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Biomedical subjects

T Inada

Publications and source records attributed to T Inada.

At least 199 records · Page 11Linked to original sources
PubMed1989

Temperature-sensitive lethal mutant of era, a G protein in Escherichia coli.

The era gene of Escherichia coli encodes a GTP-binding protein which has similarities to elongation factor Tu and the Saccharomyces cerevisiae RAS protein. To investigate its function, mutations affecting era were isolated. A mini-Tn10 insertion, which truncated 22 amino acids from the COOH end of Era, did not affect cell growth. By using this mini-Tn10 insert as a coselectable marker, a temperature-sensitive lethal era mutant was isolated by localized mutagenesis using P1 phage transduction. A single-base G to A change was found at position 23, causing a tyrosine residue to be substituted for the cysteine residue at position 8 (era-770), in addition to the COOH-terminal mini-Tn10 disruption. Both alterations were necessary for the temperature-sensitive phenotype. Purified Era-770 mutant protein exhibited reduced binding to GTP compared with that of the wild-type Era protein.

Amino Acid Sequence↗
PubMed1989

Antitumor activity of 7-N-(2-((2-(gamma-L-glutamylamino) ethyl) dithio) ethyl) mitomycin C (KW2149) against human tumor xenografts serially transplanted into nude mice.

The antitumor activity and toxicity of 7-N-(2-((2-(gamma-L-glutamylamino) ethyl) dithio) ethyl) mitomycin C (KW2149) were evaluated using a human tumor xenograft--nude mouse system, and compared with those of the maternal compound, mitomycin C. The maximum tolerated dose of KW2149 was estimated to be 15 mg/kg by bolus intraperitoneal or intravenous injection, at which a remarkable reduction of spleen weight was observed, suggesting bone marrow suppression by this agent. A bolus injection of KW2149 seemed to be more effective than a divided injection schedule, when a total of 15 mg KW2149/kg was administered to mice bearing breast (MX-1) and colon (Co-4) carcinomas. The antitumor activity of KW2149 was dose-dependent, and the difference in antitumor effect according to route of administration was minimal. The antitumor spectrum of KW2149 was essentially identical to that of mitomycin C administered intraperiotoneally as a bolus at a dose of 6 mg/kg.

Adenocarcinoma↗
PubMed1989

[Severe aplastic anemia accompanied with abnormality of T cell subset and appearance of anti-BI antibody].

A 66-year-old female was diagnosed to have severe aplastic anemia. Remission was not achieved by the ALG-oxymethorone therapy, and she was in need of RBC multitransfusion. After receiving a total of 42 units (16,800 ml) of red blood cells, it was found that her serum agglutinated strongly her own group BI cells at 4 degrees C. This agglutination disappeared in DTT solution. An eluate from her red cells also agglutinated BI panel cells, whereas Bi, O I, O i cells failed to react. It was apparent that the cold agglutinin in her serum had special affinity for I cells, which also contain B. Analysis of lymphocyte subset in peripheral blood showed T 3 (CD 3) 70.18%, T 4 (CD 4) 70.92%, T 8 (CD 8) 7.08%, T 4/T 8 = 10.1, T4 (+)2H4(+)/T4(+)2H4(-) = 1.05. Although relationship between appearance of anti-BI antibody and relative increment of CD 4 positive cells was not clear, we considered that these findings were caused by an abnormal autoimmune reaction in the patient with aplastic anemia.

ABO Blood-Group System↗
PubMed1989

[Aggressive natural killer cell leukemia/lymphoma--possible existence of a new clinical entity originating from the third lineage of lymphoid cells].

