ライフサイエンスコーパス: tuft

1 in a distance-dependent manner from soma to tuft.

2 y form cellular adhesions with the capillary tuft.

3 veral types of neurons as well as the apical tuft.

4 tive activity in the distal apical dendritic tuft.

5 occurrence of bleeding from an iris vascular tuft.

6 correlated calcium transients throughout the tuft.

7 pregulated and co-localized with neovascular tufts.

8 g proliferation of endothelial cells (EC) in tufts.

9 knotted' morphology to pathological vascular tufts, abnormal cell motility and altered filopodia dyna

10 CPI203, exhibit greater than 90% decrease in tuft and enteroendocrine cells in both crypts and villi

11 domains defines a novel pathway required for tuft and enteroendocrine differentiation and provides an

12 g networks in stem, Paneth, enteroendocrine, tuft and goblet cells, as well as enterocytes.

13 pt progenitors to promote differentiation of tuft and goblet cells, leading to increased frequencies

14 S) in humans with collapse of the glomerular tuft and marked hyperplasia of the parietal epithelial c

15 iented migration of PECs into the glomerular tuft and their acquisition of CD44 and beta1 integrin ex

16 he generation and spread of apical dendritic tuft and trunk regenerative activity.

17 Simultaneous apical dendritic tuft and trunk whole-cell current-clamp recordings revea

18 ub-bands have been hypothesized to represent tufted and mitral cell networks, respectively.

19 Furthermore, tufted and not mitral cell responses to odor mixtures be

20 ll classes in layers 2/3, 4, and the slender-tufted and thick-tufted pyramidal cells of layer 5 using

21 age of excitatory inputs mediated by mitral, tufted, and external tufted cells, and, in turn, they in

22 on, although the expressions of enterocyte-, tuft- and goblet-cell specific markers are largely not a

23 hared with those of infantile hemangioma and tufted angioma of children, but features of the clinical

24 mall vessels within the dermis, resembling a tufted angioma.

25 ge; other vascular tumors include congenital tufted angiomas (TAs), kaposiform hemangioendotheliomas

26 Iris vascular tufts are rare iris stromal vascular hamartomas.

27 Transient, spindle-like "REM beta tufts" are described in the EEG of healthy subjects, whi

28 phthalmologists to be aware of iris vascular tufts as a cause for spontaneous hyphaema, independent o

29 thy mice, about two-thirds of the glomerular tufts became LacZ positive during the regenerative phase

30 region, resulting in a decoupling of distal tuft branches from each other while at the same time eff

31 dendritic Ca(2+) spikes on different apical tuft branches of individual layer V pyramidal neurons in

32 nal Institute on Drug Abuse and the Lifespan/Tufts/Brown Center for AIDS Research from the National I

33 n conclusion, repopulation of the glomerular tuft by parietal cells may represent a compensatory resp

34 li in murine kidneys and sized the capillary tufts by combining in vivo fluorescence labeling of endo

35 ighted magnetic resonance imaging scans from tufted capuchin monkeys (5 male, 15 female).

36 s dynamically during naturalistic feeding in tufted capuchins (Sapajus apella).

37 an anointing resource given to two groups of tufted capuchins, we tested predictions derived from the

38 Volume rendering also revealed within the tuft cell an elegant network of interconnected tubules.

39 metaplasias from the mice were analyzed for tuft cell and biliary progenitor markers, including SOX1

40 Our findings identify an additional tuft cell effector function and suggest context-specific

41 cases, the extracellular signals controlling tuft cell effector function are unknown, but signal tran

42 ine interleukin-25, which indirectly induces tuft cell expansion by promoting interleukin-13 producti

43 We found that tuft cell expansion reduced chronic intestinal inflammat

44 (ILC2s), which subsequently drive increased tuft cell frequency.

45 icle, we review the current understanding of tuft cell immune function in the intestines, airways, an

46 These cytospinules project from the tuft cell into the nuclei of neighboring epithelial cell

47 s there are several disagreements related to tuft cell lineage commitment and function.

48 ing is sufficient to induce expansion of the tuft cell lineage, and ectopic stimulation of this signa

49 nsights, numerous questions remain regarding tuft cell lineage, diversity and effector mechanisms and

50 Cell death, inflammation, and tuft cell markers were downregulated in fat-1 mice in re

51 ow-level EE gene expression but co-expressed tuft cell markers, Lgr5 and Ascl2, reminiscent of label-

52 We assessed microbe dependence of tuft cell populations using microbiome depletion, organo

53 , to study interactions between microbes and tuft cell populations.

