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1 ethylome in primary T cells of patients with systemic sclerosis.
2 cells and skin transcriptome changes, as in systemic sclerosis.
3 een in patients with the autoimmune disease, systemic sclerosis.
4 n 156 patients with severe diffuse cutaneous systemic sclerosis.
5 link between epidermal c-Rel expression and systemic sclerosis.
6 is and of other fibrotic disorders including systemic sclerosis.
7 in progressive vasculopathy in patients with systemic sclerosis.
8 atment of pulmonary arterial hypertension in systemic sclerosis.
9 pecimens of skin and lung from patients with systemic sclerosis.
10 lung injury, including that associated with systemic sclerosis.
11 of morbidity and mortality in patients with systemic sclerosis.
12 s as potential therapeutic interventions for systemic sclerosis.
13 the vascular manifestations associated with systemic sclerosis.
14 leading cause of mortality in patients with systemic sclerosis.
15 general population and >90% of patients with systemic sclerosis.
16 ease and severe skin disease associated with systemic sclerosis.
17 ase-modifying therapies for the treatment of systemic sclerosis.
18 released in a higher amount in patients with systemic sclerosis.
19 the sera of patients with diffuse cutaneous systemic sclerosis.
20 s a concern in an autoimmune disease such as systemic sclerosis.
21 therapies promise to have a major impact in systemic sclerosis.
22 on on platelet contributions, in general, to systemic sclerosis.
23 aggregation in different forms and stages of systemic sclerosis.
24 atibility complex haplotypes associated with systemic sclerosis.
25 ciencies of these surrogates in the study of systemic sclerosis.
26 d with immune-mediated conditions, including systemic sclerosis.
27 atins may be effective therapeutic agents in systemic sclerosis.
28 sociation (P = 8.5 x 10(-22); OR = 4.3) with systemic sclerosis.
29 he faSScinate phase 2 trial in patients with systemic sclerosis.
30 l class of genes involved in pathogenesis of systemic sclerosis.
31 , including systemic lupus erythematosus and systemic sclerosis.
32 ures, whose pathogenesis may be similar with systemic sclerosis.
33 tions in five large cohorts of patients with systemic sclerosis.
34 CXCL4 predicted the risk and progression of systemic sclerosis.
35 rticipants, the nailfolds in 2 patients with systemic sclerosis, 1 patient with dermatomyositis, and
36 ) has been implicated in driving fibrosis in systemic sclerosis, a mechanism-derived gene expression
37 osus affects from 161,000 to 322,000 adults, systemic sclerosis affects 49,000 adults, and primary Sj
40 st potential efficacy of imatinib in diffuse systemic sclerosis, although adverse events are common.
41 ical and histopathological similarities with systemic sclerosis, an autoimmune disease whose risk is
44 g pathways and mediators that are altered in systemic sclerosis and contribute to tissue damage allow
45 entially regulated between diffuse cutaneous systemic sclerosis and controls and correlated with modi
46 vels of CXCL4 were elevated in patients with systemic sclerosis and correlated with the presence and
48 Here, we review the clinical features of systemic sclerosis and describe the best practice approa
49 ession profiling studies of animal models of systemic sclerosis and explanted fibroblasts have helped
50 proteome of patients with diffuse cutaneous systemic sclerosis and identified differentially express
51 ling and participates in the pathogenesis of systemic sclerosis and idiopathic pulmonary fibrosis.
52 s aberrantly expressed in lesional tissue in systemic sclerosis and in a murine model of scleroderma.
53 s with diffuse systemic sclerosis or limited systemic sclerosis and interstitial lung disease who wer
54 the prototypic fibrotic autoimmune condition systemic sclerosis and is known to induce collagen I exp
57 allmark of many fibrotic diseases, including systemic sclerosis and pulmonary, liver, and kidney fibr
59 sma levels of CXCL4 protein with features of systemic sclerosis and studied the direct effects of CXC
60 eir receptor has been noted in patients with systemic sclerosis and systemic lupus erythematosus with
61 tic studies on stem cell transplantation for systemic sclerosis and their implications for clinical p
62 complications are important in scleroderma (systemic sclerosis) and include scleroderma renal crisis
63 c lupus erythematosus, rheumatoid arthritis, systemic sclerosis, and anti-neutrophil cytoplasmic anti
64 s in these mediators have been identified in systemic sclerosis, and may account for the characterist
67 chronically elevated endogenous IFNs such as systemic sclerosis are strongly associated with PAH.
