ライフサイエンスコーパス: IVD

1 IVD calcification is an often overlooked disc phenotype

2 IVD calcification is not a rare finding in ageing or in

3 IVD were predominantly more likely (in descending order

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

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

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

7 displacement and strain patterns in adjacent IVDs in vivo by coupling magnetic resonance imaging (MRI

8 us and nucleus pulposus cells of young-adult IVD expressed osterix, but aging and compression reduced

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

10 laboratory-developed tests (LDTs) alongside IVD assays.

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

12 pecificity, and overall agreement of the AMG IVD assay were 100%, 99.9%, and 99.9%, respectively.

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

14 Surprisingly, we also found evidence for an IVD in fossil reptiles, including non-avian dinosaurs, i

15 o approach regulatory considerations when an IVD is converted from EUA to non-EUA status.

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

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

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

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

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

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

22 eas no significant changes in mean MChVD and IVD were observed (p > 0.05).

23 ted correlation between measures of pain and IVD degeneration highlights the need to evaluate pain or

24 oS in FVG was 2.9 and 3.3 days after SVD and IVD respectively, and the pooled regional proportion of

25 For BV, the specificity of the Aptima IVD assay (86.3%) was higher than the Affirm assay (60.6

26 As IVD calcification has implications for the management an

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

28 ifferences exist in the interactions between IVD degeneration and pain.

29 females have distinct relationships between IVD degeneration and pain using an in vivo rat model.

30 , SVD were 75,497 (69.1% out of all births), IVD were 7,281 (6.7%), OCS were 26,467 (24.2%) and UCS w

31 n, and the ability to split eluates for both IVD and LDT testing.

32 * = 0.94 [95% CI, 0.88 to 1.0]), followed by IVD-drawn quantitative [corrected] blood culture (Q* = 0

33 one-step five-plex RT-ddPCR assay with a CE-IVD RT-qPCR kit revealed a very high concordance and a h

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

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

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

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

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

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

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

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

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

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

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

45 thways are altered in cells from degenerated IVDs.

46 d gene and protein expression in degenerated IVDs as compared to non-degenerated IVDs.

47 enerated IVDs as compared to non-degenerated IVDs.

48 ls from nondegenerated, but not degenerated, IVDs.

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

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

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

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

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

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

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

56 deficiency of isovaleryl-CoA dehydrogenase (IVD).

57 3 days post instrumental vaginal deliveries (IVD).

58 livery (SVD), instrumental vaginal delivery (IVD), overall CS (OCS) and urgent/emergency CS (UCS).

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

60 BC test (in vitro diagnostic medical device [IVD]).

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

62 of EPI-CE, a CE-marked in-vitro diagnostic (IVD) assay, specifically developed for use in European c

63 rove the performance of in vitro diagnostic (IVD) assays due to the reduction of nonspecific protein

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

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

66 ray of highly sensitive in vitro diagnostic (IVD) real-time PCR assays for respiratory viruses, inclu

67 italium (AMG) assay, an in vitro diagnostic (IVD) TMA test that targets 16 s rRNA of M. genitalium An

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

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

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

71 ave potential as rapid in vitro diagnostics (IVDs), but the complexity of workflows, interpretation o

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

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

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

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

76 Intervertebral disc (IVD) degeneration activates the differentiation of prehy

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

78 Intervertebral disc (IVD) degeneration and consequent low back pain (LBP) are

79 nce is a contributor to intervertebral disc (IVD) degeneration and low back pain.

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

81 ck pain, the cascade of intervertebral disc (IVD) degeneration is initiated by the disappearance of n

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

83 is closely linked with intervertebral disc (IVD) degeneration, a prevalent age-dependent chronic dis

84 Back pain is linked to intervertebral disc (IVD) degeneration, but clinical studies show the relatio

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

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

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

88 ia and IFT80 protein in intervertebral disc (IVD) development, maintenance, and degeneration are larg

89 Intervertebral disc (IVD) disease (IDD) is a complex, multifactorial disease.

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

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

92 The intervertebral disc (IVD) has long been considered unique to mammals.

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

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

95 ted injury to the mouse intervertebral disc (IVD) is often used to recapitulate the degenerative casc

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

97 Degeneration of the intervertebral disc (IVD) results in a range of symptomatic (i.e., painful) a

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

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

100 xpression in pathologic intervertebral disc (IVD) tissues.

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

102 acellular matrix of the intervertebral disc (IVD), disc height loss, and inflammation.

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

104 elatinous region of the intervertebral disc (IVD).

105 with pathologies of the intervertebral disc (IVD).

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

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

108 ected in isolated goat intervertebral discs (IVD).

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

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

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

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

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

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

115 ed in cilia loss in GP and EP, and disrupted IVD structure with disorganized and decreased GP, EP, an

116 gion of NEMO, called the Intervening Domain (IVD), is conserved between NEMO and optineurin.

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

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

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

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

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

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

123 rted IPF GWAS loci, five (DPP9, DSP, FAM13A, IVD, and MUC5B) were significantly associated (P < 0.05/

124 of LoS > ED was 64.4% for SVD and 32.0% for IVD.

125 Similar patterns were obseved also for IVD.

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

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

128 veloping cell-based regenerative therapy for IVD regeneration.

129 Furthermore, IVD calcification may also affect the vertebral endplate

130 dology for the clinical validation of future IVD tests for this organism.

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

132 ompared to Fluc in monitoring gADSCs in goat IVDs.

133 mpression of old (18 mo) IVD induced greater IVD degeneration.

134 ions mimicking the osmolality of the healthy IVD, which was abrogated by TonEBP knockdown.

