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1 nflammatory myopathy (i.e., polymyositis and dermatomyositis).
2 human autoimmune settings including juvenile dermatomyositis.
3 tissue of adult dermatomyositis and juvenile dermatomyositis.
4 ontributions to the pathogenesis of juvenile dermatomyositis.
5 e type 1 interferon pathway for treatment of dermatomyositis.
6 rse effects in patients with polymyositis or dermatomyositis.
7 ts, 54 with inflammatory myopathies, 14 with dermatomyositis.
8  juvenile idiopathic arthritis, and juvenile dermatomyositis.
9 losporin in children with new-onset juvenile dermatomyositis.
10 inent data from adults with polymyositis and dermatomyositis.
11 c control of the immune response in juvenile dermatomyositis.
12 perimysial blood vessels in 10 patients with dermatomyositis.
13 small vessel occlusion in untreated juvenile dermatomyositis.
14 ear cells from children with active juvenile dermatomyositis.
15 d genetics play in the evolution of juvenile dermatomyositis.
16 derstanding the etiopathogenesis of juvenile dermatomyositis.
17  disability for adults with polymyositis and dermatomyositis.
18 imately 25% of patients with polymyositis or dermatomyositis.
19 enes are very strongly associated with adult dermatomyositis.
20 h juvenile idiopathic arthritis and juvenile dermatomyositis.
21  the 198 developed cancer after diagnosis of dermatomyositis.
22 d in serum of patients with polymyositis and dermatomyositis.
23 is of perifascicular muscle fibre atrophy in dermatomyositis.
24 atory myopathy, and the typical skin rash of dermatomyositis.
25 ammatory myopathies such as polymyositis and dermatomyositis.
26 flammatory demyelinating polyneuropathy, and dermatomyositis.
27 er inclusion body myositis, polymyositis, or dermatomyositis.
28 wide association study has been performed in dermatomyositis.
29 a differentiation-associated gene 5-positive dermatomyositis.
30  the diagnostic utility of autoantibodies in dermatomyositis.
31 ties between muscle and skin inflammation in dermatomyositis.
32  an important role in systemic sclerosis and dermatomyositis.
33 s a disease activity marker specifically for dermatomyositis.
34 e all manifestations of skin inflammation in dermatomyositis.
35 ifestations, and therapy for skin disease in dermatomyositis.
36 ad in regions of muscle fiber abnormality in dermatomyositis.
37 ans independently scored 10 children (9 with dermatomyositis, 1 with polymyositis; ages 4-15 years) t
38 d 3 pairs of monozygotic twins with juvenile dermatomyositis, 11 families with other siblings or rela
39 tigen in the human connective tissue disease dermatomyositis [14,15].
40  erythematosus (SLE); 17 had polymyositis or dermatomyositis; 16 had scleroderma; eight had ankylosin
41  erythematosus (3.06 [95% CI 1.78-4.90]) and dermatomyositis (2.64 [95% CI 0.86-6.17]) but not for sy
42 h to allow separate statistical analysis (47 dermatomyositis, 223 controls).
43  was characterized by a higher proportion of dermatomyositis (69% of adult Mestizos versus 35% of adu
44                                           In dermatomyositis, a multiorgan disease, evidence exists t
45 ells contribute to the pathogenesis of adult dermatomyositis, a photoinduced autoimmune skin disease.
46  association of this polymorphism with adult dermatomyositis, a photosensitive disease that exhibits
47                       Patients with juvenile dermatomyositis, a systemic autoimmune disease, displaye
48  be organized under two headings--amyopathic dermatomyositis (ADM) and classic dermatomyositis (CDM).
49  who developed classic cutaneous findings of dermatomyositis along with proximal muscle weakness and
50 e frequency of the -308A allele was 0.26 for dermatomyositis and 0.14 for controls (p = 0.014).
51                    Fifty adult patients with dermatomyositis and 239 healthy, race-matched controls w
52 ion may influence the relative prevalence of dermatomyositis and anti-Mi-2 autoantibodies in the US.
53                                      In both dermatomyositis and Duchenne dystrophy, C5-b9 deposits c
54 ment-induced microangiopathy is important in dermatomyositis and in the rare disorder, necrotizing my
55 ears, with particular focus on polymyositis, dermatomyositis and inclusion body myositis.
