Cephalic tetanus in a nontraumatized patient with left facial palsy.
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Deglutition Disorders↗
Biomedical subjects
S Imamura
Publications and source records attributed to S Imamura.
Age-related alterations in the auditory brainstem responses and the compound action potentials in guinea pigs.
The auditory brainstem response (ABR) and the eight nerve compound action potential (CAP) were measured using click click stimuli to investigate the age-related alteration in the auditory function in 66 guinea pigs consisting of four age groups. With advancing age, a gradual elevation of the thresholds in both the ABR and CAP was clearly seen, together with the prolonged latencies for waves I, II, III, and IV to clicks at 95 dBpeSPL in the ABR. There were some individual differences in either threshold elevation or latency prolongation of both the ABR and CAP in aged guinea pigs. These findings suggest that the effect of individual differences on degenerative aging processes of the auditory system should be considered in selected aged animals, although a significant elevation of the neural auditory threshold is clearly found with advancing age as a whole.
Action Potentials↗
Spontaneous autoimmune skin lesions of MRL/n mice: autoimmune disease-prone genetic background in relation to Fas-defect MRL/1pr mice.
The autoimmune-prone MRL/Mp-lpr/lpr (MRL/lpr) mouse is characterized by the lpr mutation, which is a defect in the Fas antigen. Since Fas mediates apoptosis, this defect results in CD4-CD8- double negative T-cell proliferation, lupus nephritis, and macroscopic lupus erythematosus-like skin lesions. The control counterpart of MRL/lpr mouse is the MRL/Mp-+/+ (MRL/n) mouse, which lacks the lpr mutation and is almost normal during the first 6 mo of life. The lpr mutation, however, accelerates autoimmune phenomena in MRL/lpr mice. Thus, it is important to investigate autoimmune diseases like systemic lupus erythematosis in relation to the autoimmune disease-prone genetic background of MRL/n mice. We found that skin lesions in aged MRL/n mice had unique characteristics. The first characteristic is spontaneous occurrence, and the second is epidermal cell nuclear immunostaining with IgGs by direct immunofluorescence. The skin lesions in aged MRL/n mice showed milder inflammation than in MRL/lpr mice. A homogeneous pattern of epidermal cell nuclear staining was always associated with nuclear staining in kidney cells and also correlated with the in vitro binding of sera to keratinocytes cultured from newborn MRL/n mice. These results suggest that the skin lesions of aged MRL/n mice are a good model for certain types of cutaneous lupus erythematosus and also can provide new insights into the long-standing controversy whether epidermal cell nuclear staining occurs in vivo.
Aging↗
Human cutaneous dendritic cells migrate through dermal lymphatic vessels in a skin organ culture model.
The capacity to migrate from peripheral tissues, where antigen is encountered, to lymphoid organs, where the primary immune response is initiated, is crucial to the immunogenic function of dendritic cells (DC). The skin is a suitable tissue to study migration. DC were observed to gather in distinct nonrandom arrays ("cords") in the dermis upon culture of murine whole skin explants. It is assumed that cords represent lymphatic vessels. Using a similar organ culture model with human split-thickness skin explants, we investigated migration pathways in human skin. We made the following observations. 1) Spontaneous emigration of Langerhans cells took place in skin cultured for 1-3 d. Nonrandom distribution patterns of strongly major histocompatibility complex class II-expressing DC (cords) occurred in cultured dermis. A variable, yet high (>50%) percentage of these DC coexpressed the Birbeck granule-associated antigen "Lag." Ultrastructurally, the cells corresponded to mature DC. 2) Electron microscopy proved that the dermal structures harboring the accumulations of DC (i.e., cords) were typical lymph vessels. Moreover, markers for blood endothelia (monoclonal antibody PAL-E, Factor VIII-related antigen) and markers for cords (strong major histocompatibility complex class II expression on nonrandomly arranged, hairy-appearing cells) were expressed in a mutually exclusive pattern. 3) On epidermal sheets we failed to detect gross changes in the levels of expression of adhesion molecules (CD44, CD54/ ICAM-1, E-cadherin) on keratinocytes in the course of the culture period. The reactivity of a part of the DC in the dermal cords with Birbeck granule-specific monoclonal antibody "Lag" suggests that the migratory population is composed of both epidermal Langerhans cells and dermal DC. We conclude that this organ culture model may prove helpful in resolving pathways and mechanisms of DC migration.
