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1                       Here we show that post-lesional AAV-assisted co-expression of two soluble prote
2 GABAergic) transmission has been reported in lesional acquired epilepsies (gliomas, hippocampal scler
3  1829 differentially expressed genes/DEGs in lesional AD and 662 DEGs in nonlesional AD, vs healthy s
4 )COL18A1(+) subpopulation that was unique to lesional AD and expressed CCL2 and CCL19 cytokines.
5 antly, immune activation extends well beyond lesional AD because nonlesional skin and the blood compo
6                This is the first report of a lesional AD phenotype using RNA-seq and the first direct
7                                          The lesional AD samples were characterized by expansion of i
8                                              Lesional AD skin shows a NK-cell dysregulation, which de
9 dysregulated genes in lesional psoriasis and lesional AD skin with 81% of AD dysregulated genes being
10                      We sought to define the lesional AD transcriptome using RNA-seq and compare it u
11 y of the T-cell receptor (TCR) repertoire in lesional AD, and its relation to nonlesional skin remain
12 ere higher than those of type 1 (IFNG(+)) in lesional AD, whereas this ratio was slightly diminished
13 unction (CLDN8) genes were primarily seen in lesional AD.
14 regulation of Cldn-4 in nonlesional, but not lesional, AD skin.
15 formed microarray and RT-PCR profiling of 27 lesional and 17 nonlesional scalp samples from patients
16  sequencing of the beta-TCR repertoire in 29 lesional and 19 nonlesional AD biopsies, compared to six
17                   As a result, we found peri-lesional and contralateral activations basically overlap
18 arametric classification was performed using lesional and global thresholds.
19           This ability to measure changes in lesional and healthy-appearing skin provides a new pathw
20 s were also differentially expressed between lesional and HV skin.
21 ifferences in collagen d-spacing between non-lesional and malignant tissues.
22 liative (seizure reduction) measure for both lesional and non-lesional forms of epilepsy.
23 s of P. acnes isolates recovered from paired lesional and non-lesional skin of PMH patients.
24 identification of biomarkers present in both lesional and non-lesional skin that correlate with psori
25  activated macrophages were observed in both lesional and non-lesional skin, but were elevated in les
26 ed distinct immune and barrier signatures in lesional and nonlesional AD and psoriasis skin, suggesti
27                           Nevertheless, both lesional and nonlesional AD showed a highly polyclonal T
28 t epidermal and dermal genomic signatures of lesional and nonlesional AD skin and normal skin compare
29                                              Lesional and nonlesional AD skin biopsies were collected
30  of the epidermal and dermal compartments of lesional and nonlesional AD skin compared with normal sk
31 xpression by immunohistochemical analysis of lesional and nonlesional cartilage from human and rodent
32 tially expressed proteins between paired PPR lesional and nonlesional explants.
33                                              Lesional and nonlesional skin biopsies were collected fr
34         We processed routine skin swabs from lesional and nonlesional skin from 40 patients with AD a
35                                  We assessed lesional and nonlesional skin from 59 patients with mode
36 rmed to separate the epidermis and dermis of lesional and nonlesional skin from patients with AD and
37 l DNA was analyzed from swabs collected from lesional and nonlesional skin in a double-blind, placebo
38 t a global transcriptome of tape strips from lesional and nonlesional skin of adults with moderate-to
39 kines were significantly elevated in both AD lesional and nonlesional skin of all patients regardless
40 A total of 20 tape strips were obtained from lesional and nonlesional skin of patients with AD and ps
41                         Genomic profiling of lesional and nonlesional skin of patients with atopic de
42                   We aimed to provide global lesional and nonlesional skin profiles of infants/toddle
43                                         Both lesional and nonlesional skin showed a stable "core" sig
44                                         Both lesional and nonlesional skin showed significant dysregu
45 samples and biopsies were obtained from both lesional and nonlesional skin to identify changes relate
46 lated differentially expressed genes between lesional and nonlesional skin to the AD transcriptome.
47 ubstudy where punch biopsies were collected (lesional and nonlesional skin) between baseline and 12 w
48 e mRNA and small RNA transcriptome in blood, lesional and nonlesional skin, and the SOMAscan platform
49 , the sharing of top abundant clones between lesional and nonlesional skin, and their persistence aft
50  and an increase in resting NK cells in both lesional and nonlesional skin, which was reverted by bot
51 cripts were differentially expressed between lesional and nonlesional skin.
