PubMed Health⌕ Search

Biomedical subjects

K Higuchi

Publications and source records attributed to K Higuchi.

At least 73 records · Page 4Linked to original sources
PubMed1993

Development of congenic strains of mice carrying amyloidogenic apolipoprotein A-II (Apoa2c). Apoa2c reduces the plasma level and the size of high density lipoprotein.

A congenic strain of mice with amyloidogenic apolipoprotein A-II (Apoa2c) on the genetic background of the amyloidosis-resistant SAM-R/1 strain was produced by 12 generations of backcrossing. Genome mapping using endogenous murine leukemia proviral markers was done in the congenic strain, termed R1.P1-Apoa2c. We confirmed that only a small region surrounding the apoA-II gene on chromosome 1 was transferred from the genome of the donor SAM-P/1 strain. The level and particle size of plasma high density lipoprotein were decreased in R1.P1-Apoa2c mice compared to those in the progenitor SAM-R/1 mice. The function of apoA-II can be studied using this strain of mice.

Amyloidosis↗
PubMed1993

Low plasma apolipoprotein AII levels in human and mouse amyloidosis with mutant transthyretin (Met-30) gene.

We measured the serum apolipoprotein levels in patients with familial amyloidotic polyneuropathy (FAP). The serum apolipoprotein AII levels were much lower than those of the control subjects, while the levels in asymptomatic carriers of the FAP gene were normal. Other plasma apolipoprotein levels, such as apolipoproteins AI, B, CII, CIII, and E, were all within normal ranges. The decrease of apolipoprotein AII in the plasma of FAP patients correlated with the progression of the disease. In a transgenic mice model of FAP carrying human variant transthyretin gene (Met-30), serum apolipoprotein AII levels were decreased in 1.5-year-old mice compared with control mice, while the 3-month-old mice had normal levels. These results suggest that apolipoprotein AII may play an important role in lipid metabolism or amyloid formation in patients with FAP.

Adult↗
PubMed1993

Ten-year survey of the intellectual deficits in children with acute lymphoblastic leukemia receiving chemoimmunotherapy.

Effects of chemoimmunotherapy, including cranial irradiation for central nervous system (CNS)-directed therapy, on children with acute lymphoblastic leukemia (ALL) were investigated. Fifty-five children with ALL in continuous complete remission (> 5 yr) and without evidence of current or past CNS diseases were evaluated in this retrospective study. Using standard measures of intelligence (IQ), we repeatedly (1-4 times/person; mean 2.1 times) evaluated IQ in the cohort of patients for the mean follow-up time of 9.7 yr, ranging from 5.4 to 15.8 yr. Fifty-five patients received the total number of 118 IQ testings and 40 patients received them more than twice. Patients were examined periodically at intervals of 1.4 to 10.0 yr (mean 4.8 yr) following diagnosis. Most of the published studies dealt with single IQ testing, and long-term follow-ups were not enough to assess the consequent IQ change. This report confirms and extends the previous findings: decreased IQ was related to age at diagnosis and irradiation (< 5 yr of age at diagnosis), irradiation-examination interval, and female sex. Further long-term follow-up study will be needed in these groups, since their IQs are still on the decline even after 10 yr of diagnosis.

Adolescent↗
PubMed1993

Gastrointestinal AAPOAII and systemic AA-amyloidosis in aged C57BL/Ka mice. Amyloid-type dependent effect of long-term immunosuppressive treatment.

The light microscopic and immunohistochemical features of a novel localized senile amyloidosis in the gastrointestinal tract of C57BL/Ka mice are described. Senile gastrointestinal amyloidosis was predominantly found in the lamina propria of the ileum, cecum and stomach and infrequently in other segments of the gastrointestinal tract. The Congo red affinity of the senile amyloid was sensitive to potassium permanganate pretreatment. The amyloid did not react with anti-AA and anti-immunoglobulin antisera, but stained positively for apoAII, a major apolipoprotein of high density lipoproteins. A similar type of amyloid, termed AApoAII, has recently been described in a systemic form of senile amyloidosis in mice. In the present study, we investigated the effect of long-term immunosuppressive treatment on the incidence of systemic AA-amyloidosis and gastrointestinal AApoAII-amyloidosis in aged C57BL/Ka mice. Gastrointestinal amyloidosis occurred in 60% of the control mice, but significantly less in mice of the immunosuppressed groups. In contrast, systemic AA-immunoreactive amyloidosis was only found in mice that were given immunosuppressive treatment. There was no codeposition of AA and AApoAII-amyloid. These findings indicate that immunosuppressive drugs have a profound effect on the incidence as well as the type of amyloidosis in C57BL/Ka mice.

Aging↗
PubMed1993

Role of leukotrienes in indomethacin-induced mucosal damage in rats.