Cell Movement↗
8-hydroxy-2'-deoxyguanosine is increased in epidermal cells of hairless mice after chronic ultraviolet B exposure.
8-Hydroxy-2'-deoxyguanosine (8-OHdG) is a mutation-prone (G:C to T:A transversion) DNA base-modified product generated by reactive oxygen species or photodynamic action. G:C to T:A transversions are observed in the p53 and ras genes of UVB-induced skin cancers of mice and in squamous and basal cell carcinomas of human skin exposed to sunlight. In the current study, 8-OHdG formation was evaluated in the epidermis of hairless mice after repeated exposure to UVB, and possible mechanisms involved were studied. Exposure of hairless mice to either 3.4 [2 minimal erythema dose (MED)] or 16.8 (10 MED) kJ/m2 of UVB three times a week for 2 wk induced a 2.5- or 6.1-fold increase, respectively, in the levels of 8-OHdG in DNA, compared to the unexposed controls. An immunohistochemical method using a monoclonal antibody specific for 8-OHdG showed stronger and more extensive staining in the nuclei of UV-irradiated epidermal cells than in those of nonirradiated cells. Western blots probed with antibodies against 4-hydroxy-2-nonenal-modified proteins confirmed the involvement of reactive oxygen species in the epidermal damage induced by chronic UVB exposure. 3-Nitro-L-tyrosine was detected in western blots in a concentration-dependent manner, suggesting that peroxynitrite derived from the reaction of nitric oxide and superoxide, both of which were probably released from inflammatory cells, was involved in modifying the DNA bases. Therefore, the formation of 8-OHdG after UVB exposure appears to be regulated by at least three pathways: photodynamic action, lipid peroxidation, and inflammation and may play a role in sunlight-induced skin carcinogenesis.
8-Hydroxy-2'-Deoxyguanosine↗
Evaluation of sialyl Lewisx antigen in the skin and the sera of patients with psoriasis vulgaris.
The roles of sialyl-Lewisx antigen were evaluated in the pathogenesis of psoriasis. Sialyl-Lewisx expression was investigated immunohistochemically in the epidermis of normal human skin and erythematous lesional skin of psoriasis vulgaris by avidin-biotin-peroxidase complex procedures. A few sialyl-Lewisx positive dendritic cells were detected in the epidermis of normal human skin. In 7 out of 9 cases of psoriasis vulgaris, the number of sialyl-Lewisx-positive epidermal dendritic cells increased in the erythematous lesion over the adjacent normal skin; there were no marked changes in the numbers of CD1a-positive cells in the epidermis between the two skin types. In the double immunofluorescence studies, more than half of the sialyl-Lewisx-positive epidermal cells in psoriatic erythema were stained with a monoclonal Lag antibody that specifically reacts with Birbeck granules and related structures of human Langerhans cells. Furthermore, we determined the changes in serum levels of sialyl-Lewisx antigens in patients with psoriasis. Although levels in the sera were not significantly elevated over those of controls, the increases correlated with the degree of disease activity. These findings suggest that sialyl-Lewisx antigen is possibly involved in the development of psoriasis.
Biopsy, Needle↗
Psychosomatic aspects of healthy young women with orthostatic dysregulation.
The Japanese Edition of the Cornell Medical Index-Health Questionnaire and the Yatabe-Guilford personality test (Y-G Test) was given to 56 young women (mean age 19.2 years) who were identified as having orthostatic dysregulation among a total of 280 healthy young women. The percentage classed as types III (possible neurotic) and IV (probable neurotic) according to the Health Questionnaire was 37.5% in the 56 with orthostatic dysregulation and 9.2% in the controls (n = 65). The percentage classed as types B and E, suggestive of emotional or psychological disturbance according to the personality test, was 59.0% in those with orthostatic dysregulation and 23.1% in the controls. These differences were statistically significant (P < 0.01). Furthermore, there was a significant correlation (P < 0.01) between the two test results for the frequency distribution of the 280 women. These results suggest a possibility that psychosomatic factors influence the occurrence of orthostatic dysregulation in young women, even if these subjects have not sought treatment for dizziness or vertigo, nor for psychosomatic disorders.
