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Biomedical subjects

S Tajima

Publications and source records attributed to S Tajima.

At least 127 records · Page 7Linked to original sources
PubMed1999

Bowen's disease showing spontaneous complete regression associated with apoptosis.

Spontaneous regression is sometimes seen in malignant skin tumours. We report a 68-year-old woman whose Bowen's disease showed spontaneous complete regression. Prominent infiltration of T cells and increased vascularity were found in the upper dermis of the regressed lesion. Strong expression of Fas (APO-1/CD95) antigen, an apoptosis-related tumour necrosis factor receptor family protein, in the primary lesion and faint expression following regression suggest the involvement of Fas-mediated apoptosis in the spontaneous complete regression of our patient's Bowen's disease.

Apoptosis↗
PubMed1999

Hyperpigmentation caused by hyperthyroidism: differences from the pigmentation of Addison's disease.

Two cases of hyperthyroidism with hyperpigmentation are presented. In both cases, hyperpigmentation was seen on the lower extremities, most strikingly on the shins, backs of the feet and the nail bed. Histology of the pigmented skin showed basal melanosis and heavy deposition of haemosiderin around dermal capillaries and sweat glands. Treatment with mercazol in both cases resulted in no significant waning of pigmentation. Distribution of hyperpigmentation, haemosiderin deposition and poor response to the treatment may be characteristic features of the pigmentation caused by hyperthyroidism, and may represent differences from the pigmentation seen in Addison's disease.

Addison Disease↗
PubMed1999

Expression of type XVI collagen in human skin fibroblasts: enhanced expression in fibrotic skin diseases.

Abundance of type XVI collagen mRNA in normal human dermal fibroblasts explanted from different horizontal layers was determined using RNase protection assays. Type XVI collagen mRNA level in the fibroblasts explanted from the upper dermis was greater than those of the middle and lower dermis. The antibody raised against the synthetic N-terminal noncollagenous region reacted with approximately 210 kDa collagenous polypeptide in the culture medium of fibroblasts. Immunohistochemical study of normal human skin demonstrated that the antibody reacted preferentially with the fibroblasts and the extracellular matrix in the upper dermis rather than those in the middle and lower dermis. Type XVI collagen mRNA level was elevated 2.3-fold in localized scleroderma and 3.6-fold in systemic scleroderma compared with keloid and normal controls. Immunofluorescent study revealed that an intense immunoreactivity with the antibody was observed in the upper to lower dermal matrix and fibroblasts in the skin of systemic scleroderma as compared with normal skin. The results suggest that expression of type XVI collagen, a member of fibril-associated collagens with interrupted triple helices, in human skin fibroblasts can be heterogeneous in the dermal layers and can be modulated by some fibrotic diseases.

Adolescent↗
PubMed1999

Differential responses of collagen and glycosaminoglycan syntheses and cell proliferation to exogenous transforming growth factor beta 1 in the developing mouse skin fibroblasts in culture.

Skin fibroblast cultures were established from mouse foetuses at days 14, 15, 16 and 18 of gestation and from newborn mice. Modulations of mitotic and biosynthetic phenotypes of the fibroblasts by transforming growth factor beta1 (TGFbeta1) were studied. Treatment of the fibroblasts with TGFbeta1 at doses of 1 and 10 ng/ml for 48 h resulted in significant stimulation of cell proliferation in the 15-, 16- and 18-day foetal fibroblasts and a slight stimulation in the 14-day foetal fibroblasts. Treatment with TGFbeta1 resulted in stimulation of collagen synthesis approximately 2-fold in the 18-day foetal and newborn fibroblasts, but failed to stimulate it in the 14-, 15- and 16-day foetal fibroblasts. TGFbeta1 stimulated glycosaminoglycan (GAG) synthesis throughout all developmental stages approximately 1.8-2.6 fold. Histological study demonstrated that skin wounds made at day 16 of gestation were replaced with normal-appearing dermis, but at day 18 the wounds left dermal fibrosis and lack of hair follicles. These results indicate that the modulations of fibroblast phenotypes (proliferation and syntheses of collagen and GAG) in response to TGFbeta1 occur at different stages of gestation. Ontogenic transitions of skin wound healing and collagen synthetic phenotype with TGFbeta1 treatment in cultured fibroblasts occurred between days 16 and 18 of gestation, suggesting that the unresponsiveness of collagen synthesis to exogenous TGFbeta1 in cell culture may be related to the phenomenon of scarless wounds in the foetus.

