Morphological changes of intraparenchymal arterioles after experimental subarachnoid hemorrhage in dogs

OBJECTIVE: Morphological and microcirculatory changes in intraparenchymal vessels after subarachnoid hemorrhage (SAH) have not yet been fully clarified. We conducted this experimental study to investigate the serial morphological changes of intraparenchymal arterioles after SAH. METHODS: SAH was produced by injecting autologous arterial blood into the cisterna magna twice at 48-hour intervals in 30 dogs. The dogs were killed 3, 7, or 14 days after SAH, and then perfusion-fixed specimens of both anterior sylvian giri were obtained by using two methods. Microvascular corrosion casts produced by arterial injection of polyester resin were examined using scanning electron microscopy, and the widths of 40 arterioles of each animal were measured. Sectioned slices from the brain surface to 500 microns deep were examined by light microscopy, and external diameter, internal diameters, and wall thickness of the arterioles at depths of 50, 200, and 500 microns from the brain surface were morphometrically evaluated in 40 arterioles of each animal. In control animals receiving cisternal injections of mock cerebrospinal fluid (n = 10) and in healthy control animals (n = 10), the same examination and evaluation were performed. RESULTS: Corrosion casts of arterioles showed tapered narrowing with folding after SAH, and the width of the arterioles significantly decreased 3 and 7 days after SAH (P < 0.01). Morphometric examination by light microscopy showed a significant decrease of internal diameter of arterioles associated with a significant increase of wall thickness at any depth from the brain surface 3 and 7 days after SAH (P < 0.05 or P < 0.01). These findings improved 14 days after SAH. Control animals receiving cisternal injections of mock cerebrospinal fluid showed no significant differences compared with healthy control animals. CONCLUSION: These results suggest that constriction of intraparenchymal arterioles occurs after SAH and may contribute to delayed cerebral ischemia.     

End-Effect of High-Speed Linear Induction Motor

This paper presents a new theory of the end-effect of a high-speed linear induction motor, an experimental proof of the theory, and several countermeasures to eliminate the end-effect. The theory is developed on the basis of a two-dimensional solution of electrodynamic equations and compared with the experimental results. The experiment has been made by use of a rotary type test facility; the maximum test velocity is 450 km/h. It is found that the theory agrees well with the experiment and that the end-effect exercises a very adverse influence on motor performance. The end-effect is investigated as functions of design parameters by making use of the theory. Some measures to counter the end-effect are proposed and discussed. A parallel-connected linear induction motor is also proposed as a measure to compensate the end-effect, and its performance is studied.     

Usefulness of a nonmachinery based system for the reinfusion of cell-free and concentrated autogenous ascitic fluid

A nonmachinery based system using gravity dependent flow for the treatment and reinfusion of ascitic fluid was developed, and its usefulness was assessed. In a preliminary study using bovine plasma, samples with protein concentrations below 5.0 g/dl were found to be treatable with this system. Bovine plasma containing blood, prepared to 0.5% hematocrit and with a protein concentration of 3.0 g/dl, was also treatable. We conducted a clinical study of 1,799 treatment sessions (1,495 using a machinery based system and 304 using a nonmachinery based system) of 343 patients with ascites refractory to various treatments. The recovery ratio of protein from the original ascitic fluid was 96% using the nonmachinery based system and 77% with the machinery based system (p < 0.01). Of 253 continuous reinfusions of ascitic fluid using the nonmachinery based system, the original ascitic fluid at protein concentrations below 2.5 g/dl was treatable. Original ascitic fluid below a hematocrit of 0.7% (protein concentration, 1.4 g/dl) was also treatable. This new procedure was simple and time and labor saving; the high recovery ratio of protein also demonstrated the usefulness of the new system.     

A case of glycogen storage disease type Ia with multiple hepatic adenomas and G727T mutation in the glucose-6-phosphatase gene, and a comparison with other mutations previously reported

We report a case of 23-yr-old man with glycogen storage disease (GSD) type Ia complicated by multiple hepatic adenomas. Analysis of the G-6-Pase gene using peripheral blood sample showed this patient to be homozygous for a G-to-T transversion at nucleotide 727 in exon 5. This mutation is prevalent among Japanese patients, suggesting that specific genotypes may correlate with different clinical courses or outcomes.     

Development of field‐emission displays

Abstract— FEDs are one of the attractive flat‐panel displays that realize high‐quality motion images and low power consumption. FEDs are constructed by using three elemental technologies: micro‐ or nano‐fabrication technology of emitters, opto‐electronic semiconductor technology of anode patterns, and vacuum packaging technology. Each of the three elemental technologies is essential to realize FEDs. The present status of each three technologies, especially the improvement of Spindt‐type field emitters, the trend of flat vacuum packages, and development of phosphors for FEDs is described in this paper.     