54 Conversely, cysLTs are dispensable for the tuft cell response induced by intestinal protists.

55 which shares 75% homology with villin, has a tuft cell restricted expression in the gastrointestinal

56 idence for activation of a succinate-induced tuft cell signaling pathway linked to Th2 immune respons

57 e find that the Pou2f3 gene is essential for tuft cell specification.

58 ld be derived from a complete account of the tuft cell ultrastructure.

59 s, and distinguished between two subtypes of tuft cell, one of which expresses the epithelial cytokin

60 ve distinct cellular lineages, including the tuft cell, whose function is unclear.

61 T(+) cells and type 17 cytokines (IL23) in a tuft cell-dependent manner.

62 s to access mitral cell (MC) and superficial tufted cell (sTC) subpopulations separately.

63 or neuron nerve terminals (input) and mitral/tufted cell apical dendrites (output).

64 ly, bulbar cholinergic enhancement of mitral/tufted cell odorant responses was robust and occurred in

65 Glomerular and mitral and tufted cell responses were sparse and locally heterogene

66 liable, short-latency firing consistent with tufted cell-mediated excitation.

67 Both tuft-cell tropism and resistance to interferon-lambda (I

68 After helminth infection, tuft-cell-derived IL-25 further activates ILC2s to secre

69 33 (IL-33), which synergized with intestinal tuft-cell-derived IL-25 to drive the expansion and activ

70 ILC2 activation requires tuft-cell-derived interleukin-25 (IL-25), but whether ad

71 cooperate with IL-25 to activate ILC2s, and tuft-cell-specific ablation of leukotriene synthesis att

72 rradiation injury, resulting in a paucity of tuft cells and acetylcholine production.

73 s (MNoV) infects a low percentage of enteric tuft cells and can persist in these cells for months fol

74 al a novel function of intestinal epithelial tuft cells and demonstrate a cellular relay required for

75 Pou2f3(-/-) mice lack intestinal tuft cells and have defective mucosal type 2 responses t

76 estinal organoids were stimulated with IL-4, tuft cells and IL-25 were induced in both WT and Raptor

77 We find that Dclk1(+) tuft cells and nerves are the main sources of acetylchol

78 Our study identifies advillin as a marker of tuft cells and provides a mechanism for driving gene exp

79 Administration of succinate to mice expanded tuft cells and reduced intestinal inflammation in TNF(De

80 protein villin (Vil1) is used as a marker of tuft cells and the villin promoter is frequently used to

81 After massive small bowel resection, tuft cells and Tm were diminished due to the diet used p

82 Dclk1 is a marker of differentiated Tuft cells and, when coexpressed with Lgr5, also marks i

83 Thus, enteroendocrine tuft cells appear essential to maintain epithelial homeo

84 Once referred to as "peculiar," tuft cells are enigmatic epithelial cells.

85 Tuft cells are ideally positioned as chemosensory sentin

86 Intestinal tuft cells are one of 4 secretory cell linages in the sm

87 Tuft cells are rare, secretory epithelial cells that gen

88 Tuft cells are specialized taste-chemosensory cells that

89 Tuft cells are the primary source of the parasite-induce

90 Our results identify intestinal tuft cells as critical sentinels in the gut epithelium t

91 s a mechanism for driving gene expression in tuft cells but not in other epithelial cells of the gast

92 Here we show that tuft cells constitutively express IL-25 to sustain ILC2

93 Tuft cells have a Th2-related gene expression signature

94 Tuft cells have the capacity to produce an unusual spect

95 fundamental questions about the function of tuft cells in immunity remain to be answered.

96 We used microscopy to quantify tuft cells in intestinal specimens from patients with il

97 We investigated the activities of tuft cells in patients with CD and mouse models of intes

98 his signalling cascade obviates the need for tuft cells in the epithelial cell remodelling of the int

99 Tuft cells in the small intestine sense and direct the i

100 stellate cells, and a new potential role of tuft cells in this disease.

