ライフサイエンスコーパス: IVD

1 The lumbar vertebral level 4/5 IVDs harvested from 15-day-, 4- and 24-month-old mice we

2 ng the known self-associating tripeptide, Ac-IVD, as a structural template.

3 Active IVD Ala282Val, Val342Ala, Arg363Cys, and Arg382Leu mutan

4 relate with age, and increase with advancing IVD degeneration.

5 to treat IVD degeneration and to ameliorate IVD-associated chronic low back pain.

6 ed from potato tubers and confirmed to be an IVD.

7 -methylbutyryl-CoA dehydrogenase (2MBCD) and IVD substrate binding pockets are nearly identical, 2MBC

8 actions of bFGF and FGF-18 in articular and IVD cartilage, the specific cell surface receptors bound

9 cts in both human articular chondrocytes and IVD tissue via upregulation of matrix-degrading enzyme a

10 ze the 3D morphology changes of endplate and IVD during aging using PPCST.

11 Concordance between the EVD and IVD images and gain or loss of colors, structures, and v

12 prevalence the underlying causes of LBP and IVD degeneration are not well understood.

13 staining for differential expression between IVD tissue regions and among various ages (1, 12 and 21

14 * = 0.94 [95% CI, 0.88 to 1.0]), followed by IVD-drawn quantitative [corrected] blood culture (Q* = 0

15 differentiated, human pluripotent stem cell (IVD hPSC)-derived cells, which may better model human ph

16 ells within the IVD, specifically, mast cell-IVD cell interactions using immunohistochemistry and 3D

17 bservational study collected 101 consecutive IVD and EVD images of skin tumors from a private dermato

18 e was generally similar to the corresponding IVD image but clearly darker, with new areas of blue in

19 f EVD images with those of the corresponding IVD images.

20 ssification and hypertrophy of EP, decreased IVD volume and increased activation of TGFbeta.

21 degenerate (pH 6.8) and severely degenerate IVD (pH 6.5 and 6.2).

22 e processes that characterize the degenerate IVD, making them a potential therapeutic target for LBP.

23 idic pH, similar to that found in degenerate IVDs, leads to the altered cell/functional phenotype obs

24 ta1 heterodimer was unaltered in degenerated IVD tissue as compared with normal IVD tissue.

25 n was significantly decreased in degenerated IVD, and the expression levels of PN-1 were correlated w

26 thways are altered in cells from degenerated IVDs.

27 ls from nondegenerated, but not degenerated, IVDs.

28 o human isovaleryl-coenzyme A dehydrogenase (IVD), an enzyme involved in the breakdown of the amino a

29 Isovaleryl-CoA dehydrogenase (IVD) belongs to an important flavoprotein family of acyl

30 Isovaleryl-CoA dehydrogenase (IVD) is a homotetrameric mitochondrial flavoenzyme which

31 Isovaleryl-CoA dehydrogenase (IVD) is an intramitochondrial homotetrameric flavoenzyme

32 deficiency of isovaleryl-CoA dehydrogenase (IVD), a nucleus-encoded, homotetrameric, mitochondrial f

33 ogenase (GCD), isovaleryl-CoA dehydrogenase (IVD), and ACAD10/11.

34 lu254 in human isovaleryl-CoA dehydrogenase (IVD), and Glu261 in human long chain acyl-CoA dehydrogen

35 deficiency of isovaleryl-CoA dehydrogenase (IVD).

36 thods for diagnosis of intravascular device (IVD)-related bloodstream infection.

37 ntestinal (GI) pathogen in vitro diagnostic (IVD) assay in a comparison between clinical and public h

38 lyclonal-antibody-based in vitro diagnostic (IVD) kit for histoplasma antigen detection was released,

39 ent assay (ELISA)-based in vitro diagnostic (IVD) procedure has been developed for human fetuin A (HF

40 OF MS systems and their in vitro diagnostic (IVD), research-use-only, and Security-Relevant databases

41 e-only (RUO) v.4.12 and in vitro-diagnostic (IVD) v.3.0 databases accurately identified 41 Mycobacter

42 Two FDA-approved (in vitro diagnostic [IVD]) hepatitis B virus (HBV) viral load assays, the man

43 nctional changes in the intervertebral disc (IVD) and interaction with endplate is essential to eluci

44 lation of articular and intervertebral disc (IVD) cartilage homeostasis.

