[Pancytopenia with significant neutropenia demonstrating the presence of leukocidin (leukolysin)].
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Biomedical subjects
Publications and source records attributed to Y Inaba.
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BACKGROUND: Despite a large number of studies, the relationship between depression and cardiovascular disease remains ambiguous. This study is the first to investigate the relationship between depression and left ventricular hypertrophy (LVH) as detected by electrocardiogram. METHODS: The subjects were 346 male Japan Self-Defense Forces personnel ages 49 to 55 years. LVH was assessed by electrocardiogram. Depression was measured by the Self-Rating Depression Scale (SDS). Other selected risk factors were measured. Odds ratios for LVH in relation to selected variables were calculated. A logistic regression analysis was used to adjust for possible confounding variables. RESULTS: High level of depression (SDS score > or = 34) showed a high risk of LVH occurrence. After adjusting for BMI, systolic blood pressure, and/or diastolic blood pressure, there was a tendency toward a positive association of LVH with high level of depression. CONCLUSIONS: Our present study demonstrated that depression is closely related to LVH. Since LVH could be a predictor of fatal cardiovascular disease, this is of direct relevance to the prescription of preventive measures.
Linear scar formation in the scalp after suturing an incision has been considered unavoidable. It was not known why scars formed even if the hair bulb was left intact. The authors developed a subcutaneous tissue-shaving method for radical treatment of bromidrosis and studied the process of hair regeneration by using thick-tissue specimens. They suggest that stem cells (lower) are located not only in the lower end of the telogen hair follicles but also in the sebaceous isthmus at the secretory opening of the sebaceous gland (upper stem cells). They found that linear scars can be prevented and existing linear scars can be surgically treated by using a relaxed suture on a scalp incision to avoid excessive pressure on the upper stem cells.
BACKGROUND: To investigate nontumorous focal enhancement (FE) with computed tomographic hepatic arteriography (CTHA) and perfusion defect (PD) with computed tomographic arterial portography (CTAP) in pericystic liver tissue. METHODS: Incidence, shape, and size of nontumorous FE on CTHA and PD on CTAP were examined in 100 consecutive noncirrhotic and 100 consecutive cirrhotic patients. RESULTS: FE was observed on CTHA in 77 noncirrhotic and 61 cirrhotic patients, whereas PD was observed on CTAP in 50 noncirrhotic and 51 cirrhotic patients. When both findings were visualized in both CT studies, the shape of the FE on CTHA was similar to the overlapping PD on CTAP in 81% of patients but was larger in 92% of patients. CONCLUSIONS: FE on CTHA and PD on CTAP are frequently noted in pericystic liver tissue. The size of FE on CTHA is often larger than PD on CTAP, although the shapes are generally the same. Size discrepancy suggests the presence of both portal supply and splanchnic venous drainage.
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Heparin inhibited haemagglutination by porcine reproductive and respiratory syndrome virus (PRRSV) and by Aujesky's disease virus, but failed to inhibit haemagglutination by parainfluenza virus type 3. The minimal inhibitory concentration of heparin required to inhibit 8 HA U of PRRSV haemagglutinin ranged from 0.1 to 1 U ml-1. Mouse erythrocytes failed to combine with the haemagglutination inhibitory factor of heparin. However, mouse erythrocytes treated with heparinase had greatly reduced agglutinability by PRRSV. The formation of a haemagglutinin-heparin complex could be observed by sedimenting heparin with the haemagglutinin. All these findings suggest that a heparin-like molecule on the surface of mouse erythrocytes serves as the virus-cell receptor.
"Minamata disease" (methylmercury poisoning), originally found in Minamata, Japan 3 decades ago, still poses a medico-socio-legal problem mostly resulting from difficulty in drawing diagnostic demarcation. To examine the efficacy of urinary beta-2-microglobulin (BMG) in identifying patients with Minamata disease, the authors studied 115 patients (63 males and 52 females) who were officially registered for compensation (registered patients); 114 patients (54 males, 60 females) currently undergoing medical evaluations for compensation (unregistered patients); and 82 control subjects (40 males, 42 females) matched for sex and age. There was no significant difference with regard to urinary BMG (corrected by creatinine) among the above three groups, although there was a parallel increase in urinary BMG and neurological scores of male patients which suggested the presence of a dose-effect relationship. Although renal tubular dysfunction manifesting hyper-beta-2-microglobulinuria has been reported in patients with Minamata disease, our findings indicate that excessive excretion of BMG is not a satisfactory diagnostic parameter for Minamata disease.