101 In particular, we discuss the role of tuft cells in type 2 immunity, norovirus infection, and

102 e, diversity and effector mechanisms and how tuft cells interface with the immunological niche in the

103 Strategies to expand tuft cells might be developed for treatment of CD.

104 ers of podocytes, nonepithelial cells (NECs; tuft cells other than podocytes), and parietal epithelia

105 These findings suggest that intestinal tuft cells play an important role in regulating the ATM

106 We determined that Dclk1 expressing tuft cells regulate the whole intestinal epithelial cell

107 The function of Dclk1 expressing tuft cells regulating intestinal epithelial DNA damage r

108 small intestine, chemosensing by epithelial tuft cells results in the activation of group 2 innate l

109 Here, we show that tuft cells secrete cysteinyl leukotrienes (cysLTs) to ra

110 Moreover, tuft cells secrete IL-25, thereby regulating type 2 immu

111 cell analytics have revealed diversity among tuft cells that extends from nasal epithelia and type II

112 stence of an ATOH1-independent population of tuft cells that was sensitive to metabolites produced by

113 agreement about the expression of villin in tuft cells there are several disagreements related to tu

114 es has provided important advances that link tuft cells to infectious diseases and the host immune re

115 worms, but not commensal protists, stimulate tuft cells to release cysteinyl leukotrienes to amplify

116 Broadly, a model has emerged in which tuft cells use chemosensing to monitor their surrounding

117 Expansion of tuft cells was associated with increased expression of g

118 Tuft cells were first discovered in epithelial barriers

119 etaR is essential for the development thymic tuft cells which regulate NKT2 via IL-25, while LTbetaR

120 inflammatory response following expansion of tuft cells with succinate administration in TNF(DeltaARE

121 until contemporaneous reports in 2016 linked tuft cells with type 2 immunity in the small intestine.

122 ased on their location and microanatomy, the tuft cells' cytospinules, and tubular network, might fac

123 Here we show that tuft cells, a rare epithelial cell type in the steady-st

124 new papers now identify a critical role for tuft cells, an epithelial cell type involved in percepti

125 inate, increased numbers of small intestinal tuft cells, and evidence for activation of a succinate-i

126 f stem, goblet, Paneth, enteroendocrine, and tuft cells, compared with control enteroids, with a conc

127 rom patients and mice had reduced numbers of tuft cells, compared with healthy individuals or wild-ty

128 the loss of TRMP5 abrogates the expansion of tuft cells, goblet cells, eosinophils, and type 2 innate

129 in Tritrichomonas muris (Tm) infected mice, tuft cells, IL-25 in epithelium and IL-13 in the mesench

130 Tuft cells, ILC2s and epithelial progenitors therefore c

131 ed by our surprising finding that intestinal tuft cells, in fact, do not express villin protein.

132 Thus, despite infecting a low number of tuft cells, NS1 secretion allows MNoV to globally suppre

133 uces a selective expansion of DCLK1-positive tuft cells, suggesting a model of feedback inhibition.

134 Atoh1-knockout mice, which have expansion of tuft cells, to study interactions between microbes and t

135 olinergic blockade inducing the expansion of tuft cells, which adopt an enteroendocrine phenotype and

136 Here we show that tuft cells, which are taste-chemosensory epithelial cell

137 DCLK1 is also used as a marker of tuft cells, which regulate type II immunity in the gut.

138 Tuft cells-rare solitary chemosensory cells in mucosal e

139 th cells are replaced by enteroendocrine and tuft cells.

140 d an increase in the abundance of goblet and tuft cells.

141 lution (4-5 nm/pixel) of specific intestinal tuft cells.

142 o drive expression of the Cre recombinase in tuft cells.

143 nge the way we identify and study intestinal tuft cells.

144 both mitral/tufted cells (MTCs) and external tufted cells (ETCs), the two major excitatory neurons th

145 lfactory bulb projection neurons, mitral and tufted cells (M/T), is modulated by pairs of reciprocal

146 naptic targets of OSNs, including mitral and tufted cells (M/TCs) and juxtaglomerular cells, form glo

147 ation of nAChRs directly excites both mitral/tufted cells (MTCs) and external tufted cells (ETCs), th

148 tuning was heterogeneous in both mitral and tufted cells (MTCs) and GCs but relatively constant with

149 ically inhibits the OB output neurons mitral/tufted cells (MTCs) by GABA release from SACs: (2) gap j

150 mouse olfactory bulb (OB), where mitral and tufted cells (MTCs) form parallel output streams of odor

151 siently inhibited the excitability of mitral/tufted cells (MTCs) that relay olfactory input to the co

152 om the mouse olfactory bulb (OB), mitral and tufted cells (MTCs).

153 reaching the cortex via inhibition of mitral/tufted cells (MTs).

