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J Tada

Publications and source records attributed to J Tada.

At least 55 records · Page 3Linked to original sources
PubMed1998

Salivary gland tissue kallikrein family and processing of growth factor precursors and proenzymes.

Four major enzymes of the tissue kallikrein family were purified from the mouse submandibular gland and characterized. The sequences indicated that they were mK1, mK9, mK13, and mK22. All four enzymes showed kinin-releasing activity, with mK1 exhibiting the highest activity. Like mK13, mK9 and mK22 also processed prorenin to give renin and/or arginyl renin, although their activities were less than that of mK13. The results suggest that tissue kallikrein family enzymes bearing higher kinin-releasing activity have lower prorenin-converting activity and vice versa. These enzymes may possibly have a physiological role in the tissue renin-angiotensin system.

Animals↗
PubMed1997

Biofilm formation of Staphylococcus aureus strains isolated from impetigo and furuncle: role of fibrinogen and fibrin.

The formation of membranous structure (thickness from the plastic tissue-culture coverslip (hematoxylin-eosin) > 1 mm; periodic acid-Schiff-positive) was more prominent with Staphylococcus aureus (S. aureus) strains isolated from impetigo (coagulase types I.V origin) than with S. aureus strains isolated from furuncle (coagulase type IV origin) (P < 0.05) in the plastic tissue-culture coverslip in human plasma after 72 h. Attachment of S. aureus cells to a plastic tissue-culture coverslip was more marked in 0-3% fibrinogen/tryptic soy broth (TSB) than in plasma (P < 0.05). The formation of the membranous structure was observed on the plastic tissue-culture coverslip with 0.3% fibrinogen/human serum but not with 0.3% fibrinogen + 5% glucose/TSB. Electron microscopy revealed abundant fibrin around S. aureus cells at 4 h and Ruthenium red-positive materials increased at 24 and 72 h in plasma. Staphylococcus aureus cell attachment to the plastic tissue-culture coverslip in plasma decreased by addition of levofloxacin (LVFX) at 1/2 minimum inhibitory concentration (MIC) and clarithromycin (CAM) at 1/4 MIC. Polysaccharide production of S. aureus cells on the plastic tissue-culture coverslip in plasma decreased with the addition of CAM at 1/4 MIC. Fibrinogen is closely related to initiation of infection but biofilm formation requires the conversion of fibrinogen to fibrin. Thus, attachment of S. aureus cells to the plastic tissue-culture coverslip, conversion of fibrinogen to fibrin by coagulase-prothrombin complex, and production of abundant glycocalyx by S. aureus cells are at least required for the production of biofilm in staphylococcal skin infection.

Anti-Bacterial Agents↗
PubMed1997

Changes in Staphylococcus aureus density and lesion severity after topical application of povidone-iodine in cases of atopic dermatitis.

A case-control study was performed to examine the efficacy of 10% povidone-iodine solution applied to atopic dermatitis patients. The density of Staphylococcus aureus on the eczematous lesions and the lesion severity before and after the topical application of povidone-iodine were compared. We found a 10-100-fold decrease in the density of S. aureus after povidone-iodine treatment in patients colonizing S. aureus at an initial density of > 1000 CFU/10 cm2. Erythema and exudation also decreased after povidone-iodine treatment in patients colonizing S. aureus at an initial density of > 1000 CFU/10 cm2. The 10% povidone-iodine solution disinfected S. aureus cells when added immediately after the cells were mixed in human plasma; however, 10% povidone-iodine solution only reduced the density of S. aureus cells by 10-100-fold when S. aureus cells were harvested after a 24 h incubation in human plasma. Staphylococcus aureus cells harvested after 24 h incubation in human plasma were often surrounded by fibrin bundles and cells circumscribed by fibrin bundles could not be disinfected with 10% povidone-iodine solution. We suggest that S. aureus cells may produce biofilm-like structures in atopic dermatitis patients and that these structures may help S. aureus cells resist the 10% povidone-iodine treatment.

Administration, Topical↗
PubMed1997

Ultrastructural localization of gap junction protein connexin 43 in normal human skin, basal cell carcinoma, and squamous cell carcinoma.

