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1 TSC also dampens the intensity of an ischemic challenge
2 TSC and apparent diffusion coefficient (ADC) were calcul
3 TSC astrocytes appeared epithelial (i.e. tightly adheren
4 TSC differed between 9.63 and 29.47%.
5 TSC has a wide variety of clinical and radiologic manife
6 TSC improves the diffusion of oxygen and glucose, and in
7 TSC is associated with autism, intellectual disability a
8 TSC is found to be more effective additive in order to m
9 TSC patients with autism display impairments in white ma
10 TSC values in normal glandular and adipose breast tissue
11 t-like cells from 29 TSC skin tumors from 22 TSC subjects and identified germline and second-hit muta
15 ciated with newly formed axons, indicating a TSC-dependence of lanceolate complex maintenance and reg
20 erilisation than to UHT processing, although TSC addition increased the sediment formed by UHT proces
23 amounts of total phenolics, anthocyanins and TSC were selected for further breeding purposes to provi
25 ntainer sterilisation, while adding DSHP and TSC made the milk more unstable during in-container ster
26 tors, we show that embryogenesis of ESC- and TSC-derived embryos-ETS-embryos-depends on cross-talk in
27 thways may have therapeutic value in LAM and TSC-related diseases, and possibly in other conditions a
29 identify a new interplay between the PKD and TSC genes, with important implications for the pathophys
32 ces throughout the United States to the ASRS TSC from December 1, 2011, through February 12, 2014.
37 tors are largely unknown in the human brain, TSC patient cortical tubers were used to uncover hyperph
42 als (3.2%) than from No CA/TSC (1.7%) and CA/TSC solution (1.7%; all P < 0.05) and was not different
43 uded rice than in rice with No CA/TSC and CA/TSC solution, and solubility increased with higher amoun
44 ition of a citric acid/trisodium citrate (CA/TSC) mixture before extrusion increases iron absorption
45 absorption was significantly higher from CA/TSC-extruded meals (3.2%) than from No CA/TSC (1.7%) and
46 lubility and dialyzability were higher in CA/TSC-extruded rice than in rice with No CA/TSC and CA/TSC
47 CA/TSC-extruded meals (3.2%) than from No CA/TSC (1.7%) and CA/TSC solution (1.7%; all P < 0.05) and
48 CA/TSC-extruded rice than in rice with No CA/TSC and CA/TSC solution, and solubility increased with h
49 Iron bioavailability nearly doubled when CA/TSC was extruded with FePP into fortified rice, resultin
50 dialyzable iron from rice meals in which CA/TSC was added at different preparation stages and from m
54 GC-1beta pathway-separate from the canonical TSC-mTOR-S6K pathway-that regulates browning of adipose
57 d expression of IL-10 and TIMP-3 in CD146(+) TSCs are regulated by JNK/signal transducer and activato
58 oprotease (TIMP)-3 was expressed in CD146(+) TSCs at 1 wk with CTGF, in contrast to control with no T
62 k of a representative trophoblast stem cell (TSC) model with the capacity for self-renewal and the ab
70 d differentiation of trophoblast stem cells (TSCs) are key factors for proper placental development a
73 ) and extraembryonic trophoblast stem cells (TSCs) in a three-dimensional scaffold to generate struct
74 ablation of Gmnn in trophoblast stem cells (TSCs) proliferating in the presence of FGF4 closely mimi
76 ein EED in F1 hybrid trophoblast stem cells (TSCs), which undergo imprinted inactivation of the pater
77 converts naive tumor cells to chemoresistant TSCs, thereby facilitating their invasiveness and progre
78 odium tartarate (DST) and trisodium citrate (TSC) in the temperature range (288.15-318.15)K from the
80 e shown that the tuberous sclerosis complex (TSC) 1-TSC2-mammalian target of Rapamycin (mTOR) and the
81 nitrosylation of tuberous sclerosis complex (TSC) 2, and inhibited dimerization of TSC2 with its inhi
82 atient with both tuberous sclerosis complex (TSC) and LAM (TSC-LAM) into induced pluripotent stem cel
85 Patients with tuberous sclerosis complex (TSC) frequently develop collagenous connective tissue ne
86 by mutations in tuberous sclerosis complex (TSC) genes and is associated with insulin resistance, de
101 re a hallmark of tuberous sclerosis complex (TSC) manifestations; however, the genesis of these abnor
102 overexpressed in tuberous sclerosis complex (TSC) mice, a PI3K-mTOR model of neurodevelopmental disea
103 rowth factor and tuberous sclerosis complex (TSC) signaling, is driven by RagC/D, and is separable fr
104 mutations in the tuberous sclerosis complex (TSC) tumor suppressor genes are associated closely with
105 Loss of the tuberous sclerosis complex (TSC) tumor suppressors results in activation of mTORC1 a
106 with loss of the tuberous sclerosis complex (TSC) tumor suppressors, which exhibit growth factor-inde
107 ific deletion of tuberous sclerosis complex (TSC), a major upstream inhibitor of mTOR, surprisingly a
111 een R2TP and the tuberous sclerosis complex (TSC), pointing to a potential link between growth signal
112 ode the proteins tuberous sclerosis complex (TSC)-1 and TSC2, which are directly involved in suppress
119 ividual anthocyanin and total sugar content (TSC) of wide range of plum cultivars was done in order t
120 minals at hair follicles while, in contrast, TSCs remain associated with hair follicles following ski
123 have been analyzed, of whom 13 had definite TSC, whereas another 7 had a possible TSC diagnosis.
