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1 stis carinii pneumonia and 1 cytomegalovirus retinitis.
2 ar degeneration, glaucoma, cataract, and CMV retinitis.
3 val of 27.0 years after the diagnosis of CMV retinitis.
4 remote graders evaluated each image for CMV retinitis.
5 ter the initial diagnosis of Cytomegalovirus retinitis.
6 megalovirus disease, notably Cytomegalovirus retinitis.
7 (17%), and the most common manifestation was retinitis.
8 ients may suggest a rise in incidence of CMV retinitis.
9 ompartmental analysis of 1 patient with HCMV retinitis.
12 ating cART and suggest that "immune recovery retinitis," a proposed immune recovery inflammatory synd
15 indirect ophthalmoscopy for diagnosis of CMV retinitis and clinical features of CMV retinitis lesions
18 to >/=100 cells/muL; rates of new-onset CMV retinitis and of worsening of CMV retinitis (either incr
20 the rates of new-onset cytomegalovirus (CMV) retinitis and worsening existing CMV retinitis in patien
22 patients who develop active cytomegalovirus retinitis as an immune reconstitution inflammatory syndr
23 ates of retinitis progression and increasing retinitis border activity among patients during the firs
24 dy was not highly sensitive in detecting CMV retinitis but may identify disease with an immediate thr
26 yndrome (AIDS) patients with Cytomegalovirus retinitis (CMVR) -related retinal detachments(RD) in an
28 t a cluster of 5 pediatric patients with CMV retinitis diagnosed in a 12-month period and compare thi
30 -onset CMV retinitis and of worsening of CMV retinitis (either increasing border activity or retiniti
32 ompare the proportion of CMV viremia and CMV retinitis in patients transplanted between January 2010
33 s (CMV) retinitis and worsening existing CMV retinitis in patients with AIDS after initiating combina
35 an ophthalmic screening protocol to diagnose retinitis in pediatric HSCT patients in the early, often
37 patients with immune recovery developed CMV retinitis in the first 6 months after initiating cART vs
38 CMV retinitis nor worsening of existing CMV retinitis in the first 6 months after initiating cART vs
50 s neither an increased rate of new-onset CMV retinitis nor worsening of existing CMV retinitis in the
52 ty for the 3 remote graders in detecting CMV retinitis on fundus photography was 30.2% (95% CI, 10.5%
55 ith paraneoplastic optic neuritis, vitritis, retinitis, or a combination thereof, but few reports of
59 ular degeneration (35), optic neuritis (18), retinitis pigmentosa (17), and diabetic retinopathy (16)
62 (n = 80) or autosomal recessive nonsyndromic retinitis pigmentosa (ARRP) (n = 47) associated with bia
63 EYS are associated with autosomal recessive retinitis pigmentosa (arRP) and autosomal recessive cone
64 otype in 4 families with autosomal recessive retinitis pigmentosa (arRP) that can be associated with
65 and neurogenic muscle weakness, ataxia, and retinitis pigmentosa (NARP), in mammalian oocytes using
69 Outer retinal degenerative diseases, such as retinitis pigmentosa (RP) and age-related macular degene
70 ness in a number of retinal diseases such as retinitis pigmentosa (RP) and atrophic age-related macul
71 ncurable blinding retinal diseases including retinitis pigmentosa (RP) and atrophic age-related macul
72 d and irreversible disease that manifests as retinitis pigmentosa (RP) and bilateral neurosensory hea
74 generation and clinical phenotypes including retinitis pigmentosa (RP) and congenital stationary nigh
75 For ill-defined reasons, CS degenerate in retinitis pigmentosa (RP) and in the transitional zone (
76 ripherin 2 (PRPH2) have been associated with retinitis pigmentosa (RP) and macular/pattern dystrophie
77 d to various retinal degenerations including retinitis pigmentosa (RP) and macular/pattern dystrophy
81 eber congenital amaurosis (LCA) and juvenile retinitis pigmentosa (RP) are severe hereditary diseases
82 oherence tomography (SDOCT) in patients with retinitis pigmentosa (RP) associated with retinitis pigm
104 ted for some RP cases.SIGNIFICANCE STATEMENT Retinitis pigmentosa (RP) is an inherited, degenerative
105 associated with the various genetic forms of retinitis pigmentosa (RP) is currently untreatable and l
110 some vision to patients blind as a result of retinitis pigmentosa (RP) or outer retinal degeneration.
