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Y Kitajima

Publications and source records attributed to Y Kitajima.

At least 127 records · Page 7Linked to original sources
PubMed1995

Evidence implicating phospholipase as a virulence factor of Candida albicans.

Three different approaches were used to investigate the role of extracellular phospholipases in the pathogenicity of Candida albicans. First, we compared 11 blood isolates of this yeast with an equal number of commensal strains isolated from the oral cavities of healthy volunteers. Blood isolates produced significantly more extracellular phospholipase activity than the commensal strains did. Second, two clinical isolates of C. albicans that differed in their levels of virulence in a newborn mouse model were compared for their ability to secrete phospholipases. The invasive strain produced significantly more extracellular phospholipase activity than the noninvasive strain did. Third, nine blood isolates were characterized for their phospholipase and proteinase production, germ tube formation, growth, and adherence to and damage of endothelial cells in vitro. These factors were analyzed subsequently to determine whether they predicted mortality in a mouse model of hematogenously disseminated candidiasis. By proportional hazard analysis, the relative risk of death was 5.6-fold higher (95% confidence interval, 1.672 to 18.84 [P < 0.005]) in the mice infected with the higher-phospholipase-secreting strains than in the low-phospholipase secretors. None of the other putative virulence factors predicted mortality. Characterization of phospholipases secreted by three of the blood isolates showed that these strains secreted both phospholipase B and lysophospholipase-transacylase activities. These results implicate extracellular phospholipase as a virulence factor in the pathogenesis of hematogenous infections caused by C. albicans.

Acyltransferases↗
PubMed1995

Cytokeratin expression patterns by one- and two-dimensional electrophoresis in pars flaccida cholesteatoma and pars tensa cholesteatoma.

Expression patterns of cytokeratins (CKs) in normal skin, in pars flaccida type cholesteatoma (PFTC), and in pars tensa type cholesteatoma (PTTC) were examined by means of one- and two-dimensional electrophoretic techniques. Both CKs 14 and 5 pair (CKs 14/5) and CKs 10/1 were found in all materials. Neither CKs 16/6 nor 19 was found in the skin. CKs 16/6 and 19 were both found in 3 out of 5 PFTCs, only CKs 16/6 in 1 out of 5 and neither CKs 16/6 nor 19 in 1 out of 5. CKs 16/6 and 19 were both found in 1 out of 3 PTTCs, only CKs 16/6 in 1 out of 3 and neither CKs 16/6 nor 19 in 1 out of 3. There was no significant difference in the CKs expression patterns between PFTC and PTTC. The expression of CKs 16/6 and 19 suggested that their matrix epithelia were hyperproliferative. However, not all of the cholesteatomas were always hyperproliferative. Patterns of the terminal differentiation of CKs 1, 5, 10 and 14 in the PFTC or the PTTC were basically the same as those in the skin. In the cholesteatoma, eack CK gradually diminished in molecular weight in the cornified layer and debris. Desmosomal proteins were abundant in skin but not in cholesteatomas.

Adult↗
PubMed1995

A hemidesmosomal transmembrane collagenous molecule, the 180-kDa bullous pemphigoid antigen (BPA II), is phosphorylated with 12-O-tetradecanoylphorbol-13-acetate in a human squamous cell carcinoma cell line (DJM-1).

We have previously shown that the 180-kD bullous pemphigoid antigen (BPAII), which is a transmembrane collagenous protein of hemidesmosomes, is distributed at adhesion sites on glass coverslips on the basal membrane forming a concentric ring, or arch pattern, in a human squamous cell carcinoma cell line (DJM-1), when studied by immunofluorescence microscopy using monoclonal antibodies to BPA II. This concentric ring/arch pattern of "footsteps" of BPA II has been shown to be collapsed in association with a transient activation of protein kinase C by treatment with 12-O-tetradecanoylphorbol-13-acetate (TPA). In the present study, therefore, the effects of TPA on the phosphorylation of BPA II was examined. DJM-1 cells, which were metabolically labelled with [32Pi], were lysed and the extracts were subjected to immunoprecipitation with anti-BPAII and anti-230 kDa bullous pemphigoid antigen (BPAI) monoclonal antibodies. The results showed that only BPA II, but not BPA I, was phosphorylated at serine residues before TPA treatment. After TPA treatment phosphorylation was prominently increased so as to generate a 190 kDa-phosphorylated peptide. This 190-kDa peptide was reacted with anti-BPA II monoclonal antibodies by immunoblotting, and it was not detected when cells were pretreated with a specific protein kinase C inhibitor (H7) before TPA treatment, suggesting that the 190 kDa peptide is phosphorylated BPAII with TPA. Prolonged treatment with TPA abolished both of 180- and 190-kDa BPA II from Triton X-100-soluble fractions. These findings suggest that the BPA II, but not BPA I, is a substrate of protein kinase C, and the generation of 190-kDa-phosphorylated BPA II has a key role in the TPA-induced collapse of the assembly of BPA II on the basal plasma membrane, probably, at hemidesmosomes.

