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Biomedical subjects

A A Mustafa

Publications and source records attributed to A A Mustafa.

At least 19 recordsLinked to original sources

Attitudes of Kuwaiti parents toward physical punishment of children.

OBJECTIVE: The major aim was to describe parental attitudes to physical punishments and examine their sociodemographic correlates. A related aim was to assess the association of parents' own experience of physical punishment with attitudes to punishment of children. METHOD: A cross-sectional survey was conducted during the second week of December, 1996 in five general clinics covering the major administrative areas of Kuwait: 337 Kuwaiti mothers and fathers with at least one living child were contacted; 95% were successfully interviewed using a structured questionnaire. RESULTS: Eighty-six percent of parents agreed with physical punishment as a means of child disciplining. Agreement with punishment was higher in case of serious misbehaviors such as stealing (63%), sniffing glue and using drugs (77%). Multiple regression results showed that parent's lower level of education and Bedouin ethnicity were positively associated with agreement on physical punishment. Larger percentages of parents who had experienced physical punishments themselves agreed with such punishment to discipline their children, but this was not statistically significant. CONCLUSIONS: In recent years education has become widespread for both sexes. An inverse association between educational level and agreement on physical beating suggest that attitudes to this form of child disciplining are changing. Those with a Bedouin ethnic background still adhere more strictly to the traditional forms of child disciplining including physical beating. There is a need for conducting research on the possible negative psychosocial impacts of physical punishment in view of findings from other countries.

Adolescent↗

Natural honey prevents ischaemia-reperfusion-induced gastric mucosal lesions and increased vascular permeability in rats.

OBJECTIVE: It has been proposed that natural honey may contain a 'sucralfate-like' substance. Recent studies have shown that sucralfate affords protection against ischaemia-reperfusion-induced injuries in the rat stomach. Therefore, the effect of honey was studied on ischaemia-reperfusion-induced gastric lesions, intraluminal bleeding, vascular permeability and non-protein sulphhydryls (NP-SH) in the rat stomach. METHODS: Rats were subjected to 30 min of gastric ischaemia in the presence of 100 mM HCl and reperfusion period of 60 min. Intraluminal bleeding was assessed macroscopically and the gastric lesions were graded microscopically under an inverted microscope. Vascular permeability was quantified by measuring spectrophotometrically the extravasated Evans blue dye in the stomach. NP-SH levels were measured spectrophotometrically. A luminol-dependent chemiluminescence method was used to assess antioxidant effects of honey in vitro. RESULTS: There were significantly more gastric lesions, more severe intraluminal bleeding, more leakage of Evans blue and depletion of NP-SH during the reperfusion period as compared to controls. Pre-treatment with honey (0.078-0.625 g/kg, orally) or dimethyl sulphoxide (0.02-0.08 g/kg, intraperitoneally) 30 min before the ischaemia-reperfusion dose-dependently reduced the gastric lesions and intraluminal bleeding and decreased the vascular permeability. Furthermore, honey reversed the ischaemia-reperfusion-induced depletion of NP-SH levels and inhibited the luminol-dependent chemiluminescence induced in a cell-free xanthine-xanthine oxidase system. CONCLUSION: These results suggest that gastric protection by honey may be a result of its antioxidant effect. It is suggested that this property of honey may be due to the presence of a 'sucralfate-like' substance.

Animals↗

Sucralfate attenuates gastric mucosal lesions and increased vascular permeability induced by ischaemia and reperfusion in rats.

Recent evidence suggests that oxygen-derived free radicals are involved in mediating gastric microvascular and parenchymal cell injuries induced by ischaemia and reperfusion. Therefore, the effect of the locally acting anti-ulcer drug, sucralfate, was studied on ischaemia and reperfusion (e.g. induced gastric lesions, intraluminal bleeding, changes in vascular permeability and non-protein sulfhydryl levels in the rat stomach). Allopurinol was used as a known standard antioxidant drug. Rats were subjected to 30 min of gastric ischaemia in the presence of 100 mmol/L hydrochloric acid and reperfusion periods of 15, 30 or 60 min duration. The gastric lesions were assessed microscopically under an inverted microscope. The vascular permeability was quantified by measuring the extravasated Evans blue in the stomach. There were significantly greater numbers of gastric lesions, intraluminal bleeding and leakage of Evans blue during all reperfusion periods as compared with those of ischaemia, with maximum effects occurring at 60 min following reperfusion. Pretreatment with sucralfate (31.25-250 mg/kg, p.o.) or allopurinol (12.5-50 mg/kg, i.p.) 30 min before the procedure, dose-dependently reduced the gastric lesions, intraluminal bleeding, and decreased the vascular permeability induced by ischaemia and reperfusion. Furthermore, sucralfate dose-dependently reverses the ischaemia and reperfusion-induced depletion of mucosal non-protein sulfhydryl levels and inhibited the superoxide radical production in both cell-free xanthine-xanthine oxidase and in the stimulated polymorphonuclear cellular systems. These results suggest that the protection produced by sucralfate against gastric injury may be due to its antioxidant effects.