The expression and localization of connexin 43 (Cx43) were investigated in normal human epidermis, pilosebaceous apparatus, basal cell carcinoma, and squamous cell carcinoma by immunofluorescence as well as by immunoelectron microscopy. In the normal epidermis the immunofluorescence was weak in the basal layer, increased in spinous layer and negative in the horny layer. In the sebaceous gland, peripheral lobular cells showed weak cell membrane dotted pattern. Cell membrane and cytoplasmic fluorescence was strong in the central lobular cells. In the lower hair follicle, the cortex, inner and outer root sheath cells showed cell membrane fluorescence. As cortical cells underwent keratinization, they lost Cx43 epitopes. Basal cell carcinoma and squamous cell carcinoma were poorly stained, and eccrine and apocrine glands were unstained. In immunoelectron microscopy, close membrane appositions of typical gap junctions were often observed in the spinous layers of the epidermis and the immunolabeling for Cx43 was seen along the gap junction structures. Circular and long gap junctions often were found in follicular root sheaths and sebaceous glands. Gold particles labeling Cx43 in these gap junctions were found on the gap junctions or localized in the cytoplasm near the gap junction membranes. Basal cell carcinoma and squamous cell carcinoma had a small number of small gap junctions, and gold particles were not only localized to gap junctions but scattered in the cytoplasm. No gap junctions were labeled in eccrine and apocrine glands. These findings confirmed that 1) long, curved or circular membrane appositions found in hair follicle and sebaceous gland are true gap junctions, 2) immature cells such as epidermal basal cells, peripheral germinative cells of sebaceous gland and basal and squamous cell carcinoma cells do not have fully developed gap junctions, and 3) Cx43 or its precursors are present in the cytoplasm as well as on poorly developed gap junctions in these immature cells. Immunofluorescence findings generally corresponded to ultrastructural distribution and structural maturity of gap junctions.

Adult↗
PubMed1997

[All-trans retinoic acid-induced myelomonocytoid differentiation in acute promyelocytic leukemia].

A 30-year-old man with a diagnosis of acute promyelocytic leukemia (APL) was admitted. Laboratory findings were as follows: WBC 32,900/microliter with 88% promyelocytes, Hb 10.4 g/dl, platelets 2.6 x 10(4)/microliter. Coagulation tests revealed DIC. Bone marrow was hypercellular with 91.8% promyelocytes which were strongly positive for peroxidase and positive for alpha-naphthyl butyrate esterase. Cytogenetic study revealed 46, XY, t(15;17) (q22:q11). He was treated with all-trans retinoic acid (ATRA) along with hydroxyurea (HU) and low-molecular weight heparin (LMH). Because his WBC increased to 93,700/microliter on day 6 of ATRA therapy, DCMP chemotherapy was given, while ATRA was withheld. He developed enterocolitis due to myelosuppression. ATRA was restarted along with granulocyte-colony stimulating factor (G-CSF). His WBC rose to 10,400/microliter with a marked, but temporary predominance of myelomonocytes both in peripheral blood and in bone marrow. These myelomonocytoid cells were positive for specific and nonspecific esterase double stainings. Then he entered complete remission. It was of interest that myelomonocytoid differentiation of APL cells was induced by ATRA. The etiology was discussed.

Adult↗
PubMed1997

[Blast crisis accompanied by severe DIC of Ph negative chronic myeloid leukemia showing t(9;16) and positive M-BCR/ABL rearrangement].

A 66-year-old woman complained of chest discomfort in January 1995. In March the accelerated phase of chronic myeloid leukemia (CML) was diagnosed. Chromosomal analysis demonstrated negative Ph and positive t(9;16) (q34;p11) with positive major BCR/ABL chimeric mRNA. Administration of hydroxycarbamide was initiated, but in May she developed high fever and severe left hypochondralgia. Her WBC was 62,100/microliter (blast 64%), and LDH was 3,590 IU/l. Bone marrow examination showed 78.6% blasts, with a nucleated cell count of 74 x 10(3)/microliter. Blasts were negative for esterase stain and partially positive for both peroxidase stain and PAS reaction. Surface marker analysis revealed that blasts were positive for CD13, CD19, CD33, CD34, and HLA-DR. A diagnosis of blast crisis was made and she was treated with the VDS-CP regimen with heparin for DIC. After temporary improvement her disease recurred rapidly with severe DIC. Treatment with low molecular weight heparin and fresh frozen plasma failed to control DIC and she died of subarachnoid hemorrhage on the 48th hospital day. This is the first veprted of case Ph-negative, M-BCR/ABL-positive CML with t(9;16) accompanied by severe DIC.

