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Biomedical subjects

N Handa

Publications and source records attributed to N Handa.

At least 91 records · Page 5Linked to original sources
PubMed1992

Elevation of 4 beta-galactosyltransferase activity for paragloboside synthesis in sera of patients with cancer.

Galactosyltransferase activities in sera of cancer patients were determined by assaying the formation of paragloboside from UDP-galactose and lactotriaosylceramide immobilized on microtiter plates by means of the enzyme-linked immunosorbent assay using a monoclonal antibody, H-11, directed to paragloboside. Enzyme properties were as follows. Optimum pH was 6.8 in cacodylate buffer, and Km values were 2 microM for lactotriaosylceramide and 29 microM for UDP-galactose. The enzyme activity was inhibited by the addition of alpha-lactalbumin. Glucose (20 mM) inhibited the enzyme activity in the presence of alpha-lactalbumin (0.1 mg/ml) but not in its absence. These enzyme properties are similar to those of bovine milk galactosyltransferase, indicating that the enzyme in the sera might be lactose synthetase. The enzyme activities in sera from patients with cancer, patients with benign disease, or a reference sample group were assayed. The activity was below the limit of detection (5.5 pmol/25 microliters serum/2 h) in the reference sample group. Remarkable elevations of the enzyme activity were observed with high incidence in patients with cancer, especially those with blood cancer (100%). A high incidence was observed in the progressive stage, and the enzyme activity was detected at stage 1 in lung, esophagus, stomach, colorectal, and testis cancer. The enzyme activity in sera from patients with benign disease was elevated in 22% of the patients. After effective therapies, the enzyme activity decreased to below the limit of detection. Release of the galactosyltransferase into culture medium of cancer cells could be demonstrated. These observations suggest that the galactosyltransferase is released from cancer tissue into the circulation. The present method for the assay of galactosyltransferase may be useful for the detection of patients with cancer and for monitoring neoplastic recurrence after therapy.

Antibodies, Monoclonal↗
PubMed1992

The characteristics of blood-brain barrier in three different conditions--infarction, selective neuronal death and selective loss of presynaptic terminals--following cerebral ischemia.

We investigated the extravasation of serum albumin using immunohistochemistry in three different conditions, i.e., infarction, selective neuronal death and selective loss of presynaptic terminals following cerebral ischemia in gerbils. In selective neuronal death, which is typically found in the CA1 neurons of the hippocampus after 5-min bilateral cerebral ischemia, selective damage of postsynaptic components with intact presynaptic sites was demonstrated by immunohistochemical examination for microtubule-associated protein 2 and synapsin I, and albumin extravasation did not become apparent before postsynaptic structures were destroyed. In cerebral infarction, which was consistently observed in the thalamus after 15-min forebrain ischemia, massive albumin extravasation was visible early after ischemia due probably to the ischemic endothelial necrosis. In selective loss of presynaptic terminals, which was detected at the molecular layer of the dentate gyrus in the contralateral, nonischemic hippocampus after unilateral cerebral ischemia, immunoreaction for albumin was not visualized. Since endothelium and glial cells were intact in morphological aspects in selective damage of both pre- and postsynaptic sites, it was thought that extravasation was facilitated by the stimulation of endothelial cells and glial cells with unknown factors that were induced by the destruction of post- but not presynaptic elements.

Albumins↗
PubMed1992

Recombinant human superoxide dismutase can attenuate ischemic neuronal damage in gerbils.

The effects of recombinant human superoxide dismutase (r-hSOD) on ischemic neuronal injury were examined. Cerebral ischemia was produced in Mongolian gerbils by occluding bilateral common carotid arteries for 5 min. Preischemic treatment with r-hSOD clearly reduced hippocampal neuronal damages while postischemic treatment did not. This result suggests that oxygen free radicals play an important role in selective vulnerability to ischemia and r-hSOD has a potential clinical usefulness against cerebral ischemia.

Analysis of Variance↗
PubMed1992

The synapsin I brain distribution in ischemia.