52 , including Th2/Th22 cells, are increased in lesional and nonlesional skin.
53 gnificantly from that in healthy controls in lesional and nonlesional skin.
54 tures immune and barrier alterations in both lesional and nonlesional skin.
55 ns with increasing disease severity, in both lesional and nonlesional skin.
56         We evaluated age-specific changes in lesional and nonlesional tissues and blood from patients
57  AD, TCR repertoire diversity was similar in lesional and nonlesional tissues, and absolute numbers o
58 ncreased AD severity (P = .03) and increased lesional and nonlesional transepidermal water loss (P =
59 unch biopsy specimens from patients with HS (lesional and nonlesional) and healthy controls between O
60 eated transcriptomic profiles for 39,042 AD (lesional and nonlesional) and healthy skin cells.
61 ling from 19 infants/toddlers (<5 years old; lesional and nonlesional) with early-onset moderate-to-s
62 ral myelin, axonal and dendrite integrity in lesional and normal-appearing tissue of the cortex and t
63 ge multiple sclerosis, their distribution in lesional and normal-appearing tissue, and their correlat
64 ompared the ability of ipsi-lesional, contra-lesional and sham cerebellar rTMS to reverse the effects
65                                              Lesional and to a lesser extent nonlesional skin showed
66 ) and epidermal (thickness, K16) measures in lesional and, even more strongly, in nonlesional AD.
67  loss/TEWL) with immune and barrier mRNAs in lesional and/or nonlesional AD (FLG/FLG2 with TEWL; r <
68 ed ultrasound, has again stirred interest in lesional approaches.In this article, we will discuss the
69 iagnostically uninformative areas within the lesional area by using RCM and coregistered dermoscopy i
70                 Quantification of the aortic lesional area stained with oil red O revealed that CKD-b
71 uantify the uninformative regions within the lesional area.
72  of both NK cells and CD3(+)CD56(+) cells in lesional as compared with nonlesional and healthy skin.
73 22, PI3/Elafin) correlated between blood and lesional as well as non-lesional skin.
74                                              Lesional, atrophy, and DT diffusion tensor MR measures o
75 s were taken from nonlesional (baseline) and lesional (baseline, days 1 and 3, and weeks 1, 2, 4, and
76  of surgically removed tissue, including non-lesional, benign and malignant tumour.
77 ional biopsies gave higher positive DIF than lesional biopsies (P = .029).
78          DIF results were positive in 14% of lesional biopsies, in 86% of perilesional biopsies, and
79 d) proteins were differentially expressed in lesional biopsy specimens from patients with AE relative
80                                           On lesional biopsy, a lichenoid infiltrate was observed in
81 n that normobaric hyperoxia may benefit peri-lesional brain and white matter following traumatic brai
82 ilepsy in patients, particularly after focal/lesional brain injury.
83  recurrent MI in diabetes is due to a higher lesional burden and/or elevated risk factors rather than
84 g of AD, or SCORAD) are detected not only in lesional but also nonlesional skin and blood, more compl
85  with significant gene expression changes in lesional but also nonlesional skin, particularly reducti
86 7 cell (IL-17A, CCL20, and CXCL1) markers in lesional but not nonlesional skin.
87        In accord with our in vitro findings, lesional caspase 1 activity was abolished in P2X7(-/-) m
88 n together, in PKDL, the enhanced plasma and lesional CCL17 accounted for the dermal homing of CD8(+)
89                            Additionally, the lesional CCR4(+)CD8(+) population was associated with an
90  reduced expression of type 2 NO synthase by lesional CD11b(+) cells.
91  attributed to its impact on atherosclerotic lesional cells such as macrophages.
92                       Moreover, apoptosis of lesional cells was unaffected, and we found no evidence
93 ed twice weekly for 14 weeks, or until total lesional clearance was observed, whichever was earlier.
94        Here, we compared the ability of ipsi-lesional, contra-lesional and sham cerebellar rTMS to re
95  0.03; n = 7), nonlocalized (p < 0.001), and lesional cortical sites (p < 0.001) when compared to non
96                  Moreover, decreases in ipsi-lesional corticospinal tract integrity and increases in
97 ory cell population and cytokine profiles in lesional cutaneous lupus erythematosus skin could affect
98 se findings from functional neuroimaging and lesional data.
