ライフサイエンスコーパス: inflamed

1 n tumors that were classically CD8(+) T cell inflamed.

2 The "inflamed" adipose tissue plays a key role in the release

3 ory CD4(+) T cells as highly enriched in the inflamed, affected region.

4 s integration of transplanted cells into the inflamed and cytotoxic region of damaged tissue.

5 ntial regulator of neutrophil recruitment to inflamed and damaged sites and plays prominent roles in

6 sion of mesenteric adipose tissue around the inflamed and fibrotic intestine.

7 oskeleton is critical for cell activation in inflamed and fibrotic tissues; however, the cytoskeleton

8 alpha Western blot/messenger RNA analysis of inflamed and healthy ankles to confirm our in vivo resul

9 tissue undergoes marked hyperplasia, becomes inflamed and invasive, and destroys the joint(1,2).

10 Copper levels are known to be elevated in inflamed and malignant tissues.

11 omics, epigenomics and genetics from matched inflamed and non-inflamed colonic mucosa [50 Crohn's dis

12 In conclusion, inflamed and non-inflamed colonic segments in both CD an

13 Although a subset of sarcomas appears inflamed and responsive to immune checkpoint blockade wi

14 immune cell counts were used to distinguish inflamed and uninflamed subgroups of depression and to i

15 and a 45-fold elevation in ROS expression in inflamed ankles compared with the ankles of healthy cont

16 y differentiated Treg cells relocated to the inflamed aorta in atherosclerosis-prone low-density lipo

17 rtiary lymph node structures, more common in Inflamed, are associated with better survival.

18 as required for arrest and diapedesis across inflamed arterial endothelium to a greater extent in non

19 tery disease (CAD), and their recruitment to inflamed arteries is implicated in events leading to mor

20 s non-toxic and chemically robust within the inflamed biological environment.

21 In humans, ESRP1 is downregulated in inflamed biopsies from inflammatory bowel disease patien

22 We recovered N. animaloris from chronically inflamed bite wounds on pectoral fins and tailstocks, fr

23 However, their formation in inflamed blood vessels produces a scaffold that supports

24 t increasing interstitial hemorrhages in the inflamed bowel or other organs.

25 window and flow cytometry showed that in the inflamed brain anti-VCAM/liposomes bind to endothelium,

26 med specific anti-VCAM/liposome targeting to inflamed brain in mice.

27 cell adhesion molecule 1 (anti-VCAM) in the inflamed brain is >10-fold greater than antibodies to tr

28 The uptake in the inflamed brain of respective untargeted IgG counterparts

29 How emotional stressors can lead to an inflamed brain that directly affects physiology and acti

30 2-fold and 5-fold elevation of uptake in the inflamed brain vs levels attained by IV injection.

31 es bind to the lumen of blood vessels in the inflamed brain within minutes after injection.

32 Anti-VCAM/LNP selectively accumulated in the inflamed brain, providing de novo expression of proteins

33 a platform for cerebrovascular targeting to inflamed brain, with the goal of normalizing the integri

34 ne (MDK) as a melanoma-secreted driver of an inflamed, but immune evasive, microenvironment that defi

35 Neutrophil elastase activity is detected in inflamed, but not healthy, colons.

36 t, it is present in plasma from mice acutely inflamed by injection of high dose of lipopolysaccharide

37 hocytes (Tregs) in mouse lung experimentally inflamed by intratracheal administration of lipopolysacc

38 at arterial regions of atherosusceptible-SS inflamed by low-dose TNFalpha.

39 ing a primate, enables macrophage imaging in inflamed cardiovascular tissues.

40 he bowel wall, which can become infected and inflamed causing diverticulitis, with potentially severe

41 ncluding those occurring in the persistently inflamed central nervous system (CNS).

42 y T cells preferentially infiltrate into the inflamed CNS resulting from the initial phase and that t

43 llowing transplantation into the chronically inflamed CNS.

44 We report that opioids from the inflamed colon activate delta-opioid receptors (DOPr) in

45 to inflammatory pathways activated in human inflamed colon and TNF-alpha-treated cells (false discov

46 In the inflamed colon of humans and mice, we found decreased le

47 ICAM-1-expressing macrophages were noted in inflamed colon tissue in a murine colitis model and in h

48 receptor (IL-7R) pathway are accumulated in inflamed colon tissues of severe CD and UC patients not

49 s repair of damaged intestinal epithelium in inflamed colon, serves as a potential therapy for IBD.

