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Biomedical subjects

J Kojima

Publications and source records attributed to J Kojima.

At least 55 records · Page 3Linked to original sources
PubMed1996

[The relationship between visual agnosia and visual pathway for perception].

We report a patient with a unique visual agnosia, who was thought to have lost visual functions except for the primary visual function. The patient was a 71-year-old woman with progressive memory loss and cerebro-cortical atrophy in MRI; her clinical diagnosis was senile dementia of Alzheimer's type. A battery of tests to detect higher visual dysfunctions was performed. First of all, we presented small dots and lines in front of the patient; the patient was able to recognize them. When a triangle, a tetragon, a cube, pieces of paper of different colors and lines of different length were presented, she was unable to recognize those objects. When pictures of her family members or filled circles of different size including small dots and lines were presented, the patient could only detect those small dots and any of lines; she could not recognize the members of her family. The cerebral blood flow was severely reduced in the occipital lobe except for the striate cortex. These data suggested that the visual function of striate cortex was preserved in this patient; the disturbance of higher visual functions was thought to be caused by the dysfunction of extra striate cortex.

Aged↗
PubMed1996

[How to determine the best combination assay by several tumor markers?].

Combination assay by several tumor markers provides more precise diagnosis of malignancy than using a single tumor marker. The best combination assay by two tumor markers is determined as follows. MINIMIZE RFP (1-SpAorB(CA, CB)) + RFN(1-SnAorB(CA, CB)), where RFP, RFN denote the loss of false positive and false negative, respectively. SpAorB (CA, CB), SnAorB (CA, CB) are specificity and sensitivity of the combination assay by tumor markers A, B with cut-off values CA, CB.

Biomarkers, Tumor↗
PubMed1995

Association between high serum total IgE levels and D11S97 on chromosome 11q13 in Japanese subjects.

The genetic linkage of atopy to chromosome 11q13 through maternally derived alleles has been previously reported. Linkage analysis in Japanese families did not confirm the existence of a major gene for atopy at this locus under the model of autosomal dominant inheritance. However, we observed a significant association between serum total IgE levels and genetic markers at this locus both in 14 Japanese atopic families and in 120 unrelated Japanese subjects. We detected eight alleles at the D11S97 locus and eight alleles in the CA/GT repeat region in the fifth intron of the Fc epsilon RI beta gene. A significantly increased frequency of the D11S97/PstI 0.96 kb allele was observed in the chromosomes of the subjects with high serum total IgE levels both in the family study (p < 0.001) and in the population study (p < 0.05). However, multipoint linkage analysis again did not show any evidence for the existence of a major gene regulating atopy on chromosome 11q13 with location scores to -35 under the model of maternal inheritance. Evidence against linkage was confirmed by the non-parametric linkage analysis, using the affected pedigree member method. Also, there was no substitution of isoleucine for leucine in the fourth transmembrane domain of Fc epsilon RI beta (Leu181), which was reported to be responsible for a subset of atopy in the British population. Therefore, the association of serum total IgE levels with chromosome 11q13 indicates that a gene or genes at this locus may contribute to the expression of high IgE levels in the Japanese population as well as in the British population, but the heterogeneity of the genetic regulation of serum total IgE levels is evident between the two populations.

Adolescent↗
PubMed1995

[Species difference on binding property of dilazep to erythrocytes and platelets].

The whole blood of human, rabbit and dog spiked with dilazep was fractionated by discontinuous density gradients of Ficoll-Paque, and the species difference of distribution to blood components was elucidated. In order to quantitatively evaluate its blood distribution, the binding property of dilazep to the isolated erythrocytes and platelets was also studied. Dilazep undergoes saturable binding to the erythrocytes. Therefore, the fitting of the data sets to binding models was carried out using the nonlinear least-square method, and binding parameters were calculated. This technique could be also applied to analyze directly the binding parameters for several whole blood components. In human and rabbit, dilazep was bound to the erythrocytes with a high affinity (human, KERY = 0.466 nM; rabbit, KERY = 0.0417 nM), however, the affinity to the erythrocytes in dog was very low. On the other hand, the binding affinity to the platelets decreased in the order of rabbit > dog > human.

Animals↗
PubMed1994

[Effects of NIK-247 on the spontaneous EEG of normal and nucleus basalis magnocellularis lesioned rats].