45 for homeostasis of the intervertebral disc (IVD) cell matrix, with physiologic and nonphysiologic lo

46 d biologic responses of intervertebral disc (IVD) cells to loading, although the mechanotransduction

47 Intervertebral disc (IVD) degeneration and associated spinal disorders are le

48 economic importance and intervertebral disc (IVD) degeneration has been implicated in its pathogenesi

49 The aetiology of intervertebral disc (IVD) degeneration remains poorly understood.

50 in the pathogenesis of intervertebral disc (IVD) degeneration.

51 and is often linked to intervertebral disc (IVD) degeneration.

52 us pulposus (NP) of the intervertebral disc (IVD) demonstrates substantial changes in cell and matrix

53 Intervertebral disc (IVD) disorder and age-related degeneration are believed

54 nucleus pulposus of the intervertebral disc (IVD) during maturation.

55 he main pathogenesis of intervertebral disc (IVD) herniation involves disruption of the annulus fibro

56 Recurrence of intervertebral disc (IVD) herniation is the most important factor leading to

57 abolic growth factor on intervertebral disc (IVD) matrix and cell homeostasis.

58 Narrowed intervertebral disc (IVD) space is a characteristic of IVD degeneration.

59 ess measurements of the intervertebral disc (IVD) taken throughout the day and their relationship wit

60 xpression in pathologic intervertebral disc (IVD) tissues.

61 ildly affected, but the intervertebral disc (IVD) was reduced or missing.

62 n this condition is the intervertebral disc (IVD), which frequently herniates, ruptures, or tears, of

63 Intervertebral discs (IVD) are essential components of the vertebral column.

64 us (NP) cells from the intervertebral discs (IVD) of bovine tails were transfected with a miR-146a mi

65 ected in isolated goat intervertebral discs (IVD).

66 derately affected, the intervertebral discs (IVDs) were either missing or incomplete.

67 date, approaches for replacement of diseased IVD have been confined to purely mechanical devices desi

68 otic environment in the intervertebral disk (IVD) as interstitial water is expressed from the tissue.

69 in the pathogenesis of intervertebral disk (IVD) degeneration.

70 Degeneration of the intervertebral disk (IVD) is a major pathological process implicated in low b

71 to be elucidated in the intervertebral disk (IVD).

72 lecular characteristics of disc cells during IVD maturation and aging still remain poorly defined.

73 ed cell/functional phenotype observed during IVD degeneration, and to investigate the involvement of

74 Each IVD consists of a central semi-liquid nucleus pulposus (

75 In this report, we describe eight IVD gene mutations identified in seven IVA patients that

76 he evaluation of a living, tissue-engineered IVD composed of a gelatinous nucleus pulposus surrounded

77 into the rat caudal spine, tissue-engineered IVD maintained disc space height, produced de novo extra

78 the acyl-CoA dehydrogenase family except for IVD and long-chain acyl-CoA dehydrogenase.

79 tified a nucleotide deletion in the gene for IVD in fibroblasts from a patient with isovaleric acidem

80 veloping cell-based regenerative therapy for IVD regeneration.

81 IVD, was reduced and the area of the future IVD contained peanut agglutinin (PNA) staining cartilage

82 ompared to Fluc in monitoring gADSCs in goat IVDs.

83 although expression was higher in herniated IVD samples and virtually nonexistent in control samples

84 in surgical tissues, particularly herniated IVD samples, and lymphocytes were expectedly scarce.

85 phage presence, and cellularity in herniated IVDs suggests a pattern of Th1 lymphocyte activation in

86 enerative disc disease (n = 25) or herniated IVDs (n = 12); nondegenerated autopsy control tissue was

87 Human IVD expressed in Escherichia coli crystallizes in the or

88 Expression of PN-1 was detected in human IVD tissue of varying grades.

89 The association of human IVD degeneration, assessed by magnetic resonance imaging

90 ly, the three-dimensional structure of human IVD has been determined.

91 xamination of the crystal structure of human IVD reveals that the C terminus is involved in tetramer

92 St-IVD2 protein was similar to that of human IVD.

93 Mast cells were upregulated in painful human IVD tissue and induced an inflammatory, catabolic and pr

94 cted mutagenesis was used to match the human IVD active site with that of potato 2MBCD.