154 f olfactory (OB) bulb mitral cells (MCs) and tufted cells (TCs) are known to depend on prior odor exp

155 use olfactory system, mitral cells (MCs) and tufted cells (TCs) comprise parallel pathways of olfacto

156 f olfactory bulb (OB) mitral cells (MCs) and tufted cells (TCs) is linked to a variety of computation

157 n olfactory bulb, the mitral cells (MCs) and tufted cells (TCs), differ markedly in physiological res

158 response patterns over time as compared with tufted cells (TCs), leading to odorant representations t

159 nd the output neurons mitral cells (MCs) and tufted cells (TCs).

160 7) was equivalent across mitral and external tufted cells and could be explained by a single pool of

161 ic and dendrodendritic circuitry in external tufted cells and mitral cells, respectively, tunes the p

162 es from their downstream synaptic partners - tufted cells and mitral cells.

163 modulation adds an excitatory bias to mitral/tufted cells as opposed to increasing response gain or s

164 ion of the raphe nuclei led to excitation of tufted cells at rest and potentiation of their odor resp

165 influence relatively large groups of MCs and tufted cells belonging to clusters of at least 15 glomer

166 ncreases the number of associated mitral and tufted cells by 40% and 100%, respectively.

167 sponse profiles in mitral cells and external tufted cells could be attributed to slow dendrodendritic

168 IFICANCE STATEMENT Olfactory bulb mitral and tufted cells display different odor-evoked responses and

169 odor discrimination learning, mitral but not tufted cells exhibited improved pattern separation, alth

170 Although external tufted cells had a 4.1-fold larger peak EPSC amplitude,

171 esynaptic afferents onto mitral and external tufted cells had similar quantal amplitude and release p

172 tor, Tbx21, which is expressed by mitral and tufted cells in the mature OB.

173 ract with the apical dendrites of mitral and tufted cells inside glomeruli at the first stage of olfa

174 d the parallel pathways formed by mitral and tufted cells of the olfactory system in mice and charact

175 ith sustained transmission, whereas external tufted cells responded transiently.

176 n with sustained responses, whereas external tufted cells responded transiently.

177 endent lateral inhibition between mitral and tufted cells that likely reflect newly described differe

178 e circuit-level differences allow mitral and tufted cells to best discriminate odors in separate conc

179 he distinct responses of mitral and external tufted cells to high frequency stimulation did not origi

180 o the mitral layer and unit firing of mitral/tufted cells was phase locked to HFO.

181 esting that the larger peak EPSC in external tufted cells was the result of more synaptic contacts.

182 tures represented by ensembles of mitral and tufted cells were overlapping but distinct from those re

183 ostsynaptic responses of mitral and external tufted cells within the glomerulus may involve both dire

184 on of spontaneous and odor-driven mitral and tufted cells' firing activity.

185 erular lateral inhibition between mitral and tufted cells' lateral dendrites whereas diverse subtypes

186 factory bulb (OB), principal neurons (mitral/tufted cells) make reciprocal connections with local inh

187 tains excitatory principal cells (mitral and tufted cells) that project to cortical targets as well a

188 uts mediated by mitral, tufted, and external tufted cells, and, in turn, they indiscriminately releas

189 ncy responses in mitral cells, compared with tufted cells, are due to weaker excitation and stronger

190 Compared to external tufted cells, mitral cells have a prolonged afferent-evo

191 cells in the olfactory bulb (OB), mitral and tufted cells, play key roles in processing and then rela

192 amic, 2-D, optogenetic stimulation of mitral/tufted cells, that virtual odors that differ by as littl

193 The activity of mitral and tufted cells, the principal neurons of the olfactory bul

194 that finely tune the activity of mitral and tufted cells, the principal neurons, and regulate odour

195 n and feedforward inhibition onto mitral and tufted cells, the principal neurons.

196 ays a role in the connectivity of mitral and tufted cells, the projection neurons in the mouse olfact

197 ayers in the olfactory bulb (OB), mitral and tufted cells, using chronic two-photon calcium imaging i

198 g the calcium indicator GCaMP2 in the mitral/tufted cells, we investigated the effect of ACh on the g

199 rons in the mouse olfactory bulb, mitral and tufted cells, which send olfactory information to distin

200 cortex but not in olfactory bulb mitral and tufted cells.

201 ctive output onto interneurons and principal tufted cells.

202 nsient response profile, typical of external tufted cells.

