ライフサイエンスコーパス: TCM

1 TCM and TEM cells also required lymphoid tissue to mount

2 TCM caused a 5.7-fold induction of the -517-bp promoter

3 TCM exhibit greater plasticity and proliferative capacit

4 TCM is characterized by changes in cardiomyocyte and mit

5 TCM(Null) (TLR4(Null), CD14(Null), MD2(Null)), TLR4(Hi),

6 TCM-derived (m)C patterns are associated with reduced ex

7 TCMs enhanced IFN and LAM antiviral activities and impro

8 TCMs had a greater beneficial effect (P = 0.0003) than I

9 TCMs had a similar beneficial effect when compared with

10 The 2-TCM and the Logan analyses are accurate methods to estim

11 HABs than in MABs, and estimates from the 2-TCM and the Logan analyses were highly correlated.

12 The 2-TCM best described the regional kinetics of (18)F-DPA-71

13 tly correlated with that calculated by the 2-TCM.

14 newly methylated F1 Ler segment may act as a TCM source in a process comparable to paramutation in ma

15 This is, at least in part, mediated by a TCM-induced up-regulation and enhanced binding of C/EBPb

16 ell clone generated in the skin, an abundant TCM cell clone bearing the identical TCR was present in

17 Among the active TCMs, we discovered that baicalein, a specific flavonoid

18 e (-317/-304 bp) abolished both baseline and TCM-induced activities.

19 L497Y-S750Q mutations abolished all CTZ and TCM actions without disrupting CX614 activity.

20 CTZ and TCM further slowed desensitization of L/Y mutant recepto

21 Results indicate that CTZ and TCM target deactivation and agonist potency independentl

22 Null), CD14(Null), MD2(Null)), TLR4(Hi), and TCM(Hi) cells and human bronchial epithelial cells with

23 ired for their homeostatic proliferation and TCM-mediated suppression of allograft rejection.

24 s CD62Lhigh central memory T cells (TCM) and TCM cells after L. monocytogenes infection, and both sub

25 ge about all the differences between TEM and TCM cells that may influence tumor treatment outcomes.

26 at distinguish them from circulating TEM and TCM cells.

27 ls upregulate Bcl-6 and co-initiate TFH- and TCM-like gene programs, including expression of the cyto

28 ment and reversal of HIV-1 latency in TN and TCM CD4(+) T cells and suggest that each subset should b

29 TN and TCM cells are distinct cell populations distinguished by

30 on of HIV-1 integration sites between TN and TCM cells that accounted for these observed differences.

31 s direct infection of highly purified TN and TCM cells to address differences in the establishment an

32 to naive and central memory T cells (TN and TCM), hypoxia enhances the proliferation, viability, and

33 HIF1A mRNA in glycolytically inactive TN and TCM.

34 tivity compared with that observed in TN and TCM.

35 n be distinguished by their localization, as TCM home to secondary lymphoid organs and TEM circulate

36 n also required the presence of TGFbeta1, as TCM cells expressed TGFbeta1 while neutralizing TGFbeta1

37 of bismuth shields; and (f) with organ-based TCM and one bismuth shield.

38 Organ-based TCM provided superior image quality to that with bismuth

39 A combination of organ-based TCM with one bismuth shield reduced the dose by 47.0%.

40 h one bismuth shield, 30.4% with organ-based TCM, and 30.2% with a global reduction in tube current.

41 one bismuth eye shield; (c) with organ-based TCM; (d) with reduced tube current to yield the same dos

42 Because TCM are located within B cell follicles in the spleen wh

43 sion profiling revealed similarities between TCM-exposed hMSCs and CAFs.

44 totally 222 parameters integrated from both TCM practice and modern clinical tests.

45 , was determined from a fragment produced by TCM.

46 Both bystander TCM and naive T cells, but fewer TEM cells, migrated to

47 eover, the suppression mediated by bystander TCM cells was largely dependent on IL-15, as IL-15 was r

48 aive counterparts, suggesting that bystander TCM cells have an advantage over their naive counterpart

49 Thus, bystander TCM, but not TEM, CD8+ T cells are potent suppressors ra

50 l-CoA, is used to initiate tetracenomycin C (TCM C) biosynthesis.

51 trate the safety and feasibility of CD19 CAR TCM therapy after HSCT.