Effects of oral administration of NIK-247 (9-amino-2,3,5,6,7,8-hexahydro-1H-cyclopenta-[b] quinoline monohydrochloride monohydrate) and THA (9-amino-1,2,3,4-tetrahydroacridine hydrochloride hydrate) on the EEG of normal and nucleus basalis magnocellularis (NBM) lesioned rats were examined. NIK-247 at 1 mg/kg and 3 mg/kg did not show any effects on the EEG of normal rats, but NIK-247 at 10 mg/kg significantly lowered the total power of the cortical EEG in normal rats. THA at 3 mg/kg and 10 mg/kg also decreased the total power of cortical EEG in normal rats. In the NBM-lesioned rats, decreases of delta wave activity as well as the total power of cortical EEG were observed with both NIK-247 and THA at 3 mg/kg, respectively. The arousal effects of these two drugs were comparable to the effect of physostigmine, suggesting the central cholinergic effects of both NIK-247 and THA.

Administration, Oral↗
PubMed1994

Effect of NIK-247 on basal concentrations of extracellular acetylcholine in the cerebral cortex of conscious, freely moving rats.

We studied the effect of orally administered NIK-247 (9-amino-2,3,5,6,7,8-hexahydro-1H-cyclopenta[b]quinoline monohydrochloride monohydrate) on basal extracellular acetylcholine (ACh) concentrations in the rat cerebral cortex using microdialysis without the addition of cholinesterase inhibitor to the perfusion fluid and radioimmunoassay for ACh. In addition, the effect of oral administration of NIK-247 on acetylcholinesterase (AChE) activity in rat cerebral cortex was determined. The mean basal ACh content in the perfusate from the cerebral cortex of freely moving rats was 123.2 +/- 21.8 fmol/30 min (n = 7). NIK-247 (2.5-10.0 mg/kg, p.o.) increased the ACh content of the perfusate in a dose-dependent manner. NIK-247 at 10 mg/kg significantly increased the ACh content in the perfusate from 0.5 to 2.5 hr after administration, and the maximum increase was attained at 1 hr after administration. 9-Amino-1,2,3,4-tetrahydroacridine (5 mg/kg, p.o.) and physostigmine (0.5 mg/kg, i.p.) significantly increased the ACh content in the perfusate from 1 to 2 hr and from 0.5 to 1.5 hr after administration, respectively. AChE activities in the cerebral cortex were about 32% and 12% below the control value at 1 hr and 3 hr after administration of NIK-247 at 10 mg/kg, respectively. These findings demonstrate that NIK-247 increases extracellular ACh concentration and inhibits AChE activity in the cerebral cortex after oral administration, and they suggest that NIK-247 facilitates central cholinergic transmission.

Acetylcholine↗
PubMed1994

A patient with chronic hepatitis C who simultaneously developed interstitial pneumonia, hemolytic anemia and cholestatic liver dysfunction after alpha-interferon administration.

Following a three-week administration of alpha-interferon (IFN-alpha), a 62-year-old woman with chronic hepatitis C manifested fever and dyspnea and showed diffuse infiltrative opacities on chest roentgenograms. Her laboratory data included results of anemia with reticulocytosis, a decreased complement level and hepatitis with elevated ALP, LDH and gamma-GTP. Because laboratory data also revealed a positive lymphocyte stimulation test for IFN-alpha, this cytokine was considered to be responsible for the development of interstitial pneumonia, hemolytic anemia and cholestatic liver dysfunction due to its immunomodulatory effects. Although these three disorders have been reported to develop singly after IFN-alpha therapy, this is the first report of a patient in whom these disorders occurred simultaneously.

Anemia, Hemolytic, Autoimmune↗
PubMed1994

[A trial of setting of the reference intervals of thrombin antithrombin III complex and fibrin.fibrinogen degradation products in pregnant women].

Activity of coagulation and fibrinolysis during pregnancy differed greatly from that during a nonpregnant period. We examined the reference intervals by mean +/- 2 standard deviations for thrombin antithrombin III complex (TAT), total FDP (T-FDP), FDP-E, D-dimer before and after delivery. The reference intervals obtained were as follows: TAT (micrograms/l): 1.0-4.8 for 1st trimester, 2.0-10.2 for 2nd trimester, 2.8-14.2 for 3rd trimester, 2.6-16.3 for full term pregnancy, 0-10.5 for post partum. T-FDP (micrograms/ml): 1.5-4.2 for 1st trimester, 1.8-5.6 for 2nd trimester, 1.9-8.5 for 3rd trimester, 2.9-9.7 for full term pregnancy, 2.4-9.0 for post partum. FDP-E(ng/ml): 26.4-98.0 for 1st trimester, 42.4-176.7 for 2nd trimester, 53.1-222.5 for 3rd trimester, 82.4-297.9 for full term pregnancy, 56.9-240.6 for post partum. D-dimer (micrograms/ml): 0.2-2.0 for 1st trimester, 0.6-3.8 for 2nd trimester, 0.6-4.3 for 3rd trimester, 0.7-6.8 for full term pregnancy, 0.6-5.7 for post partum. Further studies are needed to determine the borderline values to determine the clinical abnormality, with a comparison of the reference intervals with the pathologic laboratory data.