Allopurinol↗

Differential effects of fluoxetine on isoprenaline-stimulated water intake in ethanol-treated rats: a role for beta-adrenoceptors.

We examined the effects of subchronic (4 days) administration of the 5-hydroxytryptamine (5-HT) re-uptake inhibitors, fluoxetine, fluvoxamine and zimelidine and the noradrenaline-uptake inhibitor, desipramine, on isoprenaline-induced water drinking in rats treated with ethanol. These rats demonstrated significant increases in water drinking as compared to control rats that had received only i.p. injections of distilled water (P < 0.01). Administration of fluoxetine (5-20 mg/kg daily i.p., for 4 days) dose-dependently decreased water intake as compared to that of rats treated with ethanol only. In contrast, fluvoxamine, zimelidine (10 mg/kg i.p.) and desipramine (5 mg/kg i.p.) produced no significant effects on water intake. Pretreatment of animals with spiperone, methysergide, ritanserin, zacopride and BRL 43694A, together with fluoxetine, failed to reverse the inhibitory effect of the latter on isoprenaline-stimulated water intake. The results of the present study indicate that the action of fluoxetine on isoprenaline-stimulated water drinking in ethanol-treated rats may be mediated by an action on beta-adrenoceptors.

Analysis of Variance↗

Prevalence of camel brucellosis in Libya.

Sera of 967 camels of both sexes were tested for antibodies to Brucella using the Rose Bengal plate test, serum agglutination test and the complement fixation test. The prevalence of positive sera was 4.1 per cent. Samples collected for cultural examination revealed 9 isolates. Five isolates were from milk samples, 3 from aborted foetuses and one from a vaginal swab. All isolates were identified and biotyped as Brucella melitensis biovar 1.

Agglutination Tests↗

Field-oriented trial of the Chinese Brucella suis strain 2 vaccine on sheep and goats in Libya.

The Chinese Brucella suis S2 vaccine was studied in a flock of sheep and goats in field conditions. The locally-produced vaccine was orally administered in the form of a drench to 446 ewes, 50 lambs and 20 adult goats. After vaccination, abortion and excretion of the vaccine strain in vaginal discharges or in milk did not occur. Serological tests became positive in 92% of animals at 4 wk post-vaccination and declined to near nil after 1 yr. The protection conferred by the vaccine against a double virulent B melitensis conjunctival challenge which infected 10/10 control ewes was on average 53% in ewes (32/60) and 71% in goats (5/7). Abortion rates were respectively 100% (7/7) in control ewes versus 44% (25/57) and 28% (2/7) in vaccinated ewes and goats. The vaccine was thus found to be safe, antigenic and reasonably protective against the challenge dose used.

Abortion, Veterinary↗

Verapamil enhances the inhibitory effect of diclofenac on the chemiluminescence of human polymorphonuclear leukocytes and carrageenan-induced rat's paw oedema.

Diclofenac dose-dependently (1.25, 2.5 and 5 mg/kg, i.p.) inhibited the oedema produced by carrageenan in the rat's paw. This anti-inflammatory effect was enhanced by the co-administration of various doses (10, 20, and 30 mg/kg i.p.) of verapamil. Diclofenac or the calcium channel blocker, verapamil, when added separately, inhibited the chemiluminescence (CL) response of isolated human polymorphonuclear leukocytes (PMNs) stimulated by either the soluble agent, phorbol myristate acetate, (PMA) or by particulate opsonized zymosan (OPZ) in a dose-dependent manner. When verapamil was combined with diclofenac, in vitro, the inhibitory effect on PMA or OPZ-induced CL response was synergistic. This inhibitory effect on either diclofenac or verapamil on the isolated PMNs was readily reversible when the PMNs were washed with phosphate buffered saline (PBS). Additionally, diclofenac or verapamil did not significantly affect the viability of PMNs. It is concluded that verapamil enhances the anti-inflammatory effect of diclofenac in vivo and potentiates its inhibitory effect on the CL of isolated human PMNs in vitro.