125 entification rate for patients with definite TSC was 85%, but only 29% for the ones with a possible T
126 he current findings demonstrate that delayed TSC treatment improves outcomes in experimental models o
127 rofiles highly similar to blastocyst-derived TSCs, with comparable methylation and H3K27ac patterns a
130 n unusual biphasic expression profile during TSC differentiation and thus may be pivotal in balancing
132 inactive X-linked genes in WT and Eed (-/-) TSCs suggests that PRC2 acts as a brake to prevent induc
133 2 targets that remain repressed in Eed (-/-) TSCs are depleted for active chromatin characteristics i
135 a classical biallelic inactivation of either TSC genes (TSC1, hamartin or TSC2, tuberin), an event th
140 teric modulators (an mGluR5 NAM and PAM) for TSC, using a mutant mouse model with neuronal loss of Ts
141 s and that HMGA2 activation was required for TSC mesenchymal tumorigenesis in genetically engineered
143 serve as a potential therapeutic target for TSC and other diseases with dysregulated mTOR activity.
147 ion, we found that stem cells generated from TSC patients had a very high rate of integration of the
150 the transcription factor networks governing TSC identity and opportunities for studying the epigenet
151 uppress IGFBP7, and this stimulates IGF1R(+) TSCs to express FGF4, inducing a feedforward FGFR1-ETS2
152 on of genes whose translation is abnormal in TSC may provide insights to previously unidentified ther
153 sis, which was also increased at baseline in TSC-deficient cells and was not affected by rapamycin tr
154 The role of mesenchymal-derived cells in TSC tumorigenesis was investigated through disruption of
155 chondrial damage, and necrotic cell death in TSC-deficient cells in a highly synergistic and cell con
156 To study aberrations of early development in TSC, we generated induced pluripotent stem cells using d
159 uggest that measures to limit UV exposure in TSC children and adults should reduce the frequency and
161 a result of mutations in TSC1/TSC2 genes in TSC patients, because we observed the reactivation of ma
165 ions for the effects of mTORC1 inhibitors in TSC, cancers, and the many other disease settings influe
166 ignalling has not been fully investigated in TSC-associated tumours and it has been uncertain whether
169 ful therapeutic potential for mGluR5 NAMs in TSC, which warrants clinical exploration and the continu
172 re employed to promote tumor pathogenesis in TSC and identify a novel, critical pathway for potential
173 ibutes to pathologic dendritic patterning in TSC in an mTOR-independent, ERK1/2-dependent manner.
175 uppressed by the RIP1/RIP3/MLKL signaling in TSC-deficient cells, and could be a promising therapeuti
176 addition, modulation of Sox21 expression in TSCs affected lineage-specific differentiation, based on
177 ression and CRISPR/Cas9-mediated knockout in TSCs showed that high Plet1 levels favour differentiatio
178 shift in preferred Elf5-binding partners; in TSCs, Elf5 interaction with Eomes recruits Tfap2c to tri
180 hair follicles are tiled and that individual TSCs host axonal endings of more than one LTMR subtype.
