, MAK-2, and the scaffold protein HAM-5) to specialized cell fusion structures termed coni

201 me measure was posttreatment remission rate (HAM-D score </=7).

202 n symptoms (Hamilton Depression Rating Scale HAM-D) at 4 weeks (p < 0.001) but not 4-h after first do

203 mprovements in total Hamilton Anxiety Scale (HAM-A) scores at each week (P < .05) and at weeks 4 thro

204 dpoints included the Hamilton Anxiety Scale (HAM-A), Hamilton Depression Rating Scale (HDRS(17)), and

205 ures were the Hamilton Anxiety Rating Scale (HAM-A) and the Hamilton Depression Rating Scale (HAM-D).

206 The Hamilton Anxiety Rating scale (HAM-A) and Visual Analog Scale for Pain were defined a p

207 M-D), and the Hamilton Anxiety Rating Scale (HAM-A).

208 The Hamilton Depression Rating Scale (HAM-D 17-item version and Maier subscale, which focuses

209 he 17-item Hamilton Depression Rating Scale (HAM-D) (primary outcome) or a score of <or=5 on the 16-i

210 he 17-item Hamilton Depression Rating Scale (HAM-D) and the proportion of patients with remissions (H

211 res on the Hamilton Depression Rating Scale (HAM-D) and/or Beck Depression Inventory (BDI).

212 he 17-item Hamilton Depression Rating Scale (HAM-D) between the CP-316,311 and placebo groups.

213 he 24-item Hamilton Depression Rating Scale (HAM-D) score after the ECT course; the prespecified noni

214 who had a Hamilton Depression Rating Scale (HAM-D) score of 18 or greater received escitalopram, 10

215 de and had Hamilton Depression Rating Scale (HAM-D) scores >/=14 were randomly assigned to 16 session

216 effects on Hamilton Depression Rating Scale (HAM-D) scores over time while controlling for treatment

217 nd 17-item Hamilton Depression Rating Scale (HAM-D) scores.

218 he 17-item Hamilton Depression Rating Scale (HAM-D) total score was the primary outcome.

219 he 17-item Hamilton Depression Rating Scale (HAM-D) was 7 or higher at baseline.

220 he 17-item Hamilton Depression Rating Scale (HAM-D), administered by raters blinded to treatment.

221 he 17-item Hamilton Depression Rating Scale (HAM-D), and did not respond to one to three adequate ant

222 ement, the Hamilton Depression Rating Scale (HAM-D), and the Hamilton Anxiety Rating Scale (HAM-A).

223 he 24-item Hamilton Depression Rating Scale (HAM-D), and the secondary efficacy outcome was score on

224 ore on the Hamilton Depression Rating Scale (HAM-D), but HAM-D score independently predicted poorer T

225 cluded the Hamilton Depression Rating Scale (HAM-D), the Hamilton Anxiety Rating Scale, and the Beck

226 he 17-item Hamilton Depression Rating Scale (HAM-D), the Montgomery-Asberg Depression Rating Scale (M

227 he 24-item Hamilton Depression Rating Scale (HAM-D), which was administered three times per week.

228 he 17-item Hamilton Depression Rating Scale (HAM-D).

229 S) and the Hamilton Depression Rating Scale (HAM-D).

230 he 17-item Hamilton Depression Rating Scale (HAM-D).

231 he 17-item Hamilton Depression Rating Scale (HAM-D).

232 A) and the Hamilton Depression Rating Scale (HAM-D).

233 he 17-item Hamilton Depression Rating Scale (HAM-D).

234 he 17-item Hamilton Depression Rating Scale (HAM-D).

235 ne 17-item Hamilton Depression Rating Scale (HAM-D-17) score 15 and baseline biomarker data (interleu

236 he 17-item Hamilton Depression Rating Scale (HAM-D-17) was the main outcome used in analysis of the o

237 he 17-item Hamilton Depression Rating Scale (HAM-D-17), Montgomery-Asberg Depression Rating Scale (MA

238 nge in the Hamilton Depression Rating Scale (HAM-D-24) score.

239 he 17-item Hamilton Depression Rating Scale (HAM-D; scores range from 0 to 52, with higher scores ind

240 remission (Hamilton Depression Rating Scale [HAM-D] score </=7 at weeks 10 and 12), and 24 had treatm

241 nd 21-item Hamilton Depression Rating Scale [HAM-D] score <or =8) at two consecutive weekly visits fo

242 RS] or the Hamilton Depression Rating Scale [HAM-D]) and self-report scales (the Quick Inventory of D

243 l ratings (Hamilton Depression Rating Scale [HAM-D], Symptom Checklist-90 Revised [SCL-90-R]), respec

244 0.017) and higher depression rating scores (HAM-D P = 0.020, SCL-90-R depression P = 0.008).