The role of leukotriene (LT) in the pathogenesis of indomethacin-induced gastric mucosal damage was investigated in rats. After administration of indomethacin, LTB4 and sulfidopeptide LT (SPLT) content in gastric mucosa were assessed by radioimmunoassay and mucosal blood flow was measured by laser-Doppler flowmetry. Indomethacin (20 mg/kg) caused visible gastric mucosal damage. Indomethacin at this dose caused marked reduction of gastric mucosal blood flow but did not affect gastric mucosal content of LTB4 and SPLT. AA-861, a selective 5-lipoxygenase, and DS-4575 and YM-683, two different SPLT receptor antagonists, inhibited both mucosal damage and reduction of mucosal blood flow. These results suggested that endogenous LT, especially SPLT, may be involved in the indomethacin-induced mucosal damage via the reduction of gastric mucosal blood flow.

Animals↗
PubMed1993

Spontaneous amyloidosis in senile NSY mice.

Senile Nagoya, Shibata, Yasuda (NSY) mice developed amyloidosis and died from renal failure as a result of amyloidosis. NSY mice were first reported as experimental congenital diabetic mice by Shibata et al. in 1980. This study questioned whether NSY mice died from diabetic nephropathy. The authors of the present study investigated the life span and cause of death in these mice. The life span of NSY mice was found to be 618.7 +/- 72.5 days. NSY mice that lived for more than 400 days showed rising blood urea nitrogen and large amounts of amyloid deposits in the glomerulus of the kidneys. NSY mice died of renal amyloidosis. Immunological methods revealed that AApoAII was evident in the amyloid deposits of NSY mice. Apart from the kidneys, amyloid deposition was also found in the tongue, esophagus, stomach, small intestine, large intestine, rectum, lung, heart and adrenal glands. Amyloid deposits were found to a slight degree in the liver and the spleen. The most dominant amyloid deposition in NSY mice was seen in the glomerulus of the kidneys. From the point of view of amyloid depositional distribution, NSY mice were unique compared with other spontaneous amyloid mice.

Amyloidosis↗
PubMed1993

[The effect of cefaclor on the nasopharyngeal pathogens in children].

Nasopharyngeal specimens were taken from 29 children with acute otitis media, 14 children with chronic sinusitis at acute exacerbation and 2 children with streptococcal pharyngitis who had received cefaclor for 14 days. The study was designed to compare the microbiologic flora of the nasopharynx before the treatment of these diseases with that after the treatment. In this report the subjects were limited to the children who had not received antibiotics within 1 month. Pathogens detected on initial examination were 49 strains consisting of 40 strains of H. influenzae, 3 strains of S. aureus, 5 strains of S. pyogenes, and 1 strain of S. pneumoniae. Two strains were detected in 4 patients. Pathogens remained after treatment in 29 patient, with an unchanged number of pathogens in 12 patients, a decreased number in 14, and microbial substitution in 3. All of the remaining pathogens were H. influenzae, and minimum inhibitory concentration (MIC) changed in 5 of the 26 patients in whom H. influenzae was detected before and after treatment. In a patients with increased MIC, the strain changed from a sensitive strain with an MIC of lower than 3.13 micrograms/ml to a highly resistant strain with an MIC of 25.0 micrograms/ml or higher. By contrast, in 2 patients with decreased MIC, the strain changed from a highly resistant strain with an MIC of 12.5 micrograms/ml or higher to a sensitive strain with an MIC of lower than 3.13 micrograms/ml. In the other patient, MIC decreased to 3.13 micrograms/ml after it had increased from 3.13 micrograms/ml to 25.0 micrograms/ml.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1993

NC-1300, a proton-pump inhibitor, requires gastric acid to exert cytoprotection in rat gastric mucosa.

Effect of gastric acid suppression on the cytoprotective effect of a single dose of NC-1300 given intragastrically was studied. NC-1300 given intragastrically prevented gastric mucosal damage caused by absolute ethanol in rats in a dose-related manner, while the drug given subcutaneously did not. Pretreatment with NC-1300 given subcutaneously to suppress acid secretion abolished the protective effect of NC-1300 given intragastrically, but not in the presence of 0.1 N HCl. Repeated intragastric administration of NC-1300 for 7 days failed to prevent the ethanol damage. These results suggest that NC-1300 requires gastric acid to exert a protective effect against ethanol in rat gastric mucosa.

2-Pyridinylmethylsulfinylbenzimidazoles↗
PubMed1993

Reduction of increased signal intensity in the basal ganglia on T1-weighted MR images during treatment of hepatic encephalopathy.