Amino Acids↗
PubMed1994

A novel human homologue of a dead-box RNA helicase family.

Putative cDNA clones for a nuclear antigen that cross-reacts with anti-human aldolase A monoclonal antibody MAb1A2 were isolated from the HeLa lambda gt11 cDNA library and a candidate clone (clone 3) was analyzed. The cDNA has an open reading frame (ORF) of 1,317 bp encoding a novel RNA helicase belonging to the DEAD RNA helicase family. The ORF also contains a nuclear targeting signal and the epitope for MAb1A2. The putative RNA helicase has sequence similarity to Escherichia coli RNA helicase DEAD, mouse translation factor eIF-4A, and human p68 and p54.

Amino Acid Sequence↗
PubMed1994

Interferon-gamma-induced HLA-DR, but not ICAM-1, expression of human keratinocytes is down-regulated by calmodulin antagonist.

Interferon-gamma (IFN-gamma) has been shown to induce or enhance the expression of MHC class II and intercellular adhesion molecule-1 (ICAM-1) in a variety of human and murine cell types, including epidermal keratinocytes (KC). However, the expression of MHC class II and ICAM-1 molecules induced by IFN-gamma is not necessarily coordinated. We investigated the inhibitory effects of the calmodulin antagonist, W-7, and its chlorine deficient inactive analogue, W-5, on the expression of MHC class II (HLA-DR) and ICAM-1 by human KC incubated with IFN-gamma. We found that the IFN-gamma-induced expression of HLA-DR was reproducibly and dose-dependently inhibited by W-7. However, the expression of ICAM-1 was highly resistant to the inhibitory effects of W-7. Neither HLA-DR nor ICAM-1 expression was affected by W-5. These data suggest that the IFN-gamma-induced HLA-DR, but not ICAM-1, expression is mediated, if not exclusively, by calmodulin in human KC.

Calmodulin↗
PubMed1994

Antibody-binding to the 180-kD bullous pemphigoid antigens at the lateral cell surface causes their internalization and inhibits their assembly at the basal cell surface in cultured keratinocytes.

We demonstrated the effects of monoclonal antibodies to the 180-kD and 230-kD BP antigens (BPA) and of BP sera on Ca(++)-induced formation of hemidesmosomes in cultured human keratinocytes (a cell line, DJM-1) by immunofluorescence microscopy. Under low Ca++ (0.07 mM) conditions, the 180-kD and 230-kD BPAs were distributed homogeneously on the basal plasma membrane, while they formed a peculiar concentric ring or arch (ring/arch) arrangement in high-Ca++ (1.87 mM) medium. On the other hand, the apical-lateral cell membrane was stained homogeneously with antibodies to the 180-kD BPA, but not to the 230-kD BPA, both in low and high Ca++ media. The low-high Ca++ switch at first caused disappearance of the antigen from the basal plasma membrane and then formed the high-Ca++ ring/arch pattern within 3 hrs. In this system, monoclonal antibodies to the 180-kD and 230-kD BPAs and the sera from 5 BP patients, 2 pemphigus vulgaris (PV) patients, and 4 normal volunteers were added into the culture media. The addition of anti-180-kD BPA antibodies or any BP serum caused the internalization of the 180-kD BPA from the apical-lateral cell membrane and inhibited the Ca(++)-induced formation of the ring/arch pattern on the basal membrane, possibly by inhibiting the movement of the antigen from the lateral to the basal membrane to form hemidesmosomes.(ABSTRACT TRUNCATED AT 250 WORDS)

Antibodies, Monoclonal↗
PubMed1994

A possible cell-biologic mechanism involved in blister formation of bullous pemphigoid: anti-180-kD BPA antibody is an initiator.

In this short review, we summarize the results of our recent studies on the effects of anti-bullous-pemphigoid antigen (BPA) antibodies and BP sera on the hemidesmosome in cultured keratinocytes (DJM-1 cells) as examined by immunofluorescence microscopy. The 180-kD and the 230-kD BPAs localized on the basal plasma membrane showed a homogeneously dotted pattern in cells grown with low Ca2+ (0.07 mM), while they formed a peculiar concentric ring or arch (ring/arch) pattern in cells grown with high Ca2+ (1.87 mM). In addition, the 180-kD BPA was distributed also on the lateral/apical cell membrane, and the 230-kD BPA was found in the cytoplasm. The high Ca2+ ring/arch arrangement of BPAs was formed within 3 h after the low-high Ca2+ switch. Anti-180-kD BPA monoclonal antibodies (MAbs) and BP sera, but not anti-230-kD BPA MAbs, which were added into this system, caused the internalization of the 180-kD BPA from the lateral/apical cell membrane and inhibited the formation of the ring/arch pattern. These results suggest that autoantibodies to the 180-kD, but not to the 230-kD, BPAs may directly bind to the antigen on the cell surface of the basal cells and disturb the formation of hemidesmosomes. The 180-kD BPA appears to be an initiator of blister formation.