95 each other and 65 and 64% identical to human IVD, respectively.

96 ed from nondegenerated and degenerated human IVDs, expanded in monolayer, and cyclically strained for

97 We have now identified IVD sequences from seven species.

98 mutant peptides, and a previously identified IVD Leu13Pro mutant, are synthesized and imported into m

99 not be cultured routinely but rather only if IVD-related bloodstream infection is suspected clinicall

100 nts with IVA, which lead to abnormalities in IVD protein processing and activity.

101 zed the role of Noggin, a BMP antagonist, in IVD tissue and examined its effect after stimulation wit

102 hyperosmotic stress induces volume change in IVD cells and may initiate [Ca(2+)](i) transients throug

103 s occurring in patients with deficiencies in IVD activity.

104 Expression of the alpha5beta1 heterodimer in IVD tissue was examined by immunohistochemistry and poss

105 rough the mitochondrial apoptotic pathway in IVD cells.

106 iltrate and elicit a degenerate phenotype in IVD cells, enhancing key disease processes that characte

107 Recombinant HTRA1 induced MMP production in IVD cell cultures through a mechanism critically depende

108 nvestigate the role of integrin signaling in IVD cells during mechanical stimulation and to determine

109 tigate the role of beta-catenin signaling in IVD tissue function.

110 ve, we discuss imperatives for incorporating IVD hPSCs into drug discovery and the associated challen

111 146a appears to protect against IL-1 induced IVD degeneration and inflammation.

112 TGFbeta resulting in EPs hypertrophy-induced IVD space narrowing provides a pharmacologic target that

113 nstrate that the mechanical overload-induced IVD degeneration is mediated through the mitochondrial a

114 The invertebrate IVDs are more closely related to the mammalian enzymes t

115 s and annulus fibrosus regions of all lumbar IVDs were assessed by means of principal frequency analy

116 notochord remnants with aging in the lumbar IVDs of BALB/c mice.

117 Mouse IVD predicted amino acid sequences are 95.8 and 89.6% id

118 The mouse IVD gene spans approximately 17 kb and contains 12 codin

119 rder, we have cloned and sequenced the mouse IVD genomic and cDNAs.

120 The resulting mutant IVD had detectable activity with 2-methylbutyryl-CoA and

121 The mutant IVD precursor is imported and processed to mature size,

122 hanical properties similar to that of native IVD.

123 nderstanding the signals that control normal IVD growth and differentiation would also provide potent

124 generated IVD tissue as compared with normal IVD tissue.

125 (IL-17) expression, from surgically obtained IVD tissue and from nondegenerated autopsy control tissu

126 bral disc (IVD) space is a characteristic of IVD degeneration.

127 Deficiency of IVD in humans causes isovaleric acidemia, which shows tr

128 AMTS, potentially preventing degeneration of IVD tissue.

129 e is the most accurate test for diagnosis of IVD-related bloodstream infection.

130 The overall polypeptide fold of IVD is similar to that of other members of this family f

131 Mouse models of IVD degeneration were used to investigate the role of th

132 s essential to elucidate the pathogenesis of IVD degeneration disease (IDDD).

133 role for these cells in the pathogenesis of IVD degeneration.

134 pression are involved in the pathogenesis of IVD degeneration.

135 and the role of PN-1 in the pathogenesis of IVD degeneration.

136 PCR of IVD genomic and complementary DNA was used to identify m

137 ril diameter and a more rapid progression of IVD degeneration compared with the wild type.

138 patients that result in abnormal splicing of IVD RNA.

139 found in the active site of the structure of IVD is consistent with that of CoA persulfide.

140 The structure of IVD was solved at 2.6 A resolution by the molecular repl

141 okaryotic expression, and kinetic studies of IVD mutants were conducted to characterize the molecular

142 rminal sequence implicates the C terminus of IVD in both enzyme activity and tetramer stability.

143 s, which have a phenotype similar to that of IVD cells, a number of mechanoreceptors have been identi

144 a useful therapeutic target for treatment of IVD degeneration.

145 nvestigation to improve our understanding of IVD homeostasis and repair.