69 s that can be learnt from clinical trials of systemic sclerosis-associated ILD and idiopathic pulmona
71 age (BAL) cellular profiles in patients with systemic sclerosis-associated interstitial lung disease
75 or autoimmune (polymyositis/dermatomyositis, systemic sclerosis, autoimmune hemolytic anemia, pernici
77 ransplantation (HSCT) benefits patients with systemic sclerosis but has been associated with signific
78 ve treatment option for patients with severe systemic sclerosis, but is associated with toxicity and
81 by DNA microarray from 13 diffuse cutaneous systemic sclerosis (dSSc) patients enrolled in an open-l
85 oposed that play a role in susceptibility to systemic sclerosis; firstly the maintenance of immune to
86 skin and pulmonary function in patients with systemic sclerosis for up to 2 years and is preferable t
87 date major histocompatibility complex-linked systemic sclerosis genetics, we performed genotyping of
90 as a potential strategy for the treatment of systemic sclerosis has been gaining more widespread inte
91 cent studies of gene expression profiling in systemic sclerosis have demonstrated its value in diagno
92 opoietic stem-cell transplantation (HSCT) in systemic sclerosis have shown improvements in lung funct
94 specially juvenile dermatomyositis (JDM) and systemic sclerosis; however, little is known about the p
95 Among patients with early diffuse cutaneous systemic sclerosis, HSCT was associated with increased t
96 een concluded: the nonmyeloablative American Systemic Sclerosis Immune Suppression versus Transplant,
97 allele for systemic lupus erythematosus and systemic sclerosis in non-Hispanic white or Chinese subj
98 ransplantation (HSCT) have shown efficacy in systemic sclerosis in phase 1 and small phase 2 trials.
111 ibutions of platelets to the pathogenesis of systemic sclerosis is likely substantial and may not be
112 of non-lethal complications associated with systemic sclerosis is substantial and is likely to becom
114 n several inflammatory skin diseases, yet in systemic sclerosis, it can occur in all regions of the d
115 roblast in diverse fibrotic lesions, such as systemic sclerosis; kidney, liver, and lung fibrosis; an
116 vascular manifestations of limited cutaneous systemic sclerosis (lcSSc) and in the prevention of the
117 , a common complication of limited cutaneous systemic sclerosis (lcSSc), is associated with alteratio
118 studies with rituximab in diffuse cutaneous systemic sclerosis lend support that B cells may be impo
119 diseases, including the pulmonary fibroses, systemic sclerosis, liver cirrhosis, cardiovascular dise
122 derstanding of the disease in the context of systemic sclerosis may lead to novel diagnostic and ther
123 were aged younger than 60 years with diffuse systemic sclerosis, modified Rodnan skin scores (mRSS) o
124 temic lupus erythematosus (SLE) (n = 7,241), systemic sclerosis (n = 5,642), or other systemic autoim
125 Pulmonary arterial hypertension complicating systemic sclerosis occurs commonly and portends a poor p
128 kin fibroblasts from individuals with either systemic sclerosis or recessive dystrophic epidermolysis
129 idosis or collagen vascular diseases such as systemic sclerosis or rheumatoid arthritis; however, eac
132 d coding and non-coding genes in relation to systemic sclerosis pathogenesis with a specific focus on
135 assays of CD4(+) and CD8(+) T cells from 24 systemic sclerosis patients and 24 matched controls were