Animals↗
PubMed1999

Analysis of elastin metabolism in patients with late-onset focal dermal elastosis.

Late-onset focal dermal elastosis has recently been described as new clinical entity characterized by pseudoxanthoma elasticum-like eruptions and an accumulation of normal-appearing elastic fibres in the dermis. Elastin and collagen contents of the skin of 2 patients were 2- and 1.4-fold higher than in the skin of controls, respectively. A focal accumulation of elastin but not of fibrillin-1 was observed by immunohistochemical staining. The levels of type I and III collagen and elastin mRNAs isolated from cultured patient fibroblasts were elevated 2-3-fold compared with control fibroblasts. There was no significant change in the excretion of elastin peptides in the urine of patients and controls. These results suggest that the focal accumulation of elastic fibres in the patient skin may be related to overexpression of elastin rather than to altered degradation of elastin.

Age of Onset↗
PubMed1999

Xenopus maintenance-type DNA methyltransferase is accumulated and translocated into germinal vesicles of oocytes.

In vertebrates, DNA methylation plays an important role in the regulation of gene expression and embryogenesis. DNA methyltransferase, which catalyzes the introduction of a methyl group at the 5th position of cytosine in the CpG sequence, is highly accumulated in mouse oocytes and is excluded from nuclei [Carlson et al. (1992) Genes Dev. 6, 2536-2541]. In this study, we examined the expression level and localization of Xenopus DNA methyltransferase in oocytes during oogenesis. The DNA methyltransferase protein was detectable in stage III oocytes and increased thereafter, until the oocytes had matured. The rate of DNA methyltransferase synthesis rapidly increased after stage IV oocytes. Different from in mouse oocytes, DNA methyltransferase was equally distributed in the nuclear and post-nuclear fractions, in stage VI oocytes. DNA methyltransferase translocated into nuclei was uniformly localized in the nuclear matrix, and the accumulated DNA methyltransferase in stage VI nuclei had DNA methylation activity.

Animals↗
PubMed1999

Axonal degeneration of peripheral facial nerve in a patient with progressive hemifacial atrophy.

We report a case of a 23-year-old woman with progressive hemifacial atrophy. She showed an atrophic change on the left side of her face for 8 years. A skin biopsy obtained from the lesion revealed the fibrotic changes in the deep dermis and adipose tissue with infiltrations of lymphocytes and plasma cells. She underwent the augmentation using a deepithelialized anteromedial thigh flap with endoscopic assistance. A specimen of the peripheral facial nerve taken from the region adjacent to the skin lesion during the operation showed atrophy of neurofibers with vacuole degeneration. On an electron microscopic examination, a high degree of degeneration of myelinated and unmyelinated axons was observed. These findings may provide direct evidence that atrophic changes of nerve fibers are closely related with the pathology of this disease.

Adult↗
PubMed1999

Keloids have continuous high metabolic activity.

The adenosine triphosphate (ATP) content of keloids and scars resected from patients was demonstrated by high-performance liquid chromatography. The surface color of hypertrophic scars was red or pink and that of atrophic scars was white. The ATP content of red scars was (in mmol/g protein) 1.06 +/- 0.14, of pink scars 0.12 +/- 0.02, of white atrophic scars 0.19 +/- 0.06, and of keloids 1.06 +/- 0.19. The longer the elapsed time after the trauma, the lower the level of ATP in scar tissues (correlation coefficient = -0.506; p = 0.005 by Spearman's rank correlation). However, ATP levels in keloids were still high 10 years after the injury. Fibroblasts and fibrocytes in keloids and scars were counted in histologic preparations stained with hematoxylin and eosin. The average number of fibroblasts in a definite area (56 x 10(-4) mm at a magnification of x400) was 4.8 in keloids, 5.1 in red scars, 2.4 in pink scars, and 1.3 in white atrophic scars. The number of fibrocytes in the same area was 0.4 in keloids, 0.4 in red scars, 2.3 in pink scars, and 1.3 in white atrophic scars. These results indicate that keloids and red hypertrophic scars have higher ATP levels and contain more fibroblasts than pink or white scars, and they also suggest that the levels of ATP and the number of fibroblasts decrease when red hypertrophic scars change into atrophic scars. In keloids, ATP and fibroblasts seem to remain at high levels for a long time.

Adenosine Triphosphate↗
PubMed1999

The YXXL sequences of a transmembrane protein of bovine leukemia virus are required for viral entry and incorporation of viral envelope protein into virions.