56                   Most data for treatment of dermatomyositis and juvenile dermatomyositis are from an
57 n found abundantly in muscle tissue of adult dermatomyositis and juvenile dermatomyositis.
58 alpha, are present in substantial numbers in dermatomyositis and may account for most of the cells pr
59 ime of onset with the relative prevalence of dermatomyositis and myositis autoantibodies in 380 patie
60                            All patients with dermatomyositis and polymyositis (> or =15 years old) we
61                                              Dermatomyositis and polymyositis are associated with can
62                                              Dermatomyositis and polymyositis are treatable disorders
63 ratios (SIR) for individual cancer sites for dermatomyositis and polymyositis separately, using natio
64  syndromes of chronic inflammatory myopathy (dermatomyositis and polymyositis) may have in certain in
65                                      In both dermatomyositis and polymyositis, risk of malignant dise
66 re is increasing evidence of autoimmunity in dermatomyositis and polymyositis, with strong correlatio
67 nd, placebo-controlled therapeutic trials of dermatomyositis and polymyositis.
68 of specific cancer types in individuals with dermatomyositis and polymyositis.
69  tissues in patients with SS from those with dermatomyositis and provide a relative weighting of the
70                  In individual patients with dermatomyositis and some with polymyositis, a blood type
71  fundamental mechanistic differences between dermatomyositis and subacute cutaneous lupus erythematos
72       Children and adolescents with juvenile dermatomyositis and systemic lupus erythematosus also ex
73 tibodies found in the serum of patients with dermatomyositis and systemic lupus erythematosus, is rap
74 nous cyclophosphamide in refractory juvenile dermatomyositis and tacrolimus ointment for the dermatol
75 erstanding of autoantibodies associated with dermatomyositis and the autoimmune necrotizing myopathie
76 r with autoantibodies found in patients with dermatomyositis and the autoimmune necrotizing myopathie
77  genetics of children affected with juvenile dermatomyositis and the impact these genes have on disea
78                                  Advances in dermatomyositis and the juvenile idiopathic inflammatory
79 rproducing TNFalpha-308 A variant with adult dermatomyositis and with subacute cutaneous lupus erythe
80 tities, but is primarily made up of juvenile dermatomyositis and, to a lesser degree, juvenile polymy
81 ith systemic illnesses (lupus erythematosus, dermatomyositis), and the skin changes of potentially fa
82 r siblings or relatives with polymyositis or dermatomyositis, and 2 families with inclusion body myos
83 ents with systemic sclerosis, 1 patient with dermatomyositis, and a healthy volunteer were scanned us
84 ific information from children with juvenile dermatomyositis, and includes pertinent data from adults
85 mes (the most common forms are polymyositis, dermatomyositis, and inclusion body myositis) are system
86 on inflammatory myopathies are polymyositis, dermatomyositis, and inclusion body myositis.
87 roup of diseases that includes polymyositis, dermatomyositis, and inclusion body myositis.
88 i myopathy, nemaline myopathy, polymyositis, dermatomyositis, and inclusion body myositis].
89       Systemic lupus erythematosus, juvenile dermatomyositis, and juvenile localized scleroderma stan
90 cirrhosis, Sjogren syndrome, systemic lupus, dermatomyositis, and neonatal lupus.
91  with inclusion-body myositis, polymyositis, dermatomyositis, and neurogenic muscle atrophy, but it i
92 ce of systemic lupus erythematosus, juvenile dermatomyositis, and other primary systemic vasculitides
93 antibody-associated vasculitis, polymyositis/dermatomyositis, and primary Sjogren's syndrome.
94 sitis (anti-SAE autoantibodies) and juvenile dermatomyositis (anti-p155/140 autoantibodies) (anti-MJ
95 ntibodies have been described in adult-onset dermatomyositis (anti-SAE autoantibodies) and juvenile d
96 or treatment of dermatomyositis and juvenile dermatomyositis are from anecdotal, non-randomised case
97 ients with HL, sensorimotor neuropathies and dermatomyositis are more frequent in NHL.
98 phil cytoplasmic antibodies+ vasculitis, and dermatomyositis are noteworthy but must be interpreted w
99 histocompatibility complex in early juvenile dermatomyositis are reported.