136 l randomized, controlled phase 2 trial in 19 systemic sclerosis patients and a large randomized phase
137 mer group, AKA were present in 4 of 20 (20%) systemic sclerosis patients and in 3 of 12 (25%) ankylos
139 oding RNAs are deregulated in skin tissue of systemic sclerosis patients suggesting a novel class of
140 ospective analyses of independent cohorts of systemic sclerosis patients treated with autologous stem
142 healthy human skin disappear in the skin of systemic sclerosis patients, and CD34(-), podoplanin(+),
143 is dysfunctional at the epigenetic level in systemic sclerosis patients, indicating that hypomethyla
148 ion of a type I collagen receptor would make systemic sclerosis platelets more susceptible to binding
151 with pulmonary hypertension (166 SScPAH, 49 systemic sclerosis-related pulmonary hypertension with i
153 y patient with polymyositis/dermatomyositis, systemic sclerosis, rheumatoid arthritis, or Sjogren's s
157 Gastrointestinal tract (GIT) involvement in systemic sclerosis (scleroderma, SSc) is the most common
158 nderstanding of fibrosis and vasculopathy in systemic sclerosis, scleroderma (SSc) largely mediated t
161 c-Rel subunits within lesional psoriatic and systemic sclerosis skin revealed abnormal epidermal expr
163 te disease phenotypes in fibrillin-1 mutated systemic sclerosis (SS) and dextran-sulfate-sodium-induc
164 n extra-cutaneous organ system involved with systemic sclerosis (SSc) affecting approximately 90% of
166 To assess health values in subjects with systemic sclerosis (SSc) and determine variability expla
167 occurs in approximately 90% of patients with systemic sclerosis (SSc) and has a major impact on healt
168 owth factor (CTGF; CCN2) is overexpressed in systemic sclerosis (SSc) and has been hypothesized to be
169 data for elucidating the molecular basis of systemic sclerosis (SSc) and its various clinical manife
170 ltured dermal fibroblasts from patients with systemic sclerosis (SSc) and nephrogenic systemic fibros
171 the importance of interleukin-13 (IL-13) in systemic sclerosis (SSc) and other fibrotic diseases, it
173 aberrant Wnt signaling has been linked with systemic sclerosis (SSc) and pulmonary fibrosis, we soug
174 ers (CTDs), including Marfan syndrome (MFS), systemic sclerosis (SSc) and Tight-skin (Tsk) mice.
175 e, incidence, survival, and risk factors for systemic sclerosis (SSc) and to compare these data to pr
176 tivation of the Smad1 pathway in fibrosis in systemic sclerosis (SSc) and to determine whether this p
177 increased in a large cohort of patients with systemic sclerosis (SSc) and whether OPN contributes to
179 for maintaining persistent organ fibrosis in systemic sclerosis (SSc) are not known but emerging evid
180 at Wnts might contribute to skin fibrosis in systemic sclerosis (SSc) by affecting the differentiatio
184 blood cells (PBMCs) from some patients with systemic sclerosis (SSc) express an interferon-alpha (IF
185 and to determine the sensitivity of cultured systemic sclerosis (SSc) fibroblasts to Akt inhibition.
186 study was undertaken to examine responses of systemic sclerosis (SSc) fibroblasts to sphingosine 1-ph
187 btained from a small number of patients with systemic sclerosis (SSc) has been reported as confirmati
188 ells responsible for the intimal fibrosis in systemic sclerosis (SSc) has not been fully identified.