We examined the distribution of synapsin I in the gerbil brain and investigated ischemic damage of presynaptic terminals immunohistochemically by using this protein as a marker protein of synaptic vesicles. The reaction for synapsin I in normal gerbil brain is exclusively localized in the neuropil, and other brain structures such as neuronal soma, dendrites, axon bundles, glia and endothelial cells exhibited little immunoreactivity. In a reproducible gerbil model of unilateral cerebral ischemia, ischemic loss of synapsin I immunoreactivity in the affected hemisphere was confined to the area exhibiting overt infarction, where the breakdown of this protein was also confirmed by the immunoblot analysis, and noted much later than that of microtubule-associated protein 2 immunoreactivity, which was demonstrated in neuronal soma and dendrites. In the non-affected hemisphere, selective damage of presynaptic terminals due to Wallerian degeneration and subsequently occurring resynaptogenesis at the molecular layer of the dentate gyrus were clearly demonstrated as a loss and recovery of immunoreaction for synapsin I, respectively. In a gerbil model of bilateral cerebral ischemia, immunoreaction for synapsin I was persistently preserved after seven days to two months recirculation following a brief period of global forebrain ischemia in the CA1 region of the hippocampus, where delayed neuronal death was consistently observed.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1992

Right-sided diaphragmatic hernia following group B streptococcal pneumonia and sepsis.

A case of right-sided diaphragmatic hernia following group B streptococcal pneumonia and sepsis is reported herein. The clinical course was characteristic. The position of the right hemidiaphragm was initially normal. After an antecedent group B streptococcal infection, an abnormal shadow indicating either pneumonia or a pleural effusion on the chest x-ray was recognized and an elevation of the bowel and liver into the right hemithorax gradually appeared. Repair of the hernia was indicated and the postoperative result was excellent. The relationship between a delayed-onset diaphragmatic hernia and a group B streptococcal infection is still unknown. Increased intrathoracic pressure caused by mechanical ventilation coupled with an abnormal lung compliance due to inflammation may have resulted in the delayed herniation. Among various methods for diagnosis applied, chest x-ray and ultrasonography were noninvasive and useful.

Hernia, Diaphragmatic↗
PubMed1992

Silent cerebral infarction as a form of hypertensive target organ damage in the brain.

The incidence, number, size, and location of silent cerebral infarction on 0.1 T magnetic resonance imaging was investigated in 66 hypertensive patients (63 +/- 9 years old; mean +/- SD) and 42 age-matched normotensive subjects (61 +/- 9 years old) to determine the clinical significance of hypertension in silent cerebral infarction. Cerebrovascular risk factors and the severity of hypertensive changes in other major target organs were also investigated. The incidence of silent infarction in hypertensive patients (47%) tended to be higher than that of normotensive subjects (33%) and increased significantly with advancing age. In hypertensive patients, a significantly higher incidence of silent lesions was noted in patients with hypertensive changes in major target organs (72-73% in patients with organ involvement versus 33-39% in those without). The average number of lesions in hypertensive patients was significantly higher than that in normotensive subjects (6.0 versus 2.1), and the lesions in the hypertensive patients were more frequently detected in the brain areas supplied by perforating arteries than those in normotensive subjects (47% versus 24%). These results clearly demonstrate that silent cerebral infarction is frequently seen in older hypertensive patients, especially when moderate hypertensive changes are noted in major target organs, and suggest that hypertensive arterial changes play a crucial role in the occurrence of silent infarction.

Aged↗
PubMed1992

Prevalence of carotid atherosclerosis in diabetic patients. Ultrasound high-resolution B-mode imaging on carotid arteries.

OBJECTIVE: To quantitatively assess atherosclerosis of the carotid artery in subjects with and without diabetes. RESEARCH DESIGN AND METHODS: Ultrasound high resolution B-mode imaging of carotid arteries was conducted on 71 nondiabetic subjects without hyperlipidemia or hypertension and 295 diabetic patients to determine IMT of the arterial wall. RESULTS: IMT was linearly related with age in nondiabetic (IMT = [0.0087 x age] + 0.3318) and diabetic subjects (IMT = [0.0155 x age] + 0.32450). The regression coefficient for age was significantly greater in diabetic than nondiabetic subjects. IMT (mean +/- SD) of diabetic subjects aged 20-29 was significantly greater than that of nondiabetic subjects aged 20-29 (0.73 +/- 0.27 vs. 0.52 +/- 0.07 mm, P less than 0.01). Multivariate regression analysis of 275 NIDDM patients indicated smoking, hyperlipidemia, duration of diabetes, hypertension, and age were factors determining thickness of the carotid arterial wall. CONCLUSIONS: Diabetes, along with age, hyperlipidemia, smoking, and hypertension, aggravates carotid atherosclerosis.

