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961.
To investigate whether the receptor blockades of angiotensin II type 1 and aldosterone receptors can prevent renal tissue injury in relation to the renal tissue mRNA levels of peroxisome proliferation-activated receptors-gamma (PPAR-gamma) and transforming growth factor-beta (1) (TGF-beta(1)) in spontaneously hypertensive rats (SHR) given N(G)-nitro-L-arginine methyl ester (L-NAME), which is considered a model of malignant hypertension. This study was performed in 5 groups of 17-week-old male SHR treated for 3 weeks as follows: group 1, control; group 2, L-NAME (50 mg/L in drinking); group 3, L-NAME plus aldosterone antagonist, spironolactone (SPRL, 100 mg/kg/day); group 4, L-NAME plus angiotensin II type 1 receptor blocker, telmisartan (TELM, 3 mg/kg/day); group 5, L-NAME plus combination therapy (COMB) with low-dose TELM (1 mg/kg/day) and SPRL (100 mg/kg/day). Urinary protein excretion and the glomerular injury score were significantly reduced in the SPRL, TELM, and COMB groups as compared with the L-NAME group, while significant blood pressure reduction was observed only in the TELM group. In the TELM and COMB groups, the perivascular cell infiltration and fibrosis area were significantly reduced together with the PPAR-gamma mRNA increase and TGF- beta(1) mRNA decrease. The urinary excretion of nitric oxides was significantly recovered and the wall to lumen ratio of the interlobular artery was significantly reduced only in the COMB group compared with the L-NAME group. Combined administration of 1 mg/kg/day telmisartan and 100 mg/kg/day spironolactone is thought to be effective in alleviating hypertensive renal injuries independently of blood pressure changes. The anti-inflammatory and antifibrotic effects due to PPAR-gamma activation and TGF-beta(1) inhibition may participate in the renoprotection of this combination therapy. 相似文献
962.
963.
Kawakubo Y Kamio S Nose T Iwanami A Nakagome K Fukuda M Kato N Rogers MA Kasai K 《Psychiatry research》2007,152(2-3):261-265
Neurobiological mechanisms for social skills acquisition in schizophrenia remain largely unknown. We investigated whether an electrophysiological index of cognitive function predicts the degree of training-related social skills improvement in schizophrenia. Thirteen patients with schizophrenia underwent assessment of mismatch negativity (MMN) event-related potentials, followed by participation in a 3-month social skills training. Larger right frontal/temporal MMN current density values elicited by across-phoneme change were significantly associated with individual degrees of improvement in total social skills scores as assessed by a structured role play test. Although preliminary, these results suggest that phonetic MMN could be an index of social skills acquisition in patients with schizophrenia. 相似文献
964.
Aihara M Ida I Yuuki N Oshima A Kumano H Takahashi K Fukuda M Oriuchi N Endo K Matsuda H Mikuni M 《Psychiatry research》2007,155(3):245-256
Dysregulation of the hypothalamic-pituitary-adrenocortical (HPA) axis is one of the most prominent neurobiological findings in major depressive disorder (MDD). The relationship of regional brain metabolism to HPA axis dysfunction in depressed patients, however, is still unclear. In this study, to examine the clinical pharmacotherapeutic effects on HPA axis function and brain metabolism in MDD patients, we performed the combined dexamethasone (DEX)/corticotropin-releasing hormone (CRH) test on 24 antidepressant-free patients with MDD a few days after positron emission tomography (PET) with a radiotracer, [(18)F]-fluorodeoxyglucose (FDG). Moreover, 10 patients who responded to pharmacotherapy were re-tested. 75% of unmedicated MDD patients exhibited a heightened cortisol response to the DEX/CRH test, and thus were defined as non-suppressors. Non-suppressors showed a marked hypometabolism in the medial prefrontal cortex as compared with suppressors. After successful pharmacotherapy, enhanced cortisol responsiveness normalized. Prior to treatment of the unmedicated MDD, a significant hypometabolism in various frontal regions and a significant hypermetabolism in the right hippocampus and parahippocampal gyrus were observed compared with controls. Metabolic activity in treatment responders showed a normalizing pattern in almost all the areas that had been characterized by metabolic abnormality at baseline except for the medial prefrontal cortex. These results indicate that depressed patients remitted with antidepressant treatment were accompanied by resolution of HPA dysregulation and alteration of regional glucose metabolism in the prefrontal cortical, limbic and paralimbic regions. 相似文献
965.
Yokoyama S Watanabe J Iwata K Ikuta N Haji T Usui N Taira M Miyamoto T Nakamura W Sato S Horie K Kawashima R 《Neuropsychologia》2007,45(5):989-996
We used functional magnetic resonance imaging (fMRI) to investigate whether activation in Broca's area is greater during the processing of passive versus active sentences in the brains of healthy subjects. Twenty Japanese native speakers performed a visual sentence comprehension task in which they were asked to read a visually presented sentence and to identify the agent or the patient in the sentence by pressing a button. We found that the processing of passive sentences elicited no greater activation than that of active sentences in Broca's area. However, passive sentences elicited greater activation than active sentences in the left frontal operculum and the inferior parietal lobule. Thus, our neuroimaging results suggest that deficits in the comprehension of passive sentences in Japanese aphasics are induced not by lesions to Broca's area, but to the left frontal operculum and/or the inferior parietal lobule. 相似文献
966.