Adolescent↗
PubMed1994

[An improved method for determination of C-peptide levels in serum: pretreatment of test samples with anti-insulin antibody insolubilized with magnetic particles].

RIA using anti-C-peptide antibody has been employed for determination of C-peptide in serum. However, the level by this method is a sum of the levels of C-peptide and proinsulin, because anti-C-peptide cross-reacts with proinsulin. This time we developed an improved assay for C-peptide, in which a test sample is pretreated with anti-insulin antibody to eliminate proinsulin in samples before C-peptide assay. The assay procedure is composed of 3 steps; the first is the incubation of test serum with anti-insulin antibody insolubilized with magnetic particles to form a complex of proinsulin-anti-insulin antibody, the 2nd step is the centrifugation of the mixture to eliminate the complex and the last step is the assay for C-peptide by use of RIA kit in the supernatant. The assay is simple, sensitive and reproducible. Serum C-peptide level by this method is not influenced by the presence of proinsulin in test serum, even when as high as 9 ng/ml of proinsulin is contained. This assay revealed that a patient with insulinoma had normal level of serum C-peptide in spite of the extremely high level of proinsulin.

C-Peptide↗
PubMed1993

[Newly developed method by the use of factor Y assay for the detection of the lupus anticoagulant].

A New method for the detection of lupus anticoagulant was developed. Plasma factor V activities using tissue thromboplastin (simplastin auto-SA) and partial thromboplastin (platelin excel LS-LS) were measured simultaneously. Furthermore, the ratio of the two activities was calculated (SA/LS ratio) as a marker of lupus anticoagulant. The normal range of SA/LS ratio was 0.79-1.39 (mean +/- 3SD). The high SA/LS ratios were detected in all of 15 patients with positive lupus anticoagulant, in 3 (5.8%) of 52 SLE patients with normal activated partial thromboplastin time, in 2 (28.7%) of 7 patients with hemophilia, in 1 (33.3%) of 3 patients with factor VIII inhibitor and in 4 (3.3%) of 122 patients with various diseases, respectively. All of 15 patients with liver dysfunction, 54 patients under warfarin treatment and 8 patients under heparin treatment had normal SA/LS ratio.

Factor V↗
PubMed1992

Visual and oculomotor functions of monkey subthalamic nucleus.

1. Single-unit recordings were obtained from the subthalamic nuclei of three monkeys trained to perform a series of visuooculomotor tasks. The monkeys were trained to fixate on a spot of light on the screen (fixation task). When the spot was turned off and a target spot came on, they were required to fixate on the target quickly by making a saccade. Visually guided saccades were elicited when the target came on without a time gap (saccade task). Memory-guided saccades were elicited by delivering a brief cue stimulus while the monkey was fixating; after a delay, the fixation spot was turned off and the monkey made a saccade to the remembered target (delayed saccade task). 2. Of 265 neurons tested, 95 showed spike activity that was related to some aspects of the visuooculomotor tasks, whereas 66 neurons responded to active or passive limb or body movements. The task-related activities were classified into the following categories: eye fixation-related, saccade-related, visual stimulus-related, target- and reward-related, and lever release-related. 3. Activity related to eye fixation (n = 22) consisted of a sustained spike discharge that occurred while the animal was fixating on a target light during the tasks. The activity increased after the animal started fixating on the target and abruptly ceased when the target went off. The activity was unrelated to eye position. It was not elicited during eye fixation outside the tasks. The activity decreased when the target spot was removed. 4. Activity related to saccades (n = 22) consisted of a phasic increase in spike frequency that was time locked with a saccade made during the tasks. The greatest increases occurred predominantly after saccade onset. This activity usually was unrelated to spontaneous saccades made outside the task. The changes in activity typically were optimal in one direction, generally toward the contralateral side. 5. Visual responses (n = 14) consisted of a phasic excitation in response to a visual probe stimulus or target. Response latencies usually were 70-120 ms. The receptive fields generally were centered in the contralateral hemifield, sometimes extending into the ipsilateral field. The receptive fields included the foveal region in seven neurons; most of these neurons responded best to parafoveal stimulation. Peripheral stimuli sometimes suppressed the activity of visually responsive neurons. 6. Activity related to target and reward (n = 29) consisted of sustained spike discharge that occurred only when the monkey could expect a reward by detecting the dimming of the light spot that he was fixating.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1992

[Randomized trial-comparing UFT and FT in the treatment of advanced hepatocellular carcinoma (second report: well controlled study on patients with transcatheter arterial embolization) Osaka Research Society for Liver, Gallbladder and Pancreas].

