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1 s as well as in infiltrating immune cells in diseased tissue.
2 IHC, and ELISA in all samples of healthy and diseased tissue.
3 cular targets of disease are isolated in the diseased tissue.
4 action and show that pHLIP can target acidic diseased tissue.
5 iver nanoparticles to the endothelium of the diseased tissue.
6 atment hemispherectomy, allowing sampling of diseased tissue.
7 as a stimulus for targeted drug delivery to diseased tissue.
8 time and are able to actively migrate to the diseased tissue.
9 mical analysis of crystallized structures in diseased tissue.
10 1 human and 89 mouse tissue types, including diseased tissue.
11 ve ion mode in normal tissue relative to the diseased tissue.
12 ecific Treg and Tconv cells were enriched in diseased tissue.
13 eagents targeting intracellular processes in diseased tissue.
14 e medicine holds great promise for repair of diseased tissue.
15 in biological properties between normal and diseased tissue.
16 the characteristic amyloid fibrils found in diseased tissue.
17 multipotent stem cells to regenerate lost or diseased tissue.
18 ficant difference between the normal and the diseased tissue.
19 detect pathogenic microbes in primary human-diseased tissue.
20 sts, which also stain positively for CD68 in diseased tissue.
21 ailed comparison of proteins from normal and diseased tissue.
22 accumulated in a periductal distribution in diseased tissue.
23 tch-3 expression appeared to be increased in diseased tissue.
24 all vessels within the portal tract septa of diseased tissue.
25 cellular biological processes in normal and diseased tissue.
26 and functional contrast between healthy and diseased tissue.
27 IL-6 production by fibroblasts derived from diseased tissue.
28 rting a greater proportion of osteoid in the diseased tissue.
29 te to the deficiency of nNOS activity in the diseased tissue.
30 y the absence of nerve ganglion cells in the diseased tissue.
31 a greater abundance of pathogenic genera in diseased tissue.
32 e generation of cell models from healthy and diseased tissue.
33 g continual efferocytosis and the removal of diseased tissue.
34 cific microanatomical domains in healthy and diseased tissue.
35 knowledge of target expression levels in the diseased tissue.
36 onse and enhance therapeutic delivery to the diseased tissue.
37 e identified, with T7 and T8 enriched in the diseased tissue.
38 racellular matrix or to deliver a payload to diseased tissue.
39 lymer chains to favour their accumulation in diseased tissue.
40 mechanotransductive processes in normal and diseased tissue.
41 we aim to study the molecular signature of a diseased tissue.
42 stered nanomaterials and prevent delivery to diseased tissue.
43 growth can be exploited in treating aged and diseased tissues.
44 ggers massive metabolic reprogramming in the diseased tissues.
45 rol recruitment of pathogenic lymphocytes in diseased tissues.
46 ical roles of sodium channels in healthy and diseased tissues.
47 y of glucocorticoid signaling in healthy and diseased tissues.
48 veloping agents to target the endothelium in diseased tissues.
49 patial cholesterol metabolism in healthy and diseased tissues.
50 ge-scale studies of chromatin from normal or diseased tissues.
51 s known about NeuPSA expression in normal or diseased tissues.
52 individual subjects, including of normal and diseased tissues.
53 en therapies that will regenerate and repair diseased tissues.
54 utic and imaging agents to select organs and diseased tissues.
55 evelopment is selectively targeting drugs to diseased tissues.
56 ive properties that accumulate in normal and diseased tissues.
57 uently seed fibrillation and deposition into diseased tissues.
58 y of other imaging and therapeutic agents to diseased tissues.
59 overcome the issues of harvesting cells from diseased tissues.
60 ent for this cellular treatment strategy for diseased tissues.
61 nd proliferations driven by an Ag present in diseased tissues.
62 en proteases and their cognate inhibitors in diseased tissues.
63 t also disrupts vascular barrier function in diseased tissues.
64 late monocyte adhesion and infiltration into diseased tissues.
65 man CD40, which is expressed by a variety of diseased tissues.
66 flows (IFs) are present in both healthy and diseased tissues.
67 ng vectors specific for endothelial cells in diseased tissues.
68 ize the composition of the ECM of normal and diseased tissues.
69 y effective for molecularly "fingerprinting" diseased tissues.
70 ivery of radioisotopes or chemical agents to diseased tissues.
71 vely proteinase-resistant isoform (PrPSc) in diseased tissues.
72 s for the delivery of therapeutic genes into diseased tissues.
73 ne structural parameters were altered in all diseased tissues.
