In our study, the diagnosis of cirrhosis was made by TE instead of biopsy. However, several studies have demonstrated that TE is highly reliable for the diagnosis of cirrhosis in

HCV-monoinfected patients with or without HIV infection.13, 14, 16 Finally, we present data from a large, prospective cohort of HIV/HCV-coinfected patients with compensated cirrhosis diagnosed using the same method, TE, which avoids potential biases of previous cohorts, and prospectively followed and managed by a uniform management protocol. These are the strengths of our study. Compound Library cost In summary, LS, assessed by TE, is an independent predictor of the development of hepatic decompensations, HCC and liver-related mortality in HIV/HCV-coinfected patients with compensated cirrhosis, and provides find more additional prognostic information to that provided by CTP or MELD scores. In our opinion, this observation provides new evidence to consider incorporating sequential measurements of LS by TE to the routine daily clinical care of HIV/HCV-coinfected patients. In fact, the measurement of LS may help us to identify those patients at very high risk of decompensation

and death. Also, HIV/HCV-coinfected patients bearing an LS ≥ 40 kPa should probably be seen more frequently. Finally, future studies should evaluate if LS is also an independent prognostic marker in patients with decompensated cirrhosis and if sequential assessment of LS in patients with cirrhosis results in a mortality benefit. If so, it may be added to CTP and MELD scores in the decision to consider patients to be referred to a liver transplantation program. The authors thank Carmen Almeida from the Hospital Universitario de Valme, Seville, for helpful advice in statistical analyses. Additional Supporting Information may be found in the online version of this article. “
“Autophagy is a catabolic process that degrades proteins and damaged organelles to promote cell survival. Mitophagy is a selective form of autophagy

specific for degradation of mitochondria. Acetaminophen (APAP) overdose causes liver injury by inducing necrosis following mitochondrial damage, and we previously demonstrated that pharmacological induction of autophagy by rapamycin protected against APAP-induced liver injury in mice by degrading damaged Bumetanide mitochondria. However, the mechanism for this mitochondria removal by autophagy is unknown. Parkin, an E3 ligase, has been shown to be required for mitophagy induction in cultured mammalian cells following mitochondrial depolarization, but its role in vivo is not clear. The purpose of this study was to investigate the role of Parkininduced mitophagy in protection against APAP-induced liver injury using wild type (WT) and Parkin knockout (KO) mice. Parkin translocated to mitochondria in WT mouse livers after APAP treatment followed by mitophagy induction.