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1 s with complicated urinary tract infections (cUTIs).
2 RQoL that have been studied in patients with cUTIs.
3 ts give rise to dental anomalies and aplasia cutis.
4 ltrate should not be interpreted as leukemia cutis.
5 nt failure and mortality among patients with cUTIs.
6 he proposed medical therapies for calcinosis cutis.
7 g for the subcutis (2.7x-14.2x) than for the cutis (1.9x).
8 siform eczema, 30.6%; eczema, 23.5%; xerosis cutis, 10.6%; palmoplantar pustulosis, 5.3%; psoriasis,
9                            Additionally, A(3)CuTiS(4) (A = Na, K, Rb) displays direct band gap behavi
10 minescence lifetimes of 2.3-8.6 mus, and K(3)CuTiS(4) has a PLQY of 5.19%.
11 taneous lesions of VEXAS syndrome, 4 had MDS-cutis, 5 had idiopathic SS, and 5 had LC.
12          Erythrophagocytosis (70%), leukemia cutis (58%), and disseminated intravascular coagulation
13 RF8) were also commonly negative in leukemia cutis (acute myeloid leukemia in the skin), a tumor that
14                                   Calcinosis cutis affects 20-40% of patients with systemic sclerosis
15  leads to autosomal recessive hyperelastosis cutis, also known as hereditary equine regional dermal a
16                                              cUTIs and pyelonephritis are associated with high antimi
17         The pathophysiology and treatment of cUTIs and pyelonephritis are driven more by host factors
18 he non-linear viscoelastic behavior of cheek cutis and subcutis to inform anatomically-accurate compu
19 ulk RNA sequencing analysis reveals that MDS-cutis and VEXAS syndrome lesions display closely related
20 y pattern shared between VEXAS syndrome, MDS-cutis, and refractory idiopathic SS skin samples.
21 ts BTB domain, and mutations in TFAP2A cause cutis aplasia in individuals with branchiooculofacial sy
22 autosomal-dominant disorder characterized by cutis aplasia of the scalp; minor anomalies of the exter
23 terized by congenital limb defects and scalp cutis aplasia.
24        Complicated urinary tract infections (cUTIs) are responsible for a major share of all antibiot
25 history of SLE who presented with calcinosis cutis at the time of SLE diagnosis developed a large, ul
26 es have led to the identification of aplasia cutis-causing mutations in genes that have previously no
27  characterized by the combination of aplasia cutis congenita (ACC) and terminal transverse limb defec
28                                      Aplasia cutis congenita (ACC) is a congenital epidermal defect o
29                                      Aplasia cutis congenita (ACC) manifests at birth as a defect of
30 der characterized by the presence of aplasia cutis congenita (ACC) of the scalp vertex and terminal l
31 ic contracture (CVIC) and unilateral aplasia cutis congenita (ACC) type VII of the forearm presents a
32 ion disorder consisting primarily of aplasia cutis congenita of the vertex scalp and transverse termi
33 nch-American-British type M5a) with leukemia cutis developed in a patient 6 weeks after the initiatio
34  oral step-down therapy for the treatment of cUTIs, driven by a lower rate of asymptomatic bacteriuri
35 d proteinosis (LP), also known as hyalinosis cutis et mucosae or Urbach-Wiethe disease (OMIM 247100)
36                              Beare-Stevenson cutis gyrata syndrome (BSS) is a human genetic disorder
37                              Beare-Stevenson cutis gyrata syndrome (MIM 123790) is an autosomal domin
38 on of FGFR2 mutations in the Beare-Stevenson cutis gyrata syndrome.
39 cts of the FGFR2 Y394C mutation evidenced by cutis gyrata, acanthosis nigricans, and craniosynostosis
40 aracterized by the furrowed skin disorder of cutis gyrata, acanthosis nigricans, craniosynostosis, cr
41 iffer, Apert, Jackson-Weiss, Beare-Stevenson cutis gyrata, and Antley-Bixler syndromes, and Kleeblaat
42 tion of UTIs, with the common rationale that cUTIs have a higher risk of recurrence or chronification
43                           Pyelonephritis and cUTIs have emerged as infection models for the study of
44        Recent data on therapy for calcinosis cutis highlights that more prospective studies are neede
45 lesional skin samples of VEXAS syndrome, MDS-cutis, idiopathic SS, LC, and healthy controls using bul
46 had cutaneous lesions of VEXAS syndrome, MDS-cutis, idiopathic SS, or LC.
47 terized by facial lesions resembling aplasia cutis in a preauricular distribution along the line of f
48                                   Calcinosis cutis is common in several connective tissue diseases bu
49 Recently described myelodysplasia cutis (MDS-cutis) is a cutaneous manifestation of myelodysplasia in
50                                              Cutis laxa (CL) is a condition characterized by redundan
51                                              Cutis laxa (CL) is a heterogeneous group of genetic and
52 , age-related macular degeneration (AMD) and cutis laxa (CL), but the biochemical basis for the patho
53 y of diseases, ranging from retinopathies to cutis laxa (CL).