50 ased on morphological characteristics of the inflamed colon.

51 s and genetics from matched inflamed and non-inflamed colonic mucosa [50 Crohn's disease (CD); 80 ulc

52 Biopsy samples of inflamed colonic mucosa from patients and mice with coli

53 utrophil elastase (NE) have been reported in inflamed colonic mucosal tissue.

54 In conclusion, inflamed and non-inflamed colonic segments in both CD and UC differ in mi

55 ntracted structures were not observed in the inflamed colons of AKAP12 knockout (KO) mice.

56 proinflammatory cyto/chemokine production in inflamed colons.

57 To mimic an inflamed condition, RANKL upregulation in human mandibul

58 f myelomonocytic cell recruitment in acutely inflamed contexts.

59 In the lymphoid organs and inflamed corneal tissues, MDSCs were phenotypically char

60 Monocyte recruitment to inflamed coronary arteries is initiated by high affinity

61 adhesion and transmigration in the TNF-alpha-inflamed cremaster muscle and a prolongation of chemokin

62 ak formation in postcapillary venules of the inflamed cremaster muscle at sites of neutrophil extrava

63 airs leukocyte adhesion and extravasation in inflamed cremaster muscle venules in comparison with con

64 Intravital microscopy of TNFalpha-inflamed cremaster muscles in Myo1e-deficient mice revea

65 ng intravital confocal microscopy applied to inflamed cremaster muscles.

66 The repair of inflamed, demyelinated lesions as in multiple sclerosis

67 te blood cell transcriptional biomarkers for inflamed depression seems warranted.

68 forced binary clustering of cell counts: the inflamed depression subgroup (n = 81 out of 206; 39%) ha

69 may be mechanistically distinct subgroups of inflamed depression.

70 hat shape Th1 and Th2 cell navigation of the inflamed dermis.

71 express LTB(4) receptors (R) in vitro and in inflamed draining lymph nodes.

72 antly higher (64)Cu-alphaCD11b uptake in the inflamed ears in the acute inflammation phase than the c

73 hat has been isolated several times from the inflamed ears of Zebu cattle in Eastern Africa, where it

74 umulation of infiltrating macrophages in the inflamed ECM and propose P5 peptide as a potential inhib

75 Deleterious effects of Tr-OxPLs on inflamed ECs stimulated with CM were associated with fur

76 also required for neutrophil adhesion on the inflamed endothelial layer.

77 orporated into liposomes, designed to target inflamed endothelium, shows reduced atherosclerosis and

78 Tregs can undergo prolonged migration on the inflamed endothelium.

79 mune response to bacterial infection in this inflamed environment is poorly understood.

80 ty of bacteria to persist within chronically inflamed environments.

81 chanism of loss of function of exosomes from inflamed EPCs is still obscure.

82 ess responses, and successful performance on inflamed fibrotic kidney.

83 uses to aid in colonizing and persisting in inflamed gastric tissue.

84 ated with low tumor mutational burden/T cell-inflamed gene expression signature (GES) or high immunos

85 The T cell-inflamed GEP contained IFN-gamma-responsive genes relate

86 s and eventually defining a pan-tumor T cell-inflamed GEP in 220 patients with 9 cancers.

87 urvival in corneal allograft recipients with inflamed graft beds.

88 differed (P < 0.05) from baseline within the inflamed group were ferritin (elevated day 3), hepcidin

89 une cells, we observed that macrophages from inflamed gut acquire an anti-inflammatory/reparative pro

90 metabolism and epithelial repair in virally inflamed gut and as a potential mitochondrial target for

91 difficile to repurpose toxic heme within the inflamed gut as a shield against antimicrobial compounds

92 its metabolism to catabolize L-serine in the inflamed gut in order to maximize its growth potential.

93 mprinted with gut tropism and migrate to the inflamed gut.

94 intestinal microenvironments and immunity in inflamed gut.

95 an intestinal antibodies in both healthy and inflamed gut.

96 growth advantage against competitors in the inflamed gut.

97 shed in vitro and the effects of micro-EI on inflamed hAF cells were evaluated using the micro-EI-chi

98 oncept study, a model involving degenerative inflamed human annulus fibrosus (hAF) cells was establis

99 Recruitment on inflamed human aortic endothelium or rVCAM-1 under fluid

100 Mice carrying inflamed human arteries were treated with tofacitinib or

101 Msx2 expression was detected in healthy and inflamed human gingival tissues.

102 Inflamed human hepatocytes attracted neutrophils more ef

103 while transplant sarcomas resemble the most inflamed human sarcomas.

