Facial impaling on a scythe.
Explore the source record for details and available documents.
Biomedical subjects
Publications and source records attributed to L Eroğlu.
Explore the source record for details and available documents.
A mid-plantar ulcer was successfully reconstructed with an extended V-Y flap incorporating part of the flexor digitorum brevis muscle to achieve more volume and increase the safety of the flap. This flap can be used as a reliable alternative to other techniques to repair a moderately sized defect of the plantar midfoot.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Moclobemide (MOC), a selective and reversible MAO-A inhibitor, was claimed to have both anxiolytic and anxiogenic properties. Therefore, we assessed whether: (1) acute and subchronic (10 days) MOC treatments, in doses which display antidepressant activity, affect the performance of rats in the elevated plus-maze that provides detection of both anxiolytic and anxiogenic properties in the same experimental conditions; (2) the alpha 2 antagonist yohimbine (YOH), which increases noradrenaline (NA) release, is able to modify the effects of MOC treatments in the elevated plus-maze. The results showed that MOC, at doses of 10 and 20 mg kg-1 i.p. either acutely or subchronically administered, significantly reduced the immobility time in the forced swimming test in rats. In other words, it displayed antidepressant activity. In the elevated plus-maze, acutely administered MOC (20 mg kg-1 i.p.) significantly increased both the percentage of open arm entries and the time spent in open arms, while only the former parameter was increased in response to 10 mg kg-1 i.p. MOC treatment. Thus, the anxiolytic action of MOC at a dose of 20 mg kg-1 i.p. was more prominent. Subchronically administered MOC at both doses significantly increased the two parameters. Hence, it can be stated that anxiolytic action of subchronically administered MOC appears to be more pronounced. Acutely administered YOH (0.5 mg kg-1 i.p.) showed anxiogenic effect in the elevated plus-maze. However, in both acutely and subchronically MOC-treated animals, YOH failed to exert its anxiogenic effect. This implies the importance of NA-gic activity in the MOC-induced anxiolytic action.
Explore the source record for details and available documents.
Methylene blue (MB) has been intermittently used in manic depressive illness over the past century. However, to our knowledge, it has not been studied in the behavioural animal models. The present study was designed to evaluate whether the intravenous (i.v.) administration of MB in a dose range of 1.87-60 mg kg-1 would affect the performance of rats in the elevated plus-maze and the forced swimming (FST) tests. In the plus-maze, MB in doses ranging from 3.25 to 30 mg kg-1 significantly increased the percentage of open arm entries and exhibited an inverted U-shaped dose-response curve. Over a dose range, 7.5-30 mg kg-1, MB also increased time spent in open arms. These data suggest that MB has anxiolytic properties. On the other hand, MB, at doses of 15 and 30 mg kg-1 significantly decreased the immobility time in the FST and behaved as an antidepressant compound in these doses. As known, MB has prominent effects on the nitrergic system; Nitric oxide (NO) produced from L-arginine by the enzyme NO-synthase (NOS) activates soluble guanylyl cyclase (sGC) and exerts its effects on tissues through cGMP. MB acts as a direct inhibitor of NOS as well as of sGC. It also inactivates NO extracellularly through generation of superoxide anions. Thus, it can be speculated that NOS-NO-cGMP pathway may be involved in the antidepressant and anxiolytic actions of MB, and this may lead to search for new antidepressant and anxiolytic compounds.
Explore the source record for details and available documents.
There have been several reports that convulsions, although rare, occur in patients who received fluoroquinolones. In this study, conducted for the evaluation of the convulsant action of fluoroquinolones, the effect of ofloxacin and ciprofloxacin on pentylenetetrazol-induced convulsions were investigated in mice. Mice were pretreated intraperitoneally (IP) with saline, ofloxacin (20 or 80 mg/kg) or ciprofloxacin (20 or 80 mg/kg) 30 minutes before subcutaneous (SC) administration of pentylenetetrazol (40 or 60 mg/kg). In another experiment, diazepam (5 mg/kg) was injected (IP) in mice alone or in combination with ofloxacin (80 mg/kg) 30 minutes before pentylenetetrazol (40 mg/kg) administration (SC). In each experiment mice were observed over the following hour for the incidence and onset of clonic convulsions. Results showed that both doses of ofloxacin increased the incidence of clonic convulsions induced by 40 mg/kg pentylenetetrazol. This effect, however was only significant in the higher dose and inhibited by diazepam. On the other hand, a similar proconvulsant effect by ciprofloxacin could not be demonstrated.
