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Biomedical subjects

S Imamura

Publications and source records attributed to S Imamura.

At least 181 records · Page 10Linked to original sources
PubMed1994

Erythema nodosum-like eruption in sarcoidosis.

Two cases of sarcoidosis with tender, erythematous nodules on the legs are reported. The cutaneous lesions were clinically similar to those of erythema nodosum, but histologically showed non-caseating epithelioid granulomas. A review of 14 cases of this particular sarcoid eruption reported in Japan showed that 13 had ocular involvement as in our cases. In the light of the high frequency of ocular involvement, a skin biopsy should be considered in patients presenting with erythema nodosum-like eruptions situated on the legs.

Adult↗
PubMed1994

Susceptibility to UVB light in cultured keratinocytes of cutaneous lupus erythematosus.

In this study, we investigated UVB-light-induced cytotoxicity and the binding of antibodies to extractable nuclear antigens on cultured keratinocytes from patients with cutaneous lupus erythematosus (LE). Keratinocytes from cutaneous LE patients showed a higher susceptibility to single-dose UVB light irradiation compared to keratinocytes from normal controls. The binding of antibodies to U1RNP and Ro/SS-A antigens on cultured keratinocytes was induced by UVB light and more up-regulated when cultured keratinocytes were reacted with autologous sera. Antibody-dependent cellular cytotoxicity (ADCC) was induced when cultured keratinocytes irradiated with UVB light were combined with autologous sera, using peripheral mononuclear cells of normal controls. Immunohistochemical studies of skin biopsy specimens from patients with systemic LE revealed an increased number of epidermal Langerhans cells at the peripheral sites of skin lesions and a relative dominance of infiltrative CD8-positive lymphocytes in the central area of skin lesions. Based on these findings we suggested that ADCC mechanisms were involved in the development of skin lesions, and the distribution of Langerhans cells and infiltrated CD8 cells were responsible for the expansion and persistence of lesions.

Antibody-Dependent Cell Cytotoxicity↗
PubMed1994

Production of monoclonal antibodies against the N-terminal noncollagenous domain of type VII collagen encoded by epidermolysis bullosa acquisita antigen cDNA.

Eleven monoclonal antibodies were produced against the human N-terminal noncollagenous domain of type VII collagen. All antibodies were specifically bound to the epidermal basement membrane zone and did not cross-react with other dermal collagens. A binding of these antibodies was investigated with various species and revealed that the reactivities of each monoclonal antibody against rat, mouse, human and guinea pig skin differ from each other. These data may suggest that type VII collagen is antigenic to immunized small animals, i.e. the rat and mouse, and that there are multiple antigenic determinants on type VII collagen.

Animals↗
PubMed1994

Ultrastructural localization of E-cadherin cell adhesion molecule on the cytoplasmic membrane of keratinocytes in vivo and in vitro.

We examined the ultrastructural localization of E (epithelial)-cadherin cell adhesion molecules by immunoperoxidase electron microscopy on the epithelium of mouse intestine, epidermis of human skin, and cultured human keratinocytes. The in vivo studies demonstrated that E-cadherin was present at the intermediate junction but not at the desmosome of the mouse intestinal single epithelium, and was found on the cytoplasmic membranes of keratinocytes with condensation in the intercellular space of the desmosomes, except for the basal surface of the basal cells. In vitro studies demonstrated that keratinocytes cultured in medium containing a low Ca2+ concentration (0.1 mM) lacked the tight connection through desmosomes, and that E-cadherin showed diffuse distribution and dot-like accumulation around the free surface of the cytoplasmic membrane. In culture medium containing a high concentration of Ca2+ (0.6 mM), keratinocytes formed desmosomal adhesion structures in which E-cadherin was accumulated. The free surface of the keratinocytes in this medium showed weaker distribution and a lesser amount of dot-like accumulation of E-cadherin than that in a low Ca2+ condition. These findings suggest that the distribution pattern of the E-cadherin cell adhesion molecules on the keratinocytes is different from that on the single epithelium of the intestine, and that E-cadherin on the cytoplasmic membrane of the keratinocytes shifts to the desmosomes under physiological conditions, participating in adhesion in association with other desmosomal cadherins.

Cadherins↗
PubMed1994

Postinflammatory bronchiectatic cavity observed by fibreoptic bronchoscopy.

A 55 year old female, complaining of bloody sputum and fever, was referred to our institution. The chest roentgenogram on admission revealed a large thin-walled cavitary shadow in the right upper lobe. We could clearly observe the inner surface of the postinflammatory bronchiectatic cavity in the right B3 bronchus by fibreoptic bronchoscopy. This is the first case in which interesting bronchoscopic findings of a bronchiectatic cavity could be directly observed.