99       Routine use of WB/BC dosimetry without lesional dosimetry provided no OS advantage when compare
100 sion: Routine use of WB/BC dosimetry without lesional dosimetry provided no OS advantage when compare
101 oid hormone, although the impact of reducing lesional dosimetry requires attention and further invest
102 onal oxidative stress and necrosis, improved lesional efferocytosis, and thicker fibrous caps.
103 ected, and we found no evidence of defective lesional efferocytosis.
104  no granulomas were observed and only single lesional eosinophils were detected, GPTD does not resemb
105 Moreover, aberrant high BMP signaling in the lesional epidermis is mediated by a KC intrinsic mechani
106 ith refractory focal epilepsy presumed to be lesional, evaluation for surgery should be considered.
107 netic generalized epilepsy (n = 182) and non-lesional extratemporal epilepsy (n = 193).
108 esenting a 42% error) and conventional trans-lesional FFR(CT) (0.05+/-0.06; P<0.001, 37% error).
109   All investigated epilepsy types, including lesional focal epilepsy patients, showed an increase in
110 ileptic encephalopathy patients but also for lesional focal epilepsy patients.
111  Patients with genetic generalized epilepsy, lesional focal epilepsy, non-acquired focal epilepsy, an
112 reduction) measure for both lesional and non-lesional forms of epilepsy.
113 cortex that may be responsible for many 'non-lesional' forms of epilepsy.
114 weeks and approximately 70% normalization of lesional gene expression after 4 weeks.
115 he granuloma has proven difficult because of lesional heterogeneity and the limitations of animal mod
116                                Biopsies were lesional in 22% of cases (7/32), perilesional in 22% (7/
117 esolved plaque inflammation by inhibition of lesional inflammasome activation and reduced experimenta
118 entional candidate to attenuate dysregulated lesional inflammation and to restore functional recovery
119 riant, autoantibody binding is followed by a lesional inflammatory cell infiltration, and the overall
120 th a significant increase in levels of intra-lesional inflammatory markers.
121 ll group 2D (NKG2D) ligand expression in the lesional keratinocytes associated with a marked CD4+ T c
122 follicular and follicular stratum corneum of lesional KP, which correlated ultrastructurally with imp
123            Intrinsic vascular wall cells and lesional leukocytes alike can produce this cytokine.
124 ts also attenuates the EMT signature even in lesional lichen planopilaris hair follicles ex vivo.
125              Therefore, we hypothesized that lesional lipid mediator imbalance favors atheroprogressi
126                 MRI demonstrated significant lesional load in the optic radiation in MS compared to N
127 -26 reduces atherosclerotic lesion sizes and lesional macrophage accumulation.
128 2 key hallmarks of advanced atherosclerosis, lesional macrophage apoptosis and plaque necrosis, which
129  that hematopoietic Hdac9 deficiency reduces lesional macrophage content while increasing fibrous cap
130 lations of macrophages, the phenotype of the lesional macrophage is more complex and likely changes d
131 sses recent advances in our understanding of lesional macrophage phenotype and function in different
132 tes, although recent research has shown that lesional macrophage-like cells can also be derived from
133  revealed that MC1-R expression localizes in lesional macrophages and is significantly associated wit
134                                              Lesional macrophages are derived primarily from blood mo
135 crease in LRV1-induced disease severity, and lesional macrophages from these mice displayed reduced l
136                          CXCL9 expression in lesional macrophages implicates the skin as the source o
137 ges resulted in an increased total number of lesional macrophages in general and Ly6c(hi) infiltratin
138                          We demonstrate that lesional macrophages in WT mice express Axl but that Axl
139                                              Lesional macrophages take on different phenotypes depend
140 othelial cells, origins and contributions of lesional macrophages, and origins and phenotypic switchi
141 nce of apoptotic cells, or efferocytosis, by lesional macrophages, but the mechanisms underlying defe
142 n studies data were particularly enriched in lesional macrophages, endothelial, and smooth muscle cel
143 the increasing understanding of the roles of lesional macrophages, new research areas and treatment s
144 linked to cytokine and chemokine pathways in lesional macrophages, which demonstrates the potential o
145 ine atherosclerotic lesions, particularly by lesional macrophages.
146 01 [n=11], P=0.004) with a reduced amount of lesional macrophages.
147 eading to an altered number and phenotype of lesional macrophages.
148 age correlated positively with the number of lesional macrophages.
149 ly correlated with CD36 expression in aortic lesional macrophages.
