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Biomedical subjects

Y Yanagi

Publications and source records attributed to Y Yanagi.

At least 91 records · Page 5Linked to original sources
PubMed1986

A human T cell-specific cDNA clone (YT16) encodes a protein with extensive homology to a family of protein-tyrosine kinases.

We report here the isolation of a human T cell-specific cDNA clone (YT16) that encodes a protein with extensive homology to a family of transformation and proliferation-related protein-tyrosine kinases (PTK). The message size of YT16 is 2.2 kb and it encodes a protein of 507 amino acids with a mol. mass of 57,136 Daltons. The deduced protein sequence has an overall homology of about 50% to the viral oncogene products of src and yes. Around the PTK catalytic domain, the homologies increase to 70-80% between the deduced protein sequence of YT16 and those of the PTK viral oncogenes. Of special interest is the extensive homology between the deduced protein sequence of YT16 and that of a recently reported murine B and T lymphocyte-specific PTK, lskT. It is possible that YT16 either encodes the human homologue of this murine gene, or a protein with similar function(s) in T cells.

Amino Acid Sequence↗
PubMed1986

Werner's syndrome associated with cholangiocarcinoma.

A 38-year-old Japanese man had cholangiocarcinoma in association with typical features of Werner's syndrome. The replicative capacity of fibroblasts in culture was characteristically reduced, and the in vitro natural killer cell activity was deficient. He died of massive G-I tract bleeding 8 months after admission.

Adenoma, Bile Duct↗
PubMed1985

The antitumor effects of human lymphoblastoid interferon on human renal cell carcinoma in athymic nude mice.

The antitumor effects of human lymphoblastoid interferon (HLBI) on human renal cell carcinomas transplanted in nude mice, i.e., KU-2 and RCC-1, were investigated and compared with those on other human tumors, viz. HeLa (cervical carcinoma), KB (nasopharyngeal carcinoma), H.Ep#2 (laryngeal carcinoma), and MX-1 (breast cancer). A pharmacokinetic study on HLBI was also carried out in non-tumor-bearing nude mice. HLBI therapy was performed with a dose of 10(5) IU/mouse by daily SC or IT (intratumoral) injection for 2-4 weeks. Two renal cell carcinomas, KU-2 and RCC-1, proved to be highly sensitive to HLBI. The growth of these tumors was inhibited not only by IT but also by SC injection of HLBI. In contrast, HLBI exerted only a slight effect or none at all on the other human tumors, namely, MX-1, KB, H.Ep#2, and HeLa, even when given by IT injection. The data show that the antitumor effects of HLBI depend on the types of human tumors and may be relevant to the clinical observation that renal tumors are sensitive to HLBI. The serum HLBI reached a peak level of 4,390 U/ml 1 h after a single SC injection at a dose of 10(5) IU/mouse and declined with a half-life of 4 h to 128 U/ml 24 h later. This time-course was not affected by 10 consecutive daily injections of HLBI. In nude mice, the consecutive administration of HLBI at this dose level appears to result in neither accumulation nor rapid clearance due to antibody formation. From this range of serum HLBI levels and its in vitro anticellular activity, the in vivo antitumor effects of HLBI in nude mice seemed to depend on its direct anticellular action.

Animals↗
PubMed1985

Analysis of cDNA clones specific for human T cells and the alpha and beta chains of the T-cell receptor heterodimer from a human T-cell line.

We report the isolation and characterization of 19 classes of nonrearranging T cell-specific cDNA clones and two cDNA clones encoding the alpha and beta chains of the T-cell antigen receptor from a human T-cell line, Jurkat. Results indicate that the human alpha-chain gene, like its beta-chain counterpart, undergoes somatic rearrangement in T cells. In addition, it shows sequence homology to its beta-chain counterpart and immunoglobulin, indicating that the human alpha chain is also a member of the immunoglobulin supergene family. Sequence comparison suggests that the alpha chain also may be composed of variable (V), diversity (D), joining (J), and constant (C) region gene segments. The protein deduced from the cDNA sequence has a molecular weight of 29,995 and possesses six potential N-glycosylation sites. The availability of alpha- and beta-chain genes of the T-cell receptor from the same T-cell line provides tools to study their possible roles in recognition of antigens and major histocompatibility complex products by the human T-cell receptor.

Amino Acid Sequence↗
PubMed1985

Somatic rearrangement of T-cell antigen receptor gene in human T-cell malignancies.

