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1 ar pathology underlying cortical superficial siderosis.
2 he presence of cSAH and cortical superficial siderosis.
3  with environmental risk factors for hepatic siderosis.
4 ation p.Arg59* presented with severe hepatic siderosis.
5 fication of MRI-defined cortical superficial siderosis.
6 gh burden of cardiac mortality in myocardial siderosis.
7  confirmed clinical diagnosis of superficial siderosis.
8  infarcts, pyknotic neurons, and progressive siderosis.
9 d by a photosensitive dermatosis and hepatic siderosis.
10 da is a skin disease associated with hepatic siderosis.
11 (POD); successive biopsies showed increasing siderosis.
12  review possible factors contributing to the siderosis.
13 five of 73) were associated with superficial siderosis.
14 val to allow the slow development of retinal siderosis.
15 especially disseminated cortical superficial siderosis (49% vs 19%; p<0.0001).
16 ene (Hfe) have been used to generate hepatic siderosis, a nearly uniform finding in PCT.
17                Conclusion In the presence of siderosis, a transmetallation mechanism may be set off b
18  between acute cSAH and cortical superficial siderosis-a new CAA haemorrhagic imaging signature and (
19            Thus, in TM patients with cardiac siderosis, amlodipine combined with chelation therapy re
20                     The cause of the hepatic siderosis and iron overload that is common in porphyria
21                           Eight patients had siderosis and underwent chelation therapy.
22 ronic infarctions, and [on MRI] microbleeds, siderosis, and enlarged perivascular spaces) were retros
23   Cerebral microbleeds, cortical superficial siderosis, and white matter hyperintensity volume were a
24                         Cortical superficial siderosis appears to be the result of predominantly adva
25 her studies of the safety of GBCAs in severe siderosis are needed.
26         These data indicate that the hepatic siderosis associated with PCT likely results from dysreg
27                               Autopsy showed siderosis at many sites, including the implanted liver.
28 t least 1 microhemorrhage and/or superficial siderosis before initiation of lecanemab (23%).
29 le logistic regression, cortical superficial siderosis burden (OR 5.53; 95% CI 2.82 to 10.8, p<0.0001
30  relating to treatment of chronic myocardial siderosis but none relating to treatment of acute heart
31 r cerebral microbleeds, cortical superficial siderosis, centrum semiovale perivascular spaces, and wh
32 r cerebral microbleeds, cortical superficial siderosis, centrum semiovale perivascular spaces, and wh
33    Histopathologically, cortical superficial siderosis corresponded to iron-positive haemosiderin dep
34  HR, 1.6; 95% CI, 1.3-2.0; total superficial siderosis count: HR, 1.9; 95% CI, 1.3-2.6; total microhe
35  microbleeds (CMBs) and cortical superficial siderosis (CSS) are the characteristic markers of cerebr
36                         Cortical superficial siderosis describes a distinct pattern of blood-breakdow
37 e CAA were analysed for cortical superficial siderosis (focal, </=3 sulci; disseminated, >/=4 sulci),
38                Although cortical superficial siderosis has many possible causes, it is emerging as a
39 emorrhages, presence of cortical superficial siderosis, higher amyloid plaque, and elevated mean arte
40 trauma; increased conspicuity of superficial siderosis in Alzheimer disease and amyloid angiopathy; a
41  hemochromatosis (hh) gene (HFE) explain the siderosis in approximately 20% patients, suggesting that
42 tandards for evaluating cortical superficial siderosis in research studies.
43 heart failure and arrhythmia from myocardial siderosis in thalassemia major and is superior to serum
44 d ARIA-H (microhemorrhage and/or superficial siderosis) independently, assessed with the area under t
45                         Cortical superficial siderosis is an established haemorrhagic neuroimaging ma
46       These results suggest that superficial siderosis is associated with a distinct pattern of cogni
47 oid angiopathy cohorts, cortical superficial siderosis is associated with characteristic clinical sym
48                             Severe pituitary siderosis is associated with early organ dysfunction.
49                                      Hepatic siderosis is common in patients with porphyria cutanea t
50                In fact, cortical superficial siderosis is emerging as a strong independent risk facto
51                   Thus, cortical superficial siderosis is of relevance to neurologists working in neu
52 express a porphyric phenotype unless hepatic siderosis is present.
53 al nervous system infratentorial superficial siderosis (iSS) is increasingly detected by blood-sensit
54 dial T2* from 5 to 20 ms (indicating cardiac siderosis), left ventricular ejection fraction (LVEF) of
55 l lesions (microbleeds, cortical superficial siderosis, microinfarcts) and large-scale alterations (w
56 atients with severe transfusional myocardial siderosis (myocardial [m] T2* 5-<10 ms; left ventricular
57 g assessment of myocardial edema, myocardial siderosis, myocardial perfusion, and diffuse myocardial
58    ARIA-microhemorrhage and ARIA-superficial siderosis occurred in 197 participants (19.1%) and 151 p
59                                              Siderosis of interstitial trophoblasts is a novel pathol
60 tive effects are associated with superficial siderosis of the central nervous system caused by chroni
61                                  Superficial siderosis of the CNS is a rare condition, caused by depo
62  microscopy (n = 3) were conducted to verify siderosis of trophoblasts.
63 these data suggest that cortical superficial siderosis on MRI corresponds to iron-positive deposits i
64 barachnoid haemorrhage, cortical superficial siderosis or intracerebral haemorrhage.
65 microbleeds, or foci of cortical superficial siderosis) or at least one strictly lobar haemorrhagic l
66                                       Ocular siderosis (OS) is a significant cause of visual loss due
67  episodes compared with cortical superficial siderosis-positive, but cSAH-negative subjects with CAA
68                         Cortical superficial siderosis prevalence (but no other CAA severity markers)
69 iological mechanisms of cortical superficial siderosis remain elusive.
70                     Disseminated superficial siderosis (subhazard ratio [SHR] 7.45, 95% CI 4.27-12.99
71 a-thalassemia major patients with myocardial siderosis (T2* 6-20 milliseconds) and no signs of cardia
72                      We describe superficial siderosis that developed more than a decade following tr
73 d clinical, imaging and cortical superficial siderosis topographical mapping data between subjects wi
74 center, the presence of cortical superficial siderosis was an independent variable associated with la
75         The presence of cortical superficial siderosis was an independent variable associated with la
76                   Next, cortical superficial siderosis was assessed on a total of 65 Perls'-stained s
77                         Cortical superficial siderosis was assessed on ex vivo gradient echo and turb
78      Moderate-to-severe cortical superficial siderosis was associated with concentric splitting of th
79 ury, moderate-to-severe cortical superficial siderosis was associated with the presence of microinfar
80   Increased severity of cortical superficial siderosis was associated with upregulation of reactive a
81                         Cortical superficial siderosis was present on ex vivo MRI in 8/14 cases (57%)
82 rachnoid hemorrhage and cortical superficial siderosis were detected in 193 individuals (77.8%) and 1
83 CH during follow-up and cortical superficial siderosis were the main risk factors for death (odds rat
84 rohemorrhages and leptomeningeal superficial siderosis, were termed ARIA-H.
85 linical significance of cortical superficial siderosis, with a particular emphasis on cerebral amyloi