Detection limit in low-amplitude EEG measurement.

Electrocerebral inactivity for the determination of cerebral death is defined as no findings of EEG greater than the amplifier's inherent internal noise level when recording at increased sensitivity. A surface biopotential electrode contains two interfaces composed of skin gel (electrolyte) and gel electrode (metal), each forming a noise source. The power spectral density, S(f), of extremely low noise signals was obtained by means of autocorrelation and fast Fourier transformation. Interelectrode resistance, R(f), was measured with synchronous rectification. The formula of equivalent noise resistance R(n) = S(f)/4kT, where k is the Boltzmann constant and T is room temperature in Kelvin, gives a resistance that generates the thermal noise corresponding to the measured S(f). Rn/R is a parameter derived from normalization by R. When Rn/R = 1, measured noise contains thermal noise only. Meanwhile, Rn/R > 1 indicates presence of excess noise, such as 1/f, and tissue noise in addition to the thermal noise. Mean square root (Rn/R) of the scalp noise was 10.8 at 10 Hz, showing existence of excess noise. The study results suggest that it is necessary to take excess noise into consideration in the measurement of low-amplitude EEG for the determination of cerebral death.     

Modulation of infection-induced inflammation and locomotive deficit and longevity in senescence-accelerated mice-prone (SAMP8) model by the oligomerized polyphenol Oligonol.

Oligonol is produced from the oligomerization of polyphenols (typically proanthocyanidin from a variety of fruits such as lychees, grapes, apples, persimmons, etc.) and contains catechin-type monomers and oligomers of proanthocyanidins. The ability of Oligonol to affect infection-dependent eye inflammation, locomotion and longevity in senescence-accelerated prone mice (SAMP8) (a model of senescence acceleration and geriatric disorders with increased oxidative stress and neuronal deficit) was investigated. Oligonol (60mg/kg) significantly modulated the extent of inflammation scores in the eye of SAMP8 mice. Examination of the mice indicated infection with mouse hepatitis virus and pinworm (Syphacia obvelata) in both males and females and with the intestinal protozoa (trichomonad) in males. A comparison of the two groups (using log-rank test) and the difference in the mean life span between groups (using Student's t-test) indicated significant differences in survival (p=0.043) and the mean life span (p=0.033) in male SAMP8 mice. Oligonol increased the mean life span and this was statistically significant. In the open-field locomotive test, the 7-week-old SAMP8 mice crossed more than 40 partitioned lines in 1min. At 48-week-old control untreated male SAMP8 crossed 2 lines. The Oligonol-treated 48-week-old male SAMP8 mice crossed 17 lines however. The improved locomotive activity was statistically significant even after 36weeks in the Oligonol-treated male SAMP8 but this was not the case throughout the time course of the study in the Oligonol-treated female SAMP8. Thus Oligonol treatment to SAMP8 mice modulated the severity of infection-dependent inflammation, prolonged life-span and significantly improved locomotive activity indicating potential benefit to aging-associated diseases such as Alzheimer's or Parkinson's diseases. This presents potential for further research to define infection-dependent inflammation associated with degenerative conditions and the molecular mechanism of dietary antioxidant protection.     

Light and electron microscopic and autoradiographic studies onN-methyl-N-amylnitrosamine-induced rat esophageal carcinogenesis

The purpose of this study was to investigate the histogenesis of experimental tumors in the rat esophagus. Thirty rats received 0.0015% N-methyl-N-amylnitrosamine (MNAN) in the drinking water for 12 weeks. Another 30 rats received tap water. All rats then received tap water until sacrifice. Rats from each group were sacrificed immediately after MNAN administration, four weeks after, and eight weeks after. One hour before sacrifice, [³H]TdR was injected by tail vein to label proliferating cells. The entire esophagus and stomach were removed and processed for light and electron microscopy and autoradiography. The overall frequency of esophageal tumors after MNAN was 83% and did not differ significantly among the three experimental groups. Tumors were primarily papillomas and squamous cell carcinomas and occurred with equal frequency in the upper, middle, and lower thirds of the esophagus. No tumors were found in the squamous-lined forestomach. Electron microscopy revealed abundant tonofilaments, free ribosomes, and mitochondria accompanied by vacuoles. By autoradiography, esophageal epithelial proliferation was markedly stimulated in nontumorous mucosa from all three experimental groups. We conclude that MNAN ingestion for 12 weeks reliably produces papillomas and squamous cell carcinomas throughout the rat esophagus, but not in the squamouslined forestomach, and that MNAN stimulated marked epithelial proliferation which is accompanied by thickening of the epithelium in nontumorus esophageal mucosa.     