Autoantibodies↗
PubMed1994

Relationship between antigens and IgG subclasses in bullous pemphigoid.

Bullous pemphigoid (BP) is an autoimmune blistering disease characterized in part by the presence of tissue-bound and circulating antibodies (mostly of IgG) to the basement membrane zone (BMZ). We previously reported that IgG subclasses of BP antibodies were IgG1, IgG2 and IgG4, and that only BP IgG1 fixed complements. In this study, we examined whether BP IgG sub-classes bound to the same epitope of BP antigen or a different epitope. In an inhibition immunofluorescence studies, the complement fixing capability of IgG1 was inhibited by the pretreatment with IgG4 and partially inhibited by IgG2. On immunoblot analysis, IgG1 and IgG4 were bound to the same MW of BP antigen. In enzyme-linked immunosorbent assay (ELISA), the binding capability of IgG subclass fractions from patients with BP to synthetic peptide P1-2, exceeding normal IgG subclass fractions was seen in five IgG1, one IgG2 and two IgG4, from eight BP patients. The binding capability of IgG subclass fractions from the patients with BP to P1-1, exceeding the normal IgG fractions was seen in two IgG1, three IgG2 and one IgG4 from ten BP patients. On inhibition ELISA, the binding activity to P1-2 of IgG4 was partially inhibited by the pretreatment of IgG1 and IgG2. These findings suggest that BP IgG1, IgG2 and IgG4 could bind to the same epitope though considerable variation occurred between patients.

Adult↗
PubMed1994

[Glucocorticoids for dermatologic disorders].

It is a characteristic feature in the dermatologic field that topical corticosteroid is one of the most important treatments in addition to systemic corticosteroid therapy. Therefore, physicians who try to treat dermatologic disorders must understand the principles for the choice of therapy and basic methods of topical usage. Basic schedules to use corticosteroids for the treatment of autoimmune bullous diseases, collagen diseases including systemic lupus erythomatodes and related diseases, and vasculitis are described. Practical aspects of topical corticosteroids for various skin disorders are also introduced. Although corticosteroid therapy is the most effective for inflammatory skin diseases, it must be kept in mind that this therapy is only anti-symptomatic and the true cause for the skin disorder must be found.

Administration, Topical↗
PubMed1993

Isozyme-specific modules on human aldolase A molecule. Isozyme group-specific sequences 1 and 4 are required for showing characteristics as aldolase A.

Vertebrate aldolase molecules bear at least four stretches of isozyme group-specific sequences (referred to as IGS). The IGSs of the type A isozyme are known to endow the aldolase molecules with some characteristics typical of A. In order to locate the type A regions, 4 chimeric enzymes were constructed between human aldolases A and B and 5 mutant enzymes with single or double mutations in the IGS-1 region. Among engineered proteins, the chimeric enzymes bearing the type A IGS-1 to -4 (BABA34-108:306-363) and the IGS-1 and -4 (BABA34-55:306-363) exhibited similarities to isozyme A in many respects. On the other hand, neither chimeric enzyme bearing the type A IGS-1 to -3 (BAB34-108) nor that bearing the IGS-1 alone (BAB34-55) exhibited properties as isozyme A. Four mutant aldolases A (carrying single mutation in the IGS-1 region) maintained the original activity as A. Similarly, the BA306 chimera with the type B-->A substitution at positions 41 and 45 (BA306 N41K:R45S) failed to exhibit the A-like properties although the activities toward Fru-1,6-P2 and Fru-1-P significantly increased. Conclusively, the type A IGS-1, together with the IGS-4, act as indispensable modules in determining the characteristic properties of human aldolase A.

Amino Acid Sequence↗
PubMed1993

Atypical exanthema in a patient with infectious mononucleosis.

A 19-year-old male with a sore throat developed numerous, indistinct, erythematous, maculopapular lesions on the trunk. The eruptions, which mimicked secondary syphilis, continued for seven weeks and faded away without pigmentation or scarring. The laboratory examinations revealed lymphocytosis with atypical lymphocytes, seroconversion of Epstein-Barr virus titers, and elevation of transaminase in liver function.

Adult↗
PubMed1993

Localized bullous pemphigoid: report of a case with an immunofluorescence and electron microscopical studies on the lesional distribution of 180-KD bullous pemphigoid antigen, beta 4 integrin, and type VII collagen.