Arteriosclerosis↗
PubMed1992

[An ultrasonic study of the relationship between extracranial carotid atherosclerosis and ischemic cerebrovascular disease in Japanese].

The study is to evaluate the relationship between extracranial carotid atherosclerosis and ischemic cerebrovascular disease using noninvasive B-mode ultrasonography and X-ray computed tomography. The sensitivity of bruits for diagnosing severe carotid stenosis was also evaluated. A total of 229 consecutive Japanese patients were recruited for this study, of which 97 had chronic-stage ischemic cerebrovascular disease and remaining 132 patients had at least one risk factor for atherosclerosis. Carotid atherosclerosis was evaluated by B-mode ultrasonography. Ischemic cerebrovascular disease was assessed by history taking, neurological findings and X-ray CT examination. The severity of carotid atherosclerosis was assessed by using two indices; plaque score and maximum percentage diameter stenosis. We also evaluated whether it was ulcerated plaque or not. Plaque score was computed by summing up all carotid plaque thicknesses (mm) on both sides. According to the CT findings, cerebral infarction was divided into two types; deep subcortical infarction and cortical infarction. The incidence of cerebral infarction increased in relation to plaque score and maximum percentage stenosis. Although the incidence of cerebral infarction in patients without carotid atherosclerosis was only 33% (38/116), it in patients with moderate carotid atherosclerosis (plaque score > 5) was 59% (26/44) (p < 0.05, chi-square test). The incidence of ipsilateral infarction was revealed to be higher in patients with severe (50% or more) carotid stenosis (61%) than in cases of mild stenosis (28%) (p < 0.05). Thirteen patients had ulcerated plaques and they suffered more frequently cerebral infarction than patients without ulcerated lesions. Cortical infarction was more frequent in patients with severe carotid stenosis than in patients without carotid atherosclerosis.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1992

[Estimation of peripheral metabolism under cardiopulmonary bypass by measuring ketone bodies, lactate, and pyruvate].

Both ketone body ratio (KBR) and pyruvate/lactate ratio (P/L) are metabolic indicators related to NAD-linked dehydrogenase system according to the REDOX THEORY. In order to estimate the peripheral metabolic state under the cardiopulmonary bypass (CPB) which is considered to be a moderate and controllable shock state, we measured the pyruvate (P), lactate (L) and ketone bodies (acetoacetate [ACA], 3-hydroxybutyrate[HOB]) pre, during, and post-CPB in 20 open heart surgical patients (Group 1). We also measured ketone bodies in another group (Group 2: 22 patients) of elective coronary artery bypass surgery (CABG). Five patients in Group 2 who developed postoperative organ failure (Group 2-A) were compared with the other 17 cases with uneventful postoperative course (Group 2-B). In Group 1, P and L concentrations progressively increased until the end of CPB, thereafter decreased (P less than 0.001). HOB and TKB significantly increased immediately after the start of CPB, afterward which declined during CPB and returned to the control level after CPB. Both KBR and P/L regression analysis reveal the significant correlation between P/L and KBR (r = 0.51, P less than 0.001). KBR at 1 hour after CPB returned to the control level, however, P/L at 1 hour after CPB still stayed in the significant lower level than the control (P less than 0.001). KBR at the aortic declamping in group 2-A was significantly lower than that in group 2-B. In conclusion, P/L and KBR changed in relation to hemodynamic change during CPB.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1991

'Ischemic tolerance' phenomenon detected in various brain regions.