Aged↗
PubMed1996

Chronic lupoid leishmaniasis. Evaluation by polymerase chain reaction.

BACKGROUND: The cutaneous lesions in chronic lupoid leishmaniasis resemble those of lupus vulgaris, both clinically and histologically. The differential diagnosis is difficult and may depend on the detection of a few Leishmania amastigotes in the histologic sections, the growth of the promastigotes in cultures, or the identification of amastigotes by other techniques. Polymerase chain reaction was used to detect Leishmania amastigote DNA in tissue samples obtained from 65 patients with chronic lupoid leismaniasis, and the results were confirmed by Southern blot analysis. OBSERVATIONS: The histologic findings of a predominantly epithelioid cell granuloma surrounded by lymphocytic infiltrate in chronic lupoid leishmaniasis are very similar to those observed in lupus vulgaris. Extensive histologic examination of the sections in this series revealed occasional macrophages containing a few amastigotes in only 12 cases. Cultures in NNN medium yielded Leishmania promastigotes in 20 cases. Polymerase chain reaction studies using a Leishmania-specific primer identified Leishmania DNA in 30 of 63 cases, and those using a Mycobacterium tuberculosis primer were found to be negative for mycobacteria in 47 cases tested, including 11 cases with a positive tuberculin skin reaction. CONCLUSIONS: The histologic findings in chronic lupoid leishmaniasis resemble those of lupus vulgaris. Polymerase chain reaction studies were useful in identifying amastigotes in 30 (47.6%) of 63 cases. This study confirms the presence of DNA molecules of Leishmania amastigotes in samples of formalin-fixed, paraffin-embedded granulomatous tissue obtained from patients with chronic lupoid leishmaniasis.

Adolescent↗
PubMed1996

Staphylococcus aureus infection on cut wounds in the mouse skin: experimental staphylococcal botryomycosis.

Staphylococcus aureus cells were inoculated on the cut wounds in the skin of cyclophosphamide-treated mice. Biopsy specimens were taken from three mice at 1, 3, 6, 12, 24, 36, 48 and 60 h after the inoculation and were examined by light and electron microscopies. One hour after the inoculation Staphylococcus aureus cells were seen around the cut wound and deeper into the subcutaneous tissue. By 6 h after the inoculation, Staphylococcus aureus cells formed clusters of bacterial colonies. By 36 h after the inoculation inflammatory cells, mainly polymorphonuclear leukocytes and macrophages, were seen around the clusters. Electron microscopic examination revealed fibril-like structures around the Staphylococcus aureus cells at 1 h. The Staphylococcus aureus cells were enclosed in membrane-like structures at 3 h. The membrane-like structures and the fibril-like structures were positive for Ruthenium red. By 12 h after the inoculation, the membrane-like structures increased in thickness and in electron density. Inflammatory cells were seen around but outside of the membrane-like structures at 24, 36 and 48 h. At 60 h the tissues around the membrane-like structures were degenerated and almost necrotic. These results suggest that Staphylococcus aureus cells may form biofilm in dermal or subcutaneous tissues in a neutropenic condition.

Animals↗
PubMed1996

Sudoriferous acrosyringeal acantholytic disease. A subset of Grover's disease.

Three selected cases of transient acantholytic dermatosis were studied because of their definitive correlation with sweating due to fever and/ or bed-ridden situations. Biopsy specimens were serially sectioned and acantholysis was found in the acrosyringium or traced to connect to the acrosyringium in all biopsy specimens. Carcinoembryonic antigen (CEA) and eccrine gland-specific monoclonal antibody, IKH-4, were positive in acantholytic cells. Electron microscopy revealed electron dense material filling the lumen of intraepidermal eccrine ducts. This material leaked into lateral intercellular spaces of the luminal cells, passing tight junctions. Marked edema and numerous lysosomes were reminiscent of those found when eccrine acrosyringium is formed in the embryo; this suggested that an occluded and damaged eccrine intraepidermal duct was being rebuilt via lysosomal digestion.

Acantholysis↗
PubMed1996

Curvicircular intracytoplasmic membranous structures in keratinocytes of pemphigus foliaceus.