The morphologic, immunologic, genotypic, and functional properties of peripheral blood and bone marrow cells or cultured cells from two patients with a clinically aggressive non T, non B natural killer cell lymphoma/leukemia (ANKL/L) were described. The leukemic cells possessed medium to large granules in the cytoplasm, antigens against CD 38, CD 2, OKIal, and NKH-1 (N 901) monoclonal antibodies on their cell-surface, and also showed a high natural killer (NK) activity. In addition, these ANKL/L belonged to neither T-nor B-cell lineage, proved by studying clonal gene rearrangement for the T beta and T gamma receptor, and immunoglobulin. After we compared and investigated them with 9 cases of ANKL/L reported in other institutions, concerning immunophenotype, genotype and function, we reached the conclusion that the existence of ANKL/L originating from the third lineage in lymphoid cells is an obvious fact, suggesting this new clinical entity. It is important that all patients who have this type of a clinical disorder be diagnosed that there is no effective form of therapy at present.

Adult↗
PubMed1989

[A case of gastric carcinoid tumor with coexisting adenocarcinoma in the same tumor].

A case of a gastric carcinoid tumor with a coexisting adenocarcinoma in the same tumor is reported. The patient was a 71-year-old man who complained of epigastralgia. His physical examination and routine laboratory data were unremarkable. An upper GI x-ray series and the gastroendoscopic findings, however, demonstrated a Borrmann 2-like tumor of the antrum. An endoscopic biopsy specimen from the tumor revealed that it was a gastric adenocarcinoma. Therefore, a subtotal gastrectomy with a lymph node dissection was performed. The resected specimen showed a Borrmann 2-like tumor, but also that infiltration was limited to within the submucosal layer. The pathological findings revealed that the tumor contained two differential component structures (a carcinoid and an adenocarcinoma). The carcinoid and adenocarcinoma structures coexisted with transitional changes that connected both structures. Pathohistologically, it was thought that these two differential components developed from a common origin.

Adenocarcinoma↗
PubMed1989

[Studies on association between the ATL and the development of multiple malignant neoplasms--analysis of 1171 cases of hematological malignancies during the past 24 years].

A high incidence of multiple primary neoplasms has been observed in our patients with ATL in comparison to persons with other forms of hematologic malignancy who we have observed during the past 24 years (1963-1985). Five of 15 patients with ATL (33.3%) have had at least one other associated neoplasm in comparison to only 44 of 1156 patients with other forms of hematological malignancy (3.8%). The incidence figures for secondary neoplasms associated with the other hematologic malignancies were 4.3% (16/370) for acute non-lymphocytic leukemia (ANLL), 2.2% (2/90) for acute lymphocytic leukemia (ALL), 4.8% (1/21) for acute unclassifiable leukemia, 2.2% (5/225) for chronic myelogenous leukemia, 4.7% (2/43) for chronic lymphocytic leukemia, 5.9% (8/136) for malignant monoclonal gammopathy and 3.7% (10/271) for malignant lymphoma. The incidence of multiple neoplasms in patients with ATL in comparison to those with other hematological malignancies was significant (p less than 0.01 or p less than 0.001). The neoplasms associated with ATL have been adenocarcinoma of the thyroid or lung, and squamous cell carcinoma of the larynx, lip or lung. We identified ATL-derived factor (ADF) in the cytoplasm of the secondary neoplasms of the ATL patients by means of indirect immunofluoroscopy and immunohistochemical techniques utilizing anti-ADF antibody. We also identified ras p21 products in these neoplasms by means of p21 ras monoclonal antibody studies. The possibility that HTLV-I was the cause of the secondary neoplasms thus was investigated.(ABSTRACT TRUNCATED AT 250 WORDS)

Cytokines↗
PubMed1989

[Multiple myeloma following chronic neutrophilia terminated with acute monocytic leukemia (AML, M 5 b)].

A case of a 70 years old female who developed multiple myeloma during a course of neutrophilia, and later on terminated with acute monocytic leukemia (AML, M 5 b) following Melphalan therapy for five years is reported. This patient was first found to have neutrophilia in 1966, After six years, she developed monoclonal gammopathy, (IgG1 kappa type) which coexisted with the neutrophilia. She was put on Melphalan regimen for 5 years which was discontinued due to anemia, leukocytopenia and the reduction of serum IgG. By routine bone marrow examination, she was diagnosed as AMoL (AML, M 5 b) in July 1984. Thereafter, a combination chemotherapy of BH-AC, 6-MP and prednisolone was started and complete remission for the AMoL was achieved after 2 months. Sixteen months later, she relapsed and a similar combination chemotherapy for reinduction regimen was administered. However, the AMoL was resistant and after 7 months, she died of pneumonia and multiple organ failure. The association of neutrophilia with multiple myeloma, the occurrence of AMoL after prolonged Melphalan therapy for the multiple myeloma and the strategy of therapy for secondary leukemia is discussed.