150 plantation recurrence correlated with higher lesional maximum standardized uptake values: for PFS, P
151  of action of crisaborole and its effects on lesional measures of disease severity are not yet well d
152                                  At 5 years, lesional measures overtook magnetization transfer ratio
153 inal tract integrity and increases in contra-lesional medial reticulospinal tract integrity were corr
154                          The averages of all lesional median values for TBF and (18)F-FAZA V(T) were
155 xpression was also increased in inflammatory lesional morphea skin (fold change = 30.6, P = 0.006), a
156 transcriptional profiling of whole blood and lesional morphea skin, and used double-staining immunohi
157 erosclerotic lesion size by expansion of the lesional myeloid cell accumulation.
158  and derive future directions for functional lesional neurosurgery, in particularly potential trial d
159  Immune and barrier markers were measured in lesional, nonlesional, and healthy skin by quantitative
160 otropy decreased and mean diffusivity of non-lesional, normal-appearing white matter progressively in
161 lso compared with samples from patients with lesional or nonlesional AD and those with psoriasis.
162 omotes plaque stability, including decreased lesional oxidative stress and necrosis, improved lesiona
163 g accuracy (ipsi-lesional, P < 0.001, contra-lesional, P < 0.001).
164 sion' on PMEPs and swallowing accuracy (ipsi-lesional, P < 0.001, contra-lesional, P < 0.001).
165 ary outcomes were the differences in average lesional pain assessed by the Brief Pain Inventory and v
166         No significant difference in average lesional pain was observed between the study arms.
167 lesion mapping study investigating potential lesional patterns associated with headache in acute isch
168 njunctival biopsy locations were defined as "lesional," "perilesional," and "nonaffected" conjunctiva
169 ithin the atherosclerotic plaque, reactivate lesional phagocytosis and reduce the plaque burden in at
170 KC cultures grown from lesional (PP) and non-lesional (PN) biopsies of psoriasis patients and control
171  of primary monolayer KC cultures grown from lesional (PP) and non-lesional (PN) biopsies of psoriasi
172 expressed proteins in paired nonlesional and lesional PPR tissue (n = 5 patients).
173 c and proteomic profiles similar to those of lesional PPR.
174 e progression of advanced atherosclerosis or lesional processes associated with TAM receptor signalin
175                                           In lesional PRP skin samples from a single patient, upregul
176 cal imaging was conducted on lesions and non-lesional (pseudo-control) skin of 33 subjects diagnosed
177 ng correlation between dysregulated genes in lesional psoriasis and lesional AD skin with 81% of AD d
178 available TGF-beta family members within the lesional psoriatic epidermis preferentially signal throu
179 t is expressed at high levels throughout the lesional psoriatic epidermis.
180                  In a transcriptome study of lesional psoriatic skin (PP) versus normal skin, we foun
181    Furthermore, the strong IL-22 increase in lesional psoriatic skin was accompanied by a moderate in
182 ion is dysfunctional in both nonlesional and lesional psoriatic skin.
183 central vein sign, subpial demyelination and lesional rims), which are not included in the current mu
184  biopsy specimens from 5 patients with AD (4 lesional samples and 5 nonlesional samples) and 7 health
185 ellar rTMS to the ipsi-lesional side, contra-lesional side or sham while assessing PMEP amplitude or
186  pulses of 10 Hz cerebellar rTMS to the ipsi-lesional side, contra-lesional side or sham while assess
187      Upon treatment with omalizumab, >75% of lesional signatures changed to reflect nonlesional skin
188                          Two-thirds of these lesional signatures were also differentially expressed b
189                                              Lesional signatures were not modulated by treatment in n
190 e treatment resulted in early improvement in lesional signs/symptoms versus vehicle, with improvement
191 lating T cells that are primed to migrate to lesional sites at onset of inflammation are not poised f
192 nfiltrating immune cells expressed CXCL10 at lesional sites in skin of patients with BP.
193  DSS = 0) was observed in 16 (41%) psoriasis lesional sites treated with cyclosporine lipogel, 85.7%
194 esentation, the absence of CD4(+) T-cells at lesional sites was concomitant with an overwhelming infi
195 01; 95% CI, 13.77-24.51) in 59% of psoriasis lesional sites.
196 developed from separate, rather than initial lesional sites.
197 with HS, biopsy specimens were obtained from lesional skin (axilla or groin) and nonlesional skin.