Suzuki K Awata S Oyama Y Fujiyama M Takano T Sugawara A Matsuoka H 《Progress in neuro-psychopharmacology & biological psychiatry》2007,31(4):956-958
We report the case of a 70-year-old man with Addison's disease who developed severe agitated depression resulting in life-threatening medical conditions. The depression was treated safely with electroconvulsive therapy (ECT) combined with steroid cover. Administration of steroid cover just before each ECT session may increase safety of the ECT procedure in psychiatric patients with Addison's disease. 相似文献
967.
Kainic acid (KA)-induced status epilepticus (SE) produces hippocampal neuronal death, which varies from necrosis to apoptosis or programmed cell death (PCD). We examined whether the type of neuronal death was dependent on KA dose. Adult rats were induced SE by intraperitoneal injection of KA at 9 mg/kg (K9) or 12 mg/kg (K12). Hippocampal neuronal death was assessed by TUNEL staining, electron microscopy, and Western blotting of caspase-3 on days 1, 3 and 7 after SE induction. K12 rats showed higher a mortality rate and shorter latency to the onset of SE when compared with K9 rats. In both groups, acidophilic and pyknotic neurons were evident in CA1 at 24h after SE and neuronal loss developed from day 3. The degenerated neurons became TUNEL-positive on days 3 and 7 in K9 rats but not in K12 rats. Caspase-3 activation was detected on days 3 and 7 in K9 rats but was undetectable in K12 rats. Ultrastructural study revealed shrunken neurons exhibiting pyknotic nuclei containing small and dispersed chromatin clumps 24h after SE in CA1. No cells exhibited apoptosis. On days 3 and 7, the degenerated neurons were necrotic with high electron density and small chromatin clumps. There were no ultrastructural differences between the K9 and K12 groups. These results revealed that differences in KA dose affected the delayed cell death (3 and 7 days after SE); however, no effect was seen on the early cell death (24h after SE). Moderate-dose KA induced necrosis, while low-dose KA induced PCD. 相似文献
968.
Sachiko Maeda Kazuho Sakamoto Isao Matsuoka Takahiro Iwamoto Junko Kimura 《Journal of pharmacological sciences》2009,109(4):565-572
The expression levels of the Na+/Ca2+ exchanger type 1 (NCX1) change under various cardiac pathophysiological conditions, but the mechanism is unknown. We previously demonstrated that lysophosphatidylcholine (LPC) increased NCX1 expression by activating RhoB in H9c2 cardiomyoblasts. Conversely, fluvastatin (Flv), a 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitor, decreased NCX1 mRNA and protein expression by inhibiting RhoB. RhoB can be isoprenylated by either geranylgeranylpyrophosphate (GGPP) or farnesylpyrophosphate (FPP). Here we investigated which of GGPP or FPP is involved in the NCX1-increasing effect of LPC. When LPC was added with GGPP to the Flv-treated H9c2 cells, NCX1 mRNA was increased to a level significantly higher than that in the control cells. Only GGPP, but not FPP, allowed LPC to increase NCX1 mRNA in the presence of Flv. Furthermore, geranylgeranyltransferase 1 inhibitor (GGTI), but not farnesyltransferase inhibitor (FTI), inhibited the LPC-induced NCX1 mRNA increase. We conclude that geranylgeranylation, but not farnesylation, of RhoB mediates LPC-induced NCX1 mRNA increase in H9c2 cells. 相似文献
969.
Shigeyuki Yamada Xiu Quan Zhang Nobuhiro Matsuoka Troy Badger William H. Barry 《Toxicology and applied pharmacology》2009,236(1):71-77
Aims
Our goal was to determine if clinically relevant concentrations of aqueous extract of cigarette smoke (CSE) have direct deleterious effects on ventricular myocytes during simulated ischemia, and to investigate the mechanisms involved.Methods
CSE was prepared with a smoking chamber. Ischemia was simulated by metabolic inhibition (MI) with cyanide (CN) and 0 glucose. Adult rabbit and mouse ventricular myocyte [Ca2+]i was measured by flow cytometry using fluo-3. Mitochondrial [Ca2+] was measured with confocal microscopy, and Rhod-2 fluorescence. The mitochondrial permeability transition (MPT) was detected by TMRM fluorescence and myocyte contracture. Myocyte oxidative stress was quantified by dichlorofluorescein (DCF) fluorescence with confocal microscopy.Results
CSE 0.1% increased myocyte contracture caused by MI. The nicotine concentration (HPLC) in 0.1% CSE was 15 ng/ml, similar to that in humans after smoking cigarettes. CSE 0.1% increased mitochondrial Ca2+ uptake, and increased the susceptibility of mitochondria to the MPT. CSE 0.1% increased DCF fluorescence in isolated myocytes, and increased [Ca2+]i in paced myocytes exposed to 2.0 mM CN, 0 glucose (P-MI). These effects were inhibited by the superoxide scavenger Tiron. The effect of CSE on [Ca2+]i during P-MI was also prevented by ranolazine.Conclusions
CSE in clinically relevant concentrations increases myocyte [Ca2+]i during simulated ischemia, and increases myocyte susceptibility to the MPT. These effects appear to be mediated at least in part by oxidative radicals in CSE, and likely contribute to the effects of cigarette smoke to increase myocardial infarct size, and to decrease angina threshold. 相似文献970.
Takashi Uehara Tomiki Sumiyoshi Tomonori Seo Hiroko Itoh Tadasu Matsuoka Michio Suzuki Masayoshi Kurachi 《Psychopharmacology》2009,206(4):623-630