104 from a circulating pool of T cells into non-inflamed human skin in vivo.

105 ironment of ES closely resembled that of non-inflamed human skin.

106 - and nanosized implant-related particles in inflamed human tissues around titanium and ceramic denta

107 In inflamed human tissues, we often find intact eosinophili

108 We showed the existence of an inflamed ICC subtype, which is potentially treatable wit

109 We revealed the existence of an inflamed ICC subtype, which is potentially treatable wit

110 Inflamed ileal tissues from patients and mice had reduce

111 Levels of IFNL are increased in serum and inflamed ileal tissues from patients with CD and associa

112 elevated in absorptive enterocytes from the inflamed ileal tissues of Crohn disease patients compare

113 increased cell death at the crypt bottom in inflamed ileum samples.

114 ve few additional mutations yet also have an inflamed immunophenotype and should respond to ICI thera

115 d, to a lesser degree, the arterial wall are inflamed in HIV, inflammation in these tissues is not cl

116 rum into Simian immunodeficiency virus (SIV)-inflamed intestinal lumen.

117 AMT-101 was taken up by inflamed intestinal mucosa and activated pSTAT3 in the l

118 we show that, relative to healthy controls, inflamed intestinal tissues from patients with IBD expre

119 ) 17 cell pathway molecules are increased in inflamed intestinal tissues of patients with IBD.

120 robial stimulation in mice, prominent in the inflamed intestine of humans, and essential for tissue r

121 In the inflamed intestine of patients with IBD, there was a dec

122 Specifically, in the inflamed intestine, monocyte ablation was shown to ameli

123 monoclonal antibodies from both healthy and inflamed intestines bound phylogenetically unrelated bac

124 cate a monocytic origin of CD11c(+) cells in inflamed islets and suggest that therapeutic regulatory

125 Ccl5 and Ccl8 were persistently elevated in inflamed islets and the influx of CD11c(+) cells was par

126 tion while increasing Tregs in the remaining inflamed islets.

127 ompared with nontransgenic NOD TLOs found in inflamed islets.

128 defective clearance of neutrophils from the inflamed joint and failed arthritis resolution.

129 The uptake of radiolabeled 28H1 in inflamed joints (percentage injected dose) correlated wi

130 C5orf30 is highly expressed in inflamed joints and is a negative regulator of tissue da

131 nexpectedly, at extramedullary sites: in the inflamed joints and spleen.

132 Four days after BMNC treatment, inflamed joints had 24% higher macrophage counts with 10

133 is from ultrasound-guided synovial biopsy of inflamed joints in a well characterized clinical cohort

134 significant uptake of an IRDye800CW agent in inflamed joints of a collagen antibody induced arthritis

135 most abundant immune cells found in actively inflamed joints of patients with rheumatoid arthritis (R

136 The presence of this cytokine in the inflamed joints of patients with rheumatoid arthritis (R

137 e responses and were clearly enriched within inflamed joints of SpA patients where they act as major

138 cells, reduced accumulation of Treg cells in inflamed joints, and loss of inhibitory activity.

139 of subsets of macrophages within healthy and inflamed joints, and study the roles of these macrophage

140 ate that IL-4 limits neutrophil migration to inflamed joints, and that CSF3 combined with IL-4 or IL-

141 e to autologous BMNC injection in normal and inflamed joints.

142 e synovium, possibly by expressing CXCL10 in inflamed joints.

143 he immunoregulatory function of ILC2s in the inflamed liver remains elusive.

144 is an important driver of the activation of inflamed LN stromal cells, through metabolic reprogrammi

145 , and interstitial macrophages, which in the inflamed lung expressed the IL-25 receptor and produced

146 rophage numbers in the infarcted myocardium, inflamed lung regions, and atherosclerotic plaques using

147 -2 and MHC-II colocalization was observed in inflamed lung tissue and IDLA cells of AT-II cellular or

148 the upregulation of MHC-II on AT-II cells in inflamed lung tissue.

149 rectly affecting the migration of ILC2s into inflamed lung tissues.

150 oxp3(+) Tregs are rapidly mobilized into the inflamed lung tissues.