We investigated the effects of mild and non-lethal ischemic insult on neuronal death following subsequent lethal ischemic stress in various brain regions, using a gerbil model of bilateral cerebral ischemia. Single 10-min ischemia consistently caused neuronal damage in the hippocampal CA1, CA2, CA3 and CA4, layer III/IV of the cerebral cortex, dorsolateral part of the caudoputamen and ventrolateral part of the thalamus. On the other hand, in double ischemia groups, 2-min ischemic insult 2 days before 10-min ischemia exhibited significant protection in the CA1 and CA3 of the hippocampus, the cerebral cortex, the caudoputamen and the thalamus. Five-min ischemic insult 2 days before 10-min ischemia also showed protective effect in the same areas as those of 2-min ischemia except for the CA1 region of the hippocampus, while 1-min ischemic insult exhibited no protective effect in any brain regions. In the immunoblot analysis, both 2- and 5-min ischemia caused increased synthesis of heat shock protein 72 (HSP 72) in the hippocampus, but 1-min ischemia did not. The present study demonstrated that the 'ischemic tolerance' phenomenon was widely found in the brain and also suggested that ischemic treatment severe enough to cause HSP 72 synthesis might be needed for induction of 'ischemic tolerance'.

Animals↗
PubMed1991

Effect of TRK-100, a stable orally active prostacyclin analogue, on platelet function and plaque size in atherothrombotic strokes.

Patients with carotid atheromatous lesions were prospectively studied with indium-111 platelet imaging, platelet aggregability and B-mode real-time ultrasound tests to determine the short-term effects of orally active prostacyclin analogue TRK-100 (40 micrograms, three times daily for 4 weeks). To establish baseline values, all patients underwent indium-111 platelet imaging, platelet aggregation study and B-mode ultrasound. The results were positive for carotid plaque and platelet accumulation. Visual analysis showed repeated platelet scintigrams to be unchanged in five patients without antithrombotic therapy; repeated ultrasound studies showed no change in eight of ten plaques, while one showed progression and one regression of the plaque. In five TRK-100 treated patients, five of seven lesions with platelet accumulation at the baseline became negative, and two remained unchanged during the treatment; repeated B-mode ultrasound tests indicated eight of nine plaques remained unchanged, while one showed plaque size reduction. Quantitative analysis demonstrated that, TRK-100 significantly reduced the ADP aggregation (1 microM) from 55.2 +/- 21.3% to 24.0 +/- 14.7% (+/- SD; p less than 0.05) and the platelet accumulation index (25.7 +/- 17.2% vs 10.4 +/- 10.4%; p less than 0.05). However, there was no significant reduction in plaque scores during TRK-100 therapy compared with the baseline (2.70 +/- 2.75 mm vs 2.51 +/- 2.58 mm). The data obtained suggested that short-term TRK-100 therapy has an inhibitory effect on platelet accumulation in carotid atheroma but does not cause significant changes in plaque size.

Administration, Oral↗
PubMed1991

Temporal profile of serum albumin extravasation following cerebral ischemia in a newly established reproducible gerbil model for vasogenic brain edema: a combined immunohistochemical and dye tracer analysis.

We investigated the temporal profile of the extravasation of serum albumin in a reproducible gerbil model of unilateral cerebral ischemia, using immunohistochemical and dye-tracer techniques to evaluate albumin accumulation and the occurrence of active extravasation, respectively. After 30 min of cerebral ischemia and subsequent reperfusion, immunostaining for albumin became visible in the lateral part of the thalamus during the first 3 h, and then expanded to other brain regions up to 24 h. At both 24 h and 3 days after reperfusion, massive extravasation of albumin was noted in the whole ischemic hemisphere, and this had decreased again by 7 days after reperfusion. The extent and the degree of albumin immunopositivity were almost the same in all animals examined at each period after reperfusion. The extravasation of Evans blue, which was allowed to circulate for 30 min before death, was limited to the lateral part of the thalamus during the first 6 h of reperfusion. In the circumscribed area of massive albumin extravasation, many neurons were immunopositive for albumin; most of these neurons appeared to be intact and also showed immunostaining for microtubule-associated protein 2. The current investigation clearly demonstrated that (1) albumin extravasation was produced with reliable reproducibility in this model, (2) the lateral part of the thalamus was the region most vulnerable to ischemic blood-brain barrier damage, and (3) many apparently intact neurons in the ischemic region were positive for albumin.