52 pathy or tachycardia-induced cardiomyopathy (TCM) has been known for decades as a reversible form of

53 In conclusion, among CD4 TCM cells in PB of aviremic patients on cART, pTfh cells

54 peripheral blood and contain a subset of CD4 TCM cells expressing chemokine receptor CXCR5 similar in

55 CD4(+) TCM cells of sooty mangabeys (SMs), a natural host for S

56 s and RMs and the association between CD4(+) TCM levels and the main virologic and immunologic marker

57 IV DNA increase postdepletion in both CD4(+) TCM and TEM in progressor RMs but decrease in the CD4(+)

58 increased percentages of circulating CD4(+) TCM cells, (ii) increased levels of CD4(+) T cells in th

59 h of time of SIV infection needed for CD4(+) TCM cells to fall to half of their initial levels is <16

60 ir lower susceptibility to infection, CD4(+) TCM cells of SIV-infected SMs are lost with kinetics 20

61 ART despite lower infection levels of CD4(+) TCM and TSCM cells than those seen in pathogenic SIV inf

62 n SIV-infected RMs, and the extent of CD4(+) TCM cell proliferation is associated positively with CD4

63 mechanistic link between the loss of CD4(+) TCM cells and disease progression.

64 tenance of the prohomeostatic role of CD4(+) TCM cells as features distinguishing nonprogressive from

65 lly and longitudinally, the levels of CD4(+) TCM cells in a large cohort of SMs and RMs and the assoc

66 ranslates into increased stability of CD4(+) TCM cells in natural versus nonnatural hosts has not yet

67 mportance of long-term maintenance of CD4(+) TCM homeostasis during HIV/SIV infection.

68 SMs translate into a better-preserved CD4(+) TCM compartment.

69 ermore, the fraction of proliferating CD4(+) TCM cells is significantly lower in SIV-infected SMs tha

70 ess susceptible to SIV infection than CD4(+) TCM cells of RMs.

71 or this cell loss, we also found that CD4(+) TCM cells increase their level of proliferation upon SIV

72 We found that the CD4(+) TCM compartment is significantly more stable in SIV-infe

73 n progressor RMs but decreased in the CD4(+) TCM of 4 out of 5 controllers.

74 in progressor RMs but decrease in the CD4(+) TCM of controllers.

75 istent with a model whereby intrahepatic CD8 TCM cells, being maintained by IL-15-mediated survival a

76 -lived, mainly owing to the inability of CD8 TCM cells to survive in the IL-15-deficient milieu.

77 CD122 (IL-15Rbeta), which suggests that CD8 TCM cells depend on IL-15 for maintenance.

78 and clonotypically diverse CD4(+) and CD8(+) TCM populations might potentially improve adaptive immun

79 s engineered from enriched CD4(+) and CD8(+) TCM subsets and expressing a second-generation CD19 CAR

80 in Lck constitutive activity between CD8(+) TCM and TEM are due to differential regulation by SH2 do

81 The CD4(+)/CD8(+) TCM-derived CD19 CAR T cells (NHL2) exhibited improvemen

82 ell products engineered from enriched CD8(+) TCM subsets, expressing a first-generation CD19 CAR cont

83 In vitro, CD8(+) TRM cells, but not CD8(+) TCM cells, demonstrated increased mitochondrial oxidativ

84 EM cell epitopes, but not with "SYMP" CD8(+) TCM cell epitopes, induced a strong CD8(+) T cell-depend

85 EM cell epitopes, but not with "SYMP" CD8(+) TCM cell epitopes, induced a strong protective HSV-speci

86 such as effector/memory (CD4(+)TEM and CD8(+)TCM) and regulatory (T reg) T cells.

87 ates central and effector memory CD8 T cell (TCM and TEM, respectively) homeostatic proliferation, ma

88 omising effect on the central memory T cell (TCM) population (both CD4(+) and CD8(+)) in adult and ol

89 as central and transitional memory T cells (TCM and TTM, respectively).

90 ifferentiated central memory CD8(+) T cells (TCM cells) (CD45RA(low) CCR7(high) CD44(low) CD62L(high)

91 onofunctional central memory CD8(+) T cells (TCM cells) (CD45RA(low) CCR7(high) CD44(low) CD62L(high)

92 as well as CD62Lhigh central memory T cells (TCM) and TCM cells after L. monocytogenes infection, and

93 apidly expand CD8(+) central memory T cells (TCM) during the acute phase of the primary response that

94 y T cells (T(EM)) to central memory T cells (TCM) following vaccination.