151 ithin a hypoxic inflamed niche; in contrast, inflamed lung treatment with IL-4 accelerated resolution

152 phages and bronchial epithelial cells in the inflamed lung, suggesting that an innate RGMb-neogenin a

153 and following neutrophil recruitment to the inflamed lung.

154 mmatory monocytes from granulocytes in their inflamed lungs.

155 ytes and DCs migrate from the blood into the inflamed lungs.

156 olong their presence in both the healthy and inflamed lungs.

157 atory effect when cultured in tandem with an inflamed lymphocyte population.

158 We found that miR-124-3p promoted the anti-inflamed M2 polarization in microglia, and microglial ex

159 Ongoing pain from inflamed masseter muscle was also reduced in KI mice, an

160 he maintenance of mechanical hyperalgesia of inflamed masseter muscle.

161 IEC nearly abrogated fibrosis development in inflamed mice.

162 typically have high mutation burdens and an inflamed microenvironment and thus are poised to respond

163 However, whether quantifying T cell-inflamed microenvironment is a useful pan-tumor determin

164 ion, rendering platelets gate-keepers of the inflamed microvasculature.

165 ters neutrophil:lymphocyte ratio, leading to inflamed milieu in acute heart failure.

166 a mechanism of Nur77-dependent clearance of inflamed mitochondria to alleviate inflammation.

167 endothelial cell-derived exosomes (TNFalpha inflamed mouse cardiac endothelial cell-derived exosome)

168 attracted neutrophils more effectively than inflamed mouse hepatocytes because of the greater induct

169 multinucleated cells at the bone surface of inflamed mouse joints.

170 etecting adenomas against the backdrop of an inflamed mucosa (e.g. in ulcerative colitis) remains exc

171 TL1A expression is increased in inflamed mucosa and associated with fibrostenosing Crohn

172 erexpressed MFSD2A not only localized to the inflamed mucosa but also restored the ability of the end

173 fic ISLR and ETS1 significantly increased in inflamed mucosa of human IBD patients and in human color

174 cells that present DQ2.5-glia-alpha1a in the inflamed mucosa.

175 nflammatory or immuno-oncology treatments of inflamed multi-cellular tissues and the tumor microenvir

176 r to the human settings were not seen in the inflamed murine dermis.

177 carditis, (18)F-FOL shows specific uptake in inflamed myocardium containing macrophages expressing FR

178 Uptake of (18)F-FOL in inflamed myocardium was efficiently blocked by a nonlabe

179 glia, which enhances the sensitivity of the inflamed neurons as well as nearby uninjured afferents,

180 ls had a survival advantage within a hypoxic inflamed niche; in contrast, inflamed lung treatment wit

181 phenotypically distinct from the B cells in inflamed nodes, which are known to accumulate in joint-d

182 cally starting in early adulthood, cutaneous inflamed nodules, abscesses and pus-discharging tunnels

183 gain the ability to access both healthy and inflamed nonlymphoid tissues.

184 atients maintain what grossly looks like non-inflamed, normal skin in the face of massive inflammator

185 nd is not detected in plasma from moderately inflamed obese mice.

186 d-derived suppressor cells (MDSCs), populate inflamed or cancerous tissue and block immune cell effec

187 nd cellular biomarker profiles often seen in inflamed or cancerous tissues.

188 lls of an autoreactive T-cell clone found in inflamed organs, while maintaining active adaptive immun

189 esignated PD-L1 platelets) accumulate in the inflamed pancreas and may suppress the activity of pancr

190 Importantly, signal enhancement of the inflamed pancreas correlates strongly and significantly

191 es strong, selective contrast enhancement of inflamed pancreatic tissue in a mouse model (caerulein/L

192 on of PB, contralateral or ipsilateral to an inflamed paw [1 h, 1 d, or 5-6 d after intraplantar inje

193 dorsal root ganglion neurons innervating the inflamed paw, and augmented TRP channel-mediated calcium

194 beta-endorphin levels increased in the inflamed paw, and this increase and the antihyperalgesic

195 ted responses in nociceptors innervating the inflamed paw, but not in those innervating healthy tissu

196 udy was the histologic classification of the inflamed peri-implant soft tissue around ceramic implant

197 idence to assess the impact of the amount of inflamed periodontal tissue on the levels of systemic in

198 educed the number of SETD1-positive cells in inflamed periodontal tissues, restored periodontal tissu

199 h high expression of CCR5, which keeps DC in inflamed peripheral tissues.

