Zinc and an N-terminal extra stretch of the ferredoxin from a thermoacidophilic archaeon stabilize the molecule at high temperature.

Ferredoxin from the thermoacidophilic archaeon Sulfolobus sp. strain 7 has a 36-residue extra domain at its N-terminus and a 67-residue core domain carrying two iron-sulfur clusters. A zinc ion is held at the interface of the two domains through tetrahedral coordination of three histidine residues (-6, -19 and -34) and one aspartic acid residue (-76) [Fujii, T., Hata, Y., Oozeki, M., Moriyama, H., Wakagi, T., Tanaka, N. & Oshima, T. (1997) Biochemistry 36, 1505-1513]. To elucidate the roles of the novel zinc ion and the extra N-terminal domain, a series of truncated mutants was constructed: G1, V12, S17, G23, L31 and V38, which lack residues 0, 11, 16, 22, 30 and 37 starting from the N-terminus, respectively. A mutant with two histidine residues each replaced by an alanine residue, H16A/H19A, was also constructed. All the mutant ferredoxins had two iron-sulfur clusters, while zinc was retained only in G1 and V12. The thermal stability of the proteins was investigated by monitoring A408; the melting temperature (Tm) was approximately 109 degrees C for the natural ferredoxin, approximately 109 degrees C for G1, 97.6 degrees C for V12, 89.0 degrees C for S17, 89.2 degrees C for G23, 89.3 degrees C for L31, 82.1 degrees C for V38, and 89.4 degrees C for H16A/H19A. Km and Vmax values of 2-oxoglutarate:ferredoxin oxidoreductase for natural ferredoxin, G1, S17 and L31 were similar, suggesting that electron-accepting activities were not affected by the deletion. The combination of CD and fluorescent spectroscopic analyses with truncated mutant S17 indicated that not only the clusters but also the secondary and tertiary structures were simultaneously degraded at a Tm around 89 degrees C. These results unequivocally demonstrate that the zinc ion and certain parts, but not all, of the extra sequence stretch in the N-terminal domain are responsible not for function but for thermal stabilization of the molecule.

[A case of hepatocellular carcinoma (HCC) with bleeding due to duodenal perforation by the tumor].

On June 11, 1986, a 70-year-old man was introduced to our hospital because of an elevated AFP and hepatomegaly. He was diagnosed as having an HCC in the left medial segment and a transcatheter arterial embolization (TAE) was able to reduce his AFP level. In December, 1986, repeated tarry stool was noted, and he was readmitted to hospital on January, 28, 1987, because of severe anemia. An ordinary X-ray revealed an abnormal gas shadow in the right upper abdomen. A subsequent endoscopic examination showed a tumoral mass protruding into the duodenal lumen through a duodenal perforation. After death an autopsy revealed that the perforation was due to the expansive growth of the tumoral mass to the duodenum.

Computer tomography of congenital absence of the left lobe of the liver.

Computed tomography of absence of the left lobe of the liver is described. Liver scintigraphy may be misinterpreted as indicating tumor of the left lobe. Computed tomography correctly identifies absence of the left lobe and compensatory hyperplasia of the caudate lobe. Two illustrative cases with a peculiar "tongue-like projection" of the caudate lobe are presented.

[Splenic metastasis of hepatocellular carcinoma].

It is known that hepatocellular carcinoma (HCC) frequently metastasises to various organs, but metastasis to the spleen is quite rare. We experienced two cases of splenic metastasis of HCC revealed by ultrasonography (US) or computed tomography (CT) and confirmed by autopsy. We report the morphological characteristics of the US or CT findings in these two cases. The first patient was a 68-year-old woman who was admitted with the chief complaint of abdominal fullness. US revealed a hypoechoic lesion in the liver and spleen. She died of hepatic failure about a month later, and splenic metastasis of HCC was confirmed by autopsy. The second patient was a 61-year-old man who was admitted with the chief complaint of swelling a cervical lymph nodes. US showed a mosaic pattern of a mass lesion in the spleen. The patient died of hepatic failure about two weeks later, and metastasis of HCC to the spleen was confirmed by autopsy.