Animals↗

Mechanisms of L-NG-nitro arginine methyl ester-induced antinociception in mice: a role for serotonergic and adrenergic neurons.

1. The mechanisms involved in the antinociceptive action of L-NG-nitro arginine methyl ester (L-NAME) were investigated in mice. 2. Intraperitoneal administration of L-NAME produced a dose-dependent antinociception in the tail-flick, hot-plate and phenyl-p-quinone-induced writhing tests. 3. Pretreatment with the catecholamine depletors 6-hydroxydopamine (5 micrograms i.c.v.) or reserpine (5 mg/kg i.p.) or the serotonin synthesis inhibitor, p-chlorophenylalanine methyl ester (200 mg/kg i.p. on 2 consecutive days) resulted in a significant decrease in the antinociceptive effect of L-NAME. 4. Similarly, pretreatment with the selective alpha 1-adrenoceptor antagonist prazonin (2.5 mg/kg, i.p.), or the non-selective alpha-adrenoceptor blocker, phentolamine (5 mg/kg, i.p.) antagonized the antinociceptive effect of L-NAME. 5. However, the administration of the selective alpha 2-adrenoceptor antagonist, idazoxan (2.5 mg/kg i.p.) was without effect. 6. Likewise, pretreatment with the serotonin 5-HT2 receptor blocker, ketanserin (1 mg/kg, i.p.), the D2 dopamine receptor antagonist (+/-) sulpiride (30 mg/kg, i.p.) or the opioid antagonist naloxone (5 mg/kg, i.p.) did not inhibit the antinociceptive effect of L-NAME. 7. These results suggest that L-NAME produces antinociception in the mouse probably by an action on adrenergic and serotonergic synapses.

Adrenergic alpha-Antagonists↗

Enhancement of imipramine-induced rat brain beta-adrenoreceptor desensitization by subacute co-administration of trazodone, zimelidine, quipazine or 5-hydroxytryptophan.

The present work was undertaken to characterize the role of serotonin in the regulation of beta-adrenoceptors utilizing isoprenaline-induced water drinking in the rat. For this purpose, a serotonin precursor, 5-hydroxytryptophan (24.3 mg/kg/day, PO), the serotonin neuronal uptake blockers, trazodone (18.5 mg/kg/day, PO), or zimelidine (14.6 mg/kg/day, PO) or a serotonin agonist, quipazine (12.6 mg/kg/day, PO) were administered either alone or in combination with imipramine for a period of 4 days. While none of these drugs alone showed any significant effect in attenuating the effects of isoprenaline-induced water drinking, their co- administration with imipramine did produce a significant reduction in isoprenaline-induced drinking. Simultaneous injection of the serotonin synthesis inhibitor, p-chlorophenylalanine (200 mg/kg/day, IP), has resulted in blockade of this acceleration of desensitization of beta-adrenoceptors produced by the subacute co-administration of trazodone or quipazine with imipramine. The selective 5HT2 receptor antagonist ketanserin (4 mg/kg/day/ IP) significantly inhibited the attenuation of the isoprenaline-induced drinking attained by the co-administration of quipazine with imipramine, while methysergide (2 mg/kg/day, IP) which blocks both 5HT1 and 5HT2 receptors failed to produce a significant effect on this response. These results indicate that the inhibition of the synaptosomal uptake of serotonin by quipazine seems to be more pertinent than its serotoninergic agonistic effect in the desensitization of central beta-adrenoceptors in the rat. Thus, it can be concluded that noradrenaline and serotonin are both required for the process of the desensitization of central beta-adrenoceptor systems by antidepressants.

5-Hydroxytryptophan↗

Rapid desensitization of central beta-adrenoceptors in rat after subacute treatment with imipramine and calcium entry blockers.