The cytoplasmic domain of an envelope transmembrane glycoprotein (gp30) of bovine leukemia virus (BLV) has two overlapping copies of the (YXXL)2 motif. The N-terminal motif has been implicated in in vitro signal transduction pathways from the external to the intracellular compartment and is also involved in infection and maintenance of high viral loads in sheep that have been experimentally infected with BLV. To determine the role of YXXL sequences in the replication of BLV in vitro, we changed the tyrosine or leucine residues of the N-terminal motif in an infectious molecular clone of BLV, pBLV-IF, to alanine to produce mutated proviruses designated Y487A, L490A, Y498A, L501A, and Y487/498A. Transient transfection of African green monkey kidney COS-1 cells with proviral DNAs that encoded wild-type and mutant sequences revealed that all of the mutated proviral DNAs synthesized mature envelope proteins and released virus particles into the growth medium. However, serial passages of fetal lamb kidney (FLK) cells, which are sensitive to infection with BLV, after transient transfection revealed that mutation of a second tyrosine residue in the N-terminal motif completely prevented the propagation of the virus. Similarly, Y498A and Y487/498A mutant BLV that was produced by the stably transfected COS-1 cells exhibited significantly reduced levels of cell-free virion-mediated transmission. Analysis of the protein compositions of mutant viruses demonstrated that lower levels of envelope protein were incorporated by two of the mutant virions than by wild-type and other mutant virions. Furthermore, a mutation of a second tyrosine residue decreased the specific binding of BLV particles to FLK cells and the capacity for viral penetration. Our data indicate that the YXXL sequences play critical roles in both viral entry and the incorporation of viral envelope protein into the virion during the life cycle of BLV.

Amino Acid Sequence↗
PubMed1999

Elastic nevus with normal expression of elastin and elastin-related proteins mRNAs.

A 3-year-old Japanese girl presented with disseminated white papules on the trunk. A biopsied specimen of the lesional skin revealed a focal accumulation of elastic fibers in the mid to deep dermis. No skeletal involvement was detected. This case was considered to be elastic nevus without systemic involvement. Since an elevated elastin expression in the fibroblasts of typical Buschke-Ollendorff syndrome (BOS) has been reported, elastin and elastin-related protein mRNA levels in the cultured patient fibroblasts were determined. There were no significant differences of steady-state levels of elastin, fibrillin 1 and microfibril-associated glycoprotein 1 mRNAs between patient and matched control fibroblasts. Elastic nevus without skeletal involvement may be etiologically different from typical BOS.

Blotting, Northern↗
PubMed1999

Leopard syndrome associated with hyperelastic skin: analysis of collagen metabolism in cultured skin fibroblasts.

We present a patient with Leopard syndrome and hyperelastic skin. Biochemical analysis using cultured skin fibroblasts showed normal type III and V collagen synthesis, lysyl hydroxylation level of type I procollagen and processing of pro-alpha(1) and alpha(2)(I). Our results suggest that molecular defects of hyperelasticity in Leopard syndrome are not related to abnormal collagen metabolism, although not all steps of collagen synthesis have been investigated.

Abnormalities, Multiple↗
PubMed1999

A Japanese case with Frasier syndrome caused by the splice junction mutation of WT1 gene.

The Wilms' tumor suppressor gene, WT1, plays an important role in the development of the urogenital system and also subsequent normal function of this system. Recently, the splice mutations in intron 9 of WT1 gene have been detected in Frasier syndrome, which is characterized by streak gonads, pseudohermaphroditism, slowly progressive nephropathy and frequent development of gonadoblastoma. Here to elucidate the molecular basis in a Japanese patient of Frasier syndrome, WT1 gene was analyzed by polymerase-chain-reaction (PCR) and direct sequencing. We identified the splice junction mutation in intron 9 of WT1, which is recognized as a mutation hot-spot in intron 9. This finding concludes that 1) the mutation in intron 9 might be the cause of Frasier syndrome, and 2) the mutation hot-spot in Japanese and Caucasian patients is similar.

Adolescent↗
PubMed1999

An adult case with an abnormal right ventricular structure causing intraventricular pressure gradient and a history of aphthous stomatitis and thrombophlebitis.

