Masato Funaoka

Fulminant hepatitis caused by hepatitis C virus during treatment for multiple sclerosis

A 55-year-old woman was treated at our hospital for multiple sclerosis. Therapy consisted of glucocorticosteroids and cyclosporin. In the 7th week after these drugs were discontinued the patient developed acute liver failure due to fulminant hepatitis (FH) and died. Post-mortem examination showed massive liver necrosis. Serologic examination was negative for hepatitis B virus-related markers. Anti-hepatitis C virus (anti-HCV) antibody and serum HCV RNA were negative on admission, but HCV RNA appeared concurrently with the onset of FH. Although HCV infection rarely causes FH, it was considered to be the cause of FH in this patient, since there were no other causes of acute liver injury. We suspect that underlying immunologic abnormalities in conjunction with HCV infection may have precipitated the FH.

Tauroursodeoxycholic acid enhances phagocytosis of the cultured rat Kupffer cell

Background: Ursodeoxycholic acid is used in the treatment of acute and chronic intrahepatic cholestasis because it ameliorates cholestasis and protects hepatocytes. However, few studies have examined the effect of bile acids on the function of Kupffer cells.

Hepatic cyst with intracystic bleeding: contrast-enhanced sonographic findings.

Intracystic bleeding is a relatively rare complication of hepatic cysts, which is very difficult to diagnose by conventional sonography (US). Hence, a new US technique has been sought for this purpose. We present the case of a hepatic cyst with intracystic bleeding in which contrast-enhanced US showed microbubbles oozing from the cyst wall into the cystic cavity. Contrast-enhanced US is now an important diagnostic tool for diagnosing liver tumors, but contrast-enhanced US findings relating to intracystic bleeding have not been reported. Our observations suggest that this technique may be a useful new diagnostic tool for this purpose.

Malignant triton tumor in a patient with neurofibromatosis type 1

We report a case of neurofibromatosis type 1 (NF1) complicated by a malignant triton tumor (MTT), with an emphasis on B-mode sonographic (US) and contrast-enhanced US (CEUS) findings. To the best of our knowledge, this is the first report describing CEUS findings of MTT. The mass was poorly demarcated and composed of an internal echogenic area and an outer hypoechoic zone. CEUS findings showed the outer zone to be strongly enhanced, and the internal area was very poor in blood flow because of necrotic tissues.

Rupture of liver metastasis: report of a case with an emphasis on contrast-enhanced US

We present a case of liver metastasis from an uterine leiomyosarcoma in which contrast-enhanced ultrasonography (CEUS) helped determine the bleeding point and prevented a delay in devising diagnostic and therapeutic strategies. CEUS allowed us to differentiate active from nonactive bleeding on the basis of presence or absence of contrast extravasation in the ascites. CEUS is the first examination performed when liver tumor rupture is suspected. Reference to the preangiographic CEUS results is expected to provide a road map for angiography.

Purification and characterization of cytoplasmic dynein of rabbit liver

Cytoplasmic dynein is a microtubule-dependent motor protein, which plays a role in intracellular transport. However, there have been few studies regarding the role of cytoplasmic dynein in the liver. Purification of cytoplasmic dynein from rabbit liver took advantage of the affinity of microtubule-dependent motor proteins for microtubules. Purified dynein contained heavy chain (450 kDa), intermediate chain (75 kDa), light chains (45-58 kDa) and dynactin (150 kDa). The subunit composition was consistent with previously reported data on brain cytoplasmic dynein. Microtubules prepared from bovine brain were driven by purified cytoplasmic dynein from rabbit liver, and movements of microtubules were visualized by video-enhanced differential interference contrast microscopy. The mean velocity of the motile microtubules was 1.09 +/- 0.13 microns/s. Our study provides evidence of rapid intracellular transport in hepatocytes controlled by cytoplasmic dynein.

Mobile echoes in liver cysts: a form of range-ambiguity artifact.

Faint moving echoes are occasionally encountered in large hepatic cysts, as an example of range‐ambiguity artifacts. The aim of this article is to describe the pattern of these intracystic mobile echoes, to analyze the mechanism of their formation, and to discuss options to clear them.

Enhancement of kinesin-driven microtubule gliding by bile acids

Abstract We tested the effects of four bile acids, taurochenodeoxycholate, taurocholate, tauroursodeoxycholate and taurodeoxycholate, on kinesin-driven microtubule motility, which may have a major influence on membrane organelle transport in cholestasis. Reconstituted microtubules were incubated with kinesin purified from rabbit liver and brain. Binding and gliding of microtubules were visualized by video-enhanced differential interference contrast microscopy. Liver and brain kinesin produced similar microtubule gliding velocities. The effect of bile acids on liver and brain kinesin was also similar. Low concentrations of the four bile acids (0.25–0.5 mM) enhanced the speed of microtubule gliding by up to 152%. Higher concentrations of taurochenodeoxycholate and taurodeoxycholate inhibited attachment, but did not slow the speed of gliding. Detachment was inhibited by the addition of tauroursodeoxycholate. ATPase activity showed no changes in the presence of low concentrations of tauroursodeoxycholate and taurochenodeoxycholate. Triton X-100, a nonionic detergent, increased microtubule gliding by up to 147% at lower concentrations, while higher concentrations (up to 5%) caused a return to normal speed without detachment. Low concentrations of bile acids in hepatocytes may enhance kinesin-driven microtubule dependent organelle transport. In contrast, higher concentrations of toxic bile acids, chenodeoxycholate and deoxycholate, associated with cholestasis may inhibit kinesin-driven motility by detaching microtubules from kinesin.