95 er, we show that central memory CD4 T cells (TCM) from HIV-infected individuals have heightened expre

96 autologous central memory-enriched T cells (TCM) transduced with lentivirus expressing CD19-specific

97 ), but not of central memory CD8(+) T cells (TCM), locally within TG, and improved protection against

98 nsidered to comprise central memory T cells (TCM), which are restricted to the secondary lymphoid tis

99 no-PET imaging human central memory T cells (TCM), which were transgenic for a myeloid peroxidase (MP

100 ompared with <20% in central memory T cells (TCM).

101 A in CD4(+) TSCM and central memory T cells (TCM-) did not significantly change.

102 y of CCR7+ L-selectin+ central memory cells (TCMs).

103 ry CD4(+) T cells, specifically the central (TCM) and transitional memory compartments, harbor the hi

104 chloroethene (TCE) 45 vol %, and chloroform (TCM) 10 vol %).

105 Blood SigmaTHM [sum of chloroform (TCM), bromodichloromethane (BDCM), dibromo-chloromethane

106 belonged to the central-memory compartment (TCM).

107 that only the purified complex complemented TCM PKS activity in protein extracts made from strains b

108 In contrast, TCM cells, but not TEM cells, mounted a robust response

109 In contrast, TCM diapedesis did not require CXCL12 but was blocked by

110 CTZ, TCM, or L/Y mutation all essentially blocked GluR1 desen

111 sduced primary CD4(+)model, and the cultured TCM(central memory) CD4(+)model.

112 ntly more effective than nCPCs, aCPC-derived TCM, or nCPC-derived exosomes in recovering cardiac func

113 argeted by nCPC-derived TCM and aCPC-derived TCM, respectively.

114 derived TCM and 513 proteins in aCPC-derived TCM.

115 r nCPC-derived TCM but none for aCPC-derived TCM.

116 sion pattern of 804 proteins in nCPC-derived TCM and 513 proteins in aCPC-derived TCM.

117 were significantly targeted by nCPC-derived TCM and aCPC-derived TCM, respectively.

118 cting 8 identified pathways for nCPC-derived TCM but none for aCPC-derived TCM.

119 esent in S. glaucescens fermentations during TCM C production, suggesting that it could contribute to

120 This enzyme was shown to be present during TCM C production and could play a role in generating mal

121 RCTs comparing either TCM formulations alone or in combination with interferon

122 Engineered TCM-derived CD19 CAR T cells were infused 2 days after H

123 IV-dependent sRNAs are required to establish TCM events.

124 After extravasation, TCMs displayed agile movement within BM cavities, remain

125 e components from Indigo naturalis, a famous TCM herb that has been widely used for the treatment of

126 As negative training samples for TCM learning we used coding and intron sequences of plan

127 archical classification model was tested for TCM syndromes prediction based on totally 222 parameters

128 (BDCM, 0.62; DBCM, 0.53; TBM, 0.54) than for TCM (0.37).

129 A is not used directly as a starter unit for TCM C biosynthesis in vivo and argue against an involvem

130 s, the BM functions as a major reservoir for TCMs by providing specific recruitment signals that act

131 l ester, which is the biomarker derived from TCM of anthrose.

132 n complex formed by the nuclear extract from TCM-treated HAFs and a probe containing this critical C/

133 nstrate that specific plant metabolites from TCMs can directly interfere with key bacterial virulence

134 romoter use from I.4 to II in cultured HAFs, TCM-induced promoter II use was found to be mediated via

135 monocytes or TLR4 expressing cell lines (HEK-TCM) abrogates the respective inflammatory signal.

136 he use of a PA projection resulted in higher TCM values for chest CT (P < .001) owing to the higher a

137 ection localizer radiography owing to higher TCM values, whereas the organ doses from PA localizer ra

138 In TCM/TCdM the methylation state of one allele is altered

139 ts in increased constitutive Lck activity in TCM to levels similar to TEM, as well as increased cytot

140 fficiently characterize active components in TCM and their targets, which may bring a new light for a

141 l growth as efficiently as hMSCs cultured in TCM nor do they show increased SDF-1 expression.

142 as increased cytotoxic effector function in TCM Collectively, this work demonstrates a role for cons

143 However, essential ingredients in TCM herbs have not been fully identified, and their prec

144 of mitochondria was predominantly present in TCM.

145 and macrophages was significantly reduced in TCM.