100   Inclusion body myositis, polymyositis, and dermatomyositis are three distinct categories of inflamm
101 articularly systemic lupus erythematosus and dermatomyositis, are also characterized by an up-regulat
102  be an important part of the pathogenesis of dermatomyositis, as it appears to be in systemic lupus e
103  erythematosus (SLE), diabetes mellitus, and dermatomyositis, as well as monogenic type I interferono
104 verse effects related to ipilimumab therapy, dermatomyositis associated with this agent has not previ
105  sequenced peptides eluted from the juvenile dermatomyositis-associated class II allele HLA-DQalpha1*
106 effective for the cutaneous complications of dermatomyositis but has been helpful in other extramuscu
107 available for evaluating the skin disease of dermatomyositis, but there is a need for new effective t
108 the reversibility of microvascular damage in dermatomyositis by intravenous immune globulin which app
109 amyopathic dermatomyositis (ADM) and classic dermatomyositis (CDM).
110 tion of -308A and HLA-DR3 in Caucasians with dermatomyositis compared to controls.
111  5) dermatopulmonary syndrome is a subset of dermatomyositis defined by specific clinical features an
112  are certainly effective in polymyositis and dermatomyositis despite the lack of randomized controlle
113 ing patients with polymyositis (PM) (n=114), dermatomyositis (DM) (n=102), myositis associated with a
114 l muscle metabolism in vivo in patients with dermatomyositis (DM) and polymyositis (PM) in order to e
115 c acidosis and stroke-like episodes (MELAS), dermatomyositis (DM) and polymyositis (PM) using pairwis
116 non-inflammatory or dystrophic controls, two dermatomyositis (DM) and two polymyositis (PM) patients
117 ts have confirmed that polymyositis (PM) and dermatomyositis (DM) are not genetically identical disea
118 have estimated that up to 20% of adults with dermatomyositis (DM) have calcinosis, which can lead to
119                                     Juvenile dermatomyositis (DM) is a chronic inflammatory myopathy
120                                              Dermatomyositis (DM) is a rare multisystem autoimmune di
121                                     Juvenile dermatomyositis (DM) is an autoimmune disease of childho
122                                              Dermatomyositis (DM) is an autoimmune disease, which is
123        Except when the diagnosis of juvenile dermatomyositis (DM) is in doubt, a case has not been ma
124       The accumulated mucin in non-Gottron's dermatomyositis (DM) lesions is primarily chondroitin-4-
125 fication of novel autoantibodies in juvenile dermatomyositis (DM) may have etiologic and clinical imp
126 ts with polymyositis (PM) than in those with dermatomyositis (DM) or other myositis syndromes.
127 (PM) and adults and children with refractory dermatomyositis (DM) were enrolled.
128             Sera from 20 adult patients with dermatomyositis (DM) were screened for autoantibodies.
129  before and after therapy from patients with dermatomyositis (DM) who improved and patients with incl
130 vidence points toward an association between dermatomyositis (DM) with malignancy.
131 -like modifier, and its enzymatic pathway in dermatomyositis (DM), an autoimmune disease primarily in
132 f the diverse entities of polymyositis (PM), dermatomyositis (DM), and inclusion body myositis (IBM),
133 ), sporadic inclusion body myositis (s-IBM), dermatomyositis (DM), and normal or disease controls.
134 symptom onset and the prevalence of juvenile dermatomyositis (DM), compared to juvenile polymyositis
135 ysed in biopsies of sIBM, polymyositis (PM), dermatomyositis (DM), dystrophic and non-myopathic muscl
136 rs of disease activity in juvenile and adult dermatomyositis (DM), especially during the active treat
137 To properly evaluate therapies for cutaneous dermatomyositis (DM), it is essential to administer an o
138  and 15 muscle samples from 44 patients with dermatomyositis (DM), polymyositis (PM), inclusion body
139 immune inflammatory muscle disorders include Dermatomyositis (DM), Polymyositis (PM), Necrotizing Myo
140                  For Caucasian patients with dermatomyositis (DM), the Gm 3 23 5,13 phenotype was a r
141 atients at the time of diagnosis of juvenile dermatomyositis (DM), to compare the RANKL:osteoproteger
142 stituents of muscle inflammation in juvenile dermatomyositis (DM).
143 tained from children diagnosed with juvenile dermatomyositis (DM).