146 of inhibition of MyD88 pathway inhibition on IVD homeostasis, suggesting a potential therapeutic bene

147 r known disease-causing genes (one PCCB, one IVD, one DBT, three PAH, one STK11, one HEXB, three DBT,

148 n 47 subjects without current low back pain (IVDs = 230; age range, 20-71 years) after obtaining writ

149 Painful IVD degeneration is associated with an acidic intradisca

150 o evaluate the immunophenotype of pathologic IVD specimens, including interleukin-17 (IL-17) expressi

151 Remarkable pathologic IVD tissue expression of IL-17 is a novel finding that c

152 ity and 79.3% specificity for the polyclonal IVD, with areas under the curve (AUCs) of 0.987 and 0.75

153 tical sensitivity relative to the polyclonal IVD.

154 xperiments indicate that the seven precursor IVD mutant peptides, and a previously identified IVD Leu

155 nuates pathologic changes of EP and prevents IVD narrowing.

156 e support a scenario in which HTRA1 promotes IVD degeneration through the proteolytic cleavage of fib

157 The Km values of purified IVD Ala282Val, Val342Ala, and Arg382Leu mutants are 27.0

158 nvariant among all of the known and putative IVDs.

159 ated further with the use of cultured rabbit IVD cells in a stretch device.

160 ers and their age-related changes in the rat IVD.

161 (microCT) methods with the aim of resolving IVD 3D microstructure whilst minimising sample preparati

162 Surgical IVD tissues were procured from patients with degenerativ

163 eron-gamma (IFNgamma) was modest in surgical IVD tissue, although expression was higher in herniated

164 was used to develop microCT for bovine tail IVD using laboratory and synchrotron sources.

165 We examined the hypothesis that IVD cells respond to hyperosmotic stress by increasing t

166 The IVD volume consistently exhibited same trend of variatio

167 ported elsewhere nine point mutations in the IVD gene in fibroblasts of patients with IVA, which lead

168 ed gt or ag dinucleotide splice sites in the IVD gene.

169 derstanding the mechanisms that maintain the IVD, current therapies do not lead to tissue regeneratio

170 ive and sensitive approach to monitoring the IVD during postnatal development.

171 e details of 3D morphological changes of the IVD and canal network in the endplate and the interactio

172 Owing to the avascular nature of the IVD and lack of understanding the mechanisms that mainta

173 ss may provide an objective biomarker of the IVD degeneration process.

174 Molecular genetic analysis of the IVD gene for 19 subjects whose condition was detected th

175 Since the mechanical competence of the IVD relies on its structural constituents, defining the

176 Cells from the three zones of the IVD, the anulus fibrosus (AF), transition zone (TZ), and

177 main of Fibromodulin (Fmod), a marker of the IVD, was reduced and the area of the future IVD containe

178 While the IVD Leu13Pro, Arg21Pro, and Cys328Arg mutant peptides ar

179 e presence and role of mast cells within the IVD, specifically, mast cell-IVD cell interactions using

180 Although the IVDs grow and differentiate after birth along with the v

181 r to be more closely related than any of the IVDs on other branches of the phylogram, while the fly a

182 function in the postnatal body and that the IVDs are signaling centers, in addition to their already

183 various sized fragments, which when added to IVD cells in culture, caused a significant increase in M

184 trategy that delivers cells and biologics to IVD injury site is needed to limit the progression of di

185 2MBCD in potato that is highly homologous to IVD is an example of convergent evolution within the acy

186 g is critical for investigations relating to IVD function and homeostasis.

187 , structures, and vessels on EVD relative to IVD images.

188 ring branched-chain substrate specificity to IVD.

189 itute for direct BMP administration to treat IVD degeneration and to ameliorate IVD-associated chroni

190 o found to be increased within HTRA1-treated IVD cell cultures as well as in disc tissue from patient

191 mediate in the folding pathway for wild type IVD has been identified in the in vitro mitochondrial im

192 drial import experiments show that wild type IVD protein rapidly and stably forms mature homotetramer

193 poral and spatial EP changes associated with IVD volume, considering them as a functional unit.

194 EP sclerosis is associated with IVD, however the pathogenesis of EP hypertrophy is poorl

195 of endplate with aging and interaction with IVD remains a technical challenge.

196 of the notochord band has been observed with IVD degeneration.

197 as well as in disc tissue from patients with IVD degeneration.

198 roughout the day and their relationship with IVD degeneration and subject age.

199 hes of the phylogram, while the fly and worm IVDs are the most divergent.