198 genes expressed in nonlesional (NLS-CSU) and lesional skin (LS-CSU) and peripheral blood were identif
199                   Transcripts upregulated in lesional skin (vs nonlesional and/or HV skin) suggested
200 1beta is significantly elevated in psoriatic lesional skin and imiquimod-treated mouse skin.
201 terleukin-1beta (IL-1beta) is upregulated in lesional skin and mononuclear donor cells exposed to rec
202     Biopsies were taken from nonlesional and lesional skin at baseline and weeks 2 and 4.
203 ase in expression of 2645 genes expressed in lesional skin between patients receiving risankizumab an
204                                              Lesional skin biopsies from SAM syndrome patients (n = 7
205   Higher expression of B7-H6 was observed in lesional skin biopsies of patients with atopic dermatiti
206                                              Lesional skin biopsy samples from 81 patients with moder
207                                              Lesional skin biopsy samples were taken from this patien
208                                           In lesional skin children showed comparable or greater epid
209  genes differentially expressed in psoriatic lesional skin from a large-scale RNA sequencing cohort.
210 bserved to be more abundant in the dermis of lesional skin from AD patients.
211    miR-10a-5p was found to be upregulated in lesional skin from patients with AD and in proliferating
212                                        Never-lesional skin from patients with psoriasis (NLP) was col
213 n FDA-approved PAR1 antagonist, on explanted lesional skin from patients with psoriasis.
214 long noncoding RNA (lncRNA) transcriptome in lesional skin from psoriasis patients before (PP) and af
215 sease hallmarks (keratin 16 and loricrin) in lesional skin from responders (P < .05).
216  analysis revealed upregulation of CD200R in lesional skin from subjects with an extrinsic AD phenoty
217 mma-induced chemokine CXCL10 is expressed in lesional skin from vitiligo patients, and that it is cri
218                 Treatment-induced changes in lesional skin gene expression profiles were evaluated us
219  treatment resulted in reduced expression of lesional skin genes associated with IL-23/IL-17 signalin
220                            Before treatment, lesional skin had lower microbial diversity and higher o
221       Dissection of the pathologic events in lesional skin has led to knowledge of important cell pop
222 ease in the cutaneous nerve fiber density in lesional skin in vivo.
223 athologic epidermal alterations in psoriatic lesional skin include increased epidermal expression of
224                                           In lesional skin keratinocyte pSTAT1 and pSTAT3 staining wa
225                Cutaneous lupus erythematosus lesional skin microarray data and RNA sequencing data fr
226 kin of 33 subjects diagnosed with psoriasis, lesional skin of 7 subjects diagnosed with eczema, and h
227 es reflected an IFN-alpha-signature, whereas lesional skin of exanthemas showed induction of TH2-asso
228 phylococcus aureus (S. aureus) isolates from lesional skin of patients with AD, produced a substantia
229                         Activated T cells in lesional skin of patients with atopic dermatitis (AD) an
230 increased at the expense of ILC2s within the lesional skin of patients with psoriasis.
231 of miR-146a and miR-146b (miR-146a/b) in the lesional skin of patients with psoriasis.
232 n CD8(+) T cells isolated from the blood and lesional skin of patients with SSc with severe skin thic
233 lates recovered from paired lesional and non-lesional skin of PMH patients.
234 ns of filaggrin and human beta-defensin 2 in lesional skin of these patients were markedly reduced.
235              Moreover, regulatory T cells in lesional skin played an important role in disease remiss
236 expressed miRNAs between healthy skin and AD lesional skin resulted in the identification of miR-335
237                              From 1 patient, lesional skin samples were taken before ustekinumab trea
238 nd a reduced epidermal hyperproliferation at lesional skin sites.
239 43 expression was significantly lower in the lesional skin than in the nonlesional skin of patients w
240 in from patients with AD was more similar to lesional skin than to nonlesional skin of patients with
241 th biochemical and structural changes in non-lesional skin that can be assessed using clinically avai
242  biomarkers present in both lesional and non-lesional skin that correlate with psoriasis severity.
243  (AD) models link epidermal abnormalities in lesional skin to cytokine activation.
244                          ASN002 reversed the lesional skin transcriptome toward a nonlesional phenoty
245 1 in the upper and lower epidermal layers of lesional skin was detected.
246  penetration not only in intact, but also in lesional skin with impaired skin barrier function is imp
247 alignant T-cell clone could be identified in lesional skin, and a significant decrease in the fractio
248 hages were observed in both lesional and non-lesional skin, but were elevated in lesional skin.