146 Increased expression of redox regulators in TCM cells inversely correlated with the generation of re

147 o define the physical meaning of yin-yang in TCM by correlating it with biochemical processes.

148 roduced per infected TN cell as per infected TCM cell.

149 s to the lungs and lymph nodes by inhibiting TCM-induced lymphangiogenesis and angiogenesis in the pr

150 we investigated Sini Decoction, a well-known TCM consisting of three herbs, as a model.

151 Thus, antigen-reactive skin TRM and LN TCM cell clones were derived from a common naive T cell

152 kin simultaneously generates skin TRM and LN TCM cells in similar numbers from the same naive T cells

153 in both CD4(+) central memory T lymphocytes (TCM) and CD4(+) effector memory T lymphocytes (TEM) in p

154 y developed transductive confidence machine (TCM) techniques, we developed a new program TSSP-TCM for

155 model system [tumor-conditioned macrophages (TCM)].

156 Compared with normal macrophages, TCMs exhibited higher p53 levels, enhanced p53 binding t

157 earing tcmK or tcmL deletion mutants to make TCM F2 in vitro, and that the molecular mass of the puri

158 the minimal set of proteins required to make TCM F2 included the ketosynthase complex (TcmKL), an acy

159 es: (1) transparency change mechanochromism (TCM), (2) luminescent mechanochromism (LM), (3) colour a

160 ence of either tumor cell conditioned media (TCM) or tumor cells.

161 negative MDA-MB-231 tumor-conditioned media (TCM) to determine the factors that may be secreted by va

162 MDA-MB-231 tumor conditioned media (TCM) was employed to accelerate spontaneous metastasis i

163 essful cases, Traditional Chinese Medicinal (TCM) formulae can achieve synergistic effects in therape

164 onal medicine, Traditional Chinese Medicine (TCM ), Ayurveda, naturopathy, chiropractic, osteopathy,

165 omarker panel, traditional Chinese medicine (TCM) drug intervention for validating the close relation

166 Traditional Chinese Medicine (TCM) has been developed for thousands of years and has f

167 Ancient traditional Chinese medicine (TCM) has effectively relied on the theory of yin-yang ba

168 Traditional Chinese medicine (TCM) practices have put forth Shenks as a promising trea

169 Traditional Chinese Medicine (TCM) treatment has been commonly used to treat Chronic H

170 ed efficacy of traditional Chinese medicine (TCM) treatment in Dutch children with asthma in areas wi

171 acteristics of traditional Chinese medicine (TCM) used to treat pediatric asthma, we conducted a nati

172 o characterize traditional Chinese medicine (TCM), as part of the "herbalome" project, with the rever

173 d treatment in traditional Chinese medicine (TCM), is a major indicator of the occurrence, developmen

174 development of traditional Chinese medicine (TCM), we conducted a systematic review and meta-analysis

175 Traditional Chinese Medicines (TCMs) have been historically used to treat bacterial inf

176 enturies with traditional Chinese medicines (TCMs).

177 T47D breast cancer cell-conditioned medium (TCM) as a model system.

178 hibitory effect of tumor-conditioned medium (TCM) on LPS-induced CCL5 expression.

179 (hMSCs) exposed to tumor-conditioned medium (TCM) over a prolonged period of time assume a CAF-like m

180 : effector memory (TEM ) and central memory (TCM ).

181 t overall generation of both central memory (TCM) and effector memory (TEM) CD8+ T cells was severely

182 mory (TEM), and longer-lived central memory (TCM) and stem cell memory (TSCM) CD8 T cells identified

183 evels of infection of CD4(+) central memory (TCM) and stem cell memory (TSCM) T cells.

184 Central memory (TCM) CD4 T cells are the major cellular reservoir for HI

185 ed the peripheral blood (PB) central memory (TCM) CD4(+) T cell subsets designated peripheral T folli

186 Central memory (TCM) CD4(+) T cells are the principal reservoir of laten

187 y cells, particularly in the central memory (TCM) cell subset.

188 affecting CCR7(+) naive and central memory (TCM) cells has the potential of treating TEM-mediated di

189 irst evidence that bystander central memory (TCM), but not effector memory (TEM), CD8+ T cells suppre

190 bited a resting phenotype of central memory (TCM), while peptide-specific CD8(+) T cells showed a mor

191 +)CD45RO(+)IL-4(+) producing central memory (TCM, CD45RO(+)CCR7(+)CD27(+); Fo = 1.1% versus 0.5%; p =

192 nctions in the presence of either metastatic TCM or metastatic tumor cells.