54 heterozygous mutation in fibulin-5 can cause cutis laxa and also suggest that fibulin-5 and elastin g
55 als present with connective tissue features (cutis laxa and inguinal hernia), craniofacial dysmorphol
56 bulin-5 with features of autosomal recessive cutis laxa and marked defects in elastic fiber formation
57 neurological findings that overlap with both cutis laxa and spastic paraplegia.
58                     Variable lipoatrophy and cutis laxa are the basis for a progeroid appearance.
59 r data provide insights into the etiology of cutis laxa diseases and will have immediate impact on di
60                          The pathogenesis of cutis laxa in this condition is poorly understood.
61                                              Cutis laxa is a condition characterized by redundant, pe
62                                    Inherited cutis laxa is a connective tissue disorder characterized
63                                     Acquired cutis laxa is a rare cutaneous manifestation of hematolo
64 ructural differences for the disease-causing cutis laxa mutants and for one AMD variant (G412E), sugg
65                                         Both cutis laxa mutants increased dimerization.
66 tosomal dominant cutis laxa, we engineered a cutis laxa mutation (single base deletion) into the huma
67                   We conclude that recessive cutis laxa mutations in fibulin-5 result in misfolding,
68 istological analysis of skin sections from a cutis laxa patient with a homozygous S227P mutation show
69 itative defects in elastin, resulting in the cutis laxa phenotype.
70 c recoil in affected tissues and explain the cutis laxa phenotype.
71          This phenotype, which resembles the cutis laxa syndrome in humans, reveals a critical functi
72 clinical and molecular spectrum of metabolic cutis laxa syndromes and further link defective extracel
73 ne fragility, resembling autosomal-recessive cutis laxa type 1B, due to EFEMP2 (FBLN4) deficiency.
74  protein 4 (LTBP4) cause autosomal recessive cutis laxa type 1C.
75                          Autosomal recessive cutis laxa type 2 (ARCL2), a syndrome of growth and deve
76  collectively denoted as autosomal-recessive cutis laxa type 3 (ARCL3).
77 r elastogenesis, lead to autosomal recessive cutis laxa types 1B and 1A, respectively.
78 tance, and a family with autosomal recessive cutis laxa was recently reported to have a homozygous mi
79 of P5CS, cause an autosomal-dominant form of cutis laxa with progeroid features.
80  properties of the elastin protein (dominant cutis laxa).
81 ompliance, severe emphysema, and loose skin (cutis laxa).
82                                   Congenital cutis laxa, a rare syndrome with marked skin laxity and
83 ndrome, cystic fibrosis, homocystinuria, and cutis laxa, among others.
84 n variants causative for an entity combining cutis laxa, arterial tortuosity, aneurysm formation, and
85 , such as alpha-1 antitrypsin deficiency and cutis laxa, caused by rare genetic variants.
86  in five families affected by mild to severe cutis laxa, dysmorphic facial features, and cardiopulmon
87 tion disease (HCDD) associated with acquired cutis laxa, renal involvement, and hypocomplementemia an
88 ic fibers, the histopathological hallmark of cutis laxa, transmission electron microscopy of the derm
89 ne fractures at birth and was diagnosed with cutis laxa, vascular tortuosity, ascending aortic aneury
90 gene mutations leading to autosomal dominant cutis laxa, we engineered a cutis laxa mutation (single
91 mpaired elastic fiber formation in recessive cutis laxa, we have investigated two disease-causing mis
92 ion and cause the connective tissue disorder cutis laxa.
93 ement in patients with post-Sweet's syndrome cutis laxa.
94 ibulin 5 mutations cause autosomal-recessive cutis laxa.
95                             All patients had cutis laxa.
96 subtypes of Ehlers-Danlos syndrome (EDS) and cutis laxa.
97 d diseases supravalvular aortic stenosis and cutis laxa.
98 s 1-5 in fibroblasts from five patients with cutis laxa.
99 otype, the rare autosomal dominant condition cutis laxa.
100            Myeloid sarcoma (MS) and leukemia cutis (LC) represent 2 well-known EM manifestations with
101                                      Aplasia cutis manifests with localized skin defects at birth and
102            Recently described myelodysplasia cutis (MDS-cutis) is a cutaneous manifestation of myelod
103  rare disease with major features of aplasia cutis of the scalp and terminal transverse limb defects.
104                                     Leukemia cutis or leukemic cell infiltration in skin is one of th
105 ytic sarcoma, subcutaneous nodules, leukemia cutis, or meningeal leukemia) at initial presentation.
106 ncomplicated infections to complicated UTIs (cUTIs), pyelonephritis and severe urosepsis.
107            It is characterized by calcinosis cutis, Raynaud's phenomenon, esophageal involvement, scl
108   Clinical features of the CREST (calcinosis cutis, Raynaud's syndrome, esophageal dysmotility, scler
109  bone marrow, the transcriptomes of leukemia cutis samples from patients with durable remission after
110        Complicated urinary tract infections (cUTIs) significantly affect patients' health-related qua
111 dicate that biomechanical alterations of the cutis, subcutis, and dermal anchoring structures are nec
112  as potential therapies to target calcinosis cutis: these should now be investigated in human studies
113  shared inflammatory environment between MDS-cutis, VEXAS syndrome, and idiopathic SS was observed, m

 
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