74 d in cultured cells as well as in normal and diseased tissues.
75 ation that have been observed in Zn(2+)-rich diseased tissues.
76 s does not accurately reflect what occurs in diseased tissues.
77 o be expressed, with few exceptions, only in diseased tissues.
78 cules to accelerate the repair of injured or diseased tissues.
79 ersistence of proinflammatory macrophages in diseased tissues.
80 ssion of these cytokine mRNAs in healthy and diseased tissues.
81 solution and comprehensive molecular maps of diseased tissues.
82 r regeneration and restoration of injured or diseased tissues.
83 ase encapsulated drugs specifically to these diseased tissues.
84 ed clocks are often observed in patients and diseased tissues.
85 to enhance maintenance and repair of aged or diseased tissues.
86 ell data, particularly when studying complex diseased tissues.
87 nable us to control nanoparticle delivery to diseased tissues.
88 ssion differences and pathway alterations in diseased tissues.
89 ion and quantification of p16Ink4a+ cells in diseased tissues.
90 insights into cell plasticity in healthy and diseased tissues.
91 for isotope fractionation between normal and diseased tissues.
92 instead primarily maintained locally within diseased tissues.
93 sible light to damage malignant or otherwise diseased tissues.
94 o the regulation of cell death in normal and diseased tissues.
95 for treating calpain dysregulation in other diseased tissues.
96 are essential components of homeostatic and diseased tissues.
97 ying the intricate pathways altered in human diseased tissues.
98 spatial characterization of both healthy and diseased tissues.
99 ed by fibroblasts in both normal tissues and diseased tissues.
100 and gene expression dynamics in healthy and diseased tissues.
101 ility for prodrug delivery and activation in diseased tissues.
102 ng of mutational heterogeneity in normal and diseased tissues.
103 implicated in promoting apoptosis in various diseased tissues.
104 target the acidic environments of different diseased tissues.
105 NA-seq data from diverse types of normal and diseased tissues.
106 proteomes and their dynamics in healthy and diseased tissues.
107 pression of specific nucleic acid sensors in diseased tissues.
108 g healthy tissues, which decreased by 75% in diseased tissues.
109 ted by unfavorable environments in aging and diseased tissues.
110 f fundamental questions about the genomes of diseased tissues.
111 tanding the function of cells in healthy and diseased tissues.
112 the enrichment of cell subset signatures in diseased tissues.
113 ministration allows for direct access to the diseased tissues.
114 is drives blood vessel growth in healthy and diseased tissues.
115 ed drugs and structure-specific targeting to diseased tissues.
116 manner, thereby promoting arteriogenesis in diseased tissues.
117 Etiology drives progenitor fate within diseased tissues.
118 fine their physiological roles in normal and diseased tissues.
119 hage consortia differed between bleached and diseased tissues.
120 een a cell and its environment in intact and diseased tissues.
121 inimizing off-target interactions toward non-diseased tissues.
122 y tissues compared with bleached portions of diseased tissues.
123 nscriptomes from a wide range of healthy and diseased tissues across children and adults indicated th
125 tact spatial context of cells in healthy and diseased tissue, adding a novel dimension to data interp
126 and mean IL-6 concentrations were highest in diseased tissues adjacent to >6 mm sulci and were signif
128 We verified expression of AFP in normal and diseased tissue and generated an affinity-optimized T-ce
129 n is in the protein that is deposited in the diseased tissue and in these cases the whole protein is
130 ides contrast enhancement between normal and diseased tissue and microscopic imaging that provides ti
132 bably opportunistic colonizers of previously diseased tissue and others which are unique species.
