Liver atrophy after percutaneous transhepatic portal embolization occurs in two histological phases: Hepatocellular atrophy followed by apoptosis

AIM To clarify the histological changes associated with liver atrophy after percutaneous transhepatic portalembolization(PTPE) in pigs and humans. METHODS As a preliminary study, we performed pathological examinations of liver specimens from five pigs that had undergone PTPE in a time-dependent model of liver atrophy. In specimens from embolized lobes(EMB) and nonembolized lobes(controls), we measured the portal vein to central vein distance(PV-CV), the area and number of hepatocytes per lobule, and apoptotic activity using the terminal deoxynucleotidyl transferase dU TP nickend labeling assay. Immunohistochemical reactivities were evaluated for light chain 3(LC3) and lysosomal-associated membrane protein 2(LAMP2) as autophagy markers and for glutamine synthetase and cytochrome P450 2 E1(CYP2 E1) as metabolic zonation markers. Samples from ten human livers taken 20-36 d after PTPE were similarly examined. RESULTS PV-CVs and lobule areas did not differ between EMB and controls at day 0, but were lower in EMB than in controls at weeks 2, 4, and 6(P ≤ 0.001). Hepatocyte numbers were not significantly reduced in EMB at day 0 and week 2 but were reduced at weeks 4 and 6(P ≤ 0.05). Apoptotic activity was higher in EMB than in controls at day 0 and week 4. LC3 and LAMP2 staining peaked in EMB at week 2, with no significant difference between EMB and controls at weeks 4 and 6. Glutamine synthetase and CYP2 E1 zonation in EMB at weeks 2, 4, and 6 were narrower than those in controls. Human results were consistent with those of porcine specimens. CONCLUSION The mechanism of liver atrophy after PTPE has two histological phases: Hepatocellular atrophy is likely caused by autophagy in the first 2 wk and apoptosis thereafter.

Left hepatic trisectionectomy for perihilar cholangiocarcinoma with a right-sided round ligament:A case report

BACKGROUND A right-sided round ligament(RSRL)is a rare,congenital anomaly of the intrahepatic portal vein,with a reported frequency of 0.2%-1.2%.For patients with perihilar cholangiocarcinoma associated with an RSRL,an accurate understanding of the vascular and biliary anatomy is indispensable.CASE SUMMARY We report a 70-year-old male with perihilar cholangiocarcinoma associated with an RSRL.After percutaneous transhepatic embolization of the left and anterior portal branches,we conducted a left trisectionectomy of the liver with extrahepatic bile duct resection and hepaticojejunostomy.The postoperative course was uneventful,and R0 resection was achieved.When the liver volume of each section was compared between 7 patients with an RSRL and 20 patients with normal portal vein anatomy,the posterior section in RSRL patients was significantly larger than that in patients with normal portal vein anatomy(median:457 mL vs 306 mL,P=0.031).In patients with perihilar cholangiocarcinoma associated with an RSRL,left trisectionectomy has several surgical advantages:(1)The posterior branch of the portal vein often ramifies independently,and the division of the portal vein is easily conducted;(2)A relatively large amount of remnant liver can be retained;and(3)The anatomy of the posterior branch of the Glissonian pedicle is similar to that in patients with normal anatomy.CONCLUSION In patients with an RSRL and perihilar cholangiocarcinoma that does not involve the posterior section,left trisectionectomy may be a favorable choice.

Mice-lacking LMP2, immuno-proteasome subunit, as an animal model of spontaneous uterine leiomyosarcoma

Uterine tumors are the most common type of gynecologic neoplasm.Uterine leiomyosarcoma(LMS)is rare,accounting for 2%to 5%of tumors of the uterine body.Uterine LMS develops more often in the muscle tissue layer of the uterine body than in the uterine cervix.The development of gynecologic tumors is often correlated with female hormone secretion;however,the development of uterine LMS is not substantially correlated with hormonal conditions,and the risk factors are not yet known.Radiographic evaluation combined with PET/CT can be useless in the diagnosis and surveillance of uterine LMS.Importantly,a diagnostic biomarker,which distinguishes malignant LMS and benign tumor leiomyoma(LMA)is yet to be established.Accordingly,it is necessary to analyze risk factors associated with uterine LMS in order to establish a method of treatment.LMP2-deficient mice spontaneously develop uterine LMS,with a disease prevalence of~40%by 14 months of age.It is therefore of interest whether human uterine LMS shows a loss of LMP2 expression.We found LMP2 expression is absent in human LMS,but present in human LMA.Therefore,defective LMP2 expression may be one of the risk factors for LMS.LMP2 is potentially a diagnostic biomarker for uterine LMS,and gene therapy with LMP2-encording DNA may be a new therapeutic approach.