We noticed intracytoplasmic membranous, annular, or circular structures in the lesion of pemphigus foliaceus and studied these by regular transmission electron microscopy and immunoelectron microscopy. These curvicircular bodies were observed in the preacantholytic keratinocytes of the blister wall as well as in acantholytic cells in 6 out of 6 patients with pemphigus foliaceus. They were absent in samples from 3 patients with pemphigus vulgaris. These structures were about 60-70 nm wide and consisted of 4 electron-dense layers. They were continuous with intact desmosomal structures and gap junctions in the periphery of the keratinocytes. These curvicircular membranous bodies were well labeled with immunogold particles for desmoglein, plakoglobin, connexin 43, and IgG. In contrast to pemphigus vulgaris, splitting of desmosomes through dissolution of intercellular desmoglea was seldom observed in all 6 specimens of pemphigus foliaceus. These findings suggest that in pemphigus foliaceus 1) curvicircular bodies are derived from internalized desmosomes and gap junctions, and 2) cell-to-cell adhesions are weakened by this internalization and acantholysis is initiated, while in pemphigus vulgaris the dissolution of desmoglea is the initial event. It is suggested that in pemphigus foliaceus the binding of autoantibody induces internalization of many intact desmosomes and gap junctions rather than splitting them.

Fluorescent Antibody Technique↗
PubMed1995

Desmosomal dissolution in Grover's disease, Hailey-Hailey's disease and Darier's disease.

Proteins involved in the formation of desmosomes and simpler adherens junctions were studied in three types of non-immune acantholytic diseases; specifically, four cases of Grover's disease (GD), one case of Hailey-Hailey's disease (HHD) and one case of Darier's disease (DD), and these were compared to two cases of immune-mediated acantholytic disease pemphigus vulgaris (PV). The proteins studied included: 1. The intracellular desmosomal proteins, desmoplakin I and II and plakoglobin; 2. The intercellular desmosomal proteins, desmoglein and CD44; and 3. vinculin, which is a major intracellular protein of the simpler aherens junctions. In GD, HHD and DD, immunostaining showed a loss of desmoplakin I and II and plakoglobin from the desmosomes, and a diffuse staining in the cytoplasm. In contrast, in pemphigus vulgaris, these proteins seemed intact and were localized to dot-like spots on the cell surface. Also, desmoglein, and CD44 were slightly affected in GD, and moderately affected in HHD and DD. Absence of desmosomal attachment plaques, the lack of labeling with desmoglein in the affected desmosomes and a diffusion of the labels into cytoplasm were demonstrated with electron microscopy using an immunogold technique. In PV, desmoglein III is one of the target antigens for the autoantibodies in this disease and was only partially preserved in a small number of lesional cells, while CD44 was mostly preserved. Vinculin was intact in GD, HHD and DD, but was lost in PV. This study, our previous work, and that of others, suggest that: 1. In GD, HHD and DD, the proteins of the desmosomal attachment plaque are primarily affected; 2. In PV, the intercellular glycoproteins are primarily involved; and 3. Simple adherens junctions are intact in GD, HHD and DD, but are damaged in PV.

Acantholysis↗
PubMed1995

[Chromosomes, morphologic subtypes and their prognostic evaluation in acute non-lymphocytic leukemia].

Cytogenetic and morphological analyses were performed on 55 adult patients (34 males, 21 females) with acute non-lymphocytic leukemia (ANLL) diagnosed between 1986 and 1992, and the results were studied with regard to therapeutic response and prognosis. Eleven patients had M1 (20%), 14 had M2 (25.5%), 14 had M3 (25.5%), 7 had M4 (12.7%), 3 had M5 (5.5%), 5 had M6 (9.1%) and one had M7 (1.8%). The overall incidence of chromosomal abnormalities were 65.5% including 10 cases (18.2%) with t (8;21), 12 (21.8%) with t (15;17), 5 (9.1%) with pseudodiploid, 3 (5.5%) with hyperdiploid, 2 (3.6%) with hypodiploid and 4 (7.3%) with abnormalities of 5 or 7 chromosomes. Outcomes were analyzed in 45 patients. 36 patients (80%) achieved complete remission (CR). All 12 patients with M2 entered CR, and they showed a significantly longer median survival than M1. The median survival of 10 patients with t (8;21) was significantly longer than that of patients with t (15;17). However, therapeutic response and prognosis did not correlate with either chromosomal status (NN, AN, or AA) or with age-groups (> or = 60, < 60). These results confirmed that morphological subtypes and certain types of chromosomal abnormality are important variables in determining the prognosis of adult patients with ANLL.