Animals↗
PubMed1991

Diagnosis of urachal anomalies in infancy and childhood by contrast fistulography, ultrasound and CT.

From 1981 to 1989 seventeen cases of pediatric patients with urachal remnants have been treated at the Fukuoka Municipal Children's Hospital (2 patent urachus, 5 urachal cyst, 9 urachal sinus, 1 urachal diverticulum). The cases of patent urachus were discovered in the neonates due to a urine discharge from the umbilicus; in the older children, cysts or sinuses accompanied by an infection led to the diagnosis of the urachal anomaly. In 8 of 11 cases, fistulography established the diagnosis. In 9 of 12 cases, ultrasound imaging was diagnostically successful, as was CT in all 3 cases that were given scans.

Child↗
PubMed1991

Carotid lesions detected by B-mode ultrasonography in Takayasu's arteritis: "macaroni sign" as an indicator of the disease.

Twenty-three patients were studied to evaluate the clinical usefulness of high resolution B-mode ultrasonography in the detection of carotid lesions in patients with Takayasu's arteritis. In each patient the carotid arteries were examined using both B-mode ultrasonography (midfrequency of 7.5 MHz) and contrast angiography. In 19 of 23 patients, B-mode ultrasonography clearly demonstrated the characteristic circumferential arterial wall thickening of either one or both sides of the common carotid arteries as a macaroni-like, diffusely thickened intima-media complex. Conversely, contrast angiography demonstrated carotid lesions in only 13 of 23 patients. These results clearly show that B-mode ultrasonography is quite sensitive and superior in the detection of the characteristic thick intima-media complex of the common carotid artery in patients with Takayasu's arteritis, when compared with contrast angiography that is usually used for the definitive diagnosis of this disease.

Adolescent↗
PubMed1991

Hyperthermia-induced neuronal protection against ischemic injury in gerbils.

We investigated the effect of hyperthermic pretreatment before induction of ischemia using a gerbil model of 5-min forebrain ischemia. A single hyperthermic treatment 18 h before ischemia exhibited a partial protective effect, and repetitive hyperthermic pretreatments at 18-h intervals before ischemia showed clear protection against neuronal death in the CA1 area of the hippocampus, whereas single hyperthermic treatment 3, 6, 24, or 50 h before ischemia exhibited little protective effect. This transient and cumulative neuroprotective effect of hyperthermic pretreatment strongly suggested the involvement of stress reactions after hyperthermia in the protective mechanism against ischemic neuronal death.

Animals↗
PubMed1991

[Silent cerebral infarction in the patients with essential hypertension].

Evidence of old cerebral infarction of magnetic resonance imaging (MRI) is common in acute stroke patients without a prior history of stroke. This experience led us to investigate the incidence of silent cerebral infarction (SCI) in the patients with essential hypertension, as well-known major predisposing factor for stroke. The incidence, number, size and localization of SCI on MRI (MARK-J, 0.1 T) and the prevalence of risk factors for stroke were investigated both in 66 hypertensive patients (WHO stage I or II; 63 +/- 9 (mean +/- S.D.) years old) and in 42 age-matched normotensive patients (61 +/- 9 years old). Risk factors selected were as follows: diabetes mellitus, hypercholesterolemia, daily alcohol intake, cigarette smoking, obesity, cardiac disease (arrhythmia and ischemic heart disease), hyperuricemia and high hematocrit. In hypertensive patients, the relationships between the incidence of SCI and hypertensive damages in major organs were also investigated. SCI was found in 45 out of the 108 subjects studied and a total of 216 SCI lesions were detected. All of the SCI lesions were localized in the subcortical white matter or in the basal ganglia. All SCI lesions were smaller than 3 cm in diameter and 201 lesions (93%) were smaller than 1 cm. The incidence of SCI tended to be higher in hypertensive patients (47%) than that in normotensives (33%) and increased significantly with advancing age in hypertensives from 26.9% in the 50s to 86.7% in the 70s, while no significant increase was noted in normotensives.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