Search PubMed⌕ Search

Biomedical subjects

K Oda

Publications and source records attributed to K Oda.

At least 595 records · Page 33Linked to original sources
PubMed1983

A hepatitis B surface antigen polypeptide (P31) with the receptor for polymerized human as well as chimpanzee albumins.

Hepatitis B virus, and hepatitis B surface antigen particles co-occurring with hepatitis B e antigen, have the receptor for polymerized human and chimpanzee albumins that may be involved in the hepatotropism of hepatitis B virus. We identified the receptor on a hepatitis B surface antigen polypeptide with a molecular size of 31,000 daltons (P31). P31 bound to polymerized albumins from human and chimpanzee, but did not react with polymerized albumins from the experimental animals without susceptibility to hepatitis B virus. P31 was composed of the major polypeptide of hepatitis B surface antigen with a molecular size of approximately 22,000 daltons (P22) and additional 55 amino acid residues coded by the pre-S region in the hepatitis B virus-specific deoxyribonucleic acid. Because P22 did not react with polymerized albumin, the sequence of 55 amino acid residues in the pre-S region appeared to bear the receptor. Polypeptides with the receptor for polymerized albumin may make an efficacious hepatitis B vaccine, because they could raise antibodies against the putative site on hepatitis B virus capable of binding with hepatocytes to initiate the infection.

Amino Acids↗
PubMed1983

[Coenzyme Q10 in cancer chemotherapy--experimental studies on augmentation of the effects of masked compounds, especially in the combined chemotherapy with immunopotentiators].

Immunopotentiators may mitigate the depression of immunological function caused by the cancer itself or by chemotherapeutics. However, it has been found that these immunopotentiators reduce the metabolic activity of the host against drugs, including "masked" chemotherapeutics, which might be activated by metabolization in the body. Reported here is the result of serial experiments carried out on the activation of cyclophosphamide (CPM) in tumor-bearing animals, pretreated with phenobarbital, a drug-metabolizing enzyme inducer, and coenzyme Q10, a physiological activator of the electron transfer system in mitochondrias, in combination with immunopotentiators. Female Donryu rats (120 g body weight) implanted with Yoshida Sarcoma cells (YS) (2.5 X 10(6) i.p.) were treated with CPM (160 mg/kg X 1 i.p.), 84 hrs after implantation; the levels of the normustard-like substances (active metabolites of CPM) were serially measured. Some of the animals were also treated with PSK (125 mg/kg X 5 i.p.), a proteinpolysaccharide immunopotentiator obtained from mycelia of the Coriolus vesicolor, or with OK-432 (10 KE/kg X 5 i.m.), a streptococcal immunopotentiator. The results obtained were as follows: The blood levels of the normustard-like substances were lowered, i.e. the CPM activation was depressed in the YS-bearing rats and the depression was markedly intensified by PSK or OK-432 administration. Phenobarbital (40 mg/kg X 3 i.p.) or coenzyme Q10 (5 mg/rat X 5 i.p.) administration could mitigate the depression of the blood levels caused by the immunopotentiators, and the combination of phenobarbital with coenzyme Q10 could recover the blood levels up to those of the YS-bearing control rats, or even higher. YS-implanted (i.p.) rats treated with CPM+ immunopotentiators+coenzyme Q10 survived longer than those treated with CPM+immunopotentiators. These findings suggest the usefulness of coenzyme Q10 for the enhancement of cancer immunochemotherapy using masked compounds combined with immunopotentiators; all the more so, because coenzyme Q10 has also an immuno-stimulating effect, moreover, it presents almost no side effects in clinical application.

Animals↗
PubMed1982

A glycopeptide containing 15 amino acid residues derived from hepatitis B surface antigen particles: demonstration of immunogenicity to raise anti-HBs in mice.

The major polypeptides composing hepatitis B surface antigen (HBsAg) particles are P-I and P-II. P-II shares the same amino acid sequence as P-I and contains an additional carbohydrate moiety of mol. wt approximately 5000. When a purified preparation of P-II was digested with Nagarse and then with Pronase P, it gave rise to a glycopeptide containing 15 amino acid residues and the carbohydrate moiety of P-II. The N-terminal amino acid sequence of the glycopeptide was determined to be Lys-Pro-Thr-Asp-Gly-Asn-. The polysaccharide moiety contained 5 moles of N-acetylglucosamine and was connected with Asn at the sixth position from the N-terminus. When mice were immunized against this HBsAg glycopeptide, they raised humoral antibodies which bound to each of three preparations of P-I derived from HGsAg particles of subtypes adw, adr and ayw, thereby indicating that the sequence of 15 amino acids in the glycopeptide would constitute a common antigenic structure of HBsAg.

Amino Acid Sequence↗
PubMed1982

The possible origin H1N1 (Hsw1N1) virus in the swine population of Japan and antigenic analysis of the isolates.

Virus isolation and serological studies on swine sera collected during 1973 to 1978 showed that H1N1 (Hsw1N1) influenza viruses first appeared in the swine population of Japan about May 1977. With the exception of one strain, both haemagglutinin and neuraminidase subunits of all the H1N1 viruses isolated from swine in Japan and from pigs imported from North America were antigenically indistinguishable from those of A/NJ/8/76 virus, suggesting the introduction of swine influenza virus into Japan with imported pigs from North America as breeding stock. Antigenic analysis of a recombinant virus by neuraminidase-inhibition tests with specific antisera to the isolated neuraminidases of A/Victoria/3/75 and A/Aichi/2/68 revealed that the neuraminidase antigen of the recombinant virus, A/swine/Kanagawa/2/78 (H1N2), was closely related to those of A/Tokyo/6/73 (H3N2) and A/Kumamoto/22/76 (H3N2) viruses.

