PubMed Health⌕ Search

Biomedical subjects

E Ichikawa

Publications and source records attributed to E Ichikawa.

At least 19 recordsLinked to original sources
PubMed2003

Association between polymorphisms in the SPINK5 gene and atopic dermatitis in the Japanese.

Atopy, which is characterized by increased levels of immunoglobulin E (IgE) against common environmental allergens, is considered the strongest predisposing factor for asthma and atopic dermatitis (AD). Mutations in the gene encoding serine protease inhibitor Kazal-type 5 (SPINK5) are responsible for Netherton syndrome, a rare skin disorder characterized by greatly elevated IgE levels with atopic manifestations. A recent study of Caucasian AD families showed that maternally derived alleles of the SPINK5 gene are associated with development of AD and asthma, suggesting the parent-of-origin effect for the development of atopic diseases in the SPINK5 gene. We studied the possible association of the SPINK5 gene for the development of atopic diseases by determining the genotypes of five polymorphisms in a Japanese population. Ttransmission disequilibrium tests revealed an association of SPINK5 polymorphisms with AD but not with asthma. Our data indicate that the SPINK5 gene is associated with AD across ethnicities.

Carrier Proteins↗
PubMed2001

Mutation and association analysis of the interferon regulatory factor 2 gene (IRF2) with atopic dermatitis.

Interferon regulatory factor 2 (IRF-2) is a member of a family of transcriptional factors involved in the modulation of cellular responses to interferons (IFNs) and viral infection as well as in the regulation of cell growth and transformation. Irf2 knockout mice show T helper 1 (Th1) cell development defect and spontaneous development of an inflammatory skin disease. To determine if there are any mutations in IRF2 associated with development of atopic dermatitis (AD), we screened for mutations in the 5' flanking and coding regions of IRF2 in AD patients and control subjects by single-strand conformational polymorphism (SSCP) analysis. We found three mutations in the promoter region ([-829C>T, -830C>T], -684C>T, and -467G>A), one silent mutation in exon 9 (921G>A), and a 10-bp deletion in the 3' untranslated region (1739[ATCCC]8>6). Among them, the -467G allele and the haplotype of the -467G, 921A, and 1739(ATCCC)8 alleles were transmitted preferentially to AD-affected children (P = 0.02 and P = 0.007, respectively). Our data suggest that IRF-2 plays some role in the development of AD in the Japanese population.

Alleles↗
PubMed2001

Hereditary complement (C9) deficiency associated with dermatomyositis.

A 28-year-old Japanese woman with hereditary complement (C9) deficiency and dermatomyositis is reported. She had a 3-year history of facial erythema and a 1-month history of progressive muscle weakness. Clinical and laboratory findings were suggestive of dermatomyositis; muscle biopsy confirmed an inflammatory myopathy. An unexpected finding, however, was the low titre of serum haemolytic complement (CH50). Treatment with prednisolone resulted in marked clinical improvement but did not affect the CH50 titre. Further investigation revealed a selective and total absence of the ninth complement component (C9), with direct DNA sequence analysis revealing a non-sense mutation at Arg95 of the C9 gene. This case demonstrates that the muscle lesions of dermatomyositis can occur in the presence of a complement defect that would prevent the formation of the C5b-9 membrane attack complex.

Adult↗
PubMed2001

Sugar-modified nucleosides in past 10 years, a review.

In the search for effective, selective, and nontoxic antiviral and antitumour agents, a variety of strategies have been devised to design nucleoside analogs. These strategies have involved several formal modifications of the naturally occurring nucleosides, especially, alteration of the carbohydrate moiety. Since the naturally occurring purine nucleoside analog oxetanocin A and its derivatives have been found to be effective as anti-HIV-1 and anti-herpes virus agents in 1986, the syntheses of different types of sugar-modified nucleoside analogs have been reported. In this review we will give an overview of the sugar-modified nucleosides synthesized since the late 1990 according to their structural types along with the synthetic routes of some selected nucleosides.

Antiviral Agents↗
PubMed2000

Eccrine syringofibroadenoma in a patient with a burn scar ulcer.

A 72-year-old woman with a burn scar on the calves of both legs developed an ulcer on her right heel, surrounded by multiple verrucous nodules and plaques. She had experienced similar verrucous lesions on both legs in the burn scar areas. Although the clinical diagnosis was Marjolin's ulcer, histologically the ulcer region showed thick fibrous tissue without any atypical epithelial cells. The verrucous lesions were consistent with the diagnosis of eccrine syringofibroadenoma (ESFA). Moreover, an ESFA-like growth pattern was seen in the elevated margin of the ulcer. Our findings suggest that these lesions developed as a result of reactive eccrine duct hyperplasia followed by skin tissue remodelling.