A cDNA clone representing the gene encoding the beta chain of the human T-cell antigen receptor has been isolated recently. By using fragments of this cDNA as hybridization probes in Southern blot analysis of restriction endonuclease-digested genomic DNA, we have now examined the structure of the gene in DNA from 26 patients with acute leukemia and from 23 normal individuals. We have found that the T-cell antigen receptor gene has undergone somatic rearrangement in 14 of 14 patients with the phenotypic diagnosis of T-cell acute lymphoblastic leukemia. In this group of patients, similar patterns of rearrangement appear to occur in different patients. This finding suggests that there is either a limited repertoire of possible rearrangements or an association between the development of leukemia and specific patterns of rearrangement. DNA from 6 patients with acute myeloblastic leukemia, 6 patients with non-B, non-T acute lymphoblastic leukemia, and 23 nonleukemic individuals showed no rearrangement or polymorphism. One case of T-cell acute lymphoblastic leukemia, however, showed rearrangement of both the T-cell receptor beta chain and the constant region of the immunoglobulin gene. Studies with mixtures of DNAs from leukemic bone marrow cells and cultured skin fibroblasts, as well as with remission and relapse marrow DNAs from the same patients, indicate that this technique can detect 1% leukemic cells in a mixed population. In addition, DNA from the marrow of a patient in relapse contains a similar rearrangement to that found in the marrow sample taken at the time of diagnosis, which suggests that the original clone of leukemic cells was responsible for relapse. Our results indicate that assessment of rearrangement of the T-cell antigen receptor gene will be valuable in the diagnosis and management of leukemia and can be used to evaluate clonality in T-cell neoplasia.

Chromosome Mapping↗
PubMed1985

[Capgras syndrome--observations in 2 schizophrenic patients].

Two additional cases of Capgras syndrome were reported. In these schizophrenic patients, the abrupt hatred against family members seemed to contribute largely to the genesis of the syndrome in addition to delusional background. At the same time, the importance of delusional retrospective interpretation in these patients as well as in the previously reported case was discussed.

Capgras Syndrome↗
PubMed1984

The human T cell antigen receptor is encoded by variable, diversity, and joining gene segments that rearrange to generate a complete V gene.

A cDNA clone YT35 , synthesized from poly(A)+ RNA of the human T cell tumor Molt 3, exhibits homology to the variable (V), joining (J), and constant (C) regions of immunoglobulin genes. We have isolated and sequenced the germ-line V and J gene segment counterparts to YT35 from a human cosmid library, and these failed to encode 14 nucleotides of the cDNA clone between the V and J regions. We postulate that these 14 nucleotides are encoded by a third gene segment analogous to the diversity (D) gene segments of immunoglobulin heavy chain genes. This T cell antigen receptor V gene appears to be assembled from three gene segments, V, D, and J, and accordingly most closely resembles immunoglobulin heavy chain V genes.

Amino Acid Sequence↗
PubMed1984

Reversal of multidrug resistance by non-antitumor anthracycline analogs.

It was found that three synthetic anthracycline analogs lacking not only antitumor activity but also calcium-antagonizing action possessed an activity to potentiate vincristine cytotoxicity against vincristine-resistant P388 leukemia. ID-8279, one of these analogs, significantly reversed resistance to vincristine and daunorubicin by increasing their intracellular accumulation.

Animals↗
PubMed1978

[Analgetic and antipyretic activity of SL-573 (author's transl)].

Potency of analgetic activity of SL-573 was between that of indomethacin and aminopyrine in chemical stimulation tests. The analgetic activity of SL-573 was 3.2 times as potent as that of aminopyrine in the phenylquinone writhing test, 4.1 times as potent as aminopyrine in the acetic acid writhing test and 6.3 times as potent as aminopyrine in the Randall and Selitto test. Thus the analgetic activity of SL-573 appears to be comparable etic to that of codeine. SL-573, unlike narcotic analgesics, showed common properties to known antipyretic analgesics and anti-inflammatory agents in the following points. (1) Analgetic activity was not evident in the mechanical stimulation or in the heat stimulation tests. (2) The analgetic activity was not antagonized by naloxone. (3) SL-573 showed no antagonistic effect to morphine. (4) Tolerance to the analgetic activity of SL-573 was not observed after a one week pretreatment with this compound. (5) SL-573 had no effect on the evoked potentials recorded from cells in the pain pathway of CNS and the site of action of analgetic effect was considered to be in peripheral sites of the sensory neurons. The antipyretic activity of SL-573 was equal to that of aminopyrine in febrile rabbits and 4 times as potent as that of aminopyrine in febrile rats. This compound did not affect normal body temperature of rabbits and rats, this observation being similar to that noted with antipyretic analgesics and nonsteroidal anti-inflammatory agents.

Afferent Pathways↗
PubMed1978

[Anti-inflammatory activity of SL-573 (author's transl)].