Bronchi↗
PubMed1994

Synergistic interaction between class I antiarrhythmic drugs and halothane in depressant effects on ventricular activation in a canine myocardial infarction model.

Previous studies have showed that halothane has depressed ventricular activation in a canine myocardial infarction model. It is also well known that class I antiarrhythmic drugs depress ventricular activation in the infarcted myocardium. In the present study, we examined whether some electrophysiologic interactions between halothane and two class I antiarrhythmic drugs, lidocaine and procainamide, occur in a canine myocardial infarction model. Halothane, lidocaine and procainamide prolonged the activation time in the infarcted zone, and the combination of halothane and either lidocaine or procainamide markedly prolonged the activation time or blocked the delayed activation in the infarcted zone. Although the mechanism of the interaction is not clear, the present results suggest a synergistic interaction between halothane and class I antiarrhythmic drugs. Therefore, care should be taken that doses of class I antiarrhythmic drugs during halothane anesthesia will not be an overdose.

Animals↗
PubMed1994

Electrophysiologic interaction between class I antiarrhythmic drugs and volatile anesthetics in depressant effects on ventricular activation in a canine myocardial infarction model.

Previous studies showed that volatile anesthetics depressed ventricular delayed activation in a canine myocardial infarction model. It is well known that class I antiarrhythmic drugs depress the ventricular activation in the infarcted myocardium. In the present study, we examined the electrophysiologic interaction between volatile anesthetics (sevoflurane, isoflurane) and class I antiarrhythmic drugs (lidocaine, procainamide) in effects on the ventricular delayed activation in a canine myocardial infarction model. The conduction time of the premature stimulation-induced ventricular excitation was measured in both normal and infarcted zones of the ventricle. An interval from the premature stimulus artifact to the epicardial activation was measured on bipolar electrograms as an index of conduction time, i.e., activation time. In the infarcted zone, the volatile anesthetics and class I antiarrhythmic drugs prolonged the activation time in the infarcted zone, and the combination of the volatile anesthetics and the class I antiarrhythmic drugs markedly prolonged the activation time or blocked the delayed activation. In the normal zone, a similar synergistic interaction was observed, but the effect of these drugs was less compared with that in the infarcted zone. From these results, possible mechanisms to explain the synergistic interaction were discussed.

Anesthetics↗
PubMed1994

[Clinical evaluation of controlled hypotensive anesthesia with MR7S1].

Efficacy, safety and the optimal dose of MR7S1, an injectable preparation of sodium nitroprusside, were studied in 37 patients (ASA class I and II) under nitrous oxide-oxygen-enflurane anesthesia. MR7S1 was administered by intravenous infusion. The dose of MR7S1 was increased gradually starting from 0.25 micrograms.kg-1.min-1 to the dose which could achieve the target value of systolic blood pressure (80-100 mmHg). Thereafter this dose level was maintained. During the period in which the dose was increased, the blood pressure was reduced in proportion to the rate of administration. With the rate of administration of 1.0 to 3.0 micrograms.kg-1.min-1, a significant decrease in systolic blood pressure (SBP) was observed compared with the pretreatment level of SBP. During the maintenance period, the SBP was maintained around 80 to 100 mmHg at a rate of administration of 0.25 to 3.5 micrograms.kg-1.min-1. Two out of 37 patients showed a slight decrease in PaO2, but these values returned to normal without any treatment. These findings suggest that MR7S1 is a useful agent to control blood pressure for the hypotensive anesthesia.

Adult↗
PubMed1994

[A study of the relationship between diabetic neuropathy and diabetic retinopathy].

To evaluate the relationship between diabetic neuropathy and retinopathy, we examined autonomic nervous function, postural hypotension, nerve conduction velocity and coefficient of variation of R-R intervals. Forty-five non-insulin dependent diabetic cases were classified as no diabetic retinopathy (group A), simple diabetic retinopathy (group B) and proliferative diabetic retinopathy (group C). These groups did not differ in age or gender. The rate of postural hypotension (depression of systolic blood pressure over 30 mmHg) was 0% in group A, 7% in group Bs and 53% in group C. Nerve conduction velocity in both motor and sensory nerve was delayed over 20% in 0% of group A, 8% of group B, and 33% of group C. In CVR-R, 11% of group A and 7% of group B were decreased, and 44% (during rest) and 33% (during deep breathing) of group C was decreased. Between groups A and B there was no statistical difference. But group C had statistically significant difference from other groups, particularly in postural hypotension. Peripheral neuropathy might be closely related to diabetic retinopathy.

Adult↗
PubMed1994

Gene alterations and clinical characteristics of xeroderma pigmentosum group A patients in Japan.