Adult↗
The amino acids of Escherichia coli enterotoxin B subunit involved in binding to Bio-Gel A-5m or to the glycoprotein from mouse intestinal epithelial cells.
We determined whether Arg13, Met31, and Ser95 of the heat-labile enterotoxin B subunit (LT-B) might be involved in Lt-B binding to oligosaccharides, which did not bind to the B subunit of the cholera toxin (CT-B). Three LT-B mutants, R13H, M31L, and S95A were prepared by substituting three amino acid residues that differ in CT-B. These mutants formed a pentamer and exhibited the same binding ability to the GM1 ganglioside as native LT-B. Although these mutants did not bind to Bio-Gel A-5m, they did bind to the glycoprotein from mouse intestinal cells in the order R13H > M31L > S95A. These data suggest that Ser95, Met31, and Arg13 are important for LT-B binding to Bio-Gel A-5m, and that although Ser95 is also partially responsible for LT-B binding to the glycoprotein, Arg13 has no significant involvement in it.
Animals↗
Purification and characterization of a prolidase from Aureobacterium esteraromaticum.
An EDTA-insensitive prolidase (proline dipeptidase, EC 3.4.13.9) was isolated from a cell-free extract of Aureobacterium esteraromaticum IFO 3752. The enzyme was purified almost to homogeneity using acetone precipitation, hydrophobic chromatography, ion-exchange chromatography, and gel-permeation chromatography. The enzyme has a molecular weight of about 440,000 by gel permeation chromatography, and about 40,000 by SDS polyacrylamide gel electrophoresis. The isoelectric point was 4.6. The enzyme hydrolyzed aminoacylprolines such as Ser-Pro. Thr-Pro, Gly-Pro, Ala-Pro, Ile-Pro, Leu-Pro, and Pro-Pro. It also hydrolyzed Gly-Hyp and Pro-Hyp. The rate of hydrolysis for Pro-Hyp was the highest among the substrates tested. Optimum pH for hydrolyzing Pro-Hyp was 9.0 and the enzyme was stable in the pH range from 5 to 10. The optimum temperature was estimated to be 45 degrees C using 10 min of reaction. At least 90% of the initial activity remained after 30 min of incubation at 60 degrees C. p-Chloromercuribenzoic acid and o-phenanthrolin inhibited the enzyme's activity while EDTA did not. Addition of Mn2+ ion did not stimulate activity. These results suggest either that the metal ion in the enzyme may be tightly bound to the polypeptide chain, or that the enzyme is not a metallo-enzyme but a thiol-enzyme.
Amino Acid Sequence↗
Generalized pustular psoriasis in Japan: two distinct groups formed by differences in symptoms and genetic background.
A multi-center study for investigating generalized pustular psoriasis was carried out in Japan in order to clarify the prevalence, the etiology, and the standard therapy. Through questionnaires, 541 cases of patients with generalized pustular psoriasis and related disorders were collected, and the history, the precipitating factors, the symptoms and the laboratory findings were analyzed from medical records. The statistic analysis revealed that 902 (+/- 102.2) patients with generalized pustular psoriasis were expected at the time, and that the prevalence of generalized pustular psoriasis in Japan was 7.46/million. Of 541 patients with generalized pustular psoriasis, 208 cases had the recurrent episodes of symptoms with generalized pustules which had been referred to von Zumbusch type pustular psoriasis or to the acute form of generalized pustular psoriasis. Two hundred and eight patients were further subdivided into two groups: one with a preceding history of ordinary psoriasis (pso+ generalized pustular psoriasis; 65 cases) and another without a psoriasis history (pso- generalized pustular psoriasis; 143 cases). Subdivision into the two groups defined that the onset of pustular outbreak was earlier in the pso- generalized pustular psoriasis group. It was also pointed out that the precipitating factors were different, as the pso- generalized pustular psoriasis group was more frequently affected after infections, and that the pso+ generalized pustular psoriasis group was more frequently affected by preceding corticosterold therapy. HLA analysis of 92 cases with von Zumbusch type generalized pustular psoriasis confirmed that A2, B14, B35 phenotypes were weakly correlated, and when 92 cases were subdivided into the two groups, the pso+ generalized pustular psoriasis group revealed a statistically significant correlation with A1 (p < 0.01), B37 (p < 0.02) and DRw10 (p < 0.05), which was closely related with psoriasis vulgaris patients in Japan. Both clinical surveillance and genetic analysis have disclosed the heterogeneity of von Zumbusch type generalized pustular psoriasis, as there exist two types; one is closely related to psoriasis and the other not.