Disappearance of Philadelphia chromosomes after remission induction in lymphoid crisis of chronic myelogenous leukemia]

The authors report a rare case of chronic myelogenous leukemia (CML) in which the Ph1 clone disappeared after remission induction of lymphoid crisis. A 58-year-old man was admitted to our hospital because of fever in July 1988. The white cell count was elevated. Bone marrow aspirate showed hypercellularity with myeloid hyperplasia. In the chromosomal analysis, Ph1 chromosomes were detected in 100% of bone marrow cells analysed. Diagnosis of CML was made and treatment was initiated with recombinant interferon-alpha 2a. Hematological remission without cytogenetic improvement was achieved. In March 1990 he developed lymphoid crisis with proliferation of CD10-positive cells. The chromosomal analysis revealed additional abnormalities including, 45, X, -Y, t(9;22) (q34;q11), +1, -8. With vincristine 0.6 mgX4, pirarubicin 15 mgX4, dexamethasone 40 mgX4 therapy complete remission was obtained. In December 1990 the Ph1 positive clone completely disappeared judging from normal karyotypes in the chromosomal analysis and the disappearance of M-bcr gene rearrangement.     

Effect of phosphatidylcholine, phosphatidylethanolamine and lysophosphatidylcholine on the protein C/protein S anticoagulation system.

Phosphatidylserine is known to significantly accelerate the blood coagulation reaction. In a previous communication submitted for publication, we demonstrated that phosphatidylcholine, phosphatidylethanolamine and lysophosphatidylcholine showed effects on the blood coagulation reaction using the factor Xa-prothrombin reaction system, and discuss a new function of membrane phospholipids. The present study examined the role of phospholipids in the blood coagulation regulatory reaction (anticoagulation system), by studying the effects of phospholipids on the protein C/protein S reaction. We have established quantitative methods for measuring activated protein C activity and protein S activity, and used them to measure their activity after the addition of liposomes with different phospholipid compositions. We found that phosphatidylcholine inhibited activated protein C and protein S activities in a dose-dependent manner, as in the factor Xa-prothrombin reaction system. On the other hand, phosphatidylethanolamine and lysophosphatidylcholine showed no effect on activated protein C activity. Phosphatidylethanolamine inhibited and lysophosphatidylcholine accelerated coagulation activity in the factor Xa-prothrombin system, but such effects were not observed in the protein C/protein S reaction system. The coagulation and anticoagulation reactions are exquisitely balanced by thrombin, with a role both as a procoagulant and anticoagulant. Therefore, it is understandable that phosphatidylethanolamine and lysophosphatidylcholine show different effects in the factor Xa-prothrombin and protein C/protein S reaction systems. It appears that coagulation and anticoagulation reactions are co-ordinated and controlled by changes in phospholipid composition of the cellular membrane where the coagulation reaction takes place.     

Gadolinium-based balloon angioplasty for pulmonary artery stenosis in an infant with a right isomerism.

We report here the first described case of utilizing gadolinium-based contrast material as the contrast agent during a catheter intervention treatment for pulmonary artery stenosis. The patient, a male infant with complex heart disease associated with a right isomerism, had a history of severe allergic reaction to iodine-containing contrast agents. A combination of digital subtraction angiography and a gadolinium contrast agent, however, provided us with good-quality images both before and after balloon angioplasty without any associated complications. This method should therefore be considered as an alternative angiographic procedure in children with a high risk of iodine-related allergic complications.