戻る
「早戻しボタン」を押すと検索画面に戻ります。 [閉じる]

コーパス検索結果 (１語後でソート)

通し番号をクリックするとPubMedの該当ページを表示します
1 amilial Mediterranean fever (FMF)-associated AA amyloidosis.
2 k in our understanding of the development of AA amyloidosis.
3 e an explanation for the lysosomal origin of AA amyloidosis.
4 is review summarizes current knowledge about AA amyloidosis.
5 sk of early CVD in patients with FMF-related AA amyloidosis.
6 entire cohort was 19 years from diagnosis of AA amyloidosis.
7 us findings that short HS fragments preclude AA amyloidosis.
8 ss the initial events in the pathogenesis of AA amyloidosis.
9 isate slows the decline of renal function in AA amyloidosis.
10 ized chiefly by arthralgia, skin rashes, and AA amyloidosis.
11 s for overall survival and kidney failure in AA amyloidosis.
12 i) the form is biochemically classifiable as AA amyloidosis.
13 amilial Mediterranean fever (FMF)-associated AA amyloidosis.
14 om a mouse and a human patient with systemic AA amyloidosis.
15  the inflammation-related disease amyloid A (AA) amyloidosis.
16 ved to play a role in the disease Amyloid A (AA) Amyloidosis.
17 A) has been linked to the disease amyloid A (AA) amyloidosis.
18 se or systemic light chain (AL) or reactive (AA) amyloidosis.
19 SAF-1 plays a key role in the development of AA amyloidosis, a consequence of chronic inflammation.
20 idney is involved in almost 100% of cases of AA amyloidosis, a rare disease caused by persistent infl
21 iple organs resulting in reactive amyloid A (AA) amyloidosis, a consequence of rheumatoid arthritis,
22                                Patients with AA amyloidosis and age >=65 years, eGFR <45 ml/min per 1
23 rvival between the patients with FMF-related AA amyloidosis and glomerulonephropathies (GN) to define
24 cy and safety of eprodisate in patients with AA amyloidosis and kidney involvement.
25 igns of inflammation and a long-term risk of AA amyloidosis and overt lymphoproliferation.
26 es, fever, arthralgia, and in some subjects, AA amyloidosis, and have been mapped to chromosome 1q44.
27 -overexpressing mice spontaneously developed AA amyloidosis at the age of 14 mo or older.
28                 Prognostic stratification in AA amyloidosis can be easily made by staging systems, si
29                                              AA amyloidosis can be induced in mice experimentally thr
30                                   Therefore, AA amyloidosis can be thought of as a consequence of lon
31 the rapid onset of renal failure in clinical AA amyloidosis following acute exacerbation of inflammat
32                Patients with newly diagnosed AA amyloidosis from the Pavia (n=233, testing cohort) an
33 al transplant recipients with FMF-associated AA amyloidosis (group 1) and propensity score-matched tr
34     However, its role in the pathogenesis of AA amyloidosis has thus far remained obscure.
35 nally, observations from a clinical trial in AA amyloidosis have generated hypotheses about the relat
36 t been considered prior to presentation with AA amyloidosis in 23 patients (50%).
37 ble of selectively imaging systemic visceral AA amyloidosis in a murine model of the disease.
38   We report 2 further cases of patients with AA amyloidosis in HIDS, both of whom developed dialysis-
39 F-1 transgenic mice rapidly developed severe AA amyloidosis in response to azocasein injection, indic
40 r 12-117 months in 80 patients with systemic AA amyloidosis in whom serum SAA concentration was measu
41                                              AA amyloidosis is a life-threatening complication of the
42                                     Systemic AA amyloidosis is a worldwide occurring protein misfoldi
43                                              AA amyloidosis is associated with higher risk of mortali
44                                              AA amyloidosis is the most serious potential complicatio
45                                     Clinical AA amyloidosis is typically preceded by many years of ac
46                                   Amyloid A (AA) amyloidosis is a complication of chronic inflammator
47                          Systemic amyloid A (AA) amyloidosis is a serious complication of chronic inf
48                        Inflammation-related (AA) amyloidosis is a severe clinical disorder characteri
49 e SAF family, is abundantly present in human AA amyloidosis patients.
50 of this unique in vivo experimental model of AA amyloidosis provides the means to assess the therapeu
51                                     Clinical AA amyloidosis rarely involves the heart, but amyloidoti
52                                              AA amyloidosis remains a challenging and serious late co
53 es of 20 patients with FMF and biopsy-proven AA amyloidosis that were transplanted between 1995 and 2
54                                           In AA amyloidosis, the expression of cytokines, particularl
55       SAA is a protein precursor of reactive AA amyloidosis, the major complication of chronic inflam
56 an time to progression to ESRF from onset of AA amyloidosis was 3.3 years (interquartile range [IQR]
57 was 5 years; median age at presentation with AA amyloidosis was 38 years.
58                                Recurrence of AA amyloidosis was diagnosed in 2 patients during the fi
59                                Recurrence of AA amyloidosis was diagnosed in 21 patients (group 1a) a
60                                Recurrence of AA amyloidosis was diagnosed in 21 patients (group 1a),
61 -1 is directly linked to the pathogenesis of AA amyloidosis, we have developed a SAF-1 transgenic mou
62                      Using a murine model of AA amyloidosis, we have examined the in vivo amyloid rea
63 namic turnover, and outcome is favourable in AA amyloidosis when the SAA concentration is maintained