The subcutaneous (s.c.) administration of isoprenaline to rats produced a dose-dependent increase in water drinking which was effectively antagonized by propranolol. This dipsogenic response was significantly inhibited after the intraperitoneal (i.p.) administration of imipramine (15 mg/kg/day), together with either of the following calcium entry blockers, for four days: diltiazem (15 mg/kg/day), verapamil (10 mg/kg/day), nifedipine (10 mg/kg/day) or nicardipine (15 mg/kg/day). Simultaneous injection of the inhibitor of the synthesis of serotonin, p-chlorophenylalanine (200 mg/kg/day, i.p.), did not affect this attenuation of the isoprenaline-induced response. Similarly, the selective 5-HT2 receptor agonist, 1-(2,5-dimethoxy-4-methylphenyl)-2-aminopropane (DOM) or the 5-HT2 receptor antagonist, ketanserin, had no significant effect on the attenuation of isoprenaline-induced drinking behaviour. The inhibition of isoprenaline-induced drinking, was, however, effectively attenuated after treatment of the animals with 6-hydroxydopamine (2.5 micrograms) or clonidine (30 micrograms), injected intracerebroventricularly (i.c.v.). These results indicate that the calcium entry blockers accelerate the desensitization of central beta-adrenoceptors possibly by an action on central adrenoceptors of the rat.

1-Propanol↗

Bromocriptine-induced hypothermia in Balb/C mice: its possible mechanism of action.

1. Administration of bromocriptine (0.1-2.5 mg/kg, i.p.) to mice produced hypothermia. 2. Pretreatment with the alpha 1-adrenoceptor blocker, prazosin (2.0 mg/kg, i.p.) or the alpha 2-adrenoceptor antagonist yohimbine (2.5 mg/kg, i.p.) had no effect on this response. 3. The inhibitor of catecholamine synthesis, alpha-methyl-p-tyrosine, and the muscarinic antagonist, atropine (10 mg/kg, i.p.) failed to alter the hypothermia. 4. Pretreatment with the dopamine (DA) receptor antagonists haloperidol (0.02 mg/kg, i.p.) or cis-flupenthixol (0.01 mg/kg, i.p.) completely blocked this response while trans-flupenthixol (0.05 mg/kg, i.p.) was inactive. 5. Depletion of 5-HT in the brain by p-chlorophenylalanine reduced the hypothermic response. 6. Similarly, pretreatment with the serotonergic (5-HT) receptor blocker ketanserin (1 mg/kg, i.p.) attenuated the hypothermia and at a dose of 2 mg/kg (i.p.) it completely blocked the hypothermic response. 7. Methysergide (5 mg/kg, i.p.) was also effective in antagonizing the hypothermia. 8. It was concluded that both DA and 5-HT mechanisms are involved in bromocriptine-induced hypothermia in mice.

Acetylcholine↗

Acceleration of rat brain beta-adrenoceptor subsensitivity following the coadministration of histamine receptor antagonists with imipramine.

Systemic administration of isoprenaline to rats produced a dose-dependent increase in water drinking which was effectively blocked by propranolol. This dipsogenic effect was significantly inhibited by the subacute (4 days) administration of imipramine (18.1 mg/kg/day) together with either the H1-histamine receptor antagonist, chlorpheniramine (0.1 or 1.32 mg/kg/day), or the H2-histamine antagonist, cimetidine (1.91 mg/kg/day) or ranitidine (0.60 or 1.51 mg/kg/day). The oral subacute administration of imipramine alone had no significant effect on this behavior. However, chronic ingestion of imipramine alone (21 days) caused a significant reduction in the isoprenaline-induced behavior. It is concluded that the desensitization of central beta-adrenoceptors, as evidenced by inhibition of isoprenaline-induced drinking, can be accelerated following the oral subacute co-administration of imipramine with either H1- or H2-histamine receptor antagonists. It is also seems the central histamine receptors may partially contribute towards the mechanism of antidepressant effect of imipramine.

Animals↗

Study on the renal and cardiovascular activities of aminouracil derivatives.

The synthesis of five 4-aminouracil derivatives has been described. These compounds, which are chemically related to xanthines, were tested for possible diuretic activity. The increase in urine output by compounds I, III, and V was comparable to that produced by caffeine in an equimolar dose (5 x 10(-3) M). On the isolated rabbit's heart (Langendorff's preparation), compounds I, III, and V (5 x 10(-5) M) significantly increased the amplitude of contractions without having any significant effect on heart rate. Only these three compounds (4.4 x 10(-8) M) relaxed the isolated rabbit thoracic aorta and rat anococcygeus smooth muscle which were precontracted with norepinephrine (4 x 10(-8) M). This action was not antagonized by atropine, propranolol, or methylene blue, ruling out the involvement of acetylcholine, beta receptors, or endothelium-derived relaxing factor (EDRF). The relaxant effect, however, was reversed by the addition of calcium chloride, suggesting that this relaxation may be due to inhibition of the entry of extracellular calcium into the cells.