In the carrageenin-induced edema test in rats, the anti-inflammatory activity of SL-573 was 1.6 times as potent as those of phenylbutazone (PB) and ibuprofen (IP), 3.3 times as potent as that of mefenamic acid (MF) and 6.7 times as potent as that of mepirizole (MP). In the yeast-induced edema test in rats, SL-573 showed equipotent activity with IP, the activity of which was 4 times as potent as that of MP. In the dextran-induced edema test in rats, the anti-inflammatory activity of SL-573 was significantly higher than those of IP and MP. SL-573 showed no anti-inflammatory activity in the formalin-induced edema test in rats in the same way as seen with IP and MP. SL-573 markedly inhibited the increase in capillary permeability in mice induced by intraperitoneal administration of acetic acid, and its activity was 12 times as potent as that of PB and 17 times as potent as that of MF. SL-573 showed anti-granuloma activity neither systemically nor locally. SL-573 showed equi-potent activity with PB in the adjuvant arthritis test in rats and had little effect on the healing process of the skin wound in rats. The effect of SL-573 on the carrageenin-induced edema was not diminished in the adrenalectomized rats. The gastric bleeding effect of SL-573 was significantly weaker than that usually seen in nonsteroidal anti-inflammatory drugs. SL-573 did not induce intestinal perforation even at the high dose of 800 mg/kg. Additionally, SL-573 showed a protective effect on the indomethacin-induced intestinal lesions. These pharmacological profiles of SL-573 were considered to be quite characteristic as compared with those of known nonsteroidal anti-inflammatory agents.

Adrenalectomy↗
PubMed1978

[Antipyretic activity of SL-573 (II) (author's transl)].

Antipyretic activity of SL-573 was not influenced by age and sex difference in rats. The combined effect of other drugs on antipyretic activity of SL-573 was examined, using several drugs which might be clinically applicable. Cefazolin sodium, ampicillin sodium, codeine phosphate, hydrochlorothiazide and haloperidol did not show any significant effect on antipyretic activity of SL-573. Diazepam itself showed antipyretic activity, and its combined use with SL-573 resulted in an additive effect. SL-573 also showed antipyretic activity in mice with fever induced by yeast, as was seen in rats. SL-573 diminished the hyperthermic response to bacterial endotoxin and leucocytic pyrogen in rats, but not to 2, 4-dinitrophenol. Additionally, SL-573 did not inhibit the bacterial endotoxin-induced production of leucocytic pyrogen and its release in saline medium. SL-573, therefore, is considered to be a centrally acting antipyretic. Intraventricular injection of prostaglandin E2 and arachidonic acid induced a hyperthermia in mice. SL-573 clearly inhibited arachidonic acid-induced hyperthermia, but not prostaglandin E2-induced hyperthermia. Since SL-573 is known to inhibit prostaglandin biosynthesis from arachidonic acid, the prostaglandin biosynthesis inhibition may be one of the main mechanisms of antipyretic action of SL-573.

Age Factors↗
PubMed1976

Comparative metabolic study of nimetazepam and its desmethyl derivative (nitrazepam) in dogs.

1. Blood levels of nimetazepam after oral administration to dogs were relatively low at early periods after dosage and reached peak levels (7-7-7-9 mug equiv./ml) after 8 h. The time course of blood levels was similar after oral administration of its desmethyl derivative (nitrazepam) to dogs. Blood levels of the latter, however, were low compared with nimetazepam and reached a peak (5-2-6-3 mug equiv./ml) after 4 h. 2. Recoveries of nimetazepam in urine and faeces were 46 and 52% of the dose for 0-24 h, 27 and 34% for 24-48 h and 4 and 6% for 48-72 h, while those of its desmethyl derivative (nitrazepam) were 63 and 71% for 0-24 h, 12 and 21% for 24-48 h and 2 and 3% for 48-72 h. 3. At least four kinds of reaction were involved in the biotransformation of nimetazepam and its desmethyl derivative (nitrazepam): (i) demethylation at N-1 (ii) hydroxylation at C-3, (iii) subsequent glucuronic acid conjugation of 3-hydroxy derivatives and (iv) reduction of the nitro group at C-7 to an amino group. Reaction (i) proceeded very rapidly in dogs, so that the blood metabolites of nimetazepam were closely similar to those of nitrazepam. For both drugs, the major blood metabolite was nitrazepam. Reaction (ii) was rapidly followed by reaction (iii), and glucuronides were predominantly excreted in urine. Reaction (iv) as well as reaction (iii) are important in the excretion of both drugs. The subsequent acetylation of 7-amino group, however, did not occur in dogs as it did in mice and rats.

Animals↗
PubMed1975

Comparative metabolic study of nimetazepam and its desmethyl derivative (nitrazepam) in rats.

1. Nimetazepam distributed more rapidly in the brain than its desmethyl derivative (nitrazepam). The brain concentration of the active metabolites of the former was about twice that of the latter at 1h after oral administration. 2. At least four kinds of reactions were involved in the biotransformation of nimetazepam and its desmethyl derivative (nitrazepam) : (i) demethylation at N-1, (ii) hydroxylation at C-3, (iii) reduction of the nitro group at C-7 to the amino group and (iv) subsequent acetylation of the amino group. 3. The 1-N-demethylation of nimetazepam was slow compared with the other three reactions. 4. Nimetazepam was rapidly hydroxylated at C-3, while the 3-hydroxylation of its desmethyl derivative (nitrazepam) was very slow. 5. The reduction of the nitro group at C-7 and subsequent acetylation were important routes for the excretion of these drugs.

Acetylation↗