BACKGROUND AND DESIGN: The responsible gene for xeroderma pigmentosum group A was recently identified. This study was performed to detect the gene alteration of xeroderma pigmentosum group A complementing gene in 29 xeroderma pigmentosum group A patients in Japan and to analyze whether genetic alterations in the xeroderma pigmentosum group A complementing gene are related to the clinical features. RESULTS: Of 29 patients, 25 (86%) had a mutation at the splicing junction of intron 3 and exon 4 in the homozygous state that was detected by the polymerase chain reaction and the AlwN I-restriction fragment length polymorphism. Patients having a splicing mutation at intron 3 in the homozygous state develop severe skin manifestations from early infancy and severe progressive neurologic abnormalities, including sensorineural hearing impairment, brain atrophy, mental retardation, areflexia, and ataxia. Four patients were heterozygous for splicing mutation in intron 3. Among them, at least three patients showed milder skin symptoms and milder neurologic abnormalities than patients with the homozygous splicing mutation. Two patients (single-ovum twins) revealed a compound heterozygote of splicing mutation of intron 3 and a nonsense mutation of exon 6. One patient had the splicing mutation and another mutation at the last codon of exon 5, a type of mutation that has never been reported. CONCLUSION: These data indicate that different genetic alterations in the xeroderma pigmentosum group A complementing gene may induce different clinical features.

Adolescent↗
PubMed1994

Reactivation of phototoxicity test for psoralens plus ultraviolet A by low-dose methotrexate.

Reactivation of a solar burn has been reported after administration of methotrexate for cancer and psoriasis patients. We report a case of psoriasis with a similar but delayed elicitation of phototoxic reaction by administration of low-dose methotrexate one month after psoralen and long-wave ultraviolet light (PUVA) treatment. The reactivation was seen in an already receding phototoxicity test area but not in a less phototoxic, noninterval PUVA treated area, suggesting that the reactivation by methotrexate is related with the severity of light-induced skin inflammation.

Aged↗
PubMed1993

Cloning and expression of a Pseudomonas 3 alpha-hydroxysteroid dehydrogenase-encoding gene in Escherichia coli.

A bacterial strain, B-0831, which produced 3 alpha-hydroxysteroid dehydrogenase (3 alpha HSD) was isolated and identified as belonging to the genus, Pseudomonas. Molecular weights of the purified 3 alpha HSD, determined by SDS-PAGE and by chromatography on Sephacryl S-200, were about 25 and 50 kDa, respectively. A genomic library of Pseudomonas sp. B-0831, prepared in the plasmid vector pACYC184, was screened with probes based on the amino acid (aa) sequence of the protein to obtain the plasmid, p3 alpha HSD1, identified by hybridization with the probes, that contained a 2.4-kb insert from Pseudomonas DNA. When the 1.4-kb SphI fragment of p3 alpha HSD1 was inserted into the vector, pUC118, and introduced into Escherichia coli DH1 under the control of lacZ promoter in the vector, the transformants produced 200-fold more 3 alpha HSD intracellularly than Pseudomonas sp. B-0831. Sequence analysis of the 3 alpha HSD gene revealed that an ORF encoding 3 alpha HSD consists of 254 aa, with a calculated M(r) of 25,761, suggesting that the enzyme consists of homodimer subunits.

3-Hydroxysteroid Dehydrogenases↗
PubMed1993

Human smooth muscle myosin heavy chain gene mapped to chromosomal region 16q12.

The partial nucleotide sequence encoding the rod portion of the entire amino acid sequence of human smooth muscle myosin heavy chain (MHC) which corresponds to MYH11, according to Human Gene Mapping nomenclature, has been determined by cloning a complementary DNA (cDNA) and sequencing the cDNA (UMYHSM). Northern blot analysis with the UMYHSM fragment (4.3 Kb) showed that the smooth muscle MHC of the human umbilical artery is expressed in the human umbilical artery, bladder, esophagus and trachea. Southern blot analysis of human genomic DNA from human-mouse or human-Chinese hamster somatic cell hybrids demonstrated that the human smooth muscle MHC was mapped to human chromosome 16. Regional mapping of UMYHSM was performed using human cell lines with partial deletion and trisomy of chromosome 16. As a result, the human smooth muscle MHC gene segregated with 16p11-q12. In situ hybridization of biotin-labeled human smooth muscle MHC probe (UMYHSM fragment) to normal human metaphase chromosome independently showed that the human smooth muscle MHC gene (MYH11) is assigned to chromosome region 16q12. Analysis of early metaphase chromosomes showed that hybridization signals were in 16q12.1. In the human, although skeletal, cardiac, smooth muscle, and nonmuscle MHC genes are mapped to chromosomes 17, 14, 16, and 22, respectively, structural similarities of these MHC genes strongly suggest the common origin of these genes.