111 t, we assess the natural progression rate of retinitis pigmentosa (RP) over an average of three years
112 analyze the genetic and clinical findings in retinitis pigmentosa (RP) patients of Ashkenazi Jewish (
113 cing (NGS) based molecular diagnosis for 105 Retinitis Pigmentosa (RP) patients randomly selected fro
115 vel the molecular pathogenesis of an unusual retinitis pigmentosa (RP) phenotype observed in a Turkis
117 e limited published data on the phenotype of retinitis pigmentosa (RP) related to CNGB1 variants.
120 USH2A mutations are an important cause of retinitis pigmentosa (RP) with or without congenital sen
122 therapy has shown great promise in treating retinitis pigmentosa (RP), a primary photoreceptor degen
123 cells, are the most common cause of dominant retinitis pigmentosa (RP), a type of inherited blindness
124 tinal and brain pathologies, but its role in retinitis pigmentosa (RP), an inherited and largely incu
125 by congenital sensorineural hearing loss and retinitis pigmentosa (RP), and also contribute to autoso
126 retinal diseases, such as Stargardt disease, retinitis pigmentosa (RP), and atrophic age-related macu
127 viously reported to cause autosomal dominant retinitis pigmentosa (RP), and described their detailed
128 mans, such as Leber congenital amaurosis and retinitis pigmentosa (RP), are attributed to either homo
129 itary retinal degenerative diseases, such as retinitis pigmentosa (RP), are characterized by the prog
130 unrelated families with autosomal recessive retinitis pigmentosa (RP), but without extraocular invol
131 indings in patients with autosomal recessive retinitis pigmentosa (RP), cone-rod dystrophy (CRD) or c
132 individuals, it was found to segregate with retinitis pigmentosa (RP), goiter, primary ovarian insuf
133 y photoreceptor cells and cause nonsyndromic retinitis pigmentosa (RP), raising the issue of why cert
135 involved in O-mannosyl glycosylation, cause retinitis pigmentosa (RP), RP25 and RP76, respectively.
137 composed of IRD two with autosomal dominant retinitis pigmentosa (RP), two with autosomal recessive
155 phenotype groups were identified in EYS-RD: retinitis pigmentosa (RP; 85.94%), cone-rod dystrophy (C
156 d to unravel the molecular basis of sporadic retinitis pigmentosa (sRP) in the largest cohort reporte
157 tor (RPGR) gene account for >70% of X-linked retinitis pigmentosa (XLRP) and 15-20% of all inherited
158 tations in the human RP2 gene cause X-linked retinitis pigmentosa (XLRP) and cone-rod dystrophy (XL-C
159 ation (M58K) found in a family with X-linked retinitis pigmentosa (XLRP) and show that this missense
161 ges of disease in a canine model of X-linked retinitis pigmentosa (XLRP) caused by a mutation in the
163 in the pathogenesis associated with X-linked retinitis pigmentosa (XLRP) resulting from mutations in
170 ilies diagnosed as having autosomal dominant retinitis pigmentosa and 10% in families with variable c
171 itry, degenerate in retinal diseases such as retinitis pigmentosa and age related macular degeneratio
172 ntion of blinding degenerative diseases like retinitis pigmentosa and age-related macular degeneratio
173 use of untreatable blindness worldwide, with retinitis pigmentosa and cone dystrophy affecting approx
174 al degeneration and visual disorders such as retinitis pigmentosa and congenital stationary night bli
175 ndrome known as Short stature, Hearing loss, Retinitis pigmentosa and distinctive Facies (SHRF, #OMIM
176 s that BBS2 mutations can cause nonsyndromic retinitis pigmentosa and highlights yet another candidat
180 We further found that PRPF8 mutants causing Retinitis pigmentosa assemble less efficiently with the
181 lium (RPE) from an individual suffering from retinitis pigmentosa associated with biallelic variants
184 this issue in an established mouse model of Retinitis Pigmentosa caused by the P23H mutation in rhod
185 tified homozygous REEP6-E75K mutation in two retinitis pigmentosa families of different ethnicities.
