External iliac artery aneurysm and ureteric obstruction in a solitary kidney.
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Acute Kidney Injury↗
Biomedical subjects
M Raza
Publications and source records attributed to M Raza.
Therapeutic abortion in Islam: contemporary views of Muslim Shiite scholars and effect of recent Iranian legislation.
Abortion is forbidden under normal circumstances by nearly all the major world religions. Traditionally, abortion was not deemed permissible by Muslim scholars. Shiite scholars considered it forbidden after implantation of the fertilised ovum. However, Sunni scholars have held various opinions on the matter, but all agreed that after 4 months gestation abortion was not permitted. In addition, classical Islamic scholarship had only considered threats to maternal health as a reason for therapeutic abortion. Recently, scholars have begun to consider the effect of severe fetal deformities on the mother, the families and society. This has led some scholars to reconsider the prohibition on abortion in limited circumstances. This article reviews the Islamic basis for the prohibition of abortion and the reasons for its justification. Contemporary rulings from leading Shiite scholars and from the Sunni school of thought are presented and reviewed. The status of abortion in Muslim countries is reviewed, with special emphasis on the therapeutic abortion law passed by the Iranian Parliament in 2003. This law approved therapeutic abortion before 16 weeks of gestation under limited circumstances, including medical conditions related to fetal and maternal health. Recent measures in Iran provide an opportunity for the Muslim scholars in other countries to review their traditional stance on abortion.
Abortion, Therapeutic↗
Adenovirus viraemia and dissemination unresponsive to antiviral therapy in advanced HIV-1 infection.
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AIDS Dementia Complex↗
Use of rocuronium and magnesium sulphate.
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Analgesics↗
Brain death: recent ethical and religious considerations in Iran.
The Islamic Republic of Iran has a long history of medicine. The principles derived from core Islamic teachings provide a comprehensive moral, ethical, and legal framework for the practice of medicine. The issue of brain death has significant impact on the procurement of organs from cadavers. It is a major subject of debate and interest to bioscientists, legal experts, religious scholars, and the general public. Laws related to the ethical and legal aspects of cadaver organ donation from the brain dead have not been defined in many Muslim countries. This report presents recent advances in Iranian law with regard to the ethics of organ transplantation and the definition of brain death.
Brain Death↗
Some sociocultural aspects of cadaver organ donation: recent rulings from Iran.
Cultural and social factors strongly influence cadaveric organ donation and removal. In Muslim countries such as Iran, there is general public resistance to removal of organs despite clear rulings from religious leaders. Recently, some religious authorities have waived family permission and allowed cadaver organ removal even if the deceased person had not made a declaration for organ donation. Scholars have also exempted physicians from paying a legal penalty for removing organs in such cases. Cadaver organ donation is also allowed if the deceased person has made a declaration that money obtained from the recipient be spent to pay his debts or for public welfare and that the organ be used to save a life. There is no restriction on organ donation between people of different religions in normal circumstances. We conclude that these rulings should positively influence present sociocultural cadaver organ donation trends in Iran.
Cadaver↗
Impediments to implementing evidence-based mental health in developing countries.
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Developing Countries↗
Pain during injection of propofol: the effect of prior administration of ephedrine.
Propofol causes pain on intravenous injection in 28 to 90% of patients. A number of techniques have been tried to minimize propofol-induced pain, with variable results. In a randomized, double-blind, placebo-controlled trial, we compared the efficacy of ephedrine 30 microg/kg pretreatment to lignocaine 40 mg for prevention of propofol-induced pain. Ninety-three adult patients, ASA 1 and 2, undergoing elective laparoscopic cholecystectomy were randomly assigned to three groups of 31 each. Group 1 received normal saline, group 2 received lignocaine 2% (40 mg) and group 3 received 30 microg/kg ephedrine. All pretreatment drugs were made up to 2 ml. Pain at the time of propofol injection was assessed on a four-point scale: 0=no pain, 1 =mild pain, 2=moderate pain, and 3=severe pain. Twenty-seven patients (87%) of ephedrine pretreatment patients had pain during intravenous injection of propofol as compared to 24 (77%) in the normal saline group. In the lignocaine group, propofol-induced pain was observed in only 13 (42%) when compared with other study groups (P<0.05). Pretreatment with ephedrine 30 microg/kg did not attenuate pain associated with intravenous injection of propofol, nor did it improve haemodynamic stability during induction. However, pretreatment with 2% lignocaine (40 mg) was effective in attenuating propofol-associated pain.
