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Biomedical subjects

Y Niimi

Publications and source records attributed to Y Niimi.

15 recordsLinked to original sources
PubMed1992

Prevention of intimal thickening after endothelial removal by a nonpeptide angiotensin II receptor antagonist, losartan.

1. The present experiments were designed to investigate the role of local angiotensin II receptors in the myointimal proliferative response of the vascular wall after endothelial removal, by use of a novel, nonpeptide, angiotensin II receptor antagonist, losartan. 2. When administered 1 week before endothelial removal from the rabbit carotid artery and then continuously until animals were killed 6 weeks later, losartan in a dose of 10 mg kg-1 daily, p.o. had no significant effects on the carotid blood flow (CBF), mean arterial blood pressure (MBP) and heart rate (HR). 3. A full endothelial lining with increased density of regenerated endothelial cells was observed 6 weeks after the endothelial removal. These changes were unaffected by treatment with losartan. 4. Six weeks after endothelial removal, acetylcholine (ACh)- and adenosine diphosphate (ADP)-induced relaxations were greatly reduced though endothelial cells had regenerated. The reduction of the relaxations to these agonists were significantly restored by chronic treatment with losartan. The endothelial-independent, sodium nitroprusside (SNP)-induced relaxation remained unaffected in all groups. 5. There were no differences in the noradrenaline (NA)- and endothelin-1 (ET-1)-induced contractions of the carotid artery strips between vehicle and losartan-treated groups. In contrast, the contractile response of the strips to angiotensin II was significantly decreased in the losartan group, indicating the specific antagonism by chronic losartan against the angiotensin II receptor. 6. Six weeks after endothelial removal, marked myointimal proliferation resulting from new accumulation of proliferating smooth muscle cells and connective tissue was observed in the vehicle group. Losartan treatment greatly suppressed the myointimal proliferative response.7. These results suggest that the local angiotensin II receptors play a role in the myointimal proliferativeresponse of the vascular wall to removal of the endothelium.

Acetylcholine↗
PubMed1992

Identification of cicatricial pemphigoid antigens.

The nature of skin antigens defined by antibodies in patients with cicatricial pemphigoid was studied with use of the 1 mol/L of sodium chloride split skin technique and Western immunoblot analysis. Antibodies in the serum samples of three of seven patients with cicatricial pemphigoid reacted to the epidermal side of 1 mol/L of sodium chloride split skin, and antibodies in the serum sample of one patient reacted to the dermal side. With Western immunoblot analysis, three patients had antibodies to antigens in the epidermal extracts of skin. The antibodies reacted in all patients to a 160-kd antigen and in one patient to an additional 230-kd antigen. These two antigens are similar in molecular weight to the 230-kd major bullous pemphigoid antigen and to the 160-kd minor bullous pemphigoid antigen. However, while the basement membrane zone antibodies present in cicatricial pemphigoid were most often directed to the 160-kd antigen, those present in 38 patients with bullous pemphigoid reacted most often (in 34 patients [89%]) to the 230-kd antigen. None of the serum samples reacted to antigens in dermal extracts that contained the epidermolysis bullosa acquisita antigen. These results indicate that the basement zone membrane antibodies present in cicatricial pemphigoid are directed in part to epidermal antigens that are similar in molecular weight to bullous pemphigoid antigens. However, the frequency of reactions to different basement membrane zone antigens differs in the two diseases, which may account for the clinical differences between the two conditions.

Autoantibodies↗
PubMed1991

Identification of basement membrane zone antigens defined by antibodies that react to both the epidermal and dermal side of 1 M sodium chloride split skin.

Some individuals have basement membrane zone (BMZ) antibodies that react to both the epidermal and dermal side of skin split with 1 M NaCl. To examine the significance of this combined staining pattern, we tested sera from 185 different, sequential, patients with BMZ antibodies for reactivity to normal human skin split with 1 M NaCl. Six sera (3.2%) stained both the epidermal and dermal sides of split skin, 173 (93.5%) stained only the epidermal side, and 6 (3.2%) only the dermal side. All six sera with a combined staining pattern yielded the same pattern when tested with three different specimens of skin, indicating that this pattern is reproducible. By immunoblot analysis, five (83%) of the six combined staining sera reacted to a 160-kD antigen present only in epidermal extracts of normal skin, one reacted in addition to a 230-kD epidermal antigen, and one did not react to either epidermal or dermal extracts. In contrast, five (83%) of the six sera with dermal staining reacted to a 290-kD antigen present only in dermal extracts. Eighteen (90%) of twenty representative epidermal staining sera reacted to a 230-kD epidermal antigen and seven (35%) sera (five with the 230-kD antibody and two without) also reacted to the 160-kD epidermal antigen. Affinity purified antibody to the 160-kD antigen defined by combined staining sera reacted to the BMZ of normal human skin. These results indicate that the combined staining pattern on 1 M NaCl split skin is due to the presence of a distinctive antibody response directed predominantly to a 160-kD BMZ antigen located on the epidermal side of the split skin and to an as yet unidentified BMZ antigen located on the dermal side.

Aged↗
PubMed1990

Epidermolysis bullosa acquisita. Incidence in patients with basement membrane zone antibodies.

We examined the incidence of epidermolysis bullosa acquisita in patients with circulating basement membrane zone antibodies. Serum samples from 100 sequential patients with basement membrane zone antibodies were tested by indirect immunofluorescence against 1 mol/L sodium chloride split skin and by Western immunoblot against epidermal and dermal extracts of skin. Ninety-two (92%) serum samples stained only the epidermal side of split skin, 5 (5%) stained only the dermal side, and 3 (3%) stained both sides. Four of the 5 serum samples with dermal staining but none of the serum samples with epidermal or combined staining reacted with the 290-kd epidermolysis bullosa acquisita antigen by Western immunoblot. These results indicate that approximately 5% of unselected patients with basement membrane zone antibodies have epidermolysis bullosa acquisita or bullous lupus erythematosus rather than bullous pemphigoid.