249 pecies, bacteria enriched in human psoriatic lesional skin, has increased IL-1beta and dermal gammade
250                                           In lesional skin, microbiome types consisted predominantly
251                                        In AD lesional skin, miR-335 expression is aberrantly lost.
252 margination in the upper stratum spinosum in lesional skin, suggesting impaired intercellular adhesio
253  and non-lesional skin, but were elevated in lesional skin.
254 2 (IL-23p19/IL-8/S100A12) mRNA expression in lesional skin.
255 , STAT3 signaling, and cell proliferation in lesional skin.
256 otic treatment inhibits malignant T cells in lesional skin.
257  cytokines, levels of which are increased in lesional skin.
258 ed between blood and lesional as well as non-lesional skin.
259 ytokines and other inflammatory mediators in lesional skin.
260 ntly of myeloid origin, infiltrate psoriatic lesional skin.
261 ning, which was confirmed in human psoriatic lesional skin.
262  and KRT85) were significantly suppressed in lesional skin.
263 nounced changes were seen in nonlesional and lesional skin.
264  studies reveal skin microbiota shifts in HS lesional skin.
265  molecules or the numbers of immune cells in lesional skins.
266                       We show that activated lesional SMCs attract neutrophils, triggering the ejecti
267 ges, and origins and phenotypic switching of lesional smooth muscle cells.
268            Lesion quantity, mean and maximum lesional SUV, z score, and percentage of affected bone v
269  eligible for this study and had collected a lesional swab for polymerase chain reaction (PCR).
270                                              Lesional swabs were collected for real-time PCR testing
271 mplications of HLA-C*06:02 and mechanisms of lesional T cell activation in psoriasis, however, remain
272 erogenic T cell-derived interferon-gamma and lesional T cell infiltration, and was abrogated in CD4(+
273                                              Lesional T cells responded to tofacitinib with reduced p
274 nt vessel wall inflammation is maintained by lesional T cells, including the newly identified tissue-
275 ated reactions, discussing the nature of the lesional T cells, the characterization of drug-responsiv
276                      Most (87%) top expanded lesional T-cell clones were shared with nonlesional tiss
277                                     Cortical lesional T2* was compared with patients' normal-appearin
278 ecognition that host immunopathology affects lesional TB drug distribution means that pharmacokinetic
279 cent stroke studies have shown that the ipsi-lesional thalamus longitudinally and significantly decre
280 me was significantly smaller than the contra-lesional thalamus volume (t(68) = 13.89, p < 0.0001).
281                                     The ipsi-lesional thalamus volume was significantly smaller than
282 st significantly upregulated pathways in PPR lesional tissue and aligned with differently expressed p
283 c type surgical specimens into normal versus lesional tissue and low-grade versus high-grade tumors w
284                                        While lesional tissue is often visually indiscernible from nor
285                                       In non-lesional tissue the axial period of collagen is within t
286 of high levels of hypophosphorylated NRF2 in lesional tissue.
287 ties in Fabry disease were not restricted to lesional tissue; compared to healthy controls, the norma
288         The DD treponemes were isolated from lesional tissues but not from control feet or other area
289  under the cornoid lamella of PMVK-deficient lesional tissues, with incomplete differentiation of ker
290 cant percentage improvement from baseline in lesional transcriptomic profile compared with vehicle at
291 argets and the unsolved problem of bilateral lesional treatment.
292 onsistency, efficacy and side effect rate of lesional treatments for tremor are presented separately
293 , >/= 2.0; false discovery rate </= 0.05) in lesional versus nonlesional skin from 18 patients with m
294                                              Lesional vessels did not express GLUT1 or the lymphatic
295 rts describe the presence of CD8(+) T(RM) in lesional vitiligo patient skin and suggest their role as
296  greater T-cell infiltrates were observed in lesional vs nonlesional AD, TCR repertoire diversity was
297        We established the AA transcriptomes (lesional vs nonlesional: 734 DEGs [297 upregulated and 4
298 EGs [297 upregulated and 437 downregulated]; lesional vs normal: 4230 DEGs [1980 upregulated and 2250
299 cted by real-time quantitative PCR comparing lesional with perilesional or healthy skin.
300 ue in MS multiple sclerosis , whereas global lesional, WM white matter , and GM gray matter damage do

 
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