A 61-year-old man with liver cirrhosis showed a symmetrical increase in the signal intensity of the basal ganglia on T1-weighted magnetic resonance (MR) images, which was diminished after 3 months of treatment for hepatic encephalopathy. He recovered from encephalopathy with treatment, and liver dysfunction (hyperammonemia and abnormal blood coagulation) as well as the results of quantitative psychometric tests showed a marked improvement. The cause of these high signal intensity changes on T1-weighted images and the reason for their partial reversibility are not known, but hyperammonemia due to portal-systemic shunting might be closely related to these clinical observations.

Ammonia↗
PubMed1993

[Immunohistochemical study of c-erbB-2 proto-oncogene product in prostatic cancer].

The c-erbB-2 proto-oncogene product is expressed in adenocarcinomas of breast cancer and ovarian cancer, and its significance as a prognostic factor has been increasingly noted. We immunohistochemically studied the expression of c-erbB-2 proto-oncogene product using anti-c-erbB-2 gene product polyclonal antibody (Nichirei), which was produced using a synthetic peptide at the C-terminal portion as the immunogen. The subjects consisted of 52 patients with prostatic cancer who were treated at the Department of Urology, Shiga University of Medical Science, from 1982 to 1990. The expression of c-erbB-2 gene was observed in 40 of the 52 patients (76.9%). The positive rate was highest in patients with poorly differentiated cancer and in stage D2 patients, but there were no significant differences in positive rates among patients with different histological types or clinical stages. The probability that progression would occur was significantly (p < 0.05) lower in the group that tested positive for c-erbB-2 than in the group that tested negative among 33 stage D2 patients after 5 years of treatment. When cause specific survival rates were calculated using the Kaplan-Meier method, the group that tested positive had a significantly (p < 0.001) poorer outcome than the group that tested negative after 3 years and 6 months of treatment. The above results suggest that c-erbB-2 expression in prostatic cancer may be useful in predicting the prognosis of the disease.

Adenocarcinoma↗
PubMed1993

The prognostic value of the HNK-1 (Leu-7) antigen in prostatic cancer--an immunohistochemical study.

The anti-HNK-1 (Leu-7) monoclonal antibody (MAb) was revealed to be reactive with noncancerous and cancerous prostatic epithelial cells, although this antibody was originally found to be reactive against natural killer cells. However, the prognostic significance of HNK-1 antigen in prostatic cancer patients remains unknown. The expression of HNK-1 antigen on prostatic cancer was investigated immunohistochemically using the avidin-biotin-peroxidase complex (ABC) method with the anti-HNK-1 monoclonal antibody. Of the 52 patients with prostatic cancer, 49 patients (94%) showed reactivity to anti-HNK-1 MAb and the immunoreaction was associated with the histological differentiation of prostatic cancer. Well differentiated cancer showed the highest percentage of positively stained cancer cells and poorly differentiated cancer showed the lowest percentage. No statistically significant differences existed between groups classified by stage, although the more advanced cancers tended to have weaker reactions. The five-year survival rate and interval free of progression were then studied using the Kaplan-Meier method on 33 patients with stage D2 disease who had received endocrine therapy. The findings indicated that a high survival rate and a longer interval free of progression were associated with a higher fraction of positively stained cancer cells. In conclusion, the expression of HNK-1 antigen on prostatic cancer may be a useful prognostic factor in patients with prostatic cancer.

Adult↗
PubMed1993

Genetic analysis of murine senile amyloidosis.

BACKGROUND: Recent studies have suggested that not only the genotypes of apolipoprotein A-II, the precursor protein of murine senile amyloid fibrils, but also other genetic factors may contribute to the pathogenesis of murine senile amyloidosis. EXPERIMENTAL DESIGN: We investigated the mode of inheritance of murine senile amyloidosis, using 12-month-old and 14-month-old F1, F2 hybrids and backcrosses between SAM-P/1 and SAM-R/1. In SAM-P/1, the senescence process is accelerated and senile amyloidosis is evident, whereas in SAM-R/1, there is a normal aging process and no evidence of senile amyloidosis. In SAM-P/1 and SAM-R/1, the genotypes of apolipoprotein A-II are Gln/Gln and Pro/Pro, respectively, identified by restriction fragment length polymorphism of the apolipoprotein A-II gene for the restriction enzyme Cfr13I. RESULTS: Among hybrids and backcrosses, no senile amyloidosis was observed histopathologically, in Pro/Pro-type strains. Mild senile amyloidosis sparing the liver and spleen was observed in a significant percentage of Pro/Gln-type strains. Practical senile amyloidosis involving the liver and spleen was observed in all of the Gln/Gln-type strains. Quantitative fluorometric analysis with thioflavine T (Naiki H, Higuchi K, Matsushima K, Shimada A, Chen W-H, Hosokawa M, et al. Lab Invest 1990;62:768-73) revealed that the degree of murine senile amyloid fibril deposition was significantly decreased in the Gln/Gln-type hybrid and backcross strains, as compared with findings in SAM-P/1 and the degree of manifestation of accelerated senescence was significantly lower in the Gln/Gln-type hybrid and backcross strains than in the SAM-P/1. CONCLUSIONS: Murine senile amyloidosis is linked to the molecular type of apolipoprotein A-II (i.e., Gln-type apolipoprotein A-II), and is transmitted as an autosomal dominant manner with incomplete penetrance. The severity of murine senile amyloidosis is far more advanced in Gln/Gln-type strains than in Pro/Gln-type strains. Other genetic factors that determine the manifestation of accelerated senescence, may significantly contribute to the degree of murine senile amyloidosis.