Animals↗

Organ doses from cardiac and carotid digital subtraction angiography.

Estimates of mean organ doses from cardiac and carotid digital subtraction angiography (DSA) are obtained from measurements done using a Rando-Alderson tissue-equivalent phantom. Thermoluminescent dosemeter chips and discs were calibrated and used for all measurements in the primary and scattered radiation fields. Skin doses as well as mean doses received by the thyroid, lung, lens of the eye, breast, uterus and the ovaries were measured. A 30 degree right anterior oblique (RAO) cardiac DSA study produces a beam entrance dose of about 121 mGy at a rate of 0.48 mGy/frame. The highest mean organ dose from cardiac DSA was to the lung with a value of 14.4 mGy. The rest of the organs received doses below 1 mGy. In carotid DSA, the mean entrance doses resulted from the RAO, left anterior oblique, and the Towne's view projections give an average of 168 mGy at a rate of 8.4 mGy/frame. The highest mean organ dose from the three projections, 21 mGy, was received by the thyroid. The uterus and ovaries received the lowest doses from both procedures with values below 0.04 mGy. Patient and phantom surface exposures were compared using an exposure area product system. Hence, exposure conditions used for measuring organ doses on the phantom were adjusted to resemble those used for patients.

Angiocardiography↗

Antipsychotic properties of new N-(4-substituted-1-piperazinylethyl)- and N-(4-substituted-1-piperidinylethyl)-phthalimides.

A series of N-(4-phenyl- and 4-pyridyl-1-piperazinylethyl)- and N-(4-phenyl-1-piperidinylethyl)-phthalmides were synthesized and tested for antipsychotic activity. All compounds suppressed the spontaneous motor activity and the apomorphine-induced climbing in mice and pergolide-induced locomotor activity in rats, demonstrating psychotropic properties equal to the corresponding properties of sulpiride. Although the compounds, like sulpiride, were less potent than haloperidol in blocking the locomotor activities, they caused no catalepsy, a major side effect following treatment with conventional antipsychotic agents. It is likely that the new compounds produce their neuroleptic activities through inhibition of limbic dopamine receptors.

Animals↗

Interaction of some atypical antidepressants and adrenoceptor antagonists with imipramine: a behavioural study with isoprenaline-induced drinking.

The systemic administration of isoprenaline to rats produced a dose-dependent increase in drinking which was antagonized by propranolol. While oral administration of the antidepressant, imipramine, alone had no significant effect on this response, the increase was significantly inhibited by administration of imipramine together with each of the following drugs over a period of 4 days: bupropion (21.0 mg/kg/day, p.o.), a selective inhibitor of the uptake of dopamine and nomifensine (10.6 mg/kg/day, p.o.), a relatively selective dopamine and a blocker of the uptake of noradrenaline. Similarly, the combination of the selective alpha 1-adrenoceptor antagonist, prazosin (2.37 mg/kg/day, p.o.); the selective alpha 2-adrenoceptor antagonist, yohimbine (2.38 mg/kg/day, p.o.) or the non-selective alpha-adrenoceptor blocker, phentolamine (4.65 mg/kg/day, p.o.) with imipramine caused a significant inhibition of the isoprenaline-induced drinking. It is concluded that fast desensitization of central beta-adrenoceptors in the rat can be produced after the oral subacute simultaneous administration of imipramine with alpha-adrenoceptor antagonists or atypical antidepressants, such as nomifensine or bupropion.

Adrenergic alpha-Antagonists↗

Effects of disopyramide on the isolated rabbit aorta and pulmonary artery.

1. Disopyramide (8 X 10(-5)-4 X 10(-4) M) contracted the rabbit aortic strips and this could be prevented by verapamil or by omitting Ca2+ from Krebs solution. 2. Disopyramide (1.5-6 X 10(-5) M) significantly potentiated the contractile response of the rabbit aortic strips to noradrenaline, clonidine and methoxamine but not that of potassium chloride. 3. Disopyramide (2-6 X 10(-5) M) attenuated the contractile response of the rabbit pulmonary artery to transmural electrical stimulation but potentiated response to noradrenaline. Similar results were observed with the portal vein. 4. The relaxant effect of acetylcholine, on the rabbit aortic ring precontracted with noradrenaline, was blocked by disopyramide while the relaxant effect of adenosine-5'-triphosphate (ATP) was not blocked.

Animals↗