144 f low-producing MBL polymorphisms with adult dermatomyositis (DM).
145 lung disease and either polymyositis (PM) or dermatomyositis (DM).
146 nificance of the cutaneous manifestations of dermatomyositis (DM).
147 autoantibody is specifically associated with dermatomyositis (DM).
148 eases they were designed to treat, including dermatomyositis (DM).
149  found in a distinct subset of patients with dermatomyositis (DM).
150 e" is a candidate biomarker in patients with dermatomyositis (DM).
151 n implicated in the pathogenesis of juvenile dermatomyositis (DM).
152               To our knowledge, drug-induced dermatomyositis from ipilimumab has not previously been
153 y technology may also be used to distinguish dermatomyositis from the other inflammatory myopathies,
154                                           In dermatomyositis, genes induced by interferon-alpha/beta
155 ls: alopecia areata, ankylosing spondylitis, dermatomyositis, Graves' disease, Hashimoto thyroiditis,
156 y of the -308A allele was 0.27 in the entire dermatomyositis group, versus 0.14 in the controls (p =
157 tion of the heterogeneity of skin disease in dermatomyositis has already provided evidence that clini
158 e conceptual model of the pathophysiology of dermatomyositis has been based on work extending back ov
159       Type I interferon activity in juvenile dermatomyositis has been demonstrated by both global gen
160                                              Dermatomyositis has been linked to cancer, particularly
161                                              Dermatomyositis has been modeled as an autoimmune diseas
162 lesions of patients with cutaneous lupus and dermatomyositis has provided valuable information about
163                                Patients with dermatomyositis have a high rate of malignancy.
164 classification criteria for polymyositis and dermatomyositis have been suggested by a number of inves
165 evidence that patients with polymyositis and dermatomyositis have specific clinico-serological profil
166 dies; myovasculopathies, including childhood dermatomyositis; immune polymyopathies, active myopathie
167      Studies in adults with polymyositis and dermatomyositis implicate interleukin-1alpha, transformi
168  MBL variants were over-represented in adult dermatomyositis in a dose-responsive fashion (p=0.0002).
169  allele was positively associated with adult dermatomyositis in a dose-responsive fashion (p=0.0004),
170  adverse events and consider drug-associated dermatomyositis in the differential diagnosis in patient
171 utoantibodies preferentially associated with dermatomyositis include those recognizing Mi-2, MDA5, TI
172  new insights into the disease mechanisms of dermatomyositis, inclusion body myositis, and polymyosit
173 specific response in muscle in patients with dermatomyositis, inclusion body myositis, and polymyosit
174 ing intravenous immunoglobulin in refractory dermatomyositis, indicated benefit.
175        Although evidence remains strong that dermatomyositis is a disorder with an early involvement
176                                              Dermatomyositis is a microangiopathy affecting skin and
177                                              Dermatomyositis is a systemic disorder and whereas the s
178                                              Dermatomyositis is an inflammatory disorder of muscle af
179       We have previously shown that juvenile dermatomyositis is associated with the HLA-DQA1*0501 all
180  We conclude that: perifascicular atrophy in dermatomyositis is consistently associated with focal mi
181 e weakness in patients with polymyositis and dermatomyositis is due to autoimmune and inflammatory pr
182 rization of the type 1 interferon pathway in dermatomyositis is leading down a path of genomic medici
183                                              Dermatomyositis is one of the idiopathic inflammatory my
184                    The pathogenesis of adult dermatomyositis is reviewed here, with particular attent
185            Our results provide evidence that dermatomyositis is strongly associated with a wide range
186                                     Juvenile dermatomyositis is the most common of the idiopathic inf
187 nective-tissue diseases, especially juvenile dermatomyositis (JDM) and systemic sclerosis; however, l
188                                     Juvenile dermatomyositis (JDM) is a multisystem autoimmune diseas
189                                     Juvenile dermatomyositis (JDM) is an immune-mediated inflammatory
190 radiation exposure 1 month prior to juvenile dermatomyositis (JDM) may trigger the onset of disease.
191                                     Juvenile dermatomyositis (JDM), the most common pediatric inflamm
192 d have been found in high levels in juvenile dermatomyositis (JDM), which may account the frequency o
193 n how to assess the many aspects of juvenile dermatomyositis (JDM).