Adolescent↗
PubMed1990

Molecular identification of major and minor bullous pemphigoid antigens.

The skin antigens defined by basement membrane zone antibodies in 38 patients with bullous pemphigoid were analyzed by Western immunoblot. Thirty-four patients (89%) had antibodies to a major bullous pemphigoid antigen with a molecular weight of approximately 230 kD. Twelve patients (32%) had antibodies to a minor bullous pemphigoid antigen with a molecular weight of approximately 160 kD; this included four patients who did not have antibodies to the 230 kD antigen. Depending on the epidermal extract used, a variable number of patients (up to 75%) also had antibodies to minor bullous pemphigoid antigens with molecular weights of approximately 180 and 200 kD. The results of this study confirm that bullous pemphigoid antigens are heterogeneous at the molecular level. Approximately 10% of patients have antibodies directed solely to a minor bullous pemphigoid antigen.

Antigens↗
PubMed1990

Symptoms and their pattern of progression in childhood moyamoya disease.

In the series of 81 childhood moyamoya patients, the common pattern of clinical progression seen in 77 patients was revealed to be no more than four. The characteristics of each type of clinical progression were presented for a better understanding of the disease and for an initiation of early treatment of this rather rare and insidiously progressive disease. Type I (21 cases) and type II (15 cases) are cases without infarction, even in those types there are cases with poor IQ. Type III (17 cases) and type IV (24 cases) are cases with infarction and an early operation is mandatory. Types I and II are also good candidates for early operation, for IQ deterioration insidiously progress in these types and there is no way of knowing them from type III before infarctions occur. We now have effective surgical measures to improve the ischemic conditions of this disease.

Age Factors↗
PubMed1990

Identification of a 160-kD molecule as a component of the basement membrane zone and as a minor bullous pemphigoid antigen.

The antigens in normal human skin defined by antibodies in patients with bullous pemphigoid (BP) were studied by Western immunoblots. Eighteen (90%) of 20 BP sera reacted to a 230-kD antigen. Seven (35%) of the sera reacted to a 160-kD antigen. Two of these reacted only to the 160-kD antigen and five also reacted to the 230-kD antigen. Antibodies to the 160-kD antigen were not present in 25 control sera obtained from normal individuals or patients with other bullous diseases. The 160-kD antigen was present in epidermal extracts of four different specimens of normal human skin but not in dermal extracts or extracts of control cells including melanoma, fibroblasts, lung carcinoma, and colon carcinoma. Monospecific sera with antibodies to either the 230-kD or to the 160-kD antigen reacted solely to their respective target antigens, but not to both, in extracts of epidermis that contained both antigens. The 160-kD antigen broke down to a 140-kD fragment, while the 230-kD antigen was unchanged in the absence of protease inhibitors. Western blot affinity purified antibody to the 160-kD antigen bound only to the basement membrane zone on the epidermal side of 1M NaCl split skin. These results indicate that a 160-kD antigen is a normal component of the basement membrane zone of human skin. The antigen is located on the epidermal side of skin split with 1M NaCl. It is a minor BP antigen, antibodies to which are present in some patients with BP.

Antibodies↗
PubMed1989

[Case-control study of moyamoya disease].

The cause of Moyamoya disease is still unknown. We made a research about the factors closely related to Moyamoya disease through a case-control study. The number of cases studied was 66. Controls were selected from among patients' friends, matched as to sex, age and residential area. Questionnaires were sent to the cases and the respective controls by mail. The questions were about past history, developmental history, school records, habitual factors, dietary habits and pets. The first symptoms and age at onset were also surveyed in the cases. The response rate was 84.8% (56 cases) of the cases and 76.5% (101 cases) out of the 132 controls. There was no significant difference in the prevalence of tonsillitis, conjunctivitis, otitis media, and bronchitis. Odds ratio of fever of unknown origin is 2.793 and X2 is 7.213. Diseases whose odds ratio was over 1 were herpes, appendicitis, bronchitis, asthma, anemia, dental caries, head injury and drug allergy. But all of them were not significantly prevalent. Odds ratios of school records were 4-9 and X2 were 4-17 from elementary to junior high school. Odds ratio of western dishes was 2.709 and X2 was 5.189. There was no significant difference as to pets kept. We could not find overt relationships between Moyamoya disease and diseases of head and neck like tonsillitis.

Adolescent↗
PubMed1979

Twenty-four-hour secretory patterns of growth hormone, prolactin, and cortisol in narcolepsy.

Twenth-four-hour patterns of plasma GH, PRL, and cortisol concentrations concomitant with sleep stages were studied in four male patients with typical narcolepsy, aged 30--34 yr, and four normal subjects. All medications were withdrawn 2 weeks before the study. Blood was drawn every 20 min during a 24-h fasting period, except for the first sleep cycle of nocturnal sleep when samples were drawn at 5-min intevals. In all of the narcoleptics, a plasma GH peak associated with slow wave sleep at the nocturnal sleep onset was absent (n = 2) or markedly decreased (n = 2). The normal rise of PRL during sleep was present only in a narcoleptic, whereas a significant fall in plasma PRL concentrations occurred immediately after the sleep-onset rapid eye movement period and lasted 1--1.5 h in the remaining three patients. A sleep-onset rapid eye movement period occurred in all of the patients, and this abnormal phenomenon characteristic of narcolepsy was considered to be related to the suppression of GH release at the sleep onset and to the decrease of plasma PRL levels during the early part of sleep. In contrast, the normal circadian periodicity of cortisol secretion was evident in all of the narcoleptics.

Adult↗