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

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

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

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

139 Human IVD expressed in Escherichia coli crystallizes in the or

140 els in non-degenerated and degenerated human IVD tissue (with different pain intensity and chronicity

141 fined the transcriptome map of healthy human IVD by performing single-cell RNA-sequencing (scRNA-seq)

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

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

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

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

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

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

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

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

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

151 We have now identified IVD sequences from seven species.

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

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

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

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

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

157 y supports the importance of TRP channels in IVD homeostasis and pathology and their possible applica

158 s occurring in patients with deficiencies in IVD activity.

159 e expression, even though sex differences in IVD measurements were limited.

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

161 The adjusted mean LoS was higher in IVD than SVD, and although a decline of LoS > ED and mea

162 ntroduces a hybrid Agent-based (AB) model in IVD research and exploits network modelling solutions in

163 the need to evaluate pain or nociception in IVD degeneration models to better understand nervous sys

164 rough the mitochondrial apoptotic pathway in IVD cells.

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

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

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

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

169 etion; however, these levels were similar in IVDs from WT and Hmgb1 KO mice.

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

171 146a appears to protect against IL-1 induced IVD degeneration and inflammation.

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

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

174 ed up to 28 days post injury both in injured IVDs and in the IVDs adjacent to the level of injury.

175 ) macrophage (F4/80+) recruitment to injured IVDs in vivo.

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

177 erformed less SVD and 5 (A, C, D, I, J) less IVD.

178 le and female Sprague-Dawley rats had lumbar IVD puncture or sham surgery.

179 gical approach was used to access the lumbar IVD, and the injuries to the IVD were produced by either

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

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

182 genes, suggesting their role in maintaining IVD structure.

183 scription factor RUNX2, but less so in 12 mo IVD.

184 5 mo), mechanical compression of old (18 mo) IVD induced greater IVD degeneration.

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

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

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

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

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

190 hanical properties similar to that of native IVD.

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

192 generated IVD tissue as compared with normal IVD tissue.

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

194 ative approaches for the spine, awareness of IVD calcification should be raised in the spine communit

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

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

197 AMTS, potentially preventing degeneration of IVD tissue.

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

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

200 ry IFT80 is important for the maintenance of IVD cell organization and function through regulating th

201 etwork analysis visualized which measures of IVD degeneration most related to pain by sex.

202 rovides a new insight into the metabolism of IVD cells under nutrient deprivation and the information

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

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

205 pression are involved in the pathogenesis of IVD degeneration.

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

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

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

209 olic activities (including PG production) of IVD cells are restricted under the in-vivo nutrient cond

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

211 nce-associated secretory phenotype (SASP) of IVD cells.

212 patients that result in abnormal splicing of IVD RNA.

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

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

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

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

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

218 pharmacological targets for the treatment of IVD degeneration and LBP.

219 a useful therapeutic target for treatment of IVD degeneration.

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

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

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

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

224 Painful IVD degeneration is associated with an acidic intradisca

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

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

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

228 tical sensitivity relative to the polyclonal IVD.

229 amine ATP level and PG production of porcine IVD cells under prolonged exposure to hypoxia with physi

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

231 nuates pathologic changes of EP and prevents IVD narrowing.

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

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

234 nvariant among all of the known and putative IVDs.

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

236 r surgery, IVDs were evaluated by radiologic IVD height, histological grading, and biomechanical test

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

238 From this reptilian IVD, extant reptile groups and some non-avian dinosaurs

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

240 otein inhibitor, selectively kills senescent IVD cells through apoptosis.

241 c or postnatal TonEBP loss generated similar IVD changes.

242 d males, annular puncture induced structural IVD degeneration, but functional biomechanical propertie

243 Six weeks after surgery, IVDs were evaluated by radiologic IVD height, histologic

244 Surgical IVD tissues were procured from patients with degenerativ

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

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

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

248 The IVD evolved at least twice, in mammals and in extinct di

249 The IVD volume consistently exhibited same trend of variatio

250 on of TRPC6 and TRPML1 was influenced by the IVD degeneration grade.

251 the nucleus pulposus by 95%, degenerated the IVD to levels similar to aging and compression, reduced

252 d data on their presence and function in the IVD exist.

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

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

255 components, including Gli1 and Patch1 in the IVD of IFT80(fl/fl) ; Col2-creERT mice, and Gli1 and Pat

256 ntly known TRP channels are expressed in the IVD on the mRNA level, thereby revealing novel therapeut

257 regulation, may govern PG production in the IVD under restricted nutrient supply.

258 wth (PGP9.5) and sensitization (CGRP) in the IVD were also shown, suggesting a mechanism for the pain

259 ignificant increase in cell apoptosis in the IVD, and a marked decrease in expression of chondrogenic

260 the loss of notochordal cells and PG in the IVD.

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

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

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

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

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

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

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

268 Disruption of the IVD structural integrity after LPS injection was also ev

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

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

271 Calcification is not restricted to the IVD but is also observed in the degeneration of other ca

272 Collectively, compared to the IVD conceptus, evidence suggests the endometrium drives

273 cess the lumbar IVD, and the injuries to the IVD were produced by either incising one side of the ann

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

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

276 flux propagating across the cells within the IVD.

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

278 post injury both in injured IVDs and in the IVDs adjacent to the level of injury.

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

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

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

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

283 2MBCD in potato that is highly homologous to IVD is an example of convergent evolution within the acy

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

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

286 ring branched-chain substrate specificity to IVD.

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

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

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

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

291 he recently cleared in vitro diagnostic use (IVD) Aptima BV assay includes a third target (Atopobium

292 by the variant most strongly associated with IVD expression and metabolites, but with no functional e

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

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

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

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

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

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

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

300 eep, and equilibrium modulus) compared to WT IVDs; however, there was no significant effect on histop