Adolescent↗
PubMed1995

[Association of chronic neutrophilic leukemia and myeloma with fibrillar inclusions in granulocytes].

A 57 year-old-female was incidentally found to have leukocytosis in September 1988. Physical examination revealed anemia and marked hepatosplenomegaly. Her WBC count was 33,400/microliters with 95% mature neutrophils showing toxic granules. Her neutrophil alkaline phosphatase score was 482, and serum VB12 14,600 pg/ml. Serum immunoglobulin concentrations were 582 mg/dl for IgG, 3,628 mg/dl for IgA and 48 mg/dl for IgM. IgA was determined as monoclonal origin of lambda type. Bone marrow aspiration revealed a hypercellular marrow with active granulocytopoiesis and increased plasma cells. Cytogenetic study revealed normal karyotype. The bcr rearrangement was negative for bone marrow cells. An electronmicroscopy demonstrated fibrillar inclusions in granulocytes. We diagnosed this case as a chronic neutrophilic leukemia (CNL) associated with multiple myeloma. She was treated with a course of low dose busulfan without beneficial response. She was admitted for development of huge subcutaneous hematoma of left waist in October 1990. Laboratory findings were: Hb 7.0 g/dl, WBC 55, 300/microliters, Platelets 3.3 x 10(4)/microliters, and IgA 6,607 mg/dl. She required frequent transfusions. She died of pneumonia in July 1991. The peculiar fibrillar inclusions with CNL has not been reported so far. The origin and significance of such structure remains uncertain.

Female↗
PubMed1995

Mapping of the gene for Machado-Joseph disease within a 3.6-cM interval flanked by D14S291/D14S280 and D14S81, on the basis of studies of linkage and linkage disequilibrium in 24 Japanese families.

The gene locus of Machado-Joseph disease (MJD) has recently been mapped within a 29-cM subregion of 14q chromosome. We did a linkage study of 24 multigenerational MJD Japanese pedigrees, in an attempt to narrow the candidate region of this gene. Pairwise and multipoint linkage analysis, together with haplotype segregation analysis, led to the conclusion that the MJD gene is located at the 6.8-cM interval between D14S256 and D14S81 (Zmax = 24.78, multipoint linkage analysis). D14S291 and D14S280, located at the center of this interval, showed no obligate recombination with the MJD gene (Zmax = 5.93 for D14S291 and 9.99 for D14S280). A weak, but significant, linkage disequilibrium of MJD gene was noted with D14S81 (P < .05) but not with D14S291 or D14S280. These results suggest that a 3.6-cM interval flanked by D14S291/D14S280 and D14S81 is the most likely location of the MJD gene and that it is closest to D14S81.

Adult↗
PubMed1994

Staphylococcus aureus infection on experimental croton oil-inflamed skin in mice.

Staphylococcus aureus cells were inoculated on the surface of skin inflamed by application of croton oil in cyclophosphamide-treated mice. Skin specimens were taken at 1, 3, 6, 12, and 24 h inoculation and each specimen was examined by microscopy. The S. aureus cells which attached to the surface of the skin immediately after inoculation had invaded the horny layer within 1 h. The cells gradually penetrated deeper into the epidermis. Electron microscopy revealed fibril-like structures around the S. aureus cells and the cells which adhered to the horny layer and fibrin by means of Ruthenium red-positive, fibril-like structures. A combined application of 0.1% gentamicin ointment, 2% fusidic acid ointment, and clobetasol propionate ointment was more effective in decreasing the number of S. aureus cells in the lesions than was an application of clobetasol propionate ointment alone. However, a combined application of 0.1% gentamicin ointment and 2% fusidic acid ointment without clobetasol propionate ointment showed almost the same efficacy as that with clobetasol propionate ointment. Although povidone iodine killed S. aureus in vitro at a concentration of 0.01% (100 micrograms/ml) in 40 s, its in vivo efficacy was limited.

Animals↗