The determination methods of germanium (Ge) in biological specimens such as blood plasma, erythrocytes, urine, hair, nail, and other organs were established using graphite furnace atomic absorption spectrometry (GFAAS) and microwave-induced plasma mass spectrometry (MIP-MS). The detection limits of Ge standard solution were 3 ng/mL with GFAAS and 0.05 ng/mL with MIP-MS. The detection limits in organ samples depended on the type of samples and sampling amounts: 3-30 ng/g by GFAAS and 0.05-0.5 ng/g by MIP-MS. The sensitivity of GFAAS was lower than that of MIP-MS; however, it was adequate for determining Ge concentrations in specimens from patients who had ingested Ge. Samples were digested by a simple wet-ashing procedure using nitric acid and perchloric acid. To avoid the interfering effects of coexisting elements and perchloric acid residue, an extraction method using organic solvent was tried. When using MIP-MS, extraction was not necessary; however, both dilution and addition of an internal standard were needed. Special attention was required for iron-rich samples because a molecular ion of 56Fe16O was observed at nm/z72 where 2Ge was monitored. The results of Ge concentrations in human samples obtained by these methods agreed well. Interfering effects of perchloric acid, which was used for digestion and which remained in samples, were observed in both methods. Hair and nail samples from people who had ingested Ge were useful for monitoring Ge in the body. Hair samples were useful for determining past exposure to Ge when the distribution patterns from the scalp to the end of the strand were analyzed. In control subjects, Ge concentrations in the listed specimens and organs were lower than 0.1 microg/g or mL, and these low levels of Ge were able to be determined by MIP-MS in combination with the extraction method.
To investigate the effect of hepatitis delta virus (HDV) superinfection on the long-term outcome of Japanese subjects with chronic hepatitis B virus (HBV) infection, we examined the presence of antibodies to hepatitis delta antigen (anti-HD) in serial serum samples collected from 1127 subjects with chronic HBV infection. The subjects were followed for at least 36 months (mean: 121.3 months) between 1973 and 1991. Among 69 cases where anti-HD was detected, eight (12%) developed liver cirrhosis (LC) and six (9%) developed hepatocellular carcinoma (HCC). However, among 1058 cases without anti-HD, there were 43 patients (4%) who developed LC and 29 (3%) who developed HCC. The prevalence of LC and HCC was significantly higher among the cases with anti-HD than those without anti-HD. The proportion of LC and HCC per 1000 person years was 10.46 and 7.84, respectively among cases with anti-HD, and 4.05 and 2.73 among those without anti-HD, respectively. The overall relative risk of LC and HCC was 2.58 and 2.87, respectively; 95% confidence interval (CI): LC, 1.14-5.13; HCC, 1.03-6.23. These results indicate that in the Kure district in Japan, where HDV infection of persons infected with HBV is about 6%, such superinfection increases the risk of LC and HCC.
The left cerebral hemisphere of Mongolian gerbils was used to elucidate the mechanisms of brain edema which develop during cerebral ischemia and after restoration of cerebral blood flow following temporary ischemia. Water content was measured by the tissue-drying method. Sodium and potssium ion concentration was measured by flame photometry. Passage of 131I-albumin (RISA) from blood to the cerebral parenchyma was measured on a gamma scintillation counter. Our findings indicate that pure cytotoxic edema develops during ischemia and during a short period after restoration of cerebral blood flow. Vasogenic edema, which is accelerated by the leakage of plasma constitutents from blood due to blood-brain barrier damage, developed after restoration of the cerebral blood flow. After less than 1 hr of ischemia, restoration of the cerebral blood flow drastically reduced the degree of brain edema. However, restoration of the cerebral blood flow greatly worsened the brain edema following more than 3 hr of ischemia.
Mongolian gerbils were observed for the effects of beta-methasone on ischemic brain edema which developed during ischemia or after blood flow restoration. The severity of brain edema was determined by measuring water content of the ischemic cerebral hemisphere, using the wet and dry methods. Sodium and potassium ions were extracted from homogenized brains with 0.75N HNO2 and ion concentration measured by flame photometry. Passage of RISA from blood into the cerebral parenchyma, as an indicator of blood-brain barrier change, was determined with a gamma-scintillation counter. In the cytotoxic edema model, animals were killed after 9 h permanent ischemia or 3 h after 1 h ischemia. In the simultaneous cytotoxic and vasogenic edema model, the animals were killed either 20 h or 3 days following 1 h ischemia, or 3 h after blood flow restoration following 6 h ischemia. Steroid treatment was ineffective in ischemic brain edema of the cytotoxic or vasogenic type.