A 67-year-old woman with a left-sided hemiplegia had localized bullous pemphigoid demonstrating typical clinical lesions on the left pretibial skin and the radial-side skin of the right forearm. The histology showed a subepidermal blister with extensive hyperkeratosis, hypergranulosis, and acanthosis. Direct immunofluorescence revealed distinct linear deposits of IgG and C3 at the dermo-epidermal junction in the perilesional skin and in the roof of the blisters, but few deposits in nonlesional skin. Electron microscopy revealed separation in the lamina lucida. Indirect immunofluorescence of type VII collagen showed its localization in the blister floor. The distribution of the 180-KD bullous pemphigoid antigen (BPA) and beta 4 integrin, hemidesmosomal transmembrane proteins, were studied in the lesional skin by indirect immunofluorescence. Both 180-KD BPA and beta 4 integrin were localized in the blister roof. By immunoelectron microscopy, beta 4 integrin was detected in small groups on the cell surface facing the blister cavity. Since the epitope of the monoclonal antibody to 180-KD BPA used here is known to be localized at a distance of 20 to 50 nm from the membrane surface and this epitope retained in the blister roof, it appears that the blister was produced in the deep lamina lucida. The lesions were cleared with topical 0.05% clobetasole propionate ointment.

Aged↗
PubMed1993

Epidermolysis bullosa simplex, Dowling-Meara type. A report of two cases with different types of tonofilament clumping.

Two cases of the Dowling-Meara type of epidermolysis bullosa simplex (EBS) are described. Both had severe blistering at birth, which improved gradually with age. Vesicles and small bullae clustering in a herpetiform fashion were seen in both cases. One showed mild pincer deformity of the nails, and in the other the nail plates were shed after subungual blistering, but regrew without deformity. Histopathology and ultrastructural study showed cytolysis of the basal cells in both cases, but ultrastructurally different forms of tonofilament clumps were present in epidermal keratinocytes. In one case there was typical round clumping of tonofilaments, and in the other a whisk-type clumping of tonofilaments. Cultured keratinocytes from the former produced round clumps of keratin filaments, but those from the latter did not. Review of previous reports of Dowling-Meara EBS revealed that cases could also be divided into two groups in terms of the type of tonofilament clumping at an ultrastructural level. The possibility of subtyping of Dowling-Meara EBS, and possible mechanisms of the blistering in this disease are discussed.

Child↗
PubMed1993

Pustular vasculitis with clinical feature of pustular psoriasis and sternoclavicular hyperostosis.

We report the case of a 51-year-old Japanese man with a unique pustulosis. He had multiple erythematous plaques and numerous pinpoint pustules on the trunk and extremities resembling pustular psoriasis. Histologic features revealed a fully developed intraepidermal abscess filled with neutrophils and disrupted epidermal keratinocytes. Mild leukocytosclastic vasculitis was seen in the underlying dermis. A direct immunofluorescence study revealed IgM, Clq, C3 and fibrinogen deposits in the dermal vessels. The patient had also sternoclavicular hyperostosis. We think that this represents a unique type of pustular vasculitis distinct from pustular psoriasis.

Diagnosis, Differential↗
PubMed1993

Syntheses and biological activities of selenium analogs of alpha-rat atrial natriuretic peptide.

alpha-Rat atrial natriuretic peptide (7--28) (rANP (7--28)) and a series of its analogs in which half cystine residue(s) were substituted with half selenocystine residue(s) were synthesized by using the Fmoc-based solid-phase method followed by cyclization by means of dimethylsulfoxide (DMSO)-trifluoroacetic acid (TFA) oxidation. These analogs possess comparable activities in both receptor binding and cGMP accumulation in rat vascular smooth muscle cells to those of rAMP (7--28).

Amino Acid Sequence↗
PubMed1992

Structural requirements of C-type natriuretic peptide for elevation of cyclic GMP in cultured vascular smooth muscle cells.

C-type natriuretic peptide (CNP), which was recently found to be a selective ligand for one of the two known natriuretic peptide receptor guanylyl cyclases (NPR-B), potently stimulates cGMP production in cultured rat vascular smooth muscle cells (VSMC) and exerts potent antiproliferative effects on the cells. To investigate the structural requirements of CNP for stimulation of cGMP accumulation via NPR-B, we prepared CNP analogs and tested them on cultured rat VSMC. Our results indicate that only the ring portion of CNP with a disulfide bond (CNP(6-22)) participates in stimulation of cGMP accumulation, especially the sequence Leu9-Lys10-Leu11 in the ring portion executes essential roles for both elevation of cGMP and selectivity of the ligand for NPR-B. We also found a good correlation between the activities of the CNP analogs for stimulation of cGMP accumulation and inhibition of DNA synthesis.

Amino Acid Sequence↗