Amino Acid Sequence↗
PubMed1993

Amino acid sequence of heat-labile enterotoxin from chicken enterotoxigenic Escherichia coli is identical to that of human strain H 10407.

The DNA sequence of heat-labile enterotoxin from the chicken enterotoxigenic Escherichia coli 21d strain was determined by direct dideoxy sequencing of polymerase chain reaction (PCR)-amplified DNA and was compared with those of heat-labile enterotoxins from porcine and human enterotoxigenic E. coli strains EWD 299 and H 10407. The structural genes of the A and B subunits of chicken heat-labile enterotoxin were identical to those of human heat-labile enterotoxin from the human H 10407 strain. Moreover, 67 base pairs of the upstream and 60 base pairs of the downstream region of the chicken heat-labile enterotoxin gene were also identical to that of the human heat-labile enterotoxin from strain H 10407. However, the patterns of plasmids from the 21d and H 10407 strains were different. The 21d strain had no band corresponding to the 42-MDa plasmid of the H 10407 strain encoding the heat-labile enterotoxin gene but it had a smaller plasmid. These data suggest that although the DNA sequence of chicken heat-labile enterotoxin is identical to that of human heat-labile enterotoxin, the plasmid encoding the chicken heat-labile enterotoxin gene in the chicken might be different from that encoding the human heat-labile enterotoxin gene in the H 10407 strain.

Amino Acid Sequence↗
PubMed1993

Pathogenesis of lupus dermatoses in autoimmune mice. XIX. Attempts to induce subepidermal immunoglobulin deposition in MRL/Mp- +/+ mice.

The deposition of immunoglobulin (Ig) at the dermo-epidermal junction (DEJ) of the skin, frequently observed in autoimmune mouse strains, is similar to that seen in patients with systemic lupus erythematosus (SLE). MRL/Mp-lpr/lpr (MRL/lpr) mice have an autosomal recessive mutant gene, lpr, which produces massive T-cell proliferation and accelerates the onset of autoimmune diseases. MRL/Mp- +/+ (MRL/n) mice lack the lpr gene, and do not develop autoimmune disease during the first year after birth under pathogen-free conditions. To verify the mechanisms of subepidermal Ig deposition in the skin of LE, we designed an experiment in which we could induce Ig deposition in the control MRL/n mice. Intraperitoneal injection of lymphoproliferative cells of aged MRL/lpr mice induced splenomegaly and splenic granulomatous angitis in the control MRL/n mice. Lipopolysaccharide (LPS), a polyclonal B-cell activator, induced slight splenomegaly and relatively high levels of serum Ig. Dermatopathological investigation revealed mild lymphocyte infiltration without positive Ig deposition at the DEJ of MRL/n mice treated with proliferative T cells. Injection of both proliferative T cells and LPS induced 50% positivity of subepidermal Ig deposition, and high levels of serum immunoglobulins and anti-double stranded DNA (anti-dsDNA) antibodies. These changes were not observed in MRL/n mice injected with thymocytes of newborn MRL/lpr mice. Skin lesions and lupus nephritis were not demonstrated in any of the mice tested. This study suggest that both the mild inflammatory reaction and the presence of anti-dsDNA antibodies are required for the induction Ig deposition at the DEJ in the skin of LE patients.

Animals↗
PubMed1993

Immunohistochemical localization of lipocortins in normal and psoriatic human skin.

The distribution of lipocortin I, a steroid-induced inhibitory protein of phospholipase A2, was examined in normal and psoriatic human skin. Using immunoblotting analysis with specific antibody against human lipocortin I purified from human placenta, lipocortin I was detected as a 37 kDa protein in cultured epidermal cells, whole skin and epidermis. In the dermis and stratum corneum, lipocortin I was only weakly detectable by Western blotting. In contrast to normal skin, much less lipocortin I was detected by Western blotting analysis in psoriatic skin. Using immunoperoxidase immunohistochemical analysis, lipocortin I was demonstrated in the cytoplasm of keratinocytes in the upper and middle layers of the epidermis and in some infiltrating cells in the dermis in normal skin. In involved psoriatic skin, by contrast, lipocortin I was almost undetectable in the epidermis, although it was demonstrated in some infiltrating cells in the dermis. No immunostaining of lipocortin I was observed in the stratum corneum of normal or psoriatic skin. These results, together with the finding that phospholipase A2 activity is higher in psoriatic epidermis than in normal epidermis, suggest that lipocortin I plays an important role in the regulation of differentiation and proliferation of epidermal keratinocytes.

Annexin A1↗