Adenoma, Sweat Gland↗
PubMed1999

Synthesis of 2',3'-dideoxy-3'-C-(hydroxymethyl)-4'-thiopentofuranosyl nucleosides as potential antiviral agent.

1-O-Acetyl-2,3-dideoxy-3-C-(hydroxymethyl)-4-thiofuranose derivative was synthesized from (S,S)-1,4-bis(benzyloxy)-2,3-epoxybutane derived from (+)-diethyl L-tartrate and the enantiomerically pure (E)-5-(2-bromovinyl)-1-[2',3'-dideoxy-3'-C-(hydroxymethyl)-beta-D-4'- thiopentofuranosyl]uracil 4 was obtained via coupling of silylated uracil followed by palladium-mediated coupling of methyl acrylate.

Antiviral Agents↗
PubMed1998

Activation of the rat cyclin A promoter by ATF2 and Jun family members and its suppression by ATF4.

Cyclin A plays an essential role in the G1 to S phase transition in the cell cycle. The expression of cyclin A is restrained during G0 and G1, but steeply induced at the G1/S boundary. Analysis of the rat cyclin A promoter elements with the 5' sequential deletion derivatives of the promoter fused to the luciferase cDNA indicated that the ATF/CRE motif primarily determines the inducibility at G1/S. Gel shift analysis of the complex formed at the ATF/CRE site indicated that the complex was not formed with the G0/G1 cell extract, but maximally formed with the late-G1 cell extract. The complex was supershifted by anti-JunD antibody, and Western blot analysis of the immune complexes prepared with anti-JunD antibody revealed the presence of ATF2, suggesting heterodimerization of JunD with ATF2. The cyclin A promoter in a reporter plasmid was activated by nearly 10-fold in quiescent rat 3Y1 cells by cotransfection with the expression of plasmids encoding ATF2 and Jun family members. In contrast, cotransfection with the ATF4 expression plasmid suppressed the promoter activation mediated by ATF2 and Jun family members. The expression of Jun family members during G1 to S progression was induced biphasically in early and late G1 and the level of JunD increased markedly at the G1/S, while that of ATF family members was gradually increased along with the G1 to S progression. These results indicate that the cyclin A promoter activity is regulated, at least in part, by relative amounts of the ATF and Jun family members.

Activating Transcription Factor 2↗
PubMed1998

Nucleotide sequence of an alternative glucoamylase-encoding gene (glaB) expressed in solid-state culture of Aspergillus oryzae.

The DNA (glaB) and a cDNA-encoding glucoamylase produced in solid-state culture of Aspergillus oryzae were cloned using oligodeoxyribonucleotide probes derived from internal amino acid sequences of the enzyme. Comparison of the nucleotide sequences of a genomic DNA fragment with its cDNA showed the glaB gene carried three exons interrupted by two introns and had an open reading frame encoding 493 aa residues. The 5'-flanking region had a TATA box at nt -87 from the start codon and two putative CAAT sequences at nt -276 and -288. The glaB gene shared 57% homology at the aa level with the glaA gene which was cloned previously from A. oryzae. Interestingly, the glucoamylase encoded by the glaB gene had no C-terminal domain such as that proposed to have starch binding activity in Aspergillus glucoamylases. Introduction of cDNA of the glaB gene to Saccharomyces cerevisiae caused the secretion of active glucoamylase to culture medium and introduction of the glaB gene to A. oryzae increased glucoamylase productivity in solid-state culture. Northern blot analysis showed the glaB gene was expressed in solid-state culture, but not in submerged culture.

Amino Acid Sequence↗
PubMed1997

Keratin and involucrin expression in discoid lupus erythematosus and lichen planus.

In the present study, keratin and involucrin expression were studied in cutaneous lesions of discoid lupus erythematosus and lichen planus in order to gain a better understanding of the abnormal differentiation or maturation of the epidermal cells in these dermatoses. Ten specimens each from discoid lupus erythematosus and lichen planus were analyzed by immunohistochemical techniques, using a panel of monoclonal antikeratin antibodies and polyclonal anti-involucrin antibody, and five specimens each were analyzed by one- and two-dimensional gel electrophoresis and immunoblot analysis using three antikeratin antibodies. No significant difference was found between the dermatoses. The expression of differentiation-specific keratins showed a similar pattern to that in normal epidermis, and involucrin was expressed even in the lower part of the stratum spinosum. Keratins 6 and 16, which are characteristic markers of hyperproliferative states, and keratin 17 were detected in nonhyperproliferative and atrophic epidermis with hydropic degeneration and inflammatory infiltrates in the dermis. These results suggest that expression of keratins 6, 16 and 17 in discoid lupus erythematosus and lichen planus may reflect a wound healing response to the damage to the basal cell layer, or may be under the control of cytokines produced by infiltrating inflammatory cells in the dermis.

