The relationship of a neonatal care center, a pediatric neurology division and a rehabilitation center for disabled children]

In alloxan-induced diabetic rats (Wistar, females, age 3-4 months of postnatal life) the large spectrum of fatty acids in blood serum, brain cortex, medulla oblongata and liver was studied. The fatty acids, using gas chromatography, were detected as methyl esters and the methods were published previously (Smídová and al. 1994). Alloxan (Merck) administered i.p., 140 mg/kg body weight, caused immediately elevation (three times) of blood sugar levels. On the 13th day the rats were killed. The results are as follows: a) In blood serum alloxan diabetes of cca two weeks duration caused a significantly increased participation of saturated FA and decreased participation of both polyunsaturated FA (n-3 and n-6). b) In brain cortex no differences between controls and diabetic rats in the indicated groups of FA were found. c) In the medulla oblongata an increased participation of polyunsaturated fatty acids n-6 was established. d) In hepatic tissue the increased participation of saturated FA as well as a decreased participation of FA n-6 was described. Analysing the main groups of FA we found especially in n-3 and n-6 FA several significant changes in single FA (a smaller pool of arachidonic acid in blood serum as well as in liver, decreased participation of docosahexaenoic acid in the brain cortex, etc.). The purpose and possible consequences of such changes are discussed.     

Outcomes of 50 leukemia patients who received bone marrow transplants from unrelated donors]

In this study, we examined the ability of tumour necrosis factor-alpha (TNF) to stimulate the mitogen-activated protein (MAP) kinase homologues p42/44 MAP kinase, c-Jun NH2-terminal kinase (JNK) and p38 MAP kinase and its effect upon DNA synthesis in primary cultures of bovine aortic endothelial cells (BAECs). TNF strongly stimulated p38 MAP kinase and JNK activity in both a time- and concentration-dependent manner. By contrast, TNF was a very poor activator of p42/44 MAP kinase relative to the known activator of p42/44 MAP kinase in endothelial cells, adenosine triphosphate (ATP). TNF-stimulated activation of p38 MAP kinase, and MAPKAP kinase-2, a known downstream target of p38 MAP kinase, was strongly inhibited by pre-incubation with the p38 MAP kinase inhibitor SB203580, whereas the minor activation of p42/44 MAP kinase was abolished by pre-incubation of the cell with the novel MAP kinase kinase 1 inhibitor PD098059. Addition of TNF resulted in a 50-60% decrease in DNA synthesis in BAECs. Pre-incubation with PD098059 or co-incubation with ATP failed to modify the inhibitory effect of TNF upon DNA synthesis. SB203580 reduced basal DNA synthesis by approximately 50%; however, if failed to modify the inhibition mediated by TNF. These results indicate that TNF strongly activates both p38 MAP kinase, JNK and, to a minor extent, p42/p44 MAP kinase. It is likely that only one of these kinases, JNK, plays a role in the regulation of DNA synthesis in these cells.     

Vasopressin reduces taurochenodeoxycholate-induced hepatotoxicity by lowering the hepatocyte taurochenodeoxycholate content

BACKGROUND/AIMS: Vasopressin has been reported to reduce bile flow, but its effects on bile acid secretion and bile acid-related hepatotoxicity are still unclear. We therefore investigated the influence of vasopressin on the hepatotoxicity and biliary excretion of taurochenodeoxycholic acid in primary cultured rat hepatocytes and isolated perfused rat liver models. METHODS/RESULTS: 1) Addition of vasopressin to hepatocyte cultures significantly decreased lactate dehydrogenase release as compared to cultures exposed to 1 mM taurochenodeoxycholic acid alone, and also reduced intracellular taurochenodeoxycholic acid content from 19.3 +/- 2.2 to 13.0 +/- 1.6 nmol/mg protein. After 30 min of preincubation with 1 mM taurochenodeoxycholic acid, rinsing and reculture of hepatocytes in bile acid-free medium resulted in gradual decrease in the intracellular level of the bile acid, and addition of vasopressin (10(-9) M) to the reculture medium accelerated this process. 2) Superimposition of vasopressin (330 pmol/l) for 10 min on taurochenodeoxycholic acid infusion (1.0 mumol/min: 25 mumol/l) caused a rapid increase in bile flow and biliary excretion of taurochenodeoxycholic acid (697 +/- 42 vs 584 +/- 27 nmol/10 min per g liver) from perfused rat livers, and significantly reduced lactate dehydrogenase release. 3) Superimposition of the PKC blocker H-7 (5 mumol/l) on taurochenodeoxycholic acid infusion (1.0 mumol/min: 25 mumol/l) caused a gradual increase in bile flow and biliary excretion of taurochenodeoxycholic acid. Furthermore, an additional infusion of vasopressin (100 pmol/l) for 10 min in the presence of H-7 produced a greater increase in bile flow and biliary excretion of taurochenodeoxycholic acid as compared with H-7 alone (754 +/- 71 vs. 657 +/- 26 nmol/g liver). 4) Continuous infusion of vasopressin (330 pmol/l) significantly increased the late peak (10-50 min) of horseradish peroxidase excretion from perfused livers (from 8.48 +/- 1.02 to 21.7 +/- 6.02 ng/g liver). CONCLUSIONS: These findings suggest that vasopressin exerts a protective effect against taurochenodeoxycholic acid-induced hepatotoxicity by stimulating the secretion of this bile acid via intracellular vesicular transport systems.     