194  develop in 20-40% of children with juvenile dermatomyositis (juvenile DM), contributing to disease m
195 ematosis, Wegener's granulomatosis, juvenile dermatomyositis, juvenile scleroderma and autoinflammato
196 a, mixed connective tissue disease, juvenile dermatomyositis, juvenile spondyloarthropathy and system
197 ion has now been recognized in patients with dermatomyositis-like disease.
198 fferent pathways of complement activation in dermatomyositis, lupus nephritis, and necrotic muscle fi
199 iption and classification of skin disease in dermatomyositis may allow the clinician to predict more
200 se, immunotherapies to better treat juvenile dermatomyositis may become available in the future.
201 AK-RNA interference was performed in IBM and dermatomyositis mesoangioblasts.
202 egulated pathological pathway genome-wide in dermatomyositis muscle and blood.
203                                 In contrast, dermatomyositis muscle shows a dominant type I IFN patte
204 e that ISG15, which is highly upregulated in dermatomyositis muscle, does not appear to play a key ro
205 interferons alpha and beta, are prominent in dermatomyositis muscle.
206  their inducible products are upregulated in dermatomyositis muscle.
207 econd-line therapy in stiff-person syndrome, dermatomyositis, myasthenia gravis, and Lambert-Eaton my
208 lt patients with polymyositis (PM; n = 134), dermatomyositis (n = 129), or other CTDs (predominantly
209 jogren's syndrome (n = 30), polymyositis and dermatomyositis (n = 30), and progressive systemic scler
210 yositis and of an IFN-alpha/beta response in dermatomyositis, neither of which was previously describ
211 ith the relative proportion of patients with dermatomyositis (odds ratio [OR] 2.3, 95% confidence int
212 for our understanding of muscle pathology in dermatomyositis of both adults and children.
213                   We identified 618 cases of dermatomyositis, of whom 198 had cancer.
214         Ninety-six patients with adult-onset dermatomyositis or polymyositis had a baseline assessmen
215 muscle function in patients with established dermatomyositis or polymyositis receiving chronic medica
216 or rheumatoid arthritis, Sjogren's syndrome, dermatomyositis or polymyositis, or scleroderma were of
217 itis patients but in only 1/28 patients with dermatomyositis or polymyositis.
218 l haplotype; however, African Americans with dermatomyositis or with anti-Jo-1 autoantibodies shared
219 temic disease such as lupus erythematosus or dermatomyositis, or be an early symptom of a rare group
220 scular complement deposition is a feature of dermatomyositis pathology but the trigger for complement
221                                       In the dermatomyositis patient, the en face D-OCT images showed
222 from that of p155 antibody-negative juvenile dermatomyositis patients (P = 0.003).
223  antigenic target on the endothelial cell in dermatomyositis patients and the pathogenic role of the
224                                     In adult dermatomyositis patients homozygous for the wild-type TN
225                                     In adult dermatomyositis patients with one variant TNFalpha-308 A
226                                     Juvenile dermatomyositis patients with p155 autoantibody had a bi
227 tor-alpha synthesis is increased in juvenile dermatomyositis patients with the tumor necrosis factor-
228 ications for systemic and malignancy risk in dermatomyositis patients, and that there may be several
229  in the same 10, as well as in 40 additional dermatomyositis patients, we searched for vascular depos
230 myositis than in responsive polymyositis and dermatomyositis patients.
231 nd resistin have been detected in tissues of dermatomyositis patients.
