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Biomedical subjects

A Hakura

Publications and source records attributed to A Hakura.

At least 109 records · Page 6Linked to original sources
PubMed1986

Human papillomavirus type 38 isolated from patients with epidermodysplasia verruciformis.

A new type of human papillomavirus (HPV), HPV-38b, was isolated from patients with epidermodysplasia verruciformis and was molecularly cloned. This HPV was shown by hybridization experiments to have almost no sequence homology with other types of reported HPVs, but did show homology with HPV-38, which was recently isolated from a melanoma. A physical map and a rough genetic map of the organization of this HPV are presented.

Adult↗
PubMed1986

Epidemiologic aspects of epidermodysplasia verruciformis (L-L 1922) in Japan.

A survey of epidermodysplasia verruciformis (EV), a skin disease caused by human papillomavirus (HPV), was made by means of a questionnaire sent to 92 university hospitals. Replies were obtained from 68 hospitals (74% recovery) reporting 66 patients. Fewer patients were reported from north-eastern Japan than from south-western Japan. Many EV patients were from families of consanguineous marriages (44%), showing a high incidence of intra-familial onset after consanguineous marriages. The complication of malignant tumors was observed in 36 of 62 cases (58%). Malignant tumors of the skin developed at an early age in EV patients. These cancers developed predominantly in exposed areas of the skin (72%). The time from onset of skin lesions to the onset of cancer seemed to be related to the nature of the lesions in EV patients. These findings suggest that the interaction of HPVs, ultraviolet rays and host factors is associated with the development of skin carcinomas.

Adolescent↗
PubMed1985

Linear relationship between diphosphorylation of 20 kDa light chain of gizzard myosin and the actin-activated myosin ATPase activity.

The addition of large amounts of myosin light chain kinase to the reconstituted gizzard actomyosin shows diphosphorylation of 20 kDa myosin light chain. Accompanying diphosphorylation, the actin-activated myosin ATPase activity was also enhanced. The extent of diphosphorylation and the myosin ATPase activity were clearly demonstrated to be in a linear relationship. From the time course experiment, the conversion of monophosphorylated light chain into one which was diphosphorylated seemed to be a sequential process. Moreover, analyzing phospho-amino acid by using a two-dimensional electrophoresis technique revealed that monophosphorylated light chain contained phosphoserine and diphosphorylated one contained phosphothreonine in addition to phosphoserine.

Actins↗
PubMed1985

Human papillomavirus type 17 DNA in skin carcinoma tissue of a patient with epidermodysplasia verruciformis.

Epidermodysplasia verruciformis (EV) is a serious skin disease caused by certain types of human papillomavirus (HPV), because the flat wart-like lesions of EV very frequently change to malignant squamous cell carcinoma. The relation between HPV and skin carcinoma was examined by studies on an EV patient who had a squamous cell carcinoma. HPV-17 was isolated from EV lesions of this patient. With HPV-17 DNA as a probe, cellular DNA prepared from the carcinoma tissue was analyzed by Southern blot hybridization. Results showed that cells contained about 100 copies of monomeric and oligomeric extrachromosomal HPV DNA. These results suggest that HPV-17 is involved in skin carcinogenesis in EV.

DNA, Viral↗
PubMed1985

Morphological aspects on pancreatic islets of non-obese diabetic (NOD) mice.

The pancreatic islets of female non-obese diabetic (NOD) mice (a model of insulin-dependent diabetes mellitus), have been examined by both light and electron microscopy. At about the age of 2 weeks, mononuclear cells began to infiltrate in or near the islets and some of these cells were in contact with the islet cells. Following this degeneration of islet B-cells took place, the process occurring in two ways. In many cells numerous secretory granules with extremely dense cores occupied the cytoplasm. Other cells, however, were filled with low-density secretory granules and the nuclei of these cells became pycnotic. After degeneration of B-cells, the islets were effaced by numerous mononuclear cells. With the onset of the diabetic state these mononuclear cells gradually disappeared, and thereafter small islets remained. By electron microscopy, retrovirus-like particles were observed in cisternae of the rough endoplasmic reticulum in islet B-cells at all stages. With an anti-retrovirus serum (goat anti-KiMSV-NIHxeno serum), positive immunofluorescence was observed in some pancreatic islet cells of NOD mice aged 1 day and 4, 6, 8, 9, 10 and 14 weeks. It is suggested that these virus particles may be intimately related to the inflammatory reaction occurring in the islets and to the development of diabetes mellitus.

Animals↗
PubMed1985

Studies on chemical carcinogens and mutagens. XXIX. Mutagenic N-trimethylsilylmethyl-N-nitrosourea as a biological alkylating agent equivalent to N-methyl-N-nitrosourea (MNU).

N-Trimethylsilylmethyl-N-nitrosourea (TMS-MNU), a silicon analogue of N-neopentyl-N-nitrosourea (neoPNU), was assayed for mutagenicity and/or cytotoxicity on a series of E. coli B tester strains, S. typhimurium TA100, Chinese hamster V79, and cultured murine leukemia L1210 cells. All the biological activities demonstrated in this study reveal that this nitrosourea is a biological methylating agent equivalent to N-methyl-N-nitrosourea (MNU) but definitely distinguished from all the other alkylnitrosoureas examined so far, including neoPNU (the carbon analogue of TMS-MNU). The proposed molecular mechanism is that trimethylsilylmethanediazohydroxide is produced by hydrolytic activation of TMS-MNU and undergoes a nucleophilic cleavage of the Si--CH2 chemical bond at a high rate to form methanediazohydroxide (the reactive intermediate of MNU) which, in turn, methylates the informational biopolymer leading to mutagenesis.