We report a 50-year-old man with a right ventricular structure causing an intraventricular pressure gradient. He had been diagnosed as vasculo-Behçet with a history of aphthous stomatitis and thrombophlebitis. He had also been suffering from atrial flutter and mild right-side heart failure. Echocardiography showed that there was an abnormal structure attached to the right ventricular free wall and protruding into the cavity, and that it caused the pressure gradient estimated to be approximately 19 mmHg. Chest X-ray computed tomography demonstrated that the structure was partially calcified. Magnetic resonance imaging depicted the structure separating the right ventricle into two chambers. Angiographic study revealed a markedly enlarged right atrium and a filling defect at the mid-portion of the right ventricle, which divided the right ventricular cavity into two parts. Hemodynamic study showed a slightly elevated right atrial pressure (mean 7 mmHg) and a peak-to-peak intraventricular pressure difference of 18 mmHg in the right ventricle. The diastolic pressure tracing of the right ventricular low pressure chamber showed a 'dip and plateau' pattern. Although the pathological features of the abnormal right ventricular structure in this case were not fully clarified, abnormal muscle bundle and/or endocardial fibrosis, which were reported to be associated with Behçet's disease, may have contributed to its generation.

Atrial Flutter↗
PubMed1999

Reduction of operating time and blood transfusion for craniosynostosis by simulated surgery using three-dimensional solid models.

Preoperative planning of craniofacial synostosis can be achieved through the use of two- or three-dimensional (3D) computed tomography (CT) images and by 3D solid models. The advantage of using 3D models was evaluated by calculating the amount of blood transfused and the operating time for 36 craniosynostosis procedures, 21 planned with 3D models and 15 with CT images performed in the past 7 years. The use of 3D models reduced both blood loss and operating time for fronto-orbital advancement with reshaping, LeFort III advancement, and LeFort IV minus Glabellar advancement; blood loss for fronto-orbital advancement without reshaping; and operating time for total cranial reshaping.

Adolescent↗
PubMed1999

Developmental induction and villus-crypt distribution of retinol esterifying enzyme activities in chick duodenum.

Retinol absorbed and generated from dietary beta-carotene can be esterified by retinol esterifying enzyme(s) in intestinal absorptive cells. In this study, we observed the developmental changes and villus-crypt distribution of the activities of two retinol esterifying enzymes (lecithin-retinol acyltransferase (LRAT); and acyl-CoA-retinol acyltransferase (ARAT) in chick duodenum) to seek the possibility that these enzymes play distinct roles in retinol absorption and metabolism. Intestinal LRAT activity was barely expressed in embryonic stages until 2-3 d before hatching, when its activity becomes detectable; thereafter it abruptly increased to the maximal level at the third day of the posthatch period. In contrast, ARAT activity was present in the duodenum at the earliest stage examined, the 15th day of embryogenesis, and was elevated to the maximal level 3-4 d after hatching. An assay of LRAT and ARAT activities along the villus-crypt axis of the duodenum by a cryostat sectioning technique revealed that between the day of hatching and 1 d posthatch, an abrupt induction of LRAT activity occurred only in the villus region of the duodenum, where a coordinated induction of cellular retinol-binding protein, type II (CRBPII), was observed. In contrast, the rise in ARAT activity observed around the hatching period occurred at the broader portions of the villi including the area of villus-crypt junction. These observations in the developmental changes and distribution of LRAT and ARAT activities suggest that LRAT activity but not ARAT activity is closely related to the induction of CRBPII in the duodenum of developing chicks.

Acyltransferases↗
PubMed1998

Function and Conformation of Wild-Type p53 Protein Are Influenced by Mutations in Bovine Leukemia Virus-Induced B-Cell Lymphosarcoma

The mutations of the p53 gene previously represented one of several genetic changes involved in the development of bovine leukemia virus (BLV)-induced lymphosarcoma, while the effects of these mutations on the function of p53 are unknown. We identified four mutations of p53 gene in BLV-infected cattle with lymphosarcoma and demonstrated clearly the existence of two functionally distinct groups of mutants: (i) the mutant forms with substitutions at codons 241 and 242, which were mapped within an evolutionally conserved region and corresponded to the human "hot-spot" mutations, had completely lost the capacities for transactivation and growth suppression and gained transdominant repression activity in p53-null SAOS-2 cells; and (ii) the mutations at codons 206 and 207 were located outside the evolutionally conserved regions. These mutants partially retained the capacity for transactivation and growth suppression and failed to inhibit the transactivation activity of coexpressed wild-type p53, instead showing an enhancement of this activity. In addition, protein analysis using an antibody specific for the mutant form revealed that the mutations at codons 206 and 242 induced a "mutant" conformation of the bovine p53 proteins. Collectively, these results show that mutations of p53 gene in BLV-infected cattle with lymphosarcoma can potentially alter its physiological function and may play an important role in BLV-induced leukemogenesis. Copyright 1998 Academic Press.

Journal Article↗