186 etinal degeneration in XLRP.Mutations in the Retinitis Pigmentosa GTPase Regulator (RPGR) cause retin
192 th retinitis pigmentosa (RP) associated with retinitis pigmentosa GTPase regulator gene (RPGR) mutati
193 ogression rates, and interocular symmetry in retinitis pigmentosa GTPase regulator gene (RPGR)-associ
194 addition, SPATA7 directly interacts with the retinitis pigmentosa GTPase regulator interacting protei
198 y leading to decreased expression of FTO and retinitis pigmentosa GTPase regulator-interacting protei
200 horoidal neovascularization in 2.3% of eyes; retinitis pigmentosa in 1.9% of eyes; severe cough in 1.
201 etinal dystrophy in 82% (19/23), followed by retinitis pigmentosa in 14% (3/23) and cone-rod dystroph
212 d CRB1 and CRB2 gene therapy vectors in Crb1-retinitis pigmentosa mouse models at mid-stage disease.
214 deficiency is linked to human diseases like retinitis pigmentosa or myeloid neoplasia, but its genom
215 specific visual cortical gray matter loss in Retinitis Pigmentosa patients associated with their visu
216 is likely the cause of phenotype observed in retinitis pigmentosa patients carrying T17M mutation.
220 whole brain gray matter volume changes in 27 Retinitis Pigmentosa patients with partially preserved v
221 of several rhodopsin mutations identified in retinitis pigmentosa patients, including F220C and F45L,
223 Vision impairments and blindness caused by retinitis pigmentosa result from severe neurodegeneratio
225 ere autosomal recessive retinal dystrophies (retinitis pigmentosa RP64 and cone-rod dystrophy CORD16)
226 higher photosynthetic organisms, as well as Retinitis Pigmentosa Type 2-Clathrin Light Chain, a memb
227 tegies to optimize outcomes in patients with retinitis pigmentosa undergoing retinal prosthesis impla
228 disease, age-related macular degeneration or retinitis pigmentosa urgently require the development of
230 udinal imaging follow-up in 71 patients with retinitis pigmentosa was studied using the main outcome
231 ient demonstrated an unexpected diagnosis of retinitis pigmentosa with a novel variant of unknown sig
232 o groups of patients suffering from advanced retinitis pigmentosa with specific deterioration of the
233 understanding other dominant diseases (e.g., retinitis pigmentosa) caused by missense mutations in me
234 ilies with a diagnosis of autosomal dominant retinitis pigmentosa, 35 families with unspecified macul
235 e regulator (RPGR) gene are a major cause of retinitis pigmentosa, a blinding retinal disease resulti
238 ular age-related macular degeneration (AMD), retinitis pigmentosa, and diabetic retinopathy are assoc
239 nvolved in age-related macular degeneration, retinitis pigmentosa, and Leber's congenital amaurosis m
240 the proband presents with hepatic fibrosis, retinitis pigmentosa, and postaxial polydactyly; he harb
241 sing CRISPR/Cas9 to model the human disorder retinitis pigmentosa, and to introduce point mutations o
242 tics with potential applications not only in retinitis pigmentosa, but also in age-related macular de
244 macular degeneration (wet AMD), Luxturna for retinitis pigmentosa, Dextenza (0.4 mg dexamethasone int
246 tained families with a clinical diagnosis of retinitis pigmentosa, macular dystrophy, and/or pattern
248 d deletion of codon 153 (K153Delta) leads to retinitis pigmentosa, pattern dystrophy, and fundus flav
251 he RPGR gene cause a common form of X-linked retinitis pigmentosa, which often results in severe loss
252 ophy and some exhibited macular dystrophy or retinitis pigmentosa, while all presented with macular d
253 encing or high-throughput sequencing for all retinitis pigmentosa-associated genes in patients, and s
254 t use, to our knowledge, of human iPSCs with retinitis pigmentosa-causing mutations to look at pathop
288 ng patients with CMV retinitis, the rates of retinitis progression and increasing retinitis border ac
289 initis (either increasing border activity or retinitis progression) were compared between those with
291 clinic for HIV treatment had less extensive retinitis than patients in recent reports from an ophtha
292 at the time of the initial diagnosis of CMV retinitis that predicted subsequent retinal detachment i
298 al of 13.5 months after the diagnosis of CMV retinitis, whereas those with immune recovery had a mort