133 f the presence of Mig in any human normal or diseased tissue and the first description of IP-10 in ce
134 in healthy cells differs from that found in diseased tissue and, if so, whether glycosylation affect
135 t analysis of single-cell genomics data from diseased tissues and a healthy reference can reveal alte
136 d characterization of gene expression within diseased tissues and circulating cells from animal model
137 enerically applicable for targeting cells to diseased tissues and elucidating the biology of cell-cel
138 cs showed that key subsets colocalize within diseased tissues and identified additional populations s
139 both granulocyte and monocyte trafficking to diseased tissues and immune-suppressive, profibrotic tra
140 requently isolated bacteria in periodontally diseased tissues and is reported to synergize with Pg, e
142 ulated by ETS2 were prominently expressed in diseased tissues and more enriched for inflammatory bowe
143 of synthetic implants in the restoration of diseased tissues and organs is to use inert and solid ma
147 e complex mechanisms of crystal formation in diseased tissues and their interplay with the nutrients,
148 ing, pHLIP has utility as an agent to target diseased tissues and translocate molecules through the m
149 umber of functional progenitors delivered to diseased tissue, and prevents correction of underlying p
150 ly occurring differences between healthy and diseased tissues, and active targeting, which utilizes v
151 an be used to distinguish between normal and diseased tissues, and the correlations between them are
152 of the mutant form of HTT is a key aspect of diseased tissues, and the most promising therapeutic app
153 f Kv1.3(high) expressing cells in normal and diseased tissues, and to visualize the distribution of f
154 ondrial proteomics data sets from normal and diseased tissue are published, MitoMiner can be used to
156 ies when the differences between healthy and diseased tissues are small; clinically, CT image noise i
159 ric to quantifiably differentiate normal and diseased tissues based on the physical properties of the
161 he measurement of MAO activity in normal and diseased tissues, blood samples, and other biological fl
162 idative stress and apoptosis are nitrated in diseased tissues but not in normal tissues; definitive e
163 used in strategies to regenerate and repair diseased tissues, but current therapies that go directly
164 ma delta + T cells were found in half of the diseased tissues, but in none of the healthy tissues of
165 ple macrophage phenotypes are represented in diseased tissues, but we lack deep understanding of mech
166 nd imaging are designed to accumulate in the diseased tissue by exploiting the Enhanced Permeability
168 ing, targeting, and possibly treating acidic diseased tissue by using the selective insertion and fol
169 to their potential for replacing damaged and diseased tissues by differentiating into tissue-specific
170 -gradient echo magnetic resonance imaging in diseased tissues can shed light on the pathological proc
171 d IFN-alpha mRNA was significantly higher in diseased tissues compared to healthy tissues in patients
175 lux kinetics of medical agents in normal and diseased tissues could be a new strategy for tackling ch
177 their potential to deliver drugs directly to diseased tissue, decrease off-target adverse effects, an
178 , IL-31 receptor expression was increased in diseased tissues derived from an animal model of airway
180 o an imaging agent, to select patients whose diseased tissues display sufficient targeted receptors f
182 ling of the fibronectin matrix in injured or diseased tissue elicits an EDA-dependent fibro-inflammat
183 therapeutic cells are incapable of targeting diseased tissues following systemic infusion, which repr
185 tool to study the cellular heterogeneity in diseased tissues for a variety of biological problems.
186 y of nanoparticles at the molecular level to diseased tissues for therapeutic and diagnostic applicat
190 datasets as input: an expression dataset of diseased tissues from patients with a disease of interes
191 ly relevant protein processing in normal and diseased tissue-from 40 to 70% of proteins also occur in
194 itor cells for the restoration of injured or diseased tissues has garnered much interest recently, es
195 though genome-wide transcriptome analysis on diseased tissues has greatly advanced our understanding
199 decoy receptor osteoprotegerin, measured in diseased tissue homogenates were significantly higher in
200 ilar concentration pattern within normal and diseased tissue; however, the concentration pattern of I
201 identify the sequences of microorganisms in diseased tissues, i.e., to identify organisms that appea
202 TRAF proteins are expressed in normal and diseased tissue in a regulated fashion, suggesting that
203 the central nervous system and for repair of diseased tissue in conditions such as Parkinson's diseas
205 ve ions inside a cell in vitro, and inside a diseased tissue in vivo, may indicate growth or recurren
206 fferentially transcribed between healthy and diseased tissues in colorectal cancer and chronic lympho
208 key to find novel avenues for CO delivery to diseased tissues in need of treatment, without concomita
209 delivery of oligonucleotides selectively to diseased tissues in the body, and specifically to the ce
211 and imaging MS has been applied to multiple diseased tissues, including human non-small cell lung tu
212 , protein, and activity levels in normal and diseased tissues indicate targeting applicability in a v
213 the TGF-beta superfamily, is upregulated in diseased tissue, indicating that it might be a useful th
215 tion of microRNA (miRNA) in cancer cells and diseased tissues is essential for advancing our comprehe
216 hibitors prevented increased NLRP3 levels in diseased tissue, limited the production of sHLH-associat
217 tral sensitivity, and selective targeting to diseased tissue make DENAQ a prime drug candidate for vi
218 Endogenous cues that are increased in the diseased tissue may amplify the activity of CD4(+)CD28(-
221 esses through the engineering of healthy and diseased tissue models towards the treatment of hypoxia-
223 identified candidate proteins for analyzing diseased tissues near or distal to salivary glands using
226 ted antigenic stimulation and are present in diseased tissues of patients with various autoimmune dis
227 sed gene expression libraries from normal or diseased tissues offer opportunities to interrogate cell
228 (HD; i.e. preceding the lesion boundary) to diseased tissue on diseased colonies (DD; i.e. lesion fr
230 ncrease in the interstitial water within the diseased tissue or a change in the vibrational modes of
231 d plasma) and others in the proximity of the diseased tissue or cell (e.g. bile, urine, and sputum) o
232 how do human eosinophils become activated in diseased tissues or at the site of an immune response?