Adolescent↗
An acquired bullous dermatosis due to an autoimmune reaction against uncein.
A 59-year-old male showed acquired, mechanically induced, scarring blisters on the fingers, toes, scalp and abdomen, as well as in the oral cavity. Ultrastructural and immunohistochemical examination of the bullae revealed junctional epidermal-dermal separation and IgG deposits in the lamina lucida of the basement membrane zone (BMZ), where the reactivity of the 19-DEJ-1 monoclonal antibody was decreased. Anti-BMZ autoantibodies detected in his serum were reactive to the lower lamina lucida region of normal human skin. SDS-PAGE of affinity purified antigens from human keratinocytes with IgG from the patient's serum revealed three polypeptide bands at 165, 135 and 100 kDa, in reduced condition. The indirect immunofluorescence test of his serum was negative on skin cryosections from patients with lethal junctional epidermolysis bullosa. Pretreatment of normal human skin sections with the patient's serum, blocked the binding of 19-DEJ-1 monoclonal antibody but not that of the GB3 monoclonal antibody. This case is considered to be an acquired autoimmune bullous dermatosis due to an autoantibody reaction against uncein (19-DEJ-1 antigen), a component of anchoring filaments.
Antigens↗
Superior cytotoxic potency of mitoxantrone in interaction with DNA: comparison with that of daunorubicin.
The mechanism of action of the anthraquinone antileukemic drug mitoxantrone (MIT) was investigated and compared with that of daunorubicin (DNR) with emphasis on the interaction with DNA to clarify the more potent cytotoxic activity of MIT than DNR in human leukemia cells. MIT showed similar characteristics to those of the anthracyclines such as DNR in that binding of MIT to DNA was associated with reduced template activity and cleavage of DNA in HL-60 human leukemia cells. However, as compared with DNR, MIT showed an increased number of binding sites on DNA, a lower inhibition constant for DNA polymerization, and a greater DNA cleavage activity. These properties may contribute to its greater potency than that of DNR, with which MIT inhibited the proliferation of HL-60 human leukemia cells.
Antineoplastic Agents↗
Expression of four myosin heavy chain genes in developing blood vessels and other smooth muscle organs in rabbits.
At least two smooth muscle myosin heavy chain (MHC) isoforms (SM1, SM2) and two non-muscle MHC isoforms (NMA, NMB) have been detected in smooth muscles. We used the S-1 nuclease mapping procedure to study the expression of these four types of MHC mRNAs in various rabbit blood vessels, such as the aorta (Ao), pulmonary artery (PA), inferior vena cava (IVC) and ductus arteriosus (DA), and in various rabbit tissues and organs. The results demonstrated that in the blood vessels, the four types of MHC mRNA were expressed during all developmental stages in Ao and PA and that SM2 expression appeared to increase dramatically after birth. Compared to the other fetal vessels, the fetal DA contained considerably higher amounts of the four types of MHC mRNAs. SM2 was more prevalent than SM1 in the esophagus, stomach, small intestine and urinary bladder, which are often stretched and show vigorous contractile activity. SM2 expression in a smooth muscle cell appears to correlate well with the contractile ability and/or activity of the cell. Our data show that among the four types of MHC mRNAs, the expression of SM2 MHC mRNA shows great variation among different organs, blood vessel types and stages of development of Ao and PA.
Amino Acid Sequence↗
[Neurophysiological studies of minamata disease with HTLV-I associated myelopathy--a case report].
