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  • 1
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: A sensitive and specific method for determining three forms of methylarginine, i.e., NG-monomethylarginine, NG,NG-dimethylarginine, and NG,NG-dimethylarginine, in mammalian tissues was developed. After partial purification by ion-exchange chromatography, the methyl-arginines were derivatized to phenylthiocarbamyl compounds and quantitatively determined using HPLC with a reverse-phase C18 column. In rat organs, the highest concentrations of methylarginines were observed in the spleen. In rat brain, cerebellum and olfactory bulb contained large amounts of NG-monomethylarginine and NG,NG-dimethylarginine. A detailed study of the distribution of methylarginines in the bovine brain was also made, and the concentration of NG,NG-dimethylarginine was almost the same in all regions. The cerebellar gray matter, hippocampus, and hypothalamus contained large amounts of methylarginines. The distribution of methylarginines seems to parallel the distribution of nitric oxide synthase, which is known to be inhibited by NG-monomethylarginine. This may indicate that methylarginines play some role in controlling nitric oxide synthase activity.
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  • 2
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: The accumulation of inositol phosphates (IPs) in response to prostaglandins (PGs) was studied in NG108-15 cells preincubated with myo-[3H]inositol. As a positive control, bradykinin caused accumulation of IPs transiently at an early phase (within 1 min) and continuously during a late phase (15-60 min) of incubation in the cells. PGD2 and PGF2adid not significantly cause the accumulation of IPs at an early phase but significantly stimulated inositol bisphosphate (IP2) and inositol monophosphate (IP1) formation at a late phase of incubation. The maximum stimulation was obtained at 〈10−7M concentrations of these PGs. the levels being three-and twofold for IP2 and IP1 respectively. 9α, 11 β-PGF2 has a slight effect but PGE2 and the metabolites of PGD2 and PGF2α have no effect up to 10−6M. The effects of PGD2 and PGF2α were not additive, but the effect of each PG was additive to that of bradykinin at a late phase of incubation.Inositol 1-monophosphate was mainly identified in the stimulation by 10−5 M PGD2 and 10−5MPGF2a, whereas both inositol 1-monophosphate and inositol 4-monophosphate were produced in the stimulation by 10−5M bradykinin. Depletion of extracellular Ca2+ diminished the stimulatory effect of PGD2 and PGF2α and late-phase effect of bradykinin, but simple Ca2+ influx into the cells by high K+, ionomycin, or A23187 failed to cause such late-phase effects. These results suggest that PGD2 and PGF2α specifically stimulate hydrolysis of inositol phospholipids.
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  • 3
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Many reports have suggested that γ-aminobutyric acid (GABA) may play a role in organophosphate-in-duced convulsions. The balance between GABA and acetylcholine (ACh) in the brain also has been suggested by some investigators to be related to brain excitability. We examined these questions by studying the levels of GABA and ACh and the ratios of GABA to ACh in rat striata and cerebella (two major motor control areas in the CNS) after the administration of soman, an organophosphate acetylcholinesterase inhibitor also known as nerve gas. Male Sprague-Dawley rats weighing 250–300 g were injected subcutaneously with three different doses of soman: a subconvulsive dose of 40 μg/kg (approximately 30% of the ED50 for convulsions in rats), a convulsive dose of 120 μg/kg (approximately one ED50 for convulsions), and a higher convulsive dose of 150 μg/kg (approximately 120% of the ED50 for convulsions). The incidence and severity of convulsions were monitored in individual rats until they were sacrificed by focused microwave irradiation of the head at the following time points after soman administration: 4 min, a time prior to the onset of convulsions; 10 min, the time of onset of convulsions; 1 h, the time of peak convulsive activity; and 6 h, a time at which rats were recovering from convulsions. Results showed that in rat striata and cerebella, neither changes in levels of GABA and ACh nor changes in ratios of GABA to ACh were related to soman-induced convulsions, i.e., none of the changes in either levels or ratios of these two neurotransmitters were related to the initiation of, maintenance of, or recovery from soman-induced convulsions.
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  • 4
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 48 (1987), S. 0 
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: The distribution of α-(γ-aminobutyryl)-hypusine was examined in several organs of the rabbit and in the brain of the rat, rabbit, dog, ox, and monkey. The peptide occurred only in the brains, but appeared to be absent from dog brain. Concentrations were higher in the cerebral hemispheres than in other portions of the brain. No significant difference between white and gray matter was observed.
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  • 5
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Nephrology 7 (2002), S. 0 
    ISSN: 1440-1797
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
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  • 6
    ISSN: 1440-1797
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: SUMMARY: FK506-induced nephrotoxicity is characterized by a disturbance in renal haemody-namics that is attributed to an imbalance between the various modulators of renal vascular tone. It has not been well defined whether nitric oxide (NO), as an important vasoactive factor, is involved in FK506-induced nephrotoxicity. This study was designed to evaluate the involvement of nitric oxide in FK506-induced nephrotoxicity by investigating NO synthesis and NO synthase (NOS) expression in the kidney of rats treated with FK506. Male Wistar rats weighing 240–260 g, aged 11 weeks, were administered with FK506 (3.2mg/kg per day i.m.) for 4 weeks. Renal function and urinary NOx was measured using biochemical methods at the end of both 2 and 4 weeks of treatment. Expression of NOS protein and NOS mRNA in the kidney was also investigated using Western blot analysis and reverse transcription/polymerase chain reaction, respectively. FK506 administration induced nephrotoxicity, which was indicated by renal dysfunction (elevated blood urea nitrogen and creatinine, and reduced creatinine clearance, P 〈 0.05 vs control). FK506-induced nephrotoxicity was accompanied by higher urinary NOx excretion at the end of 2 weeks' treatment. In parallel with an increase in NO synthesis, increased eNOS protein and mRNA expression were also found in the renal medulla and renal cortex at week 2. the expression remained at higher levels in the renal medulla and returned to normal levels in the renal cortex at week 4. FK506 treatment induced nephrotoxicity in rats, which was accompanied by a temporal increase in NO synthesis in the kidney. Increased eNOS protein and mRNA expression were also found in the kidney of treated rats, which may be responsible for the enhanced NO synthesis.