245 gnificantly greater reduction in mean +/- SE HAM-A total score at last-observation-carried-forward en

246 , improvement in the least-squares mean (SE) HAM-D-24 scores were similar between the active (-11.1 [

247 mptom and general psychopathology subscales, HAM-A, and HAM-D than for placebo.

248 t week-by-group interaction, indicating that HAM-D scores for citalopram-treated participants decline

249 Here, we show that HAM-1 is a novel protein and define residues important f

250 alysis of ham-1 mutant embryos suggests that HAM-1 controls only neuroblast divisions that produce ap

251 The HAM-A response (63% vs 49%, respectively, P = .001) and

252 The HAM-D response and remission rates were higher for patie

253 The HAM-D score was lower in the vardenafil group (7.9) than

254 The HAM-D was administered by telephone by raters to whom tr

255 f diverse stem cell niche locations, and the HAM family is essential for all of these stem cell niche

256 8%), the BAI score (39% versus 27%), and the HAM-d score (29% versus 9%).

257 replicated in CO-MED and was similar for the HAM-D scale.

258 riterion was 50% or greater reduction in the HAM-A total score.

259 im analysis, the change from baseline in the HAM-D score at the final visit was not significantly dif

260 The least-squares mean (+/-SE) change in the HAM-D score from baseline to day 15 was -17.4+/-1.3 poin

261 uction from baseline of more than 50% in the HAM-D score, a HAM-D score of 7 or lower, and a Clinical

262 he crossover phase was the difference in the HAM-D-17 scores between active and sham DBS.

263 e individual suicide items of the MADRS, the HAM-D, and the QIDS-SR but not the BDI.

264 ificant for the primary outcome measure, the HAM-D-6.

265 However, at 6 months the HAM-D scores did not differ between groups.

266 Moreover, the HAM-induced inhibition of BRCECs was neutralized by a sp

267 ponders to treatment (>/=50% decrease of the HAM-D-17 score compared with baseline) and partial respo

268 l responders (>/=25 but <50% decrease of the HAM-D-17 score).

269 ere was a main effect of ADM over CBT on the HAM-D (beta = -0.88; P = .03) and a nonsignificant trend

270 .6; 95% CI, 0.3-2.9; P = .02) but not on the HAM-D 17-item version (treatment effect, 1.0; 95% CI, -1

271 Higher baseline scores on the HAM-D and the Quick Inventory of Depression Symptomatolo

272 Superior improvement on the HAM-D only (odds ratio=1.67) and attrition (odds ratio=1

273 erate differences between CBT and ADM on the HAM-D or BDI or in response or remission.

274 , patients scored significantly lower on the HAM-D-17 scale (13.6 [95% CI, 9.8-17.4]) than during sha

275 Main Outcome Measure Total score on the HAM-D.

276 Mixed-effects models using the HAM-D indicated that baseline depression severity does n

277 Thus, HAM-1 regulates the position of the cleavage plane, apop

278 is thus a promising therapeutic approach to HAM/TSP with the potential of being more effective than

279 4 ACs showed atrophy in a pattern similar to HAM/TSP.

280 hat CD8(+) T cells of patients with HAM/TSP (HAM/TSP patients) spontaneously degranulate and express

281 araparesis/HTLV-1-associated myelopathy (TSP/HAM).

282 lls were expanded in patients with untreated HAM compared with asymptomatic carriers (P < .001) but l

283 While HAM/TSP patients showed a higher clonal T-cell expansion

284 TBX-2, along with HAM-1, regulates the migrations of the HSNs and prevents

285 ate of the immune activation associated with HAM/TSP.

286 with low or high pVL; 19 were diagnosed with HAM, with 10 receiving anti-inflammatory therapy.

287 provide evidence that AtPDCD5 interacts with HAM proteins, suggesting that both proteins participate

288 s GM fraction was decreased in patients with HAM and correlated with the disease severity.

289 pilot study suggests that some patients with HAM have asymptomatic inflammation in the brain, which c

290 strated that CD8(+) T cells of patients with HAM/TSP (HAM/TSP patients) spontaneously degranulate and

291 y reduced in CD4(+) T cells in patients with HAM/TSP compared with healthy donors, and the expression

292 e-center, open-label trial, 12 patients with HAM/TSP were treated with doses of interferon-beta1a of

293 ng pathway was dysregulated in patients with HAM/TSP.

294 volume of distribution for the subjects with HAM (5.44 +/- 0.84) was significantly greater than that

295 Five subjects with HAM and 2 HTLV-1 asymptomatic carriers were studied.

296 mononuclear cells (PBMCs) from subjects with HAM/TSP.

297 all individuals, particularly in those with HAM, while monocytes showed increased aggregation and CD

298 chronic subtypes of ATL, or from those with HAM/TSP whose PBMCs are associated with autocrine/paracr

299 f HTLV-1-infected patients, with and without HAM but no clinical evidence of brain involvement, were

300 essant nonresponders had significantly worse HAM-D scores over time than the placebo-treated patients