Rapid Dissemination followed by Spontaneous Regression of Metastatic Hepatocellular Carcinoma after Liver Radiofrequency Thermal Ablation: A Case Report with Correlative Immune Assay.

Rapid intrahepatic and distant metastasis of hepatocellular carcinoma (HCC) after locoregional treatment for early stage tumor is very rare. Descriptions of spontaneous regression of HCC exist in case reports, but its true mechanism is unclear. Here, we describe a case of rapid dissemination with lung metastasis shortly after localized RFA treatment of HCC liver lesions, followed by spontaneous, sustained regression of those lung lesions. We also show the detection of cytotoxic T lymphocytes (CTLs) specific to hepatitis B antigens by immune assay in this patient. We propose immune-related destruction as the basis for spontaneous regression.

The effect of preoperative vitamin K on the INR in bridging therapy.

We investigated a bridging protocol using oral Vitamin K three days before scheduled surgery. 60 patients in two bridging protocols, 30 cases per protocol. The first cohort (Control group) had its warfarin held on Day-5 (five days before surgery). The intervention cohort (Vitamin K group) routinely received 2.5 mg of oral Vitamin K on Day-3 but was otherwise identically bridged. Primary outcome was INR on Day-1. Secondary outcomes included patients with INRs ≥1.5 on Day-1, bleeding episodes and elevated INR post surgery. Day-1 INR for the Vitamin K group was 1.16, vs. 1.28 for the Control group (p = 0.037). Postoperative INR was similar. Only the Control group had patients with INRs ≥1.5 on Day-1, or patients with significant bleeding. Adding Vitamin K on Day-3 leads to a safe preoperative INR and may limit other complications.

Mice devoid of Tau have increased susceptibility to neuronal damage in myelin oligodendrocyte glycoprotein-induced experimental autoimmune encephalomyelitis.

The abundant axonal microtubule-associated protein tau regulates microtubule and actin dynamics, thereby contributing to normal neuronal function. We examined whether mice deficient in tau (Tau(-/-)) or with high levels of human tau differ from wild-type (WT) mice in their susceptibility to neuroaxonal injury in experimental autoimmune encephalomyelitis, an animal model of multiple sclerosis. After sensitization with MOG35-55, there was no difference in clinical disease course between human tau and WT mice, but Tau mice had more severe clinical disease and significantly more axonal damage in spinal cord white matter than those in WT mice. Axonal damage in gray matter correlated with clinical severity in individual mice. By immunoblot analysis, the early microtubule-associated protein-1b was increased 2-fold in the spinal cords of Tau mice with chronic experimental autoimmune encephalomyelitis versus naive Tau mice. This difference was not detected in comparable WT animals, which suggests that there was compensation for the loss of tau in the deficient mice. In addition, levels of the growth arrest-specific protein 7b, a tau-binding protein that is stabilized when bound to tau, were higher in WT than those in Tau(-/-) spinal cord samples. These data indicate that loss of tau exacerbates experimental autoimmune encephalomyelitis and suggest that maintaining tau integrity might reduce the axonal damage that occurs in inflammatory neurodegenerative diseases such as multiple sclerosis.