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  • 7
    ISSN: 1440-1797
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Summary: Most cases of adult type IgA nephropathy (IgAN) have an insidious onset and asymptomatic course. However, some patients reveal recurrent macroscopic haematuria following episodes of respiratory or urinary tract infections. In order to clarify the correlation between clinical features and histological alterations or prognosis, 42 cases of early stage IgAN and 40 cases with acute exacerbation episodes were investigated and compared with a control group. Early stage cases were defined as having had a renal biopsy within 1 year after the first detection of urinary abnormalities, and had normal urinary findings within the 12 months before the first detection of urinary abnormalities. Acute exacerbation cases were defined as macroscopic haematuria or worsening of urinary abnormalities after acute infectious episodes and undergoing a renal biopsy within 120 days after the onset of these episodes. the early stage cases had better renal function and lower systolic and diastolic blood pressure than that of control group. They also showed milder changes in mesangial cell proliferation, mesangial matrix increase, totally sclerotic glomeruli, and tubulo-interstitial changes. However, it is important to note that glomerular and interstitial sclerotic changes were observed even in early stage cases. Endothelial detachment was noticed more frequently in the early stage cases. Acute exacerbation cases revealed lesions of endocapillary proliferation, mesangiolysis and endothelial detachment more frequently, although these changes were segmental in each glomerulus. There was no statistical difference in disease prognosis between cases with and without acute exacerbation. These data indicated that there are characteristic histological changes in early stage cases and acute exacerbation cases of IgAN.
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  • 8
    ISSN: 1442-2042
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Background: We used buserelin acetate ([D-Ser(But)6] LHRH), an LHRH agonist and strong blocker of LH secretion, as a treatment for prostatic cancer. It is possible that this LHRH agonist has a proliferative effect on the prostate in addition to suppressing LH secretion. The purpose of this study was to examine the proliferative effect of LHRH agonist on rat prostatic epithelial cells. Methods: We determined the optimal dose of testosterone necessary to maintain a positive level of proliferating cell nuclear antigen (PCNA) in the ventral prostatic epithelial cells of castrated Wistar rats. Testosterone-treated rats then received various doses of buserelin acetate. Castrated rats without exogenous testosterone also received buserelin acetate. The PCNA positivity was determined by immunohistochemistry with anti-PCNA monoclonal antibody. Results: The optimal dose of testosterone enanthate was 4mg at 0 and 28 days after castration. Administration of buserelin acetate on day 0 and 28 in doses of 0.1 6mg to 1.28mg significantly increased PCNA positivity in a dose-dependent manner. Administration of buserelin acetate to castrated rats without testosterone also increased PCNA positivity but there was no statistical significance. Conclusions: Buserelin acetate has a potentiating effect on the proliferation of ventral prostatic epithelial cells of castrated rat in the presence of a physiological level of exogenous testosterone. This effect may slightly influence the result of hormonal therapy by LHRH agonist.
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  • 9
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Anaesthesia 48 (1993), S. 0 
    ISSN: 1365-2044
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: A newly designed 4 FG double-lumen catheter with the second port located either 5 or 7 cm proximal to the tip was tested in five children undergoing open heart surgery. The catheter was inserted percutaneously and initially positioned in the superior vena cava, right atrium or inferior vena cava. During cardiopulmonary bypass, the tip of the catheter was repositioned manually in the left atrium across the interatrial septum. In all patients, left atrial pressure was monitored successfully while central venous pressure was monitored with the second port positioned in the superior vena cava. Removal of the catheter from the left atrium was easily performed and caused no problems.
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  • 10
    ISSN: 1369-1600
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: We tested the hypothesis that phospholipids are altered in skeletal muscles of rats exposed to ethanol for either acute (2.5 hours) or prolonged (6 weeks) periods. In acute studies, rats were dosed with saline (0.15 mmol/l; controls) or ethanol (75 mmol/kg body weight; treated). There were four groups: (A) saline (control); (B) cyanamide (an aldehyde dehydrogenase inhibitor); (C) ethanol; and (D) cyanamide+ethanol. In prolonged studies, two groups of rats were fed liquid diets containing 35% of total dietary energy as either glucose [group (E)] or ethanol [group (F)]. At the end of the treatments, membrane phospholipids were measured in soleus (Type I fibre-predominant) and plantaris (Type II fibre-predominant) muscle. In acute studies, ethanol alone [(A) vs. (C)] and cyanamide+ethanol [(A) vs. (D)] significantly increased 18:2 in plantaris (p 〈0.05), whereas in soleus none of the treatments had any effect on the phospholipids. In prolonged studies [(E) vs. (F)], there were decreases in 16:0 (p 〈0.05) and 18:1 (p 〈0.01) and increases in 18:2 (p〈0.001) in plantaris. In soleus, decreases in 18:1 (p〈0.05) and increases in 18:2 (p 〈0.01) occurred. In conclusion, alterations in the proportions of 16:0, 18:1 and 18:2 provide evidence of an altered membrane domain which may contribute to the pathogenesis of alcohol-induced muscle disease. Changes due to prolonged exposure are more profound than those in acute exposure and the preferential effects in Type II plantaris may reflect the greater susceptibility of this muscle to alcohol.
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