In both Minamata disease (MD) and HTLV-I associated myelopathy (HAM), sensory disturbance is one of the most characteristic clinical symptoms. We have examined median nerve SSEPs (MN-SEP) and posterior tibial nerve SEPs (PTN-SEP) of both patient groups, and reported their specific abnormalities. MN-SEP of MD patients never showed any conduction delay nor conduction block at the cervical cord. However, they demonstrated the initial positive cortical response with low amplitude instead of the initial negative response (N20) seen in healthy subjects. In PTN-SEP, MD patients showed the initial positive cortical response with significantly shorter latency and lower amplitude than healthy subjects. These findings have never been seen in any other diseases. On the other hand, the conduction delay and conduction block on peripheral nerve, spinal cord and/or intracranial sensory tracts have been demonstrated in many cases with HAM. The patient was a 60-year-old man. About 40 years ago, he suffered with typical clinical symptoms of MD such as cerebellar ataxia, intention tremor and sensory disturbance of upper and lower extremities, and then his condition was complicated with progressive spastic paraplegia and urinary bladder dysfunction since 30 years ago. Both MN-SEP and PTN-SEP were studied so that we could make the electrophysiological differential diagnosis of MD and HAM. His MN-SEP indicated both the conduction delay at his cervical cord and intracranial sensory tract and the initial positive potential from cephalic recording. Furthermore, his PTN-SEP demonstrated severe conduction block at the spinal cord and neither cervical response (N28) nor cortical response (P37) was evoked. In conclusion, the clinical electrophysiologic studies supported our notion that the case might be affected with both MD and HAM.
Electrophysiology↗
Missense mutation of the beta-cardiac myosin heavy-chain gene in hypertrophic cardiomyopathy.
Hypertrophic cardiomyopathy occurs as an autosomal dominant familial disorder or as a sporadic disease without familial involvement. We describe a missense mutation of the beta-cardiac myosin heavy chain (MHC) gene, a G to T transversion (741 Gly-->Trp) identified by direct sequencing of exon 20 in four individuals affected with familial hypertrophic cardiomyopathy. Three individuals with sporadic hypertrophic cardiomyopathy, whose parents are clinically and genetically unaffected, had sequence variations of exon 34 of the alpha-cardiac MHC gene (a C to T transversion, 1658 Asp-->Asp, resulting in FokI site polymorphism), of intron 33 of the alpha-cardiac MHC gene (a G to A and an A to T transversion), and also of intron 14 of the beta-cardiac MHC gene (a C to T transversion in a patient with Noonan syndrome). Including our case, 30 missense mutations of the beta-cardiac MHC gene in 49 families have been reported thus far worldwide. Almost all are located in the region of the gene coding for the globular head of the molecule, and only one mutation was found in both Caucasian and Japanese families. Missense mutations of the beta-cardiac MHC gene in hypertrophic cardiomyopathy may therefore differ according to race.
Adolescent↗
Development of autoreactivity and changes of T cell repertoire in different strains of aging mice.
Physiological changes with increasing age are generally accompanied by disorders of immunity, including autoaggression which can be seen in some syngeneic host-versus-graft reactions provoked when responder and stimulator cells are of different ages. The magnitude of the response, however, varies with the strain of mice. Footpad injection of irradiated spleen cells from 1-year-old, but not from 2-month-old, BALB/c mice (H-2d) into syngeneic young mice evoked popliteal lymph node-swelling, but this was not the case in DBA/2 (H-2d) mice. Therefore, the generation of autoreactivity was thought to be closely related to the change of T cell repertoire with age in the former strain of mice. At around 1 year of age, when only a small reduction in T cell number was observed and when a slight increase in CD8+ T cells in the periphery caused the CD4/CD8 ratio to be lower than in young mice, the proportion of V beta 8+ cells in BALB/c mice started to increase, increasing from 16% in the young to 27% in 2-year-old mice (P < 0.01). On the other hand, V beta 6+ T cells remained at the same level as in young mice throughout life. The increasing fraction of V beta 8+ T cells was characterized by a low density of T cell receptors (TcR) and it was more conspicuous in the spleen than in the peripheral blood in mice more than 1 year of age. A shift to a TcR-low population in V beta 8+, T cells was followed in a few months by a shift in V beta 6+ T cells. Although both the change of T cell repertoire and development of autoaggression may be parameters of aging, no direct correlation was demonstrated between them in experiments with cross-hybrids and recombinant inbred strains of BALB/c and DBA/2 mice. Probably, the two parameters are genetically and independently controlled. All the data taken together indicate that T cells undergo V beta-TcR-restricted changes during their life history, depending on their genetic background.