203 asts with the transient response in external tufted cells.

204 rons are similar between mitral and external tufted cells.

205 through feedforward excitation from external tufted cells.

206 ity of mitral cells but had little impact on tufted cells.

207 asing the spike output of presumptive mitral/tufted cells.

208 e principal neurons of the bulb, mitral, and tufted cells.

209 sequent wrinkling of glomerular capillaries, tuft collapse, and periglomerular fibrosis.

210 ns, although minor differences in glomerular tuft contractility and macula densa cell calcium handlin

211 g from the dental-enamel junction and enamel tufts, crack deflections, and the initiation of new crac

212 ion encoding in simultaneously imaged apical tuft dendrites and their respective cell bodies in retro

213 annels that regulate synaptic integration in tuft dendrites have, however, not been thoroughly invest

214 rons in RSCg via potent synapses onto apical tuft dendrites in L1.

215 Towards the distal tuft dendrites in upper L1, the relative inhibitory inpu

216 ent of HCN1 and GIRK1 channels in the distal tuft dendrites of both hippocampal CA1 and neocortical l

217 CaMP6s signals in the soma, trunk and distal tuft dendrites of layer 5 pyramidal neurons in the awake

218 ic contacts from L1 INs target distal apical tuft dendrites, whereas PNs primarily innervate basal an

219 -receptor-dependent calcium spikes in apical tuft dendrites.

220 tatin (SST)-positive interneurons and apical tufts dendrites of excitatory pyramidal neurons.

221 of excitatory cells, it contains the distal "tuft" dendrites of pyramidal cells (PCs) located in deep

222 gh-frequency somatic bursts or strong apical tuft depolarization.

223 The Developmental FunctionaL Annotation at Tufts (DFLAT) project aims to improve the quality of ana

224 We found that removing the apical dendritic tuft did not alter orientation-tuning.

225 ioles, LacZ-positive cells in the glomerular tuft did not express renin.

226 ed glomerular podocyte number and glomerular tuft enlargement.

227 Syndromic congenital tufting enteropathy (CTE) is a life-threatening recessiv

228 Congenital tufting enteropathy (CTE) is a severe autosomal recessiv

229 , an effect that is mediated by the external tufted (ET) cells coupled to DAT+ cells via chemical and

230 eal griseofulvin decreased both pathological tuft formation and areas of vasoobliteration compared to

231 c retinal angiogenesis, reducing neovascular tuft formation and increased avascular area, in a dose-d

232 loss, but also reduced pathological vascular tuft formation in sEH-/- mice.

233 ar zone and peripheral pathological vascular tuft formation than did their WT littermates.

234 upy layer 5A and display an apical dendritic tuft; functionally, they fire broad, adapting action pot

235 Patients with iris vascular tufts generally remain asymptomatic until presenting wit

236 gment six major renal structures: glomerular tuft, glomerulus including Bowman's capsule, tubules, ar

237 Patients at Tufts HCM Institute, from 2004 to 2017, were identified

238 n and suggest context-specific regulation of tuft-ILC2 circuits within the small intestine.

239 PEC markers were detected on the tuft in 87% of the biopsies of patients diagnosed as pri

240 rong and specific staining of the glomerular tufts in a distribution that mimicked that of the immune

241 ed in a significant reduction of neovascular tufts in oxygen-induced retinopathy, supporting the feas

242 vel of Cavin-2 expression in the neovascular tufts in the mouse model of oxygen-induced retinopathy,

243 ssels of patient-derived FVMs and angiogenic tufts in the retina of mice with oxygen-induced retinopa

244 cent protein-positive area in the glomerular tufts increased after mesangial injury.

245 of frequency-modulation of somatic output by tuft input and (simulated) calcium-channel blockage func

246 incidence detection between basal and apical tuft inputs by controlling the frequency of spike output

247 The apical tuft is the most remote area of the dendritic tree of ne

248 Here, we show that one-third of the thick-tufted layer 5 pyramidal neurons have an axon originatin

249 Accompanying knockout studies reveal that tuft-like cells are the likely progenitor of both pulmon

250 ughout the OB to cause suppression of mitral/tufted (M/T) cell firing, an effect that is mediated by

251 Here we show that individual mitral/tufted (M/T) cells sum inputs linearly across odors and

252 us samples analyzed, 4683 (81.64%) were from Tufts Medical Center (TMC), 955 (16.65%) were from Bosto

