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-D scores at the end of treatment were significantly

4 HAM/TSP patients develop antibodies to neurons.

5 HAM/TSP patients had significantly elevated levels of ne

6 HAM/TSP patients had significantly higher Ab responses f

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

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

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

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

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

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

15 17 asymptomatic carriers of HTLV-1 (AC), 47 HAM/TSP, 74 relapsing-remitting MS [RRMS], 17 secondary

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

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

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

19 re severe MDD subgroup defined a priori by a HAM-D score of at least 18 and history of 2 or more prio

20 to the native peptide in bulk PBMC of HLA-A2 HAM/TSP patients.

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

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

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

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

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

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

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

28 In the latter 2 groups, both CGI-I and HAM-D measures were significantly better in those assign

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

30 ry (BDI), Hamilton Rating Scale for Anxiety (HAM-A), the Global Assessment of Function (GAF) scale, a

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

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

33 of associated inflammatory diseases such as HAM/TSP.

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

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

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

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

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

39 Both HAM/TSP patients followed longitudinally showed thoracic

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

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

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

43 e random coefficient analyses for the HAM-D, HAM-A, CGI-S, and CGI-I all showed significant effects f

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

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

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

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

48 7-item Hamilton Rating Scale for Depression (HAM-D) rating of 18 or higher, and antidepressant-naive

49 e, and Hamilton Rating Scale for Depression (HAM-D).

50 7-item Hamilton Rating Scale for Depression (HAM-D-17).

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

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

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

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

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

56 In neuronal extracts, HAM/TSP immunoglobulin G identified heterogeneous nuclea

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

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

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

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

61 atment or time-by-treatment interaction (for HAM-D scores, P<.001, P =.16, and P =.58, respectively).

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

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

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

65 Immunoglobulin G isolated from HAM/TSP patients identified heterogeneous nuclear ribonu

66 spinal fluid-derived CTL and bulk PBMC from HAM/TSP patients by altered peptide ligands (APL) derive

67 PEDF primers amplified a single product from HAM RNA.

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

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

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

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

72 1 or BDI score >/=31), superior improvement (HAM-D or BDI decrease >/=95%), and superior response (po

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

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

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

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

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

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

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

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

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

82 e maintenance of viral-specific CD8 cells in HAM/TSP.

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

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

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

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

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

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

89 interferon-gamma, a predominant cytokine in HAM/TSP.

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

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

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

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

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

95 fected cells (mRNA/DNA ratio) were higher in HAM/TSP patients than in asymptomatic HTLV-1 carriers.

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

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

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

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

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

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

102 e responses and high HTLV-I proviral load in HAM/TSP.

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

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

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

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

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

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

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

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

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

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

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

114 vation of the IDO pathway may play a role in HAM/TSP.

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

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

117 oad also correlated with disease severity in HAM/TSP patients.

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

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

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

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

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

123 Jamaican HAM/TSP patients (n=17) were compared with patients with

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

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

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

127 infection primes human alveolar macrophages (HAM) for tumor necrosis factor alpha (TNF-alpha)-mediate

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

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

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

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

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

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

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

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

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

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

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

139 TLV-I) causing HTLV-I-associated myelopathy (HAM)/tropical spastic paraparesis (TSP)] and subcortical

140 in the disease HTLV-1-associated myelopathy (HAM/TSP).

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

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

143 basis underlying antiangiogenic activity of HAM.

144 cells was also increased in CD8(+) cells of HAM/TSP, compared with those in HLA-DR(+)CD8(+) cells of

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 Using ex vivo cultures of HAM/TSP peripheral blood mononuclear cells, we demonstra

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

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

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

151 (SP) is one of the immunologic hallmarks of HAM/TSP and is considered to be an important factor rela

152 The elucidation of the immunopathology of HAM/TSP will enhance our understanding of other HTLV-I-a

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

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

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

156 The potential mechanisms of HAM/TSP pathogenesis were assessed by examination of 2 p

157 nantly localized in the basement membrane of HAM.

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

159 ays an important role in the pathogenesis of HAM/TSP, and the HTLV-1 tax mRNA level could be a useful

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

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

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

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

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

165 mimicry plays a role in the pathogenesis of HAM/TSP.

166 ortant factor related to the pathogenesis of HAM/TSP.

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

168 s faithfully model the apoptosis response of HAM.

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

170 %), and nonresponse (62.5%) or in changes on HAM-D scores.

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

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

173 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

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

175 ted myelopathy/tropical spastic paraparesis (HAM/TSP) and chronic Lyme neuroborreliosis.

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

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

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

179 ted myelopathy/tropical spastic paraparesis (HAM/TSP) based on newly developed molecular and immunolo

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

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

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

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

184 ted myelopathy/tropical spastic paraparesis (HAM/TSP) is associated with immunoreactivity to HTLV-I t

185 ted myelopathy/tropical spastic paraparesis (HAM/TSP) proliferate spontaneously in vitro.

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

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

188 ted myelopathy/tropical spastic paraparesis (HAM/TSP), a disease that can be indistinguishable from M

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

205 /=95%), and superior response (posttreatment HAM-D or BDI score of 0) using multilevel models.

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

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

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

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

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

211 n scores remained consistent with remission (HAM-D score < or =10) in both groups for the study durat

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

244 ntially, more so with venlafaxine (mean [SD] HAM-D scores at pretreatment: IPT, 22.7 [2.7], and venla

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

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

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

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

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

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

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

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

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

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

255 8%), the BAI score (39% versus 27%), and the HAM-d score (29% versus 9%).

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

257 The random coefficient analyses for the HAM-D, HAM-A, CGI-S, and CGI-I all showed significant ef

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

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

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

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

264 zed sample, the CGI-I (P =.049), but not the HAM-D (P =.14), favored sertraline.

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

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

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

268 .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

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

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

271 ry outcome measure was rate of change on the HAM-D over the treatment period.

272 lar adverse events, as well as scores on the HAM-D scale and Clinical Global Impression Improvement s

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

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

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

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

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

278 4 ACs showed atrophy in a pattern similar to HAM/TSP.

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

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

281 n in the central nervous system (CNS) of TSP/HAM patients demonstrates the ability of HTLV-1 to cross

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

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

284 immune response to which is associated with HAM/TSP.

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

286 viral peptide/MHC complex in a patient with HAM/TSP.

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

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

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

290 Antibodies isolated from patients with HAM/TSP and monoclonal antibodies (MAbs) to HTLV-I tax s

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 ctor of disease progression in patients with HAM/TSP.

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

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

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

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