193 methylome are Trans Chromosomal Methylation (TCM) and Trans Chromosomal deMethylation (TCdM) in which

194 the processes trans-chromosomal methylation (TCM) and trans-chromosomal demethylation (TCdM).

195 roach for CLCA, the Technology Choice Model (TCM).

196 ors adapted from the temporal context model (TCM).

197 The present tissue contrast model (TCM) can be applied to "conventional," targeted, or bioc

198 sing the 1- and 2-tissue-compartment models (TCMs) as well as the Logan analysis to estimate total vo

199 omography (CT) with tube current modulation (TCM).

200 tions at the CO2 Technology Center Mongstad (TCM), Norway.

201 conducted to evaluate differences in noise, TCM curves, and organ doses, respectively.

202 sers was significantly more than that of non-TCM users in school-age children.

203 Importantly, the survival of TEM, but not TCM, CD8+ cells was reduced without MCP-1, whereas the h

204 retrospectively fulfilled common criteria of TCM, 79 patients had a diagnosis of DCM, and 91 had a di

205 L5 inhibition, and the inhibitory effects of TCM, PGE(2), and cAMP analog on LPS-induced CCL5 express

206 t a unique mechanism to secure engagement of TCM during an ongoing effector response.

207 ells differentiated to higher frequencies of TCM at low doses of MP Rapa MPs.

208 improve the cytotoxic effector functions of TCM for adoptive cell therapy applications.

209 reover, the function to eliminate a graft of TCM, but not TEM, CD8+ cells was impaired without MCP-1.

210 ng that it could contribute to initiation of TCM C biosynthesis in vivo.

211 ssification based on a proper integration of TCM and modern clinical indexes was significantly higher

212 Interestingly, the migration of TCM, but not TEM, CD8+ cells to inflammatory sites was s

213 The number of TCM users was significantly more than that of non-TCM us

214 II complex, produces TCM F2, a precursor of TCM C in Streptomyces glaucescens, and consists of at le

215 hat this results from a lower probability of TCM reaching threshold signaling owing to the decreased

216 unction, greatly increased the production of TCM F2 but could not replace TcmN as a cyclase in the re

217 PKS, was not required for the production of TCM F2 in vitro, although it could be incorporated into

218 Conversely, cytokine-driven proliferation of TCM and TSCM memory cells resulted in phenotypic convers

219 -1, whereas the homeostatic proliferation of TCM, but not TEM, CD8+ cells was weakened in MCP-1-/- mi

220 lishing the divergent effector properties of TCM and TEM.

221 ts of randomized controlled trials (RCTs) of TCM formulations reported in China in 1998-2008 for trea

222 ike EBV, includes a substantial reservoir of TCM CD4+ TH1 precursors, which continuously fuels TH1-po

223 ese pTfh cells, which constitute a subset of TCM CD4 T cells, can be readily monitored in peripheral

224 of deuterium label into the starter unit of TCM C.

225 tics and prescription patterns of the use of TCM in children with asthma.

226 e to mediate the constitutive recruitment of TCMs from the blood.

227 s with CHB, suggesting that further study of TCMs in the treatment of CHB is warranted, both in precl

228 epatitis B (CHB) in Asian countries based on TCM syndrome diagnosis, also called "ZHENG".

229 cturally related flavonoids present in other TCMs, such as quercetin, also inactivated the SPI-1 T3SS

230 cells with a central memory-like phenotype (TCM cells).

231 ze T cells toward central memory phenotypes (TCM), or to suppress immune function, depending on the c

232 The most commonly prescribed TCM formula is Ding-chuan-tang, or Xing-ren (Semen Armen

233 thase (TCM PKS), a type II complex, produces TCM F2, a precursor of TCM C in Streptomyces glaucescens

234 ovar Typhimurium, we discovered that several TCMs can attenuate this key virulence pathway without af

235 Conclusion: Some TCMs seem effective as alternative remedies for patients

236 P doses, vaccines increased antigen-specific TCM, resulting in enhanced T cell expansion measured dur

237 mokine receptor analysis, all EBNA1-specific TCM CD4+ T cells were TH1 committed.