We investigated the existence of the "no-reflow" phenomenon in focal cerebral ischemia. Regional cerebral blood flow was studied in Mongolian gerbils perfused with a carbon-black particle suspension after cerebral ischemia prior to decapitation and compared with 14C-antipyrine autoradiographic images. The correlation between the occurrence of the "no-reflow" phenomenon and systemic arterial blood pressure change was also examined. We found that the phenomenon was transient in character and that its manifestation was related to the transient fall in arterial blood pressure observed immediately after clip release and with stagnation of venous blood flow. The phenomenon disappeared in animals in which the arterial blood pressure was artificially increased after clip release.
The effect of induced hypertension on the blood-brain barrier (BBB) change in Mongolian gerbils exposed to various periods of ischemia was studied. Evans blue dye was used to determine the BBB change in animals subjected to different levels of hypertension after 3 h ischemia. Horseradish peroxidase (HRP) was used in electronmicroscopic studies of animals subjected to 30 min, 1, 3 or 6 h ischemia and subsequently exposed for 30 min to varying periods and sequences of normo- and hypertension. Furthermore, HRP-labeled vesicle counts were performed in animals from the 30-min ischemia group. Our findings revealed that hypertension, after blood flow restoration following ischemia, induces and/or accelerates BBB damage by enhancing endothelial vesicular and/or tubulo-channel transport.
Moyamoya disease presents clinically as chronic progressive ischemia in the young brain. The brain is surrounded by concentric collateral networks but all of these networks are not available as collaterals in the early stage of cerebral ischemia. The anatomical characteristics precluding their early use include the presence of the watery layer of subarachnoid fluid between the cortical and dural vessels and of a closed bony box intervening between the dural and scalp arterial networks. These barriers isolate the brain from the abundant blood flow of the external carotid system as if they were the moat (the subarachnoid fluid layer) and the walls (the skull) of a castle. Based on these concepts, we have developed a surgical procedure, the encephalo-duro-arterio-synangiosis to treat moyamoya disease in children. This operation surmounts the above mentioned two obstacles to collateral formation to the brain by perforating the castle wall and bridging the moat by granulation tissue, without injuring the collaterals which are already formed. This procedure was performed on 70 sides in 38 pediatric moyamoya patients. Revascularisation of the brain was obtained in 100 percent of the cases with varying improvement in the symptoms.
To demonstrate the BBB break-down on the CT image in the acute stage of cerebral infarction, a 3 hour continuous drip infusion of 200 ml of meglumine amidotrizoate, rather than the conventional bolus injection, was used. In this study, 22 examinations were carried out in 18 patients in whom cerebral infarction due to temporary or permanent obstruction of the cerebral artery was diagnosed by CT and angiography on admission. With each examination, the first CT was obtained prior to contrast infusion, and second immediately after the end of 3 hours of continuous contrast infusion. The EMI number was calculated at 3 regions of interest in the infarction. Within 3 days after stroke episode, 4 out of 5 patients with temporary vascular obstruction demonstrated enhancement, as well as 6 out of 9 patients with permanent vascular obstruction. Between 4 and 14 days after the stroke episode, all of 8 patients showed enhancement. To further clarify the extravasation of the contrast medium during the first 3 days of a cerebral infarction, a third CT scan was performed 3-hrs after finishing the contrast infusion in 4 patients. In these latter patients, blood was sampled at the time of each of the 3 CT series. The EMI number of the blood samples was also measured. In all 4 patients, the Gado's tissue-blood ratio (the EMI number of the CT lesion divided by that of the blood sample) was higher than 17.2% in the second, and higher than 54.7% in the third CT scan. Thus break-down of the BBB which was demonstrated by prolonged contrast infusion is an earlier event in human cerebral infarction than is usually accepted.
The functions of the interferons in the testis are unclear. We investigated the role of interferon alpha and gamma in the seminal plasma on spermatogenesis. The levels of interferon alpha and gamma were determined in the seminal plasma of 101 males including normozoospermic (n = 31), oligozoospermic (n = 57) and azoospermic men (n = 13). The correlation between such levels and clinical parameter (seminogram and serum hormone levels) was evaluated. The seminal plasma level of interferon alpha (92.0 + 110.3 ng/mL) in the normozoospermic men was significantly lower than that of oligozoospermic men (162.4 +/- 130.3 ng/mL) (p < .05). The three groups (normozoospermic, oligozoospermic, and azoospermic group) did not differ as to the level of interferon gamma. No significant correlations were observed between the levels of interferon alpha or gamma in seminal plasma and the serum levels of follicle stimulating hormone (FSH), luteinizing hormone (LH), testosterone, prolactin, or estradiol. Theses results suggest that the level of interferon alpha in the seminal plasma may be related to sperm production.