Aging↗
PubMed1993

[Dose escalation study of high dose etoposide in autologous hematopoietic stem cell transplantation].

Eight cases with poor prognosis hematological malignancies (non-Hodgkin lymphoma, 6 cases; acute non-lymphocytic leukemia, 2 cases) and nine cases with non-hematological malignancies were treated with high dose etoposide (VP16) containing regimen followed by autologous hemopoietic stem cell transplantation. Results were as follows; 1) all of three chemotherapy sensitive relapse patients with hematological malignancies continue complete remission without any cyto-reductive therapy 2) one of four refractory relapse patients continue remission 3) partial anti-tumor effect was noted in non-hematological malignancies, however, only two cases continue complete remission. Remission duration of other responders was not so long. The results disclosed the dose-limiting factor of high-dose VP16 therapy as reversible stomatitis with no related mortality, and maximal tolerated dose appears to be 60 mg/kg over 72 hr with 45 mg/kg as a safe and recommended therapeutic dose in future clinical trial. The clinical effect of dose escalation was not clearly demonstrated.

Adult↗
PubMed1993

[A case of coronary artery bypass grafting after unsuccessful PTCA in a patient with systemic lupus erythematosis].

For angina of effort in a 69-year-old male patient who had been on steroid for SLE for 7 years we performed PTCA. However, with no dilation obtained we were compelled to perform CABG. The left internal thoracic artery was anastomosed with seg. 12 and the left great saphenous vein was anastomosed sequentially with seg. 14 and seg. 4PL. Through coronary angiography performed at postoperative 2 months, the vein graft was found well patent but in the left internal thoracic artery 90%-stenosis was observed at the anastomosed part, for which PTCA was performed to have it dilated up to 25%. In patho-histological examinations, intimal hypertrophy was observed in both grafts, which seemed to suggest a possible risk factor to determine long-term prognosis. In cases of SLE, the frequency of occurrences of ischemic heart diseases is high, indicating probabilities to be taken up as serious complication from now on. Until now, however, there are few instances reported on performing CABG for patients with SLE. We are reporting here our studies of this particular case of SLE, discussing the involvement of steroids, angitis and lupus anticoagulants as causative factors of ischemic heart diseases and related issues of surgical treatments.

Aged↗
PubMed1992

Production and properties of novel human thyroid cancer specific monoclonal antibodies.

Monoclonal antibodies (TCM-7, -9 and -12) against human thyroid differentiated cancers were established by screening with human thyroid cancers, normal and benign thyroid tissue, and normal human serum protein. A monoclonal antibody (TCM-9) with strong specificity for human thyroid cancer but not for Graves' disease, adenoma or normal thyroid, was shown to recognize a 300 K protein but not to bind to native or mature human thyroglobulin. When TCM-9 was used in immunohistochemical staining tests on more than 30 types of non-thyroid lesions, no reactivity of TCM-9 was observed except with skin immature teratoma, lip squamous carcinoma and stomach adenocarcinoma, which revealed weak reactivities. TCM-9 also showed strong reactivity with two undifferentiated thyroid cancer cell lines and one tissue specimen. Thus TCM-9 is a novel monoclonal antibody against the thyroid cancer.

Adenocarcinoma↗
PubMed1992

Synaptic inhibition of accessory motoneurons evoked by stimulation of the trigeminal nerve in the cat.

Stimulation of the trigeminal nerve produced polysynaptic inhibitory postsynaptic potentials (IPSPs) in accessory motoneurons of the cat. This contrasts with the observation that dorsal cervical motoneurons responded with EPSPs to trigeminal stimulus. Stimulation of the rostral part of spinal trigeminal nucleus elicited di- or polysynaptic IPSPs in accessory motoneurons. Transection of the anterior funiculus at the upper cervical cord selectively abolished the IPSPs. The IPSPs were antagonized by systematically administrated strychnine but not bicuculline.

Accessory Nerve↗