200 oxB8 neutrophils were able to migrate to the inflamed peritoneum and to phagocytose heat-killed Candi

201 that in vivo neutrophil recruitment into the inflamed peritoneum of mice remains intact in the absenc

202 ation of so-called don't eat me molecules on inflamed phagocytes, which reduces their capacity for pr

203 port of MAA presenting as inguinal pain with inflamed phlegmonous tissue and scrotal abscess.

204 After 8 h, 1 inflamed radiocarpal and 1 normal tarsocrural joint rece

205 ulate an anti-inflammatory factor (IL-10) in inflamed Raw 264.7 cells.

206 Prss8 gene caused spontaneous colitis and an inflamed rectum at an early age and caused intestinal tu

207 tify three proteomic subtypes, two of which (Inflamed, Redox) comprise 87% of tumors.

208 istent CD11b(+) microglia/macrophages in the inflamed regions on day 30 p.i.

209 -25% of individuals, the diverticulae become inflamed, resulting in diverticulitis.

210 , displaying efficacy only on pathologically inflamed samples.

211 ved in PD pathophysiology, is upregulated in inflamed segments of Crohn's colon.

212 t the source of periostin and VCAM-1 was the inflamed sheep liver tissue.

213 t preclude the precipitation of sHLH in TLR9-inflamed SIRPalpha(-/-) mice, whereas macrophage depleti

214 xis of M0 or M2 phenotype macrophages to the inflamed site and induce M2 phenotype polarization local

215 by controlling neutrophil recruitment to the inflamed site and survival and function therein.

216 ontrast, analysis of cellular recruitment to inflamed sites provides evidence of specificity of recep

217 ic signals to direct neutrophil migration to inflamed sites through its receptor BLT1.

218 and eosinophilic recruitment to resting and inflamed sites.

219 the delivery of drug-loaded liposomes to an inflamed skeletal muscle in mice.

220 attenuates the recruitment of neutrophils to inflamed skin through reduction of chemokine production

221 IgE-bearing basophils are recruited to inflamed skin via CXCL12 and thymic stromal lymphopoieti

222 In the inflamed skin, IgE/FcepsilonRI-signalling in basophils p

223 S by promoting Treg stability and fitness in inflamed skin.

224 ulatory T cell recruitment and activation in inflamed skin; however, the role of regulatory T cells i

225 teristics between Th17 and Treg cells in the inflamed spinal cord and reveal three potential cellular

226 ociated with a profound hypoperfusion of the inflamed spinal cord.

227 and heart at a steady-state resulting in an inflamed splenocardiac axis.

228 DCAF15 disruption induced an inflamed state in leukemic cells, including increased ex

229 astric corpus; its expression in chronically inflamed stomachs (from TxA23 mice and mice with Helicob

230 In analyses of tissues from chronically inflamed stomachs of mice and humans, we expanded the de

231 rols) and TxA23 mice, which have chronically inflamed stomachs with metaplasia.

232 had distinct transcriptomes, in chronically inflamed stomachs, these cells had distinct transcriptio

233 ium to metaplastic epithelium in chronically inflamed stomachs.

234 dia that simulate nutritional aspects of the inflamed subgingival environment.

235 The inflamed subtype (11%) presented a massive T lymphocyte

236 The inflamed subtype (11%) presented a massive T-lymphocyte

237 The Inflamed subtype is enriched with neutrophils, B-cells,

238 Periodontal inflamed surface area (PISA) and FMD were assessed in al

239 sCRP) and both periodontitis and periodontal inflamed surface area (PISA) in adults with end-stage re

240 The periodontal inflamed surface area (PISA) was calculated for each par

241 parameters were recorded and the periodontal inflamed surface area (PISA) was calculated to quantify

242 ers were recorded as well as the Periodontal Inflamed Surface Area and the Periodontal Index for Risk

243 ated the response of BMNC to normal (SF) and inflamed synovial fluid (ISF).

244 fusion-weighted imaging (DWI) can depict the inflamed synovial membrane in arthritis.

245 t macrophages, infiltrating macrophages from inflamed synovium and tumor-associated macrophages.

246 clast precursor-containing population in the inflamed synovium, comprising a subset distinct from con

247 le at the same time amplifying LXA(4) in the inflamed target tissue.

248 * constitutes the major CRP species in human-inflamed tissue and allows binding of complement factor

249 ble to transport drug-loaded nanocarriers to inflamed tissue by exploiting the inherent ability of ne

250 lized delivery of immunosuppressive drugs to inflamed tissue in a non-invasive manner offers signific

251 n, mirroring macrophage metabolic changes in inflamed tissue in vivo.