Animals↗
PubMed1982

Properties of T antigen-positive phenotypic revertants isolated from SV40-transformed rat and mouse cells.

Four T antigen-positive phenotypic revertants were isolated by negative selection with BUdR from SV40-transformed rat and mouse cells which contain six and two viral genome equivalents per cell, respectively. Karyological analysis indicated that one rat and one mouse revertant had a hyperploid number of chromosomes, while the remaining two rat revertants had a subtetraploid number similar to those of the transformed parent cells. The hyperploid revertants were unable to grow in soft agar medium and were nontumorigenic in nude mice. One of the subtetraploid revertants formed large colonies at a very low frequency and induced tumors after a prolonged incubation period. These results indicate that there is a good correlation between the capacity of cells to grow without anchorage and the capacity to form tumors in nude mice and suggest that the revertant phenotype is stable in the presence of T antigen when the number of chromosomes is greatly increased as compared with that of the transformed parent cells.

Animals↗
PubMed1982

Detection of rotavirus antibody by inhibition of reverse passive hemagglutination.

A reverse passive hemagglutination inhibition (RPHI) test was developed for detecting rotavirus antibody in patients' sera. Sheep erythrocytes coated with guinea pig antibody against Nebraska calf diarrhea virus (NCDV) were readily hemagglutinated by NCDV in a reaction called reverse passive hemagglutination (RPHA). Inhibition of this RPHA reaction was used to detect the presence of rotavirus antibody in patients' sera which cross-reacted with NCDV. The sensitivity of RPHI was consistently at least 10 times greater than that of the complement fixation test for detection of rotavirus antibody in patients' sera. Since immunoglobulin M (IgM) antibody activity detected by RPHI was destroyed by pretreatment of serum with dithiothreitol (DDT), whereas DTT-resistant antibodies such as IgG remained unchanged, the titer of IgM antibody could be distinguished from that of DTT-resistant antibody by comparing the results of two RPHI tests performed with and without DTT pretreatment. From the IgM antibody response pattern, primary and secondary rotavirus infections could be distinguished.

Adolescent↗
PubMed1982

Hyponatremia without inappropriate secretion of vasopressin in a case of myxedema coma.

A 45-year-old woman with myxedema coma due to primary hypothyroidism manifested hyponatremia, impaired water excretion, and elevated urine osmolarity as well as natriuresis suggestive of a syndrome of inappropriate antidiuretic hormone secretion. However, plasma vasopressin was undetectable or very low and plasma aldosterone levels were suppressed in the presence of hyponatremia. Subsequent replacement therapy with levothyroxine caused a rapid decline in sodium clearance which was independent of the change in glomerular filtration rate, and corrected the impaired water excretion and hyponatremia. Plasma vasopressin levels returned to the normal range after the correction of hyponatremia. Thus, the results indicate that neither vasopressin nor aldosterone plays a dominant role in the pathogenesis of the hyponatremia in this patient. It appears that thyroid hormone deficiency itself caused the derangement of tubular cell function, which resulted in the development of the impaired water excretion and hyponatremia.

Coma↗
PubMed1981

Inhibitory effect of colchicine on translocation of alkaline phosphatase to the plasma membrane concomitant to its induction in rat liver.

A single injection of colchicine (1--3 mg/kg body weight) caused a remarkable induction of hepatic alkaline phosphatase, which increased linearly in the homogenate starting at 5--6 h and reached a maximum level (14-fold of the control activity) at 20--22 h after the drug treatment. In the plasma membrane, however, the increase in specific activity and the recovery of alkaline phosphatase were greatly inhibited up to 12 h after the treatment. Such an inhibitory effect of colchicine was confirmed by a combination experiment of the drug treatment with bile duct ligation; in the plasma membrane elevation of the enzyme induced by bile duct ligation was also greatly retarded by colchicine. The subcellular distribution of the enzyme activity in livers was determined among the four groups of rats with or without bile duct ligation and/or colchicine administration taken at 8 h after each treatment. In the control and the bile duct-ligated livers, the highest specific activity was observed in the plasma membrane fraction, while in the colchicine-treated livers, with or without bile duct ligation, the highest activity was found in the Golgi fractions. These results indicate that the Golgi membranes enriched with the induced enzyme were blocked by the drug to prevent migration toward the plasma membranes enriched with the induced enzyme were blocked by the drug to prevent migration toward the plasma membrane, thus demonstrating involvement of the Golgi complex in the translocation route of newly synthesized alklaine phosphatase to the plasma membrane.

Alkaline Phosphatase↗
PubMed1981

Myasthenia gravis: antibodies to acetylcholine receptor in ocular myasthenia gravis.

To improve the sensitivity of the radioimmunoassay method for anti-AChR-antibody, large amounts of sera from patients with myasthenia gravis, and higher concentrations of antigens and rabbit anti-human-IgG-antiserum, were used. These procedures enabled measurement of the titre value of over 0.04 pmol/ml serum and this value revealed a sensitivity about 10 times higher than that predicted using the previous model. Antibodies against AChR were found in 13 out of 17 ocular myasthenia patients (70%) and 35 of 37 with generalized myasthenia (90%). However, the average titre value of sera in those with ocular myasthenia was significantly lower than the value obtained in the generalized cases. Even in the patients with ptosis or ophthalmoparesis, in the early stage (less than one year) of ocular myasthenia, anti-AChR-antibodies were not detectable using this more sensitive assay method.

Adult↗