181 al tail-tip-derived fibroblasts into induced TSCs (iTSCs) and surmount the epigenetic barrier separat
183 report reprogramming mouse fibroblasts into TSCs, surmounting the first lineage barrier established
185 th tuberous sclerosis complex (TSC) and LAM (TSC-LAM) into induced pluripotent stem cells (iPSC), fol
188 as achieved, with high reproducibility (mean TSC values +/- standard deviation for the test, 36 mmol
189 sion was detected in 100% of human and mouse TSC tumors and that HMGA2 activation was required for TS
193 Taken together, this molecular catalogue of TSC serves as a resource into the origin of these hamart
194 e of second-hit mutations and development of TSC facial angiofibromas and suggest that measures to li
195 ged >/= 3 years with a definite diagnosis of TSC and increasing SEGA lesion size (>/=2 magnetic reson
197 on of mTORC1 through the combined effects of TSC and RHEB as part of a multiprotein complex localized
202 ible Cre-lox system to study the function of TSC in the remyelination of a focal, lysolecithin-demyel
205 Here we describe a novel mouse model of TSC which develops renal mesenchymal lesions recapitulat
208 mozygous mutant cells to the pathogenesis of TSC and the important role of p53 during reprogramming.
209 ted the role of HMGA2 in the pathogenesis of TSC using the TSC2(+/-) mouse model that similarly mirro
210 The mTOR-dependent, epithelial phenotype of TSC astrocytes suggests TSC1/2 and mTOR tune the phospho
215 d drugs that selectively affect viability of TSC-deficient cells, representing promising candidates f
216 e of grain-boundaries, the trap densities of TSCs are 10-100 folds lower than that of polycrystalline
218 ng strategies have enabled the generation of TSCs from fibroblasts, opening up exciting new avenues t
219 erformed genome-wide expression profiling of TSCs, embryonic stem cells, epiblast stem cells, and mou
222 thesis have selective deleterious effects on TSC-deficient cells, including in mouse tumor models.
227 tors based on CH3 NH3 PbBr3 and CH3 NH3 PbI3 TSCs show low noise of 1-2 fA Hz(-1/2) , yielding a high
235 2 complex (TSC1/2) cause tuberous sclerosis (TSC), a hereditary syndrome with neurological symptoms a
238 t anti-inflammatory roles of CTGF-stimulated TSCs that are likely associated with improved tendon hea
239 ame screen, as well as the more well studied TSC, 3-AP (Triapine), to determine whether they function
240 nxiety (STAI-T) and trauma-related symptoms (TSC-40) were collected; the disinhibition scale of the t
243 sted the relationship between BD-II, STAI-T, TSC-40, TFEQ, CWIT, and BMI with correlation analyses.
249 ng the spatial recruitment of mTORC1 and the TSC complex to Rheb at the lysosomal surface serve to in
250 ng mutations in either TSC1 or TSC2, and the TSC protein complex is an essential regulator of mTOR co
254 gene products hamartin and tuberin form the TSC complex that acts as GTPase-activating protein for R
256 This study provides new insights into the TSC transcriptomic network along with the identification
258 ean size, 31 mm +/- 24; range, 6-92 mm), the TSC of 69 mmol/kg +/- 10 was, on average, 49% higher tha
259 ke the existing methods, the validity of the TSC approach does not rely on any specific measurement e
260 lf5 are critical for normal expansion of the TSC compartment and embryonic survival, as Elf5 overexpr
261 lly suppresses lysosomal localization of the TSC complex and interaction with its target small GTPase
262 insulin stimulates acute dissociation of the TSC complex from the lysosomal surface, where subpopulat
265 plain the severe renal manifestations of the TSC/PKD contiguous gene syndrome and open new perspectiv
269 26 (ZMC1), belongs to the thiosemicarbazone (TSC) class of metal ion chelators that bind iron, copper
270 ed to uncover hyperphosphorylation unique to TSC primary astrocytes, the cell type affected in the br
272 hypomethylated and expressed in trophoblast (TSCs) stem cells are very rare and may have particularly
273 Here we describe genetic findings in two TSC patients with multiple renal tumors, each of whom ha
274 Sox21 levels were high in undifferentiated TSCs and were dramatically reduced upon differentiation.
278 Despite its oncogenic effect, cells with TSC deficiency were more sensitive to oxidative stress a
279 e report a case of a 36-year-old female with TSC presenting as massive hematuria with underlying gian
282 m hypomelanotic macules from 6 patients with TSC all exhibited reduced TSC2 protein expression, and 1
289 raphy was performed; 104 adult patients with TSC were enrolled in an observational cohort study that
290 risk markers and mortality in patients with TSC with that of individuals with or without coronary ar
294 detected in 50% (24 of 48) of patients with TSC; however, no MFF was detected in control patients (P
296 (median [range] age, 42 [19-70] years) with TSC (56%) had at least 1 connective tissue nevus on the
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