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Biomedical subjects

K Wada

Publications and source records attributed to K Wada.

At least 685 records · Page 38Linked to original sources

[Genetic studies on the ossification of the posterior longitudinal ligament].

The genetic mechanism of OPLL (ossification of the posterior longitudinal ligament) was investigated through a family study including 62 probands and 129 relatives using X-ray examination of the spine. The study showed that the prevalence of OPLL was 29.1% in men and 25.7% in women with a tendency of increase with age. As the mode of inheritance, the segregation ratio or children of probands was that of simple recessive; the segregation ratio of siblings was either simple recessive or dominant. The recurrence rate of siblings excluded polygenes; this mode of transmission and the penetrance suggested that the most probable mode of inheritance of OPLL would be simple dominant. As genetic markers, various blood groups, serum groups, and erythrocyte isozyme groups were examined in 23 patients with OPLL. Gc serum groups and EsD isozyme groups displayed some association with OPLL in comparison with the normal controls.

Adult↗

[The efficacy and limitations of laser surgery in malignant tumors].

Using rats with tumor transplanted into the subcutaneous tissue, tumor resections done with either an ordinary scalpel or a laser scalpel were compared from the viewpoints of tumor recurrence and survival time. It was found that tumor resection using the laser scalpel and laser irradiation of the field after tumor resection were effective in preventing recurrence. With this concept in mind, 286 operations involving laser surgery were performed, including 179 for malignant tumor, most of which were cancers of the liver, esophagus, stomach and colon. Laser surgery for hepatoma and other malignant tumors yielded better results than ordinary surgery. Another experimental study of PDT (photodynamic therapy) for malignant tumor of the parenchymal organs was carried out. The uptake of HpD (hematoporphyrin derivatives) by the liver was as much as 1.5 times that by the digestive tract. The concentration of HpD in the tumor tissue of WKA rats with DAB hepatic tumor was twice that in liver tissue. However, the difference in HpD concentration between the tumor tissue and liver tissue is not large enough for PDT and this point requires further study.

Animals↗

N-terminal amino acid sequences of the heavy and light chains of chicken liver cathepsin L.

Avian cathepsin L (EC 3.4.22.15) was first purified from chicken liver. The enzyme was composed of two polypeptides with Mr values of 28,000 (heavy chain) and 5000 (light chain). The two polypeptide chains of the enzyme were separated by gel filtration after cleavage of disulfide bonds. The N-terminal amino acid sequences of the heavy and light chains were (sequence in text) and (sequence in text) respectively. These sequences show high homologies with those of the N-terminal and C-terminal portions of papain, respectively. The residues of the surrounding area of cysteine-25 in the heavy chain were quite similar to those in the region around the active-site cysteine of papain.

Amino Acid Sequence↗

Combined hepatocellular and mucinous carcinoma.

A rare autopsy case of combined liver cell and bile duct carcinoma (CLBC) occurring in a 51-year-old male with alcoholic liver cirrhosis is presented. Histologically, while the primary lesion was solely composed of well differentiated hepatocellular carcinoma (HCC), intrahepatic metastases consisted of a variable admixture of HCC and cholangiocarcinoma (CC) with excessive mucin production. Interestingly, the tumor cell cluster showing a trabecular growth pattern produced both bile and mucin, thus converting from HCC to mucinous CC. It is concluded that this liver malignancy is principally HCC with a marked tendency to transform into CC. The importance of the findings, especially the simultaneous production of bile and mucin within the same cell cluster, is emphasized in terms of the classification of CLBCs.

Adenocarcinoma, Mucinous↗

Pathologic features of small hepatocellular carcinoma.

Twenty-one nodules of small hepatocellular carcinoma (HCC) were examined. Histologically, the nodules often presented formation of plump trabeculae, marked nuclear atypism, or aggressive growth comprising capsular invasion, vascular invasion, and replacement of adjacent pseudolobules. Aside from these characteristic findings of HCC, it was important to reveal the following features for the diagnosis of well differentiated type of small HCC: variable thickening or distortion of trabecular structure in association with nuclear crowding, acinar formation, selective cytoplasmic accumulation of Mallory bodies, nuclear abnormalities consisting of thickening of nucleolus, hepatic cords in close contact with bile ducts or blood vessels, and hepatocytes growing in a fibrous environment. During the invasive growth, the tumor cells may well be subtly blended with benign hepatocytes, giving rise to a pattern of "mixed cellularity". It is also emphasized that connective tissue septa of pseudolobules could be a route of rapid tumor spreading.

Carcinoma, Hepatocellular↗

Inhibition of liver acetyl-coenzyme-A carboxylase by 2-tetradecanylglutarate.

In a previous study (A. ENDO, et al., J. Antibiotics 38: 599 approximately 604, 1985), 2-alkyl glutarate and its derivatives isolated from cultures of Gongronella butleri were shown to inhibit animal acetyl-CoA carboxylase. In the present communication, the inhibition of liver acetyl-CoA carboxylase was investigated with several 2-alkyl glutarate and 2-alkyl succinate analogs. Their inhibitory potency increased with the chain length of the alkyl moiety, and 2-tetradecanylglutarate was most potent among the inhibitors tested. Kinetic analysis indicated that inhibition by 2-tetradecanylglutarate was non-competitive with respect to the substrates, ATP, HCO3- and acetyl-CoA, and competitive with respect to the allosteric regulatory citrate, giving a Ki value of 40 microM. Sucrose density gradient centrifugation analysis showed that the citrate-induced polymerization of the enzyme was inhibited by 2-tetradecanylglutarate.

Acetyl-CoA Carboxylase↗