Cell Differentiation↗
PubMed1997

Papillary eccrine adenoma: immunohistochemical studies of keratin expression.

Despite various studies, there are serious disagreements about the cellular differentiation of papillary eccrine adenoma. In the present study, 2 specimens of papillary eccrine adenoma were analyzed by immunohistochemical techniques, using a panel of monoclonal antibodies against keratins, to elucidate its differentiation. Histopathologically, the tumor was composed of multiple tubular structures lined by two or more layers of epithelial cells. The luminal cells of the tubules were flattened or cuboidal. The former were noted in large dilated tubules. The latter were usually observed in small-to-moderate-sized tubules, and formed intraluminal papillary projections in some tubules. Immunohistochemically, there were two kinds of cuboidal cells in the luminal layers of the tubules. Most of the large dilated tubules and some of the small-to-moderate-sized tubules expressed immunophenotypes similar to those of the eccrine dermal duct. The other tubular structures, including the small tubules resembling those of syringoma, expressed immunophenotypes similar to those of the transitional portions between the dermal ducts and the secretory segments of eccrine glands. From the above comparative studies, papillary eccrine adenoma is considered to differentiate towards the dermal duct and the transitional portions between the dermal ducts and the secretory segments of eccrine glands.

Adenoma, Sweat Gland↗
PubMed1997

Expression of cathepsin D and B in invasion and metastasis of squamous cell carcinoma.

To determine the involvement of proteinases with hydrolytic activity towards extracellular matrix and basement membrane, in invasion and metastasis of tumour cells, the expression of cathepsin D, an aspartic proteinase, and cathepsin B, a cysteine proteinase, was studied. Formalin-fixed paraffin-embedded specimens from 13 patients who had squamous cell carcinomas (SCC) with local recurrence, skin and/or lymph node metastasis were examined. Cathepsin D stained intensely as a granular pattern (mature enzyme) in tumour cells of 69% of primary lesions and all the secondary lesions of the patients with SCC. Cathepsin B stained more intensely in SCC cells of all of the primary and secondary lesions than in normal epidermis; staining patterns were almost diffuse (procathepsin B). Granular and diffuse patterns (mature enzyme of cathepsin D and procathepsin B, respectively) appeared in the outer and inner parts of tumour islands, respectively. The presence of the active mature form of cathepsin D and procathepsin B in metastatic skin lesions of SCC was confirmed by Western blotting analysis. The presence and localization of the active mature form of cathepsin D suggests that activated cathepsin D may be involved in the invasion and metastasis of SCC.

Blotting, Western↗
PubMed1996

A case of cutaneous malignant fibrous histiocytoma.

A 54-year-old Japanese man with cutaneous malignant fibrous histiocytoma on the back is reported. He not only had a past history of thyroid cancer 1 year prior to the onset of the skin tumor, but also had simultaneous bladder cancer. Despite the early, wide resection, the prognosis was rapid and progressive. Histologically, the primary lesion of the skin tumor was difficult to differentiate from dermatofibrosarcoma protuberans; however, the recurrent and the metastatic lesions changed in appearance.

Fatal Outcome↗
PubMed1996

Identification of major biliary and urinary metabolites of ecabapide in rats.

1. The structures of major biliary and urinary metabolites of ecabapide in rat were identified by comparison with authentic standards using lc-ms and 1H-nmr spectrometry. 2. A major metabolite was found in the bile obtained from rat after an oral dose of 14C-ecabapide and identified as the amidaldehyde derivative. In the urine, two polar metabolites were characterized as the phenolic sulphates. Further, two lipophilic metabolites were identified as alcohol derivatives, and two others as oxamic acids. 3. From these results, it was estimated that the first step in the metabolism of ecabapide in rat was oxidative N-dealkylation to produce the amidaldehyde. This amidaldehyde was further metabolized by two routes, one by reduction of the amidaldehyde into the corresponding alcohol followed by mono-demethylation and subsequent aromatic O-sulphation, the second by oxidation of the amidaldehyde into the oxamic acid followed by mono-demethylation and subsequent aromatic O-sulphation.

Animals↗