The possible role of voltage-sensitive calcium channels (VSCCs) in the anxiolytic effect of ethanol was investigated using three different doses of ethanol (0.5, 1.0 and 2.0 g/kg) with calcium agonist Bay K 8644 (0.5 mg/kg) and calcium antagonist nifedipine (5 mg/kg) in rats. Ethanol produced an anxiolytic effect in a dose-dependent manner. The Bay K 8644-potentiated anxiolytic effect of ethanol, however, Bay K 8644 did not alter anxiety when used alone. Nifedipine itself showed an anxiolytic effect but did not change the ethanol-induced anxiolytic effect. This finding may lead to the consideration of the neurochemical mechanisms of the anxiolytic effects of ethanol and nifedipine as they vary from each other.
There have been several reports that insomnia occurs in some patients who receive ofloxacin. Since almost no experimental data on ofloxacin-induced insomnia were available, this study was conducted for the evaluation of ofloxacin effects on sleep parameters in mice. In Experiment 1, mice were pretreated with ofloxacin (20 or 40 mg/kg IP) or saline 15 minutes before sodium pentobarbital (35 mg/kg IP). Experiment 2 was carried out in two days. On the first day mice were treated twice, in the morning and in the evening, with ofloxacin (20 or 80 mg/kg IP) or saline. On the second morning, mice were pretreated with the same doses of ofloxacin or saline 15 minutes before sodium pentobarbital (35 mg/kg IP). Sleep latency and sleeping time were recorded in each experiment. Results showed that ofloxacin had no apparent effect on sleep latency, but caused a shortening in sleeping time. However, this effect was significant only in the 40 and 80 mg/kg ofloxacin-treated groups.
The possible involvement of voltage sensitive calcium channels (VSCCs) in both locomotor activity and striatal homovanillic acid (HVA) alterations in acutely low (0.5 g/kg) and high (2 g/kg) dose ethanol-treated rats was investigated. Both doses of ethanol produced inhibitory effects on both locomotor activity and striatal HVA levels. Bay K 8644 significantly potentiated and nifedipine reversed the locomotor inhibitory effect of low-dose ethanol, whereas both drugs did not alter locomotor activity and striatal HVA levels, when used alone. On the other hand, both Bay K 8644 and nifedipine significantly reversed the decrease in striatal HVA levels induced by the low and high doses of ethanol.
The effect of nifedipine on serum theophylline levels in 13 female hypertensive patients having asthma on theophylline therapy has been investigated. Administration of a slow release theophylline product in a dose of 200 mg bidaily for 15 days provided a steady-state through serum theophylline concentration (11.2 +/- 2.7 micrograms/ml). After this period, 10 mg bidaily nifedipine was added to therapy and trough serum theophylline levels, pulmonary function tests and blood pressure measurements have been performed following 15 and 45 days of simultaneous use of theophylline and nifedipine. No change has been observed in serum theophylline level after 15 days of simultaneous use, however after 45 days, serum theophylline level was significantly lower (7.3 +/- 1 micrograms/ml). There were no changes in clinical responsiveness of either of these drugs.
A comparison has been made between liposome-encapsulated and free indomethacin for their anti-inflammatory activities in the carrageenan paw oedema test in rats, and their inhibitory effect on platelet aggregation induced by adenosine 5-diphosphate (ADP) in-vitro. Free indomethacin, 3 mg kg-1, strongly inhibited carrageenan-induced oedema and a similar inhibitory activity was shown by 0.3 mg kg-1 of encapsulated drug. For the inhibition of platelet aggregation, the threshold concentration of free drug was 0.559 mM. At this concentration, at least 5 min incubation was needed to achieve 12.5% and 45 min for 50% inhibition. The inhibition was much stronger with encapsulated drug, and pre-incubation of 28 microM encapsulated drug for 10 min with platelet-rich plasma before addition of ADP completely inhibited platelet aggregation.