232                                  In juvenile dermatomyositis, peptides from human skeletal myosin pla
233  with a subset of patients with polymyositis/dermatomyositis (PM/DM) complicated by interstitial lung
234 whether sera from patients with polymyositis/dermatomyositis (PM/DM) with or without interstitial lun
235 -55-kd bands, all patients with polymyositis/dermatomyositis (PM/DM), and a random selection of SSc,
236 , 121 with scleroderma, 86 with polymyositis/dermatomyositis [PM/DM]) and 248 Italian patients with a
237 sus, Wegener's granulomatosis, polymyositis, dermatomyositis, polyarteritis nodosa, or scleroderma wh
238             The inflammatory muscle diseases dermatomyositis, polymyositis and inclusion body myositi
239 ell into the typical IIM subclassifications: dermatomyositis, polymyositis and inclusion body myositi
240 pathies (IIMs) are typically subdivided into dermatomyositis, polymyositis and inclusion body myositi
241 esoangioblasts isolated from samples of IBM, dermatomyositis, polymyositis, and control muscles were
242  the results of recent therapeutic trials in dermatomyositis, polymyositis, and inclusion body myosit
243 muscle cells in the inflammatory myopathies (dermatomyositis, polymyositis, and inclusion body myosit
244 iopathic inflammatory myopathies, comprising dermatomyositis, polymyositis, and inclusion body myosit
245 iated into three major and distinct subsets: dermatomyositis, polymyositis, and inclusion-body myosit
246 BM patient sera, whereas their prevalence in dermatomyositis, polymyositis, and other neuromuscular d
247                    Classification systems of dermatomyositis, polymyositis, and the other idiopathic
248 arison, 2/15 (14%) age-matched patients with dermatomyositis, polymyositis, or necrotizing myopathy,
249 ritis; lupus; scleroderma; Sjogren Syndrome; dermatomyositis/polymyositis; unspecified/mixed CTD; oth
250 nisone plus methotrexate achieved a juvenile dermatomyositis PRINTO 20 improvement (p=0.0228).
251  proportion of patients achieving a juvenile dermatomyositis PRINTO 20 level of improvement (20% impr
252 ic systemic lupus erythematosus and juvenile dermatomyositis, remain life-threatening.
253 d Musculoskeletal and Skin Diseases Juvenile Dermatomyositis Research Registry and the National Pedia
254 py is essential, since both polymyositis and dermatomyositis respond to immunotherapeutic agents.
255 vascular membrane attack complex deposits in dermatomyositis result from activation of the classical
256 d unusual manifestations of cutaneous lupus, dermatomyositis, scleroderma, and rheumatoid arthritis.
257  the dermatologic manifestations of juvenile dermatomyositis seem promising.
258 ow the possibility that, for the first time, dermatomyositis skin disease can serve as a valid outcom
259 lases HDAC1/2, histone-binding proteins, the dermatomyositis-specific autoantigen Mi2beta, a polypept
260                             Thirty-one of 50 dermatomyositis specimens contained C5b-9 reactive endom
261 , and the LX promoter polymorphism) in adult dermatomyositis, subacute cutaneous lupus erythematosus,
262 liminary gene expression studies in juvenile dermatomyositis, systemic lupus erythematosus, and chron
263  and specific prior autoimmune (polymyositis/dermatomyositis, systemic sclerosis, autoimmune hemolyti
264 ot observed in any patient with polymyositis/dermatomyositis, systemic sclerosis, rheumatoid arthriti
265 an inflammatory myopathies (polymyositis and dermatomyositis), the early, widespread appearance of MH
266 ar to what is observed in human polymyositis/dermatomyositis, the mice developed a strong antinuclear
267 n understanding these mechanisms in juvenile dermatomyositis, the most common form of childhood infla
268                                  In juvenile dermatomyositis, the quantitative magnetic resonance ima
269 lar atrophy, and what is the relationship of dermatomyositis to systemic lupus erythematosus.
270 ols, OR = infinite; two-sided p = 0.02), but dermatomyositis was absent in cases themselves.
271                            Family history of dermatomyositis was associated with NHL (7 cases vs. 0 c
272 ation, the association of these two genes in dermatomyositis was significantly less than we previousl
273 To further understand the pathophysiology of dermatomyositis, we used microarrays, computational meth
274 sms in patients with rheumatoid arthritis or dermatomyositis were analyzed by polymerase chain reacti
275  A total of 37 patients with polymyositis or dermatomyositis were randomized (19 to creatine, 18 to p
276 factor -308A polymorphism is associated with dermatomyositis, which suggests a pathophysiologic contr
277  18 years or younger with new-onset juvenile dermatomyositis who had received no previous treatment a
278  affect as many as 20% to 30% of adults with dermatomyositis, will not be addressed in this review.
279 crosis factor-alpha, more common in juvenile dermatomyositis with the tumor necrosis factor-alpha-308
280                             They distinguish dermatomyositis with vascular pathology from other infla
281  juvenile idiopathic arthritis, and juvenile dermatomyositis, with special interest on strategies to

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