Genomic organization and mutational analysis of KVLQT1, a gene responsible for familial long QT syndrome

BACKGROUND: Turcot's Syndrome is the association of multiple adenomatous polyps of the colon with a primary tumor of the central nervous system. We present the first reported case of Turcot's Syndrome in a patient with malignant ependymomas. Recent advances in the elucidation of the genetic basis for the hereditary forms of colon cancer have provided a clearer understanding of the etiology of Turcot's Syndrome. This new information is relevant to the neurosurgical community and provides updated guidelines in the diagnosis and management of patients with this complex disease process. RESULTS: Turcot's Syndrome is related to two distinct genetic errors. The first involves a germ-line mutation in the adenomatous polyposis coli (APC) gene, which is postulated to act as a tumor suppressor gene. The second is a germ-line defect in one of a group of genes responsible for DNA nucleotide mismatch repair. CONCLUSION: The elucidation of the gene defects responsible for the hereditary forms of colon cancer has provided a clearer understanding of the molecular basis of Turcot's Syndrome. Patients with hereditary forms of colon cancer and neurologic symptoms require immediate and thorough investigation because of their significantly increased risk of developing CNS tumors. Previously healthy patients diagnosed with a CNS tumor with a family history of adenomatous polyposis coli should undergo screening and surveillance colonoscopy as the CNS lesion may precede colonic symptoms. CNS screening guidelines for asymptomatic patients with adenomatous polyposis coli requires further risk analysis studies. All patients diagnosed with Turcot's Syndrome should be tested for the gene defect, including the CNS tumor tissue to provide further data on the genetic relationship between Turcot's Syndrome and the hereditary forms of colon cancer.     

Microwave Behavior of α-Fe／Fe3B／Y2O3 Nanocomposites in GHz Range Prepared by Melt-Spun Technique

Recentemploymentofcommunicationdevices ,(e .g .,mobiletelephones ,intelligenttransportsys tems ,electronictollcollectionsystems ,localareanet worksystemsandradarsystems)hasrapidlyexpand ed .Therefore ,seriouselectromagneticinterference(EMI)problemshaveworsened .Concernfortheseproblemshaspromptedthestudyofelectromagneticwaveabsorbingmaterialswithanti electromagneticin terferencecoatings ,self concealingtechnologyandmicrowavedarkroomsforthecivilandmilitaryapplica tions .Formagneticelectromagnet…     

Improved oxygen utilization during mild exercise in heart failure

In heart failure with low cardiac output, exercise tolerance is reduced despite modulated regional blood distribution and oxygen extraction. However, low cardiac output does not necessarily lead to reduced exercise tolerance especially during mild exercise. In the present study, in order to understand the mechanisms regulating exercise tolerance in heart failure, we measured oxygen consumption (VO2) and cardiac output (CO) during both mild and intense exercise. Patients with heart failure were divided into 2 groups; group L (n = 8) consists of patients with low anaerobic threshold (AT) < 13 ml/min per kg and group H (n = 7) consisting of patients with AT > 13 ml/min per kg. At rest, VO2 was similar between groups L and H, whereas CO was lower in group L than in group H (3.5 + 0.3 vs 4.8 + 1.4 ml/min, p < 0.01). Increase in VO2 during warm-up exercise was not significant between the 2 groups (7.4 +/- 0.5 (group L) vs 6.2 +/- 0.3 ml/min per kg (group H), ns), but increase in CO was lower in group L than in group H (2.5 +/- 0.6 vs 3.4 +/- 0.4 ml/min, p < 0.01). After warm-up to the AT point, however, the increase in not only VO2 but also CO was markedly reduced in group L than in group H (VO2: 0.5 +/- 0.4 vs 3.7 +/- 0.8 ml/min per kg, p < 0.01, CO: 0.2 +/- 0.3 vs 1.1 +/- 0.3 L/min, p < 0.01). Based on these measurements, we calculated the arteriovenous oxygen difference (c(A-V)O2 difference) during exercise in individual patients using Fick's equation. The c(A-V)O2 difference was markedly increased in severe heart failure during the warm-up stage, but between the end of warm-up and the AT point, it remained at the same level as that of group H. These results suggest the presence of a unique mechanism regulating the c(A-V)O2 difference in severe heart failure patients, activation of which may, at least during mild exercise, contribute to efficient oxygen delivery to the peripheral tissues thus compensating for the jeopardized exercise tolerance in those patients.     

Analysis of adenovirus type 7 hexon hypervariable region]

The isolation of adenovirus type 7 (Ad7) has been rare in Japan in the past. However since April, 1995, many isolates of Ad 7 have been reported. In order to find the cause of Ad 7 re-emergence in Japan, we investigated the genome sequences of Ad 7 by analyzing the hexon hypervariable regions (HVRs). HVRs of genomes isolated before and after this prevalence showed little change and were closely related with each other. It was concluded that adenovirus hexon which contains HVRs is conserved in the same serotype of any genome type. At present, virus genome typing seems more suitable for comparing the differences of genomes than sequencing.