253 ren-Lawrence grades 2 or 3, were enrolled at Tufts Medical Center beginning February 11, 2013; all pa

254 of 1558 consecutive patients followed at the Tufts Medical Center Hypertrophic Cardiomyopathy Institu

255 th EFE referred to New England Eye Center at Tufts Medical Center, a tertiary care ophthalmology prac

256 ts from the outpatient dermatology center of Tufts Medical Center, enrolled from August 18, 2009, to

257 l cystoid degeneration (TCD), cystic retinal tuft, meridional fold, lattice and cobblestone degenerat

258 lium, ora serrata pearl, TCD, cystic retinal tuft, meridional fold, lattice, and cobblestone degenera

259 errata pearl, ora tooth, TCD, cystic retinal tuft, meridional fold, retinal hole, and typical degener

260 and short axon (SA) cells, as well as mitral/tufted (MT) cells carrying OB output to piriform cortex.

261 suppression in OB output neurons (mitral and tufted, MT cells).

262 te its distal location, the apical dendritic tuft of layer 5 pyramidal neurons receives substantial e

263 on of spine synapses in the apical dendritic tuft of layer V pyramidal neurons in the mPFC.

264 In bilaterians they are characterised by a tuft of long cilia and receptor cells and they are assoc

265 o gamma oscillations generated at the apical tuft of pyramidal cells.

266 idal structures), BVNs in 26 eyes (55.3%, 26 tufts of BVNs), and stalks of origin from the choroid in

267 vestigate dendritic spine dynamics in apical tufts of GFP-expressing layer 4 (L4) pyramidal neurons o

268 summarize evidence that input to the apical tufts of neocortical pyramidal cells modulates their res

269 distal apical dendrites and apical dendritic tufts of pyramidal neurons in layer I, and rarely target

270 A fibrovascular tuft on the optic nerve head with induced traction on su

271 caused marked regression of the new vascular tufts on the vitreal side with normal organization and t

272 Tuft (or brush) cells are solitary chemosensory cells sc

273 l cells (PECs) migrating onto the glomerular tuft participate in the formation of focal segmental glo

274 y focal scarring of the glomerular capillary tuft, podocyte injury, and nephrotic syndrome.

275 We identified CPMs in the Tufts Predictive Analytics and Comparative Effectiveness

276 rter 1, a presynaptic protein, in mitral and tufted projection neurons, and 5T4 in granule cells.

277 ers 2/3, 4, and the slender-tufted and thick-tufted pyramidal cells of layer 5 using a combination of

278 an 2-fold larger for L2 than L3 and L5 thick-tufted pyramidal cells.

279 ding to previously described thin- and thick-tufted pyramidal neurons, respectively.

280 e of spontaneous hyphaema from iris vascular tuft related to a documented supratherapeutic Internatio

281 rominent hematologist Dr William Dameshek of Tufts School of Medicine, Blood has published many paper

282 We found that apical tuft signals were dominated by widespread, highly correl

283 cised from distal apical dendritic trunk and tuft sites.

284 This species has a reticulate, tufted skeleton of minute monaxon spicules, characterist

285 Trichodesmium forms macroscopic, fusiform (tufts), spherical (puffs) and raft-like colonies that pr

286 IHC showed that glomerular tuft staining for cathepsin B, cathepsin C, and annexin

287 in the formation of pathological neovascular tufts that impair vision.

288 disorganized and poorly perfused neovascular tufts that mimic human ocular diseases.

289 Carolina chickadees (Poecile carolinensis), tufted titmice (Baeolophus bicolor), and white-breasted

290 who underwent lateral sinus augmentation at Tufts University School of Dental Medicine, Boston, Mass

291 elected from patients receiving treatment at Tufts University School of Dental Medicine.

292 onference convened by Harvard University and Tufts University.

293 ed by an independent evidence review team at Tufts University.

294 al, and evolutionary foundations of music at Tufts University.

295 capable of shifting the balance of principal tufted versus mitral cell activity across large expanses

296 a 1.6 mm hyphaema and multiple iris vascular tufts visible around the entire pupil.

297 ophy prevented a change in the proportion of tuft volume occupied by podocytes.

298 sited extracellular matrix on the glomerular tuft which are all hallmarks of FSGS.

299 treatment significantly reduced neovascular tufts while sparing healthy retinal vessels, thereby dem

300 gies that eliminate pathological neovascular tufts while sparing normal blood vessels are needed.