238 The tetracenomycin polyketide synthase (TCM PKS), a type II complex, produces TCM F2, a precurso

239 evelopmentally related central memory CD8 T (TCM) cells express elevated levels of CD122 (IL-15Rbeta)

240 Depletion of CD4(+) central memory T (TCM) cells dictates the tempo of progression to AIDS in

241 Central memory T (TCM) cells in lymph nodes (LNs) and resident memory T (T

242 effect on the survival of central memory T (TCM) cells in lymph nodes.

243 ing feature is that CD4(+) central memory T (TCM) cells in SIV-infected SMs are less infected than th

244 ollicular helper (TFH) and central memory T (TCM) cells.

245 by the TcmI protein from the tetracenomycin (TCM) C pathway in Streptomyces glaucescens, where a tric

246 IV-1 infected TN cells less efficiently than TCM cells.

247 EC-mediated tumor growth, we discovered that TCM-treated LEC ('tumor-educated LEC') secrete high amou

248 Given that TCM cells survive relatively longer in oxidative tumor m

249 onments, we investigated the hypothesis that TCM cells possess relatively greater antioxidative capac

250 The study results indicate that TCM treatment of children living in more polluted urban

251 Here, we report that TCM cells exhibit a relative increase compared with TEM

252 Intravital microscopy (IVM) showed that TCMs roll efficiently in BM microvessels via L-, P-, and

253 The TCM device can reversibly switch between transparent and

254 The TCM is a particularly useful tool in the development of

255 The TCM PKS activity was reconstituted with purified protein

256 At At1g64790 the TCM- and TCdM-derived (m)C patterns are maintained in th

257 al, they produced as many virions as did the TCM cells (if not more virions).

258 Examining the TCM, we quantified changes in the expression pattern of

259 cetyl-CoA, the proposed starter unit for the TCM PKS, was not required for the production of TCM F2 i

260 genes including Bcl6 and Cxcr5, but not the TCM-related genes Klf2 and Sell.

261 As an example of the applicability of the TCM, we test it against in vivo magnetic resonance micro

262 routinely believed to be unrelated with the TCM syndrome diagnosis.

263 he importance of latent infection within the TCM compartment and again focus attention on these cells

264 were generated by one-step thermochemolysis (TCM) at 140 degrees C in 5 min to provide specific bioma

265 Thus, TCM technique has produced a plant-oriented promoter pre

266 es in modern medicine could be beneficial to TCM syndrome diagnostics in an integrative way.

267 e, polarizing vaccine-induced T cells toward TCM is an intriguing strategy to enhance T cell expansio

268 larization of differentiating T cells toward TCM.

269 Adoptively transferred TCMs accumulated more efficiently in the BM than naive a

270 of cyclothiazide (CTZ), trichlormethiazide (TCM), and CX614 were compared at wild-type GluR1 and "no

271 TSSP-TCM program and annotated promoters are available at htt

272 techniques, we developed a new program TSSP-TCM for the prediction of plant promoters that also prov

273 Using TSSP-TCM program we annotated promoters in the whole Arabidop

274 7-fold for CD4(+) transitional memory [TTM], TCM, effector memory [TEM], and TSCM cells, respectively

275 We examined two loci that undergo TCM/TCdM in the Arabidopsis C24/Landsberg erecta (Ler) F

276 ed, and 57.95% (N = 26 585) of them had used TCM.

277 igated with Monte Carlo simulations by using TCM curves with fixed start angles (0 degrees , 90 degre

278 ut fewer TEM cells, migrated to DLN, whereas TCM cells exhibited faster turnover than their naive cou

279 contact hypersensitivity responses, whereas TCM cells mediated delayed and attenuated responses.

280 in TEM following TCR ligation compared with TCM Furthermore, we observed superior cytotoxic effector

281 toxic effector function in TEM compared with TCM, and we provide evidence that this results from a lo

282 Chest CT with TCM was performed after one localizer radiographic exami

283 Finally, treatment of HAFs with TCM strikingly induced C/EBPbeta expression, whereas thi

284 myocardial biopsy samples from patients with TCM and compared them with samples from patients with di

285 are warranted to characterize patients with TCM by endomyocardial biopsy more clearly.

286 significantly lower degree in patients with TCM compared with patients with DCM and ICM.

287 Patients with TCM, on the basis of clinical criteria, had stronger myo

288 d severe structural changes in patients with TCM.

289 ees ; for chest CT, a spiral trajectory with TCM was used.

290 Upon treatment with TCM, HAFs displayed a striking induction of P450arom mRN