Aged↗
PubMed1988

Conditionally lethal and recessive UGA-suppressor mutations in the prfB gene encoding peptide chain release factor 2 of Escherichia coli.

Strains carrying mutations in the prfB gene encoding peptide chain release factor 2 of Escherichia coli were isolated. prfB1, prfB2, and prfB3 were selected as suppressor mutations of a lacZ (UGA) mutation at 37 degrees C, one of which, prfB2, is temperature sensitive in growth. A prfB286 strain was selected as a conditionally lethal mutant which grows at 32 but not at 43 degrees C and was shown to have UGA-suppressor activity. All the mutations are recessive UGA-suppressors. These data indicate that release factor 2 is essential to E. coli growth and that all mutants isolated here trigger suppression of the UGA codon.

Escherichia coli↗
PubMed1988

[In vitro chemosensitivity tests of human lung small cell carcinomas--with reference to combination cancer chemotherapy].

Four human lung small cell carcinoma (SCC) cell lines were used for the experimental cancer chemotherapy with a single agent and combination method. The chemosensitivity of SCC cell lines including H-69, H-128, Lu-24 and Lu-134 were assessed by the clonogenic assay according to the method of Salmon and Humburger. Cyclophosphamide (CPA) showed the most excellent antitumor effect against these 4 strains followed by tetra-hydropyranyl adriamycin and adriamycin (ADM). In vitro combination clonogenic assay was conducted by mixing the half of the concentration of two matched drugs and the synergistic effect was evaluated according to the method of Berenbaum. Whereas the synergistic effects were frequently observed in the combination of drugs which were effective by the single usage, it was found that the combination of CPA + mitomycin C and CPA + ADM showed high efficacy rates against these cell lines in comparison with other matchings. From these findings, it was concluded that the combination chemosensitivity test in clonogenic assay might be a promising method to evaluate the chemosensitivity of the individual patient. And it was supposed that this method might be also useful as an early phase III study to predict the useful combination of newly developed antitumor agents.

Antineoplastic Combined Chemotherapy Protocols↗
PubMed1987

Genetic basis for Ia positivity and susceptibility to lactic dehydrogenase virus in macrophages of SJL/J mice.

SJL/J mice showed a higher elevation of serum lactic dehydrogenase after lactic dehydrogenase virus (LDV) infection, and a higher per cent of Ia positive and LDV infectable cultured macrophages, than several other mouse strains. Genetic studies suggested that these unique characteristics in SJL/J mice are closely linked and inherited as a single autosomal recessive trait, which is not within the H-2 gene complex.

Animals↗
PubMed1987

Induction and repair of DNA lesions in cultured human melanoma cells exposed to a nitrogen-ion beam.

Induction and repair kinetics of DNA lesions after exposure to nitrogen ions (N-ions) were studied in comparison to those after 180 kVp X-rays. DNA lesions in human melanoma cells (HMV-I) irradiated with 95 MeV N-ions (0-6 Gy, l.e.t.D = 530 keV micron-1 or with X-rays (0.9 Gy) were assayed by alkaline elution. The N-ion r.b.e. for DNA lesion induction was approximately 0.7. About 85 per cent of the lesions induced by N ions were rejoined with a time-course similar to the rejoining of DNA lesions produced by X-rays. These lesions were considered to be induced by delta-rays around the N-ion tracks. The fraction of residual DNA lesions remaining after a 6 h post-irradiation incubation was higher for N-ions than for X-rays. Unlike the case for X-rays, DNA-protein crosslinks were included in the residual DNA lesions after N-ion irradiation.

Cells, Cultured↗