scholarly journals Data on the stem cells paracrine effects on apoptosis and cytokine milieu in an experimental model of cardiorenal syndrome type II

Data in Brief ◽  
2018 ◽  
Vol 21 ◽  
pp. 1430-1434
Author(s):  
Giorgio Vescovo ◽  
Chiara Castellani ◽  
Marny Fedrigo ◽  
Grazia Maria Virzì ◽  
Giovanni Maria Vescovo ◽  
...  
Keyword(s):  
Stem Cells ◽  
Experimental Model ◽  
Cardiorenal Syndrome ◽  
Syndrome Type ◽  
Type Ii ◽  
Paracrine Effects ◽  
Cytokine Milieu

Stem cells transplantation positively modulates the heart-kidney cross talk in cardiorenal syndrome type II

2019 ◽  
Vol 275 ◽  
pp. 136-144 ◽  
Author(s):  
Giorgio Vescovo ◽  
Chiara Castellani ◽  
Marny Fedrigo ◽  
Grazia Maria Virzì ◽  
Giovanni Maria Vescovo ◽  
...  
Keyword(s):  
Stem Cells ◽  
Cross Talk ◽  
Cardiorenal Syndrome ◽  
Syndrome Type ◽  
Type Ii ◽  
Stem Cells Transplantation

scholarly journals Nonuremic Indication for Peritoneal Dialysis for Refractory Heart Failure in Cardiorenal Syndrome Type II: Review and Perspective

2013 ◽  
Vol 33 (1) ◽  
pp. 8-14 ◽  
Author(s):  
Masaaki Nakayama
Keyword(s):  
Heart Failure ◽  
Congestive Heart Failure ◽  
Peritoneal Dialysis ◽  
Maintenance Therapy ◽  
Supportive Therapy ◽  
Cardiorenal Syndrome ◽  
Syndrome Type ◽  
Type Ii ◽  
Kidney Dysfunction ◽  
Refractory Heart Failure

Cardiorenal syndrome (CRS) type II is a serious condition in which chronic cardiac abnormalities cause worsening kidney function, leading to permanent chronic kidney damage. Management of CRS type II coupled with diuretic-resistant congestive heart failure (CHF) has been an issue of dispute. However, since the early 1990s, reports indicating the clinical usefulness of peritoneal dialysis (PD) as maintenance therapy for intractable CHF in this population have been accumulating. The present manuscript reviews the mechanisms by which kidney dysfunction develops within CHF, and then examines recent experiences of PD as chronic supportive therapy for intractable CRS type II, reviews the contributing mechanisms, and discusses the rationale for using PD as a new therapeutic approach in the nonuremic setting of CHF.

scholarly journals Insights into the pathophisiology of cardiorenal syndrome type II in the rat

2013 ◽  
Vol 34 (suppl 1) ◽  
pp. P5736-P5736
Author(s):  
A. Angelini ◽  
C. Castellani ◽  
G. Virzi ◽  
M. Fedrigo ◽  
G. Thiene ◽  
...  
Keyword(s):  
Cardiorenal Syndrome ◽  
Syndrome Type ◽  
Type Ii

Can photobiomodulation associated with implantation of mesenchymal adipose-derived stem cells attenuate the expression of MMPs and decrease degradation of type II collagen in an experimental model of osteoarthritis?

2018 ◽  
Vol 33 (5) ◽  
pp. 1073-1084 ◽  
Author(s):  
Tatiane Garcia Stancker ◽  
Stella Souza Vieira ◽  
Andrey Jorge Serra ◽  
Rafael do Nascimento Lima ◽  
Regiane dos Santos Feliciano ◽  
...  
Keyword(s):  
Stem Cells ◽  
Experimental Model ◽  
Type Ii Collagen ◽  
Adipose Derived Stem Cells ◽  
Type Ii

Individual Health Trial with Ruxolitinib in Aicardi-Goutières Syndrome Type II

2019 ◽  
Author(s):  
Afshin Saffari ◽  
Stefan Kölker ◽  
Georg Friedrich Hoffmann ◽  
Andreas Ziegler
Keyword(s):  
Syndrome Type ◽  
Type Ii ◽  
Individual Health

Two Different UGT1A1 Mutations causing Crigler–Najjar Syndrome types I and II in an Iranian Family

2015 ◽  
Vol 24 (4) ◽  
pp. 523-526 ◽  
Author(s):  
Yoshihiro Maruo ◽  
Mahdiyeh Behnam ◽  
Shinichi Ikushiro ◽  
Sayuri Nakahara ◽  
Narges Nouri ◽  
...  
Keyword(s):  
Serum Bilirubin ◽  
Total Serum Bilirubin ◽  
Total Serum ◽  
Compound Heterozygous ◽  
Type I ◽  
Syndrome Type ◽  
Type Ii ◽  
Wild Type ◽  
Iranian Family ◽  
Udp Glucuronosyltransferase

Background: Crigler–Najjar syndrome type I (CN-1) and type II (CN-2) are rare hereditary unconjugated hyperbilirubinemia disorders. However, there have been no reports regarding the co-existence of CN-1 and CN-2 in one family. We experienced a case of an Iranian family that included members with either CN-1 or CN-2. Genetic analysis revealed a mutation in the bilirubin UDP-glucuronosyltransferase (UGT1A1) gene that resulted in residual enzymatic activity.Case report: The female proband developed severe hyperbilirubinemia [total serum bilirubin concentration (TB) = 34.8 mg/dL] with bilirubin encephalopathy (kernicterus) and died after liver transplantation. Her family history included a cousin with kernicterus (TB = 30.0 mg/dL) diagnosed as CN-1. Her great grandfather (TB unknown) and uncle (TB = 23.0 mg/dL) developed jaundice, but without any treatment, they remained healthy as CN-2. Results: The affected cousin was homozygous for a novel frameshift mutation (c.381insGG, p.C127WfsX23). The affected uncle was compound heterozygous for p.C127WfsX23 and p.V225G linked with A(TA)7TAA. p.V225G-UGT1A1 reduced glucuronidation activity to 60% of wild-type. Thus, linkage of A(TA)7TAA and p.V225G might reduce UGT1A1 activity to 18%–36 % of the wild-type. Conclusion: Genetic and in vitro expression analyses are useful for accurate genetic counseling for a family with a history of both CN-1 and CN-2. Abbreviations: CN-1: Crigler–Najjar syndrome type I; CN-2: Crigler–Najjar syndrome type II; GS: Gilbert syndrome; UGT1A1: bilirubin UDP-glucuronosyltransferase; WT: Wild type; TB: total serum bilirubin.

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