234 profiling technologies to compare normal and diseased tissues or to assess molecular alterations resu
236 d to image wound healing in other injured or diseased tissues, or to monitor tissue changes over time
237 mportantly, our list of chimeric RNAs in non-diseased tissues overlaps with some entries in several c
239 (ECM) in directing cell fate in healthy and diseased tissues--particularly in development, wound hea
240 infiltration of different pancreaticobiliary diseased tissues (PDAC, ampullary carcinoma, cholangioca
241 population of patients, DCs recruited at the diseased tissue produce high levels of CCL-2 and IL-8 an
242 ve pharmacodelivery of cytotoxic payloads to diseased tissues, providing an innovative platform in ch
243 oor efficiency of nanomaterial delivery into diseased tissues, redistribution of nanomaterials within
244 teomic study of human glaucoma may represent diseased tissue-related antigens and serve as candidate
248 a crucial reference set for comparisons with diseased tissue samples to map the cellular foundations
250 performed, PCR products were sequenced, and diseased tissue samples were studied for intercellular j
251 e, small sample size and a heavy reliance on diseased tissue samples, often without age-matched healt
255 been identified in periodontal disease, and diseased tissues showed elevated RANKL mRNA expression,
256 rogeneous phenotypes, and their influence on diseased tissue stability remains poorly understood.
258 s have gained popularity since the pH in the diseased tissues such as cancer, bacterial infection and
259 For most ATAC-Seq data from healthy and diseased tissues such as tumors, chromatin accessibility
262 ription that will deliver radiation doses to diseased tissues sufficient to produce an effective trea
263 tylation in our studies was only detected in diseased tissue, suggesting it may have a role in pathol
264 ins was highly restricted in both normal and diseased tissues, suggesting defined physiological roles
265 NA copy number and dynamics in any normal or diseased tissue that can be used for monitoring the effe
266 A major limitation comes from the amount of diseased tissue that can be used for research purposes.
267 lex cellular and signaling dynamics in human diseased tissue that facilitate this debilitating diseas
268 resolution downloadable images of normal and diseased tissues that are searchable through orthogonal
269 nment is an integral component of normal and diseased tissues that is poorly understood owing to its
270 ts, and by the low levels of free calcium in diseased tissues that restrict the use of annexins.
272 ments, which are based on PS-induced harm to diseased tissues, the photoinduced cycle of singlet oxyg
275 which intimately interacts with healthy and diseased tissues through resident and recruited leukocyt
277 fying protein differences between normal and diseased tissue, thus providing the opportunity to searc
278 w top-down strategy for directly employing a diseased tissue to produce biofunctional nanovesicle-bas
279 s, reactive vasculature forms in response to diseased tissues to create new niches that secrete CXCL1
285 he expression of TCC isoforms in healthy and diseased tissue was investigated using quantitative real
287 onal skin as exemplar T(H)2 and T(H)1/T(H)17 diseased tissue, we sought to clarify common and unique
288 f placenta, hemangioma, and eight normal and diseased tissues were compared by hierarchical and nonhi
289 erentiate the healthy colon tissues from the diseased tissues were identified to be in the phosphodie
291 e repository of chimeric RNAs present in non-diseased tissues, which can be used as a control dataset
292 ace of the nanoparticle and molecules in the diseased tissue, while minimizing off-target interaction
294 issue engineering aims to replace damaged or diseased tissue with a functional regenerate that restor
295 ents with TMJ disorders an option to replace diseased tissue with autologous, functional tissue.
297 delivery of an anti-inflammatory cytokine to diseased tissue (with respect to unmodified stromal cell
298 enabling discrimination between healthy and diseased tissue, with the cell-killing ability of cytoto
299 ical epithelium or in stroma adjacent to the diseased tissues, with cellular proliferation and extrac
300 e examination of a variety of developing and diseased tissues, with specific focus on the dynamics of