252 eptors are increased in the blood and within inflamed tissue of patients with rheumatic diseases, suc

253 identify and profile ILCs across healthy and inflamed tissue types.

254 neutrophils systemically circulate and enter inflamed tissue, and pharmaceutical based targeting of t

255 culature to inhibit them from migrating into inflamed tissue.

256 ukocytes for microvascular clot formation in inflamed tissue.

257 abetes by supporting macrophage retention in inflamed tissue.

258 (+) T-cell phenotypes present in chronically inflamed tissue.

259 trafollicular plasmablast development within inflamed tissue.

260 ead to enhanced recruitment of leukocytes to inflamed tissue.

261 heterogeneity between malignant, benign, and inflamed tissue.

262 signatures that suggest their recruitment to inflamed tissues and a putative role of these T cells in

263 ed immunities following their recruitment to inflamed tissues and lymphoid organs.

264 nonspecific T cells with homing capacity to inflamed tissues are associated with severe LF.IMPORTANC

265 Further, because hypoxic inflamed tissues are associated with the overexpression

266 propensity for particle accumulation in the inflamed tissues around dental implants and will help in

267 ion, including their ability to migrate into inflamed tissues during autoimmune disease.

268 gnals that control endothelial plasticity in inflamed tissues have only been partially characterized.

269 tabolic profile of macrophages isolated from inflamed tissues in immune complex (IC)-associated disea

270 ngle-cell RNA analysis of ILCs isolated from inflamed tissues indicates that RORalpha perturbation le

271 The neutrophil recruitment cascade to inflamed tissues involves elements of neutrophil rolling

272 how these cells are sustained in chronically inflamed tissues remains unclear.

273 tients expressed a unique cellular module in inflamed tissues that consisted of IgG plasma cells, inf

274 g proteins, which enter the bloodstream from inflamed tissues, also offers insight into global IFN ac

275 adhesion and recruitment of immune cells to inflamed tissues, in quantifying lung inflammation in a

276 circulating T cells with homing capacity to inflamed tissues, including the gut mucosa.

277 D-1; the former is ubiquitously expressed in inflamed tissues, whereas the latter is restricted to an

278 required for effector T cell trafficking to inflamed tissues, without affecting naive T cell entry i

279 SEMA3F in inflammatory cell retention within inflamed tissues.

280 nvironmental cues for optimal exploration of inflamed tissues.

281 rophils or lymphocytes to resting or acutely inflamed tissues.

282 influences CD4(+) effector T (Teff) cells in inflamed tissues.

283 effectors of innate immunity and enriched in inflamed tissues.

284 neonatal monocytes are capable of colonizing inflamed tissues.

285 -driver mutations in DNMT3A exhibit a highly inflamed transcriptome, which may contribute to the aggr

286 cellular immune profile, resulting in a more inflamed tumor environment with enhanced T-cell infiltra

287 mmunotherapy, factors that define the T cell inflamed tumor microenvironment are not fully understood

288 itor and anti-PD-1/PD-L1 antibody for T cell-inflamed tumors such as PDACs treated with vaccine thera

289 nresponsive patients tend to have non-T-cell-inflamed tumors that lack markers associated with the ac

290 by CD103(+) dendritic cells (DCs) in T cell-inflamed tumors.

291 By inducing an inflamed, type I IFN-enriched tumour microenvironment an

292 of neutrophil-rolling interactions with the inflamed vasculature and occurs through GEF-H1-dependent

293 ia to scan for fibrin(ogen) deposited on the inflamed vasculature and to directionally spread, to pol

294 tes shape the rheological environment in the inflamed venular microvasculature for platelet aggregati

295 y an order of magnitude higher uptake in the inflamed vs normal brain (from ~0.1 to 0.8%ID/g for lipo

296 ecause dystrophic muscles become extensively inflamed, we tested whether expressing a therapeutic tra

297 and fail to fully develop sHLH, albeit TLR9-inflamed wild-type and CD47(-/-) mice exhibited hemophag

298 uates monocyte adhesion to endothelial cells inflamed with tumor necrosis factor alpha (TNF-alpha) by

299 Overall, male animals appear to have more inflamed yet smaller plaques compared to female animals.

300 ruitment of leukocytes from blood vessels to inflamed zones is guided by biochemical and mechanical s