In a randomized trial Tegafur (FT) or Tegafur.Uracil (UFT) was administrated to 90 patients with advanced hepatocellular carcinoma for whom transcatheter arterial embolization was applied. Efficacy in the reduction of tumor size, subjective symptoms and clinical laboratory findings was comparable in both groups. However, survival rate in the UFT group was significantly higher than in the FT group in only 2 limited subgroups of patients without prior chemotherapy and with tumors found in both lobes of the liver. With respect to adverse effects, complaints about gastrointestinal tract were often noted in the UFT group, but no significant difference was found between the two groups.

Adult↗
PubMed1992

[Evaluation of 99mTc-PMT delayed imaging in diagnosis of hepatocellular carcinoma].

99mTc-PMT delayed imaging was performed on 199 patients with hepatocellular carcinoma (HCC), and 72 patients with various hepatic diseases, from which HCC should be differentiated. Of the 199 patients with HCC, 128 (64.3%) showed positive results on 99mTc-PMT images. Of these 128, 102 (51.3%) showed increased uptake of radioactivity by the hepatic tumor as compared with the surrounding non-tumorous area of the liver, and 26 (13.1%) showed equal uptake. On the contrary, only 2 (9.1%) of the 22 patients with other malignant hepatic tumors (7 with cholangiocellular carcinoma and 15 with metastatic liver tumors) showed equal uptake of 99mTc-PMT. These findings indicated that 99mTc-PMT delayed imaging was useful for increasing the specificity in diagnosis of HCC. Of the patients with HCC showing increased uptake on 99mTc-PMT images taken 5-hour after the injection of the radioisotope, 26.3%, 69.6%, and 96.0% showed intense 99mTc-PMT uptake by hepatic tumor on 1-hour, 2-hour, and 3-hour images, respectively. These findings indicated that in diagnosing HCC, 5-hour image should be taken only in the patients with a hepatic tumor showing no increased uptake of radioactivity even on 3-hour image. Moreover, the rate of HCC to take up 99mTc-PMT intensely was higher in patients with hepatic tumor showing filling defect on colloid liver image than in those showing no filling defect (p less than 0.001). The points in the assessment of radioactivity uptake by hepatic tumor on 99mTc-PMT delayed image were as follows: Overlapping of radioactivity excreted into the gall bladder or intestine with the radioactivity of the liver tumors, radioactivity retention in the non-neoplastic portion of the liver, and the radioactivity of the dilated intrahepatic bile duct were noted in 6 (2.6%), 15 (6.5%) and 9 (3.9%), respectively, among the 230 patients with focal space occupying lesions. Further, a patient of giant nodular regenerative hyperplasia showed increased uptake of 99mTc-PMT consistent with the hepatic lesion.

Carcinoma, Hepatocellular↗
PubMed1992

[A method for determination of proinsulin levels in serum using both insolubilized anti-insulin antibody and anti-C-peptide antibody].

A method is described for determination of proinsulin levels in serum. The principle of the assay is that proinsulin reacts with both anti-insulin and anti-C-peptide antibodies. The assay procedure is as follows; Anti-insulin antibody fixed to bacterial cell wall and insolubilized is incubated with test serum to form a complex of proinsulin-anti-insulin antibody (solid phase), followed by washing twice with buffer to eliminate free C-peptide. Then, glycin-HCl buffer is added to dissociate the bound proinsulin. After centrifugation, the supernatant is neutralized with NaOH and proinsulin in it is measured using RIA kit for CPR assay. The assay is simple, sensitive and reproducible. Neither insulin nor C-peptide contained in test serum influences the proinsulin levels determined by this assay. The mean +/- S.D. of the fasting serum proinsulin levels of healthy donors was 7.0 +/- 2.6 PM/l. A patient with insulinoma showed extremely high serum proinsulin level, which decreased to the normal range after extirpation of insulinoma.

Antibodies↗
PubMed1991

Electrically controlled proliferation of human carcinoma cells cultured on the surface of an electrode.

