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1 presents a potential therapeutic approach in polycystic liver disease.
2 Mutations in polycystins are a cause of polycystic liver disease.
3 tal diseases including Alagille Syndrome and polycystic liver disease.
4 gous gene models of human autosomal dominant polycystic liver disease.
5 ibitors might be used to treat patients with polycystic liver disease.
6 ese proteins might inhibit cyst expansion in polycystic liver disease.
7 regulator of cell proliferation may underlie polycystic liver disease.
8 mortalized B lymphoblasts from patients with polycystic liver disease.
9 mic reticulum (ER), cause autosomal dominant polycystic liver disease.
10 d in livers of animal models and humans with polycystic liver disease.
11 Mutations in PC2 are associated with polycystic liver diseases.
12 ts with breast abnormalities, 1 patient with polycystic liver disease, 1 patient with esophageal thic
14 nical profile of isolated autosomal dominant polycystic liver disease (ADPLD) using nonaffected famil
16 ficant cause of ESRD, and autosomal dominant polycystic liver diseases (ADPLD), which result in signi
17 in vitro key features of Alagille syndrome, polycystic liver disease and cystic fibrosis (CF)-associ
18 olycystic kidney disease, autosomal dominant polycystic liver disease, and the third form of ADPKD.
19 al history, manifestations, and treatment of polycystic liver disease are based on the disease as it
20 underdiagnosed and genetically distinct from polycystic liver disease associated with ADPKD but with
21 y-eight of the 49 individuals diagnosed with polycystic liver disease before participation in the stu
23 ith extensive hepatic involvement with adult polycystic liver disease can have an excellent outcome w
26 whereas in isolated PCLD (autosomal dominant polycystic liver disease), disrupted cell adhesion may b
27 osomal dominant polycystic kidney disease or polycystic liver disease; efficacy does not depend on si
29 ative or indeterminate diagnosis, those with polycystic liver disease had slightly higher levels of s
32 Mutations in the gene encoding SEC63 cause polycystic liver disease in humans; however, it is not c
33 al presentation and histological features of polycystic liver disease in the presence or absence of A
41 ion and biochemical properties of normal and polycystic liver disease mutant forms of hepatocystin we
42 ns were solitary giant liver cysts (n = 16), polycystic liver disease (n = 9), hydatid cyst (n = 6),
43 al hepatic fibrosis (two), cystinosis (one), polycystic liver disease (one), A-1-A deficiency (one),
44 ng mutation in hepatocystin observed in some polycystic liver disease patients produces a protein tha
45 seen in the rare inherited disorder isolated polycystic liver disease (PCLD) and are recognized as th
49 of resective and fenestration procedures for polycystic liver disease (PCLD), we present the first se
52 resent review summarizes recent knowledge on polycystic liver diseases (PCLDs), mechanisms of hepatic
57 ical trials have shown that in patients with polycystic liver disease (PLD), short-term treatment wit
59 ncreased level of intracranial aneurysms and polycystic liver disease (PLD), which can be severe and
66 d from healthy individuals and patients with polycystic liver disease to reproduce the effects of the
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