Adolescent↗
Contribution of functional voltage-gated Na+ channel expression to cell behaviors involved in the metastatic cascade in rat prostate cancer: I. Lateral motility.
Previous work suggested that functional voltage-gated Na(+) channels (VGSCs) are expressed specifically in strongly metastatic cells of rat and human prostate cancer (PCa), thereby raising the possibility that VGSC activity could be involved in cellular behavior(s) related to the metastatic cascade. In the present study, the possible role of VGSCs in the lateral motility of rat PCa cells was investigated in vitro by testing the effect of modulators that either block or enhance VGSC activity. Two rat PCa cell lines of markedly different metastatic ability were used in a comparative approach: the strongly metastatic MAT-LyLu and the weakly metastatic AT-2 cell line, only the former being known to express functional VGSCs. Using both electrophysiological recording and a motility assay, the effects of two VGSC blockers (tetrodotoxin and phenytoin) and four potential openers (veratridine, aconitine, ATX II, and brevetoxin) were monitored on (a) Na(+) channel activity and (b) cell motility over 48 h. Tetrodotoxin (at 1 microM) and phenytoin (at 50 microM) both decreased the motility index of the MAT-LyLu cell line by 47 and 11%, respectively. Veratridine (at 20 microM) and brevetoxin (at 10 nM) had no effect on the motility of either cell line, whilst aconitine (at 100 microM) and ATX II (at 25 pM) significantly increased the motility of the MAT-LyLu cell line by 15 and 9%, respectively. Importantly, at the concentrations used, none of these drugs had effects on the proliferation or viability of either cell line. The results, taken together, would suggest strongly that functional VGSC expression enhances cellular motility of PCa cells. The relevance of these findings to the metastatic process in PCa is discussed.
Aconitine↗
Potentiation of diclofenac-induced anti-inflammatory response by aminoguanidine in carrageenan-induced acute inflammation in rats: the role of nitric oxide.
OBJECTIVE: To investigate whether aminoguanidine (AG) treatment enhances the anti-inflammatory effect of diclofenac in an acute inflammation model in rats. MATERIAL AND METHODS: In 48 rats carrageenan-induced paw edema was used as an acute inflammation model. Inflammatory activity was assessed at 1.5, 3 and 6 h after sub-planter injection of carrageenan (0.1 ml of a 1% solution in 0.85% saline). The anti-inflammatory effect of diclofenac (25 mg/kg, i.p.) was studied in comparison to that of the selective inducible nitric oxide synthase (iNOS) inhibitor, AG, and of nitric oxide donor, sodium nitroprusside (SNP). RESULTS: AG, failed to inhibit inflammation during the first 3 h following carrageenan administration, but caused a slight, although statistically insignificant inhibition at 6 h. Diclofenac significantly reduced the carrageenan-induced edema in rat paw at all the time points studied. Administration of diclofenac after AG pretreatment caused significant (P < 0.001) reduction in edema that was double that of diclofenac alone 6 h after carrageenan injection. Administration of SNP as a single dose after AG pretreatment prevented any potentiation of anti-inflammatory response that was observed in the case of AG combined with diclofenac treatment. CONCLUSION: These results show that AG markedly potentiates the anti-inflammatory activity of diclofenac at 6 h and this potentiation effect is nitric oxide-dependent.
Acute Disease↗
Effect of vigabatrin on contractile response to arachidonic acid and prostaglandins in smooth muscle preparations and platelet aggregation in experimental laboratory animals.
