All issues
Volume 118 (2001)
- Issue 6 Pages 363-
- Issue 5 Pages 303-
- Issue 4 Pages 251-
- Issue 3 Pages 147-
- Issue 2 Pages 81-
- Issue 1 Pages 5-
Volume 118, Issue 4
Displaying 1-5 of 5 articles from this issue
- |<
- <
- 1
- >
- >|
Reviews
-
Kiminobu SUGAYASubject area: Others
2001 Volume 118 Issue 4 Pages 251-257
Published: 2001
Released on J-STAGE: September 27, 2002
JOURNAL FREE ACCESSWhile basal forebrain cholinergic neurons degenerate in aging and Alzheimer’s disease, the cholinergic groups of the upper brainstem are preserved. Since the brainstem reticular-like cholinergic neurons differ from the rostral cholinergic phenotype by their high expression of nitric oxide synthase (NOS) mRNA, we hypothesized that they contain biochemical mechanisms to protect themselves against self-induced damage by nitric oxide (NO). Our initial question was a source of the NO during the aging process. We found a significant correlation between cognitive function and markers for glial activation and oxidative stress using aged rats. This result indicates that oxidative stress accompanied by glial activation may be occurred in the cognitively impaired animals. We also found mitochondrial DNA (mDNA) was significantly damaged in these animals, while accumulation of oxidative damage was not evident in other molecules. Therefore, oxidative damage to the mDNA by glial activation may occur in the cells having poor protection against oxidative stress during aging. Then the dysfunction of mitochondria, induced by the mDNA damage, may induce cell death as well as produce another oxidative stress to cause neuronal damage. The damaged neurons induce further glial activation and such self-accelerated immune-like response results in progressive neurodegeneration.View full abstractDownload PDF (1048K)
Thesis
-
Yoshihiro KETO, Misako EBATA, Susumu OKABEArticle type: Others
Subject area: Others
2001 Volume 118 Issue 4 Pages 259-268
Published: 2001
Released on J-STAGE: September 27, 2002
JOURNAL FREE ACCESSHelicobacter pylori (H. pylori) infection has been recognized to be a causal factor of gastritis, ulcers and gastric cancer in man. Using Mongolian gerbils (M. gerbils), which are suitable for an H. pylori infection animal model, we examined 1) how H. pylori infection, indomethacin and their combination affects the healing of gastric ulcers and whether or not such factors provoke a relapse of healed acetic acid ulcers; and 2) whether or not eradication of the bacteria with drugs at specified times after infection prevents the development of mucosal changes, including gastric adenocarcinoma. 1) H. pylori infection significantly delayed ulcer healing 4 weeks following infection. Indomethacin treatment showed a tendency to delay ulcer healing. Ulcer healing in H. pylori-infected M. gerbils was significantly delayed by indomethacin. H. pylori infection resulted in a relapse of healed ulcers from 1 to 6 months after infection, with a gradual increase in size. Omeprazole markedly prevented the ulcer relapse caused by H. pylori infection. 2) Four or 8 months after H. pylori inoculation, eradication was performed by concurrent treatment with omeprazole + clarithromycin. Immediately after treatment ended in both the 5 and 9 month groups, it was verified that H. pylori were completely eradicated. Autopsy performed 18 months after H. pylori inoculation revealed gastric hyperplastic polyps with erosive lesions and ulcers that were grossly visible; and atrophic gastritis, intestinal metaplasia, carcinoids, and adenocarcinomas were histologically observed in the non-treated control group. In animals eradicated after 4 months and autopsied after 18 months, however, such mucosal changes were not observed. In contrast, intestinal metaplasia and mucosal atrophy was observed in animals eradicated after 8 months and autopsied after 18 months. It was concluded that 1) H. pylori infection delayed the healing of preexisting gastric ulcers and resulted in the relapse of healed ulcers, yet indomethacin had little or no effect on ulcer healing or relapse; and 2) early eradication of H. pylori infection with drug therapy can prevent severe gastric mucosal changes, to include adenocarcinomas, in M gerbils.View full abstractDownload PDF (1667K)
Technical Note
-
Kazuhiro KOHAMA, Akio NAKAMURAArticle type: Others
Subject area: Others
2001 Volume 118 Issue 4 Pages 269-276
Published: 2001
Released on J-STAGE: September 27, 2002
JOURNAL FREE ACCESSWe constructed a plasmid vector to have a 1.4-kb insert of myosin light chain kinase (MLCK) cDNA in an antisense direction to express antisense mRNA. The construct was then transfected to SM3, a cell line from vascular smooth muscle cells (VSMCs), producing a few stable transformants. We explained the methods in detail. The down-regulation of MLCK expression in the transfectants was confirmed by both Northern and Western blots. The control showed chemotactic motility to the platelet derived growth factor. However, the transfectants did not show chemotactic motility, indicating the essential role of MLCK in the motility. It was discussed that down-regulation of MLCK expression could be ultilized to discover the drug for arteriosclerosis which prevents the proliferating VSMCs from forming arterinal plaques.View full abstractDownload PDF (1074K) -
Mitsushi IKEMOTO, Masatoshi TAKITAArticle type: Others
Subject area: Others
2001 Volume 118 Issue 4 Pages 277-282
Published: 2001
Released on J-STAGE: September 27, 2002
JOURNAL FREE ACCESSIt is urgently necessary to clarify functions of uncharacterized proteins. To understand life processes, we must investigate the functions and networks of proteins expressed from genomic DNA. In the near future, microinfusion experiments will become a more important method for analyzing uncharacterized function of proteins in vivo. Here we provide a practical manual for performing microinfusion experiments in mice. We also describe our experiment in which we performed a single injection of morphine following Secreted Protein Acidic and Rich in Cysteine (SPARC) infusion into the basolateral amygdala of previously uninjected mice and found markedly enhanced locomotor activity. We discuss the utility of microinfusion experiemnts in mice.View full abstractDownload PDF (986K) -
Takanobu TANIGUCHIArticle type: Others
Subject area: Others
2001 Volume 118 Issue 4 Pages 283-288
Published: 2001
Released on J-STAGE: September 27, 2002
JOURNAL FREE ACCESSUsing a microphysiometer with synchronized valve switching, we investigated real-time acid extrusion from CHO cells, in which human alpha-1a adrenoceptor (AR) is stably expressed, in response to noradrenaline (NA). The time course of the extracellular acidification rate after stimulation had two phases: in the first phase, it transiently reached a rate several times greater than the base rate with a peak at around 10 s, and in the second, it reached to 2 times the base rate and reached a plateau in 2 min. Both phases showed concentration-dependent increase of acidification rates in response to NA, but had distinct pEC50 values: 5.6 for the transient phase and 7.2 for the steady phase. HOE642, an inhibitor of Na+-H+ exchanger (NHE) 1, inhibited the acid extrusion response in a concentration-dependent manner. HOE642 had high pIC50 values (7.3) for inhibition of the transient phase response. In contrast, it revealed the presence of two components in the steady phase response: one had high pIC50 values (8.2) and the other had low pIC50 values (6.0). As Ca2+ was depleted, the transient phase disappeared, while the steady phase was not affected. These results suggest that alpha-1a AR drives two acid extrusion sytems in CHO cells upon stimulation: one elicits the transient response that is largely mediated by a HOE642-sensitive and Ca2+-dependent NHE, presumably NHE1, and the other induces the steady acid extrusion that is mediated by NHE1 and another NHE that has low sensitivity to HOE642.View full abstractDownload PDF (567K)
- |<
- <
- 1
- >
- >|