Aging↗
Epidermal growth factor enhancement of HSC-1 human cutaneous squamous carcinoma cell adhesion and migration on type I collagen involves selective up-regulation of alpha 2 beta 1 integrin expression.
Some human neoplasms show aberrant expression or overexpression of epidermal growth factor (EGF) receptor, and the degree of the receptor expression is correlated with the malignant phenotype in certain epithelial tumors including squamous carcinoma cells. Since phenotypic transformation of cells could involve quantitative and qualitative alteration of integrin function, the effects of EGF on cell-matrix interactions were studied using HSC-1 cells, a human squamous carcinoma cell line showing EGF receptor overexpression. The EGF-treated HSC-1 cells interacted with matrix proteins differently from the untreated cells, as shown by cell adhesion and phagokinetic track assays. Among fibronectin, laminin, fibrinogen, and type I collagen, fibronectin was the most efficient substratum to promote untreated HSC-1 cell adhesion and migration. Pretreatment of the cells with 50 ng/ml EGF for 18 h selectively increased the number of spread cells and the size of the individual cell migration area on type I collagen by 250 and 400%, respectively. The same pretreatment diminished cell adhesion and migration on other substrata so that the EGF treatment converted type I collagen as the most efficient substratum for cell adhesion and migration of the HSC-1 cells. ELISA and immunoprecipitation studies showed that EGF up-regulated the expression of alpha 2 beta 1 integrin collagen receptor in a time- and dose-dependent manner by stimulating biosynthesis of alpha 2 subunit, but did not up-regulate those of the alpha 3 beta 1, alpha 5 beta 1, or alpha v beta 3 integrins. These results suggest that EGF preferentially enhances HSC-1 cell interaction with type I collagen, leading to the enhanced cellular migratory activity on the substratum, as a result of selective up-regulation of alpha 2 beta 1 integrin expression.
Antigens, CD↗
Cell surface proteolysis by serine proteinases enhances RGD-sensitive melanoma cell adhesion on fibrinogen and vitronectin.
Tumor cells avidly secrete various proteinases, and cascades of proteolytic activation occur around the cells. Therefore, cell surface receptors of tumor cells are under the constant influence of proteinases. In this study, the effects of serine proteinases on integrin-medicated cell-matrix interactions were studied in C32TG and Mewo human melanoma cells. These melanoma cells were pretreated with proteinases and their adhesive properties on various substrata were evaluated by cell adhesion assays. Paradoxically, appropriate cell surface proteolysis enhanced the RGD-sensitive cell adhesion on fibrinogen and vitronectin, but not the RGD-insensitive adhesion on type I collagen or laminin. Pretreatment of these cells with 0.1 to 1 microM of trypsin, chymotrypsin, or plasmin for 30 min at 37 degrees C increased the number of spread cells on fibrinogen and vitronectin by 200-300%. The enhancement of cell spreading was not accompanied by up-regulation of the relevant RGD-sensitive integrin expression. Analysis of the cell surface receptor by GRGDSPK-Sepharose affinity chromatography showed that trypsin treatment did not up-regulate alpha v beta 3 integrin, an RGD-sensitive receptor for fibrinogen and vitronectin in the melanoma cells, nor the induced appearance of novel receptors. Treatment of cells with 100 nM proteinases increased cell binding of both monoclonal and polyclonal antibodies against alpha v beta 3 integrin subunits by 70%, but not that of monoclonal antibody against alpha 2, alpha 3, or alpha 6 subunit, indicating that cell surface proteolysis exposed more alpha v beta 3 integrin on the cell surface. These results suggest that exposure of alpha v beta 3 integrin is a part of the mechanisms underlying the serine proteinase-induced enhancement of melanoma cell adhesion on fibrinogen and vitronectin.
Amino Acid Sequence↗