Portal and peripheral blood immunoreactive insulin concentrations after glucose infusion during gastrectomy

We evaluated portal and peripheral blood immunoreactive insulin concentrations (IRI) after glucose infusion in patients undergoing gastrectomy. Seventy-four patients were divided into following two groups: 68 received 25g glucose infusion in an hour (glucose group), and the remainder received no glucose (control group). Portal blood IRI level in glucose group was about thirty-fold higher than that in control group. However, peripheral blood IRI did not correlate with portal blood IRI in glucose group. In addition, significant negative correlation between portal blood IRI and blood glucose was observed in glucose group. Our results reveal that adequate pancreatic insulin secretion occurs after glucose infusion during gastrectomy, but peripheral blood IRI does not reflect this pancreatic insulin secretion. The results also suggest that blood glucose may be regulated by the liver under these conditions.     

Observations of seismic electromagnetic phenomena in VHF band by dual frequency method

Seismic electromagnetic (EM) phenomena have been observed at many laboratories with specially designed systems. Recently we can utilize radio receivers, personal computers, and communication systems with higher performances and reasonable cost. It is possible to observe seismic EM phenomena not only by specially designed systems but also by a simple observation system integrated by these devices and systems. We have created an observation system for seismic EM phenomena with them in the very high frequency (VHF) band, from 76 MHz to 90 MHz, assigned for FM broadcasting exclusive use in Japan. We are surrounded by many EM waves, such as broadcasting, communication usage, and man‐made noises. Thus, we have newly developed the dual frequency observation method. In this paper, we describe an observation method that can identify whether a received signal is a broadband EM wave or an artificial FM radio wave. Next, the observation results for broadband EM waves from galactic noise and solar flares are presented. Then, the observation results for FM radio waves reflected from sporadic E layer and the Leonid meteors are shown. Finally, the observation results for the detected broadband EM waves associated with the Geiyo earthquake are described. © 2006 Wiley Periodicals, Inc. Electr Eng Jpn, 155(4): 36–44, 2006; Published online in Wiley InterScience ( www.interscience.wiley.com ). DOI 10.1002/eej.20350     

BEOL工艺统合Integration--low-k Dual/Damascene的形成

1简介 当前,从成膜方法来讲,ILD loW-k材料大致上分为两类:一类是以SiCOH为代表的CVD(化学气相淀积)膜,另一类是SOD(旋转涂层)膜,它包括有机的、无机的和SiCOH.     

Arterial ketone body ratio and its modification by PGE1 in elderly patients during gastrectomy

Breeding studies are reported of a previously undescribed hereditary retinal degeneration identified in the Siberian Husky breed of dog. This disorder clinically resembles the previously reported autosomal recessive canine hereditary retinal degenerations collectively termed progressive retinal atrophy (PRA). However, the pedigree of the propositus, a male Siberian Husky, exhibited an X-linked pattern of transmission. This dog was outcrossed to three phenotypically normal female laboratory Beagles and two of their F1 daughters were bred to a phenotypically normal male Beagle, producing affected males in the F2 generation. Subsequent inbreedings produced further affected males and affected females as well. X-linked transmission was established by exclusion of alternative modes of inheritance and, consequently, the disease has been termed X-linked progressive retinal atrophy (XLPRA). This is the first reported X-linked retinal degeneration in an animal. Because of the many similarities of PRA in dogs to retinitis pigmentosa (RP) in humans, this new disease may not only represent the first animal model of X-linked RP (XLRP) but may well be a true homolog of one of the XLRP loci (RP2, RP3, RP6). It is the first retinal degeneration in dogs that can be assigned to an identified canine chromosome, and the first for which linkage mapping offers a realistic approach to proceed by positional cloning towards identifying the responsible gene locus.