The liver‐specific microRNA‐122*, the complementary strand of microRNA‐122, acts as a tumor suppressor by modulating the p53/mouse double minute 2 homolog circuitry

Alina Simerzin, Elina Zorde‐Khvalevsky, Mila Rivkin, Revital Adar, Jessica Zucman‐Rossi, Gabrielle Couchy, Tania Roskams, Olivier Govaere, Moshe Oren, Hilla Giladi, Eithan Galun – 15 June 2016 – The tumor suppressor p53 is a central regulator of signaling pathways that controls the cell cycle and maintains the integrity of the human genome. p53 level is regulated by mouse double minute 2 homolog (Mdm2), which marks p53 for proteasomal degradation. The p53‐Mdm2 circuitry is subjected to complex regulation by a variety of mechanisms, including microRNAs (miRNAs).

Prevalence of chronic liver disease and cirrhosis by underlying cause in understudied ethnic groups: The multiethnic cohort

Veronica Wendy Setiawan, Daniel O. Stram, Jacqueline Porcel, Shelly C. Lu, Loïc Le Marchand, Mazen Noureddin – 15 June 2016 – Chronic liver disease (CLD) and cirrhosis are major sources of morbidity and mortality in the United States. Little is known about the epidemiology of these two diseases in ethnic minority populations in the United States. We examined the prevalence of CLD and cirrhosis by underlying etiologies among African Americans, Native Hawaiians, Japanese Americans, Latinos, and whites in the Multiethnic Cohort.

The P2X4 purinergic receptor impacts liver regeneration after partial hepatectomy in mice through the regulation of biliary homeostasis

Aurore Besnard, Julien Gautherot, Boris Julien, Ali Tebbi, Isabelle Garcin, Isabelle Doignon, Noémie Péan, Emmanuel Gonzales, Doris Cassio, Brigitte Grosse, Bingkaï Liu, Hanaa Safya, Florent Cauchois, Lydie Humbert, Dominique Rainteau, Thierry Tordjmann – 15 June 2016 – Many regulatory pathways are involved in liver regeneration after partial hepatectomy (PH), to initiate growth, protect liver cells, and sustain remnant liver functions.

Chemokine (C‐C motif) receptor 2–positive monocytes aggravate the early phase of acetaminophen‐induced acute liver injury

Jana C. Mossanen, Oliver Krenkel, Can Ergen, Olivier Govaere, Anke Liepelt, Tobias Puengel, Felix Heymann, Sandra Kalthoff, Eric Lefebvre, Dirk Eulberg, Tom Luedde, Gernot Marx, Christian P. Strassburg, Tania Roskams, Christian Trautwein, Frank Tacke – 15 June 2016 – Acetaminophen (APAP, paracetamol) poisoning is a leading cause of acute liver failure (ALF) in humans and induces hepatocyte necrosis, followed by activation of the innate immune system, further aggravating liver injury. The role of infiltrating monocytes during the early phase of ALF is still ambiguous.

The liver‐specific microRNA‐122*, the complementary strand of microRNA‐122, acts as a tumor suppressor by modulating the p53/mouse double minute 2 homolog circuitry

Alina Simerzin, Elina Zorde‐Khvalevsky, Mila Rivkin, Revital Adar, Jessica Zucman‐Rossi, Gabrielle Couchy, Tania Roskams, Olivier Govaere, Moshe Oren, Hilla Giladi, Eithan Galun – 15 June 2016 – The tumor suppressor p53 is a central regulator of signaling pathways that controls the cell cycle and maintains the integrity of the human genome. p53 level is regulated by mouse double minute 2 homolog (Mdm2), which marks p53 for proteasomal degradation. The p53‐Mdm2 circuitry is subjected to complex regulation by a variety of mechanisms, including microRNAs (miRNAs).

A Model to predict severity of drug‐induced liver injury in humans

Minjun Chen, Jürgen Borlak, Weida Tong – 15 June 2016 – Drug‐induced liver injury (DILI) is a major public health concern, and improving its prediction remains an unmet challenge. Recently, we reported the Rule‐of‐2 (RO2) and found lipophilicity (logP ≥3) and daily dose ≥100 mg of oral medications to be associated with significant risk for DILI; however, the RO2 failed to estimate grades of DILI severity.

Predicting renal recovery after liver transplant with severe pretransplant subacute kidney injury: The impact of warm ischemia time

Heather L. Laskey, Nathan Schomaker, Kenneth W. Hung, Sumeet K. Asrani, Linda Jennings, Trevor L. Nydam, Jane Gralla, Alex Wiseman, Hugo R. Rosen, Scott W. Biggins – 15 June 2016 – Identifying which liver transplantation (LT) candidates with severe kidney injury will have a full recovery of renal function after liver transplantation alone (LTA) is difficult. Avoiding unnecessary simultaneous liver‐kidney transplantation (SLKT) can optimize the use of scarce kidney grafts. Incorrect predictions of spontaneous renal recovery after LTA can lead to increased morbidity and mortality.

Inhibition of spleen tyrosine kinase activation ameliorates inflammation, cell death, and steatosis in alcoholic liver disease

Terence N. Bukong, Arvin Iracheta‐Vellve, Banishree Saha, Aditya Ambade, Abhishek Satishchandran, Benedek Gyongyosi, Patrick Lowe, Donna Catalano, Karen Kodys, Gyongyi Szabo – 15 June 2016 – The spectrum of alcoholic liver disease (ALD) is a major cause of mortality with limited therapies available. Because alcohol targets numerous signaling pathways in hepatocytes and in immune cells, the identification of a master regulatory target that modulates multiple signaling processes is attractive.

Five‐year histological and serological follow‐up of operationally tolerant pediatric liver transplant recipients enrolled in WISP‐R

Sandy Feng, Anthony J. Demetris, Katharine M. Spain, Sai Kanaparthi, Bryna E. Burrell, Udeme D. Ekong, Estella M. Alonso, Philip Rosenthal, Laurence A. Turka, David Ikle, Nadia K. Tchao – 15 June 2016 – Pediatric liver transplant recipients arguably have the most to gain and the most to lose from discontinuing immunosuppression (IS). Whereas IS undoubtedly exerts a cumulative toll, there is concern that insufficient or no IS may contribute to allograft deterioration.

Receptor interacting protein 3 protects mice from high‐fat diet‐induced liver injury

Sanjoy Roychowdhury, Rebecca L. McCullough, Carlos Sanz‐Garcia, Paramananda Saikia, Naim Alkhouri, Ammar Matloob, Katherine A. Pollard, Megan R. McMullen, Colleen M. Croniger, Laura E. Nagy – 15 June 2016 – Multiple pathways of programmed cell death are important in liver homeostasis. Hepatocyte death is associated with progression of nonalcoholic fatty liver disease, and inhibition of apoptosis partially protects against liver injury in response to a high‐fat diet (HFD).

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