Human carcinoma cells, MKN45, were cultured on the surface of a metal-coated plastic plate electrode the potential of which was controlled. The proliferation rate and cell morphology were altered depending on the applied potential. Cell proliferation was halted in the potential range above 0.4 V vs. Ag/AgCl, although cells started to proliferate again when the applied potential was shifted from 0.4 V to 0.1 V vs. Ag/AgCl. Fluorescence probe studies indicated that the fluidity of plasma membrane decreased in association with halting of cell proliferation. These results suggest that electrical stimulation causes cells to temporarily halt proliferation, and that cell proliferation was reversibly controlled by electrode potential. The mechanism is interpreted in relation to the change of plasma membrane structure represented by membrane fluidity.

Cell Division↗
PubMed1991

Left ventricular regional relaxation and its nonuniformity in hypertrophic nonobstructive cardiomyopathy.

BACKGROUND: Regional nonuniformity has been suggested to be closely related to left ventricular (LV) relaxation in diseased heart. The purpose of the present study was to assess LV global and regional relaxation in patients with nonobstructive hypertrophic cardiomyopathy (HCM). METHODS AND RESULTS: Left ventriculography was conducted simultaneously with pressure micromanometry in 10 normal control subjects and 11 patients with nonobstructive HCM. LV silhouettes in the right anterior oblique projection were divided into eight regions, and regional wall stress during isovolumic relaxation was computed for six regions from the midventricle to the apex. In HCM patients, isovolumic relaxation time (IRT) and the time constant of LV pressure decrease (Tp) were greater than in control subjects (IRT, 84 +/- 13 versus 66 +/- 6 msec; Tp, 51 +/- 8 versus 36 +/- 5 msec, respectively; p less than 0.01). In HCM patients, the (-)dP/dt upstroke pattern was convex-downward, and dP/dt(20/60), the ratio of dP/dt values 20 and 60 msec after peak (-)dP/dt, was less than in control subjects (1.46 +/- 0.16 versus 2.15 +/- 0.14, p less than 0.01). These findings suggest that there is impaired LV relaxation in HCM patients. End-systolic regional wall stress was lower, and the time constant of regional stress decrease (Tst) was prolonged for each region in HCM patients compared with control subjects. In the HCM group, Tst tended to be more prolonged in regions with increased wall thickness than in regions with normal wall thickness (60 +/- 15 versus 50 +/- 11 msec, p less than 0.01). The coefficient of variation for Tst values in six areas of the left ventricle was calculated in each subject and was greater in HCM patients than in control subjects (13 +/- 7% versus 7 +/- 3%, p less than 0.05), indicating regional nonuniformity in Tst during isovolumic relaxation in HCM patients. CONCLUSIONS: Significant correlations existed between the coefficients of variation for Tst and Tp (r = 0.80, p less than 0.01), IRT (r = 0.79, p less than 0.01), and dP/dt(20/60) (r = -0.67, p less than 0.05) in the HCM group. Thus, regional nonuniformity is closely related to the impairment of LV relaxation in HCM.

Cardiac Catheterization↗
PubMed1991

Study on antithrombogenicity of poly[beta-(acetylsalicylyloxy)ethyl methacrylate] relative to poly(hydroxyethyl methacrylate).

The antithrombogenicity of a polymer made of aspirin bound to hydroxyethyl methacrylate (HEMA), abbreviated as ASA-polymer, was compared with that of poly(hydroxyethyl methacrylate) (PHEMA). Platelet from platelet rich plasma (PRP) incubated with ASA-polymer surface exhibited noticeable decreases in adhesion and aggregation as compared to platelets incubated with PHEMA. Low molecular weight components other than aspirin, which may be released from ASA-polymer during the incubation with PRP, or contact with ASA-polymer causing denaturation of platelets without morphological changes could be responsible for the decrease of adhesion and aggregation. Both PRP and PPP exposed to ASA-polymer-coated surfaces exhibited a much smaller partial thromboplastin time (PTT) than if exposed to PHEMA-coated surfaces; the PTT of ASA-polymer was similar to that of glass exposed plasma. With respect to the in vivo antithrombogenicity, the ASA-polymer surface led to thrombus formation. This may be due to the partial hydrolysis of the acetyl groups resulting in the formation of a negatively charged surface which in turn accelerates the coagulation cascade despite its inhibitory effects on platelet adhesion and aggregation. On the other hand, neointima formed around a thrombus layer on PHEMA-coated sutures after 14 days.

Animals↗