Laser ablation is superior to TACE in large-sized hepatocellular carcinoma: A pilot case-control study

Background:Limited therapies are available for large ( 6540 mm) unresectable hepatocellular carcinoma (HCC). Currently, the standard treatment with transarterial chemoembolisation (TACE) is unsatisfactory with high recurrence rate and limited effect on survival. Laser Ablation (LA) has emerged as a relatively new technique characterized by high efficacy and good safety. This study is aimed to evaluate the efficacy of LA in comparison to TACE in patients with large HCC. Methods: Eighty-two patients with a single HCC nodule 6540 mm (BCLC stage A or B) were enrolled in this case-control study. Forty-one patients were treated with LA and 41 patients were treated with TACE. Response to therapy was evaluated according to the mRECIST criteria. Survival was calculated with Kaplan-Meier from the time of cancer diagnosis to death with values censored at the date of the last follow-up. Results: Twenty-six (63.4%) and 8 (19.5%) patients had a complete response after LA and TACE, respectively (p < 0.001). Subsequently we stratified the HCCs in 3 categories according to the nodule size: 40-50 mm, 51-60 mm, and > 60 mm. LA resulted superior to TACE especially in nodules ranging between 51 and 60 mm in diameter, with a complete response rate post-LA and post-TACE of 75% and 14.3%, respectively (p = 0.0133). The 36 months cumulative survival rate in patients treated with LA and TACE was 55.4% and 48.8%, respectively. The disease recurrence rates after LA and TACE were 19.5% and 75.0%, respectively. Conclusions: LA is a more effective therapeutic option than TACE in patients with solitary large HCC

Aged PrP null mice show defective processing of neuregulins in the peripheral nervous system

A prion, a protease-resistant conformer of the cellular prion protein (PrP(C)), is the causative agent of transmissible spongiform encephalopathies or prion diseases. While this property is well established for the aberrantly folded protein, the physiological function of PrP(C) remains elusive. Among different putative functions, the non-pathogenic protein isoform PrP(C) is involved in several cellular processes. Here, we show that PrP(C) regulates the cleavage of neuregulin-1 proteins (NRG1). Neuregulins provide key axonal signals that regulate several processes, including glial cells proliferation, survival and myelination. Interestingly, mice devoid of PrP(C) (Prnp\u2070/\u2070) were recently shown to have a late-onset demyelinating disease in the peripheral nervous system (PNS) but not in the central nervous system (CNS). We found that NRG1 processing is developmentally regulated in the PNS and, by comparing wildtype and Prnp\u2070/\u2070 mice, that PrP(C) influences NRG1 processing in old, but not in young, animals. In addition, we found that also the processing of neuregulin-3, another neuregulin family member, is altered in the PNS of Prnp\u2070/\u2070 mice. These differences in neuregulin proteins processing are not paralleled in the CNS, thus suggesting a different cellular function for PrP(C) between the CNS and the PN

Prevalence and incidence of cholecystolithiasis in cirrhosis and relation to the etiology of liver disease

To assess prevalence and incidence of cholecystolithiasis in cirrhosis, 356 consecutive cirrhotics and 247 consecutive cases of chronic hepatitis without cirrhosis were studied by ultrasonography. Cholecystolithiasis was significantly more frequent in cirrhotics than in patients with chronic hepatitis (p lt 0.001) after stratification for age and for alcohol abuse, and its prevalence in the former was affected by Child's class (p lt 0.001) and duration (p lt 0.001) of cirrhosis and was higher in HBsAg-negative as compared with HBsAg-positive cases (36.2 vs. 11.9%) and in patients with previous alcohol abuse (41.5 vs. 28.3%), while no difference was noted in relation to sex. By multivariate analysis, duration and Child's class of cirrhosis and HBsAg-negative status were statistically associated with cholecystolithiasis. One hundred and eighty-two of the 356 cirrhotic patients without gallstones at inclusion were followed prospectively, and 21 (11.5%) of them developed cholecystolithiasis, and duration of cirrhosis and past alcohol abuse were found to be independent risk factors for gallstone development by multivariate analysis. Cirrhosis is a significant risk factor for cholecystolithiasis, except for HBsAg-positive patients who have prevalence and incidence similar to noncirrhotics. Severity and duration of cirrhosis and previous alcohol abuse are associated with an increased risk of gallstone formation