Animals↗
PubMed1984

Mutagenicity of pyridine- and quinoline-carbohydroxamic acid derivatives.

11 pyridine- and 6 quinoline-carbohydroxamic acids were tested for mutagenicity on Salmonella typhimurium TA100 and TA98. The results are compared with those obtained for benzohydroxamic acid and 4 naphthohydroxamic acids. Most of them were mutagenic on both these tester strains. Of the pyridine derivatives, pyridine-2-carbohydroxamic acid was the most potent mutagen. Quaternarization of the pyridine-ring nitrogen prevented the induction of mutation to a marked extent. Among the quinoline derivatives, quinoline-6-carbohydroxamic acid showed potent mutagenicity similar to that of 2-naphthohydroxamic acid. The present study supports the proposal made previously that the mechanism for mutagenicity of hydroxamic acids involves Lossen rearrangement of the acid conjugates produced by enzymic acylation (or perhaps phosphorylation or sulfation) of the hydroxamic acids, followed by carbamoylation of the target molecule in the cell by the resultant isocyanate. The multiplicity of factors determining the mutagenic potency of hydroxamic acids is discussed.

Hydroxamic Acids↗
PubMed1984

Occurrence of caldesmon (a calmodulin-binding protein) in cultured cells: comparison of normal and transformed cells.

Caldesmon is a calmodulin-binding and F-actin-binding protein originally purified from chicken gizzard smooth muscle. This protein binds to F-actin filaments in a Ca2+- and calmodulin-dependent "flip-flop" fashion, thereby regulating the function of actin filaments. Here we report that various lines of cultured cells contain a Mr 77,000 protein that specifically reacts with the affinity-purified caldesmon antibody raised against chicken gizzard caldesmon . Among the fibroblast proteins that had been pulse-labeled with [35S]methionine, the Mr 77,000 protein was the only protein band detected on the NaDodSO4 gel that reacted with the anticaldesmon . The subcellular distribution of the Mr 77,000 protein was investigated by the indirect immunofluorescence technique using the anticaldesmon . In all fibroblast cell lines examined, the immunofluorescence localized along the cellular stress fibers and in leading edges of the cell. In Rous sarcoma virus-transformed cells (S7-1), however, the distribution of the fluorescence changed to a diffuse and blurred appearance. These staining patterns of anticaldesmon obtained with the normal and transformed cells coincided with those of antiactin in the corresponding states, strongly suggesting the functional linkage between the Mr 77,000 protein and actin filaments. We propose to refer to this Mr 77,000 protein as caldesmon 77. The cellular level of caldesmon 77 in transformed S7-1 cells decreased to about one-third of that in their normal counterparts (cell line no. 7). Essentially the same result was obtained with normal rat kidney cells infected with the temperature-sensitive transformation mutant Schmidt-Ruppin strain of Rous sarcoma virus (68 N2 clone). The cellular level of caldesmon 77 observed at a permissive temperature (35 degrees C) was about one-third of that at a nonpermissive temperature (38.5 degrees C). These changes of caldesmon 77 in transformed cells may correlate with the loss of Ca2+ regulation in the transformed state.

Animals↗
PubMed1983

Rat mutant cells showing temperature sensitivity for transformation by wild-type Moloney murine sarcoma virus.

To clarify the cellular target(s) of onc gene products of Moloney murine sarcoma virus (Mo-MSV), we isolated seven mutant cells that exhibit temperature sensitivity for transformation by wild-type Mo-MSV from Fischer rat cell line. Five strains of these mutant cells showed normal virus production at the nonpermissive temperature when infected with Mo-MSV, suggesting that viral replication is not affected by these cellular mutations. Four of these mutants were also temperature sensitive (ts) for transformation by Kirsten murine sarcoma virus (Ki-MSV), whereas the other three mutants were not ts, suggesting that our mutants isolated with Mo-MSV can be divided into two classes as regards temperature sensitivity to transformation by Ki-MSV.

Animals↗
PubMed1983

Isolation and characterization of host range mutants of avian sarcoma virus.

Two host range mutants of avian sarcoma virus (ASV) were isolated from a clone of the Bratislava 77 strain, subgroup C (B77-C). An HR- mutant was obtained by adaptation to duck cells and showed almost the same efficiencies of transformation (e.o.t.) and growth in cultures of chick embryo fibroblasts (CEF) and duck embryo fibroblasts (DEF). An HR+ mutant showed lower e.o.t. and slower growth on DEF than on CEF. Characterization of these mutants and wild-type B77-C showed that (i) unlike the host range mutants reported previously, these mutants and wild-type B77-C have common antigenicity, (ii) the number of infective centres is almost the same for the two mutants and the wild-type, and so the adsorption and integration of these viruses are similar, and (iii) the content of viral RNA in DEF infected with HR- is increased and decreased in the case of HR+ compared with the wild-type.

Animals↗
PubMed1983

[Cellular factors participating in cell transformation].

To clarify the cellular target(s) of onc gene products of Moloney murine sarcoma virus (Mo-MSV), we isolated eight mutant cells that exhibit temperature-sensitivity for transformation by wild type Mo-MSV from F2408 (Fischer rat cell line). These mutant cells showed normal growth and normal Mo-MSV production at the nonpermissive temperature, suggesting that cellular and viral replication are not affected by these cellular mutations. These mutant cells are divided into 3 classes on the bases of temperature-sensitivity for transformation by other tumor viruses such as Kirsten sarcoma virus, Rous sarcoma virus (SRD strain), Fujinami sarcoma virus and Abelson leukemia virus. These results have suggested that several kinds of cellular factors are concerned in transformation by Mo-MSV.

Animals↗