195 n present clinically, cardiac involvement in systemic sclerosis (SSc) is a major risk factor for deat
214 ulmonary vasculature of <2 mm in diameter in Systemic Sclerosis (SSc) patients with (n = 17) and with
215 ight stimulate both of these key features of systemic sclerosis (SSc) RECENT FINDINGS: Nucleic acid c
218 amics and exercise capacity in patients with systemic sclerosis (SSc) spectrum-associated ePH treated
220 mononuclear cells (PBMCs) from patients with systemic sclerosis (SSc) to better understand the dysreg
221 t the baseline visit (V0), 203 patients with systemic sclerosis (SSc) were examined (104 whites, 39 A
224 T lymphocytes play an important role in systemic sclerosis (SSc), a connective tissue disease ch
225 CD8(+)CD28(-) T cells in the pathogenesis of systemic sclerosis (SSc), a connective tissue disorder c
226 in the peripheral blood of individuals with systemic sclerosis (SSc), a disease characterized by fib
228 ggested a role for pathogens as a trigger of systemic sclerosis (SSc), although neither a pathogen no
229 nchoalveolar lavage fluid from patients with systemic sclerosis (SSc), and in a CCL18 overexpression
230 need for effective antifibrotic therapies in systemic sclerosis (SSc), and in parallel a rapid develo
231 vement with dermal fibrosis is a hallmark of systemic sclerosis (SSc), and keratinocytes may be criti
232 ity in vitro and has long been implicated in systemic sclerosis (SSc), as expression of TGF-beta-regu
235 n (PH) is an important cause of mortality in systemic sclerosis (SSc), where it can be isolated (pulm
236 ating tight skin (Tsk(-/+)) mice, a model of systemic sclerosis (SSc), with 4F decreases inflammation
237 uss recent advances in serologic testing for systemic sclerosis (SSc)-associated antibodies with resp
238 s now been shown to reduce the number of new systemic sclerosis (SSc)-related digital ulcers in two m
239 th factor (PDGF) may play a critical role in systemic sclerosis (SSc)-related interstitial lung disea
258 data and interstitial lung disease (ILD) - a systemic sclerosis (SSc, or scleroderma) clinical phenot
259 exist in the susceptibility and severity of systemic sclerosis (SSc, scleroderma) and are responsibl
260 ry fibrosis is an important manifestation in systemic sclerosis (SSc, scleroderma) where it portends
263 African American and Caucasian patients with systemic sclerosis (SSc; scleroderma) and in healthy ind
264 and its receptor, PDGFR, promote fibrosis in systemic sclerosis (SSc; scleroderma) dermal fibroblasts
265 cted first-degree relatives within multicase systemic sclerosis (SSc; scleroderma) families are conco
269 atures and natural history of the disease in systemic sclerosis (SSc; scleroderma) patients with anti
270 leading cause of morbidity and mortality in systemic sclerosis (SSc; scleroderma), and interstitial
271 biopsy specimens obtained from patients with systemic sclerosis (SSc; scleroderma), and that specific
279 S scores comparable with scores reported for systemic sclerosis, systemic lupus erythematosus, and mu
280 ncluding systemic lupus erythematosus (SLE), systemic sclerosis, Takayasu arteritis, Wegener granulom
281 y of proteins not previously associated with systemic sclerosis that provide insight into pathogenesi
282 sorders, such as scleroderma and progressive systemic sclerosis, the direct consequences of IL-33 rel
284 have been implicated in the pathogenesis of systemic sclerosis through mechanisms beyond the previou
285 adequately represented in gene profiling of systemic sclerosis tissue due to the small amounts of RN
286 ular localization of the protein in affected systemic sclerosis tissues and demonstrated its expressi
287 lines for cardiac screening of patients with systemic sclerosis to assess treatment-related risk from
288 that have a well-documented association with systemic sclerosis to determine whether these SNPs are a
289 ess in understanding genetic associations of systemic sclerosis to explain the observed heritability.
290 ion data from skin biopsies of patients with systemic sclerosis treated with five therapies: mycophen
291 mean (+/-SD) level of CXCL4 in patients with systemic sclerosis was 25,624+/-2652 pg per milliliter,
292 ed and unequivocally effective currently for systemic sclerosis, we have come a long way in the past
293 six healthy volunteers and six patients with systemic sclerosis were imaged at 1.5-T nonenhanced FSD
294 9, 156 patients with early diffuse cutaneous systemic sclerosis were recruited and followed up until
295 -three patients with early diffuse cutaneous systemic sclerosis were studied at 11 international cent
296 thritis [RA], 12 psoriatic arthritis, and 12 systemic sclerosis) were recruited together with 12 heal
297 o cohorts of patients with diffuse cutaneous systemic sclerosis, were identified as differentially re
298 appear to operate in Sjogren's syndrome and systemic sclerosis whereas only the IRF5-TNPO3 gene-span
300 from healthy persons and from patients with systemic sclerosis who had distinct clinical phenotypes.
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