Gamma-vinyl GABA (vigabatrin; VGB), an irreversible inhibitor of GABA-transaminase, was evaluated for its effect on the contractile responses to PGE(2) or its precursor arachidonic acid (AA) in guinea pig ileum (GPI) and non-pregnant rat uterus. Rationale behind this study was the rise in gamma-aminobutyric acid (GABA) contents in the peripheral organs after treatment with GABAergic agents and extensive interconnections of neuromediators and their interactions.Indomethacin, the standard NSAID, at 6.1x10(-5) and 12.2x10(-5)M concentrations highly significantly (P<0.001) inhibited contractile responses induced by AA (4.3x10(-5)M) in the isolated GPI. Incubation of the GPI segments with VGB at different concentrations (25, 100 and 200mM) failed to inhibit AA-induced contractile responses in the same preparation. In fact, VGB at 25mM significantly (P<0.05) potentiated the contractile effect of AA 4.3x10(-5)M. Incubation of the same tissue with GABA at 13x10(-3) and 26x10(-3)M inhibited responses elicited by AA at 4.3x10(-5)M that was significant (P<0.05) only with low concentration of GABA. Conversely, a higher concentration (64x10(-3)M) of GABA was needed to antagonise PGE(2) (9.4x10(-6)M)-induced contractions in the same tissue. Almost similar results (i.e. inhibition of contractile responses to AA and PGE(2)) were obtained with isolated non-pregnant rat uterus. These findings suggested that GABA had the potential to inhibit prostaglandin (PG) synthesis and/or antagonise PGE(2) responses in isolated GPI and rat uterus. The addition of 35 or 70 micro l of rat aorta incubation medium caused a dose-dependent inhibition of ADP-induced aggregation being 21.5 and 43.5%, respectively, an indication of prostacycline (PGI(2)) contents. Pre-incubation of rat aortic tissues with VGB (96.8mM) significantly (P<0.05) reversed the anti-aggregatory activity of control aortic prostacycline on ADP-induced aggregation. These findings suggested that VGB might inhibit PGI(2) activity through the inhibition of its synthesis.
4-Aminobutyrate Transaminase↗
A comparison of hepatoprotective activities of aminoguanidine and N-acetylcysteine in rat against the toxic damage induced by azathioprine.
Azathioprine (AZA) is an important drug used in the therapy of autoimmune system disorders. It induces hepatotoxicity that restricts its use. The rationale behind this study was the proven efficacy of N-acetylcysteine (NAC; a replenisher of sulfhydryls) and reports on the antioxidant potential of aminoguanidine (AG; an iNOS inhibitor), that might be useful to protect against the toxic implications of AZA. AG (100 mg/kg; i.p.) or NAC (100 mg/kg; i.p.) were administered to the Wistar male rats for 7 days and after that AZA (15 mg/kg, i.p.) was given as a single dose. This caused an increase in the activity of hepatic aminotransferases (AST and ALT) in the serum 24 h after AZA treatment. AZA (7.5 or 15 mg/kg, i.p.) also caused an increase in rat liver lipid peroxides and a lowering of reduced glutathione (GSH) contents. In the other part of experiment, protective effects of AG and NAC were observed on AZA induced hepatotoxicity. NAC significantly protected against the toxic effects produced by AZA. Pretreatment with NAC prevented any change in the activities of both the aminotransferases after AZA. This pretreatment also resulted in a significant decline in the contents of lipid peroxides and a significant elevation in GSH level was evident after AZA treatment. In the group with AG pretreatment the activities of AST and ALT did not increase significantly after AZA when compared to control. However, the lipid peroxides and GSH levels did not have any significant difference when compared to AZA group. These observations also indicate that the improvement in the GSH levels by NAC is the most significant protective mechanism rather than any other mechanistic profile. The protective effect of AG against the enzyme leakage seems to be through the liver cell membrane permeability restoration and is independent of any effects on liver GSH contents.
Acetylcysteine↗
Boric acid enhances in vivo Ehrlich ascites carcinoma cell proliferation in Swiss albino mice.
The influence of boric acid, a boron carrier, on Ehrlich ascites carcinoma (EAC) cell-bearing mice was investigated in view of its importance in the boron neutron capture therapy and the influence of boron on proliferation and progression of cancer cells mediated by proteoglycans and collagen. The present study included the evaluation of boric acid for the effects on total count and viability of EAC cells in addition to their non-protein sulfhydryls (NP-SH) and malondialdehyde (MDA) contents as parameters for conjugative detoxication potency and possible oxidative damage. The EAC cell-bearing animals were also observed for the effect on survival, body weight changes, and histopathological evaluation of the tumors grown at the site of inoculation. The treatment with boric acid significantly increased the total number of peritoneal EAC cells and their viability. A significant increase in the body weight was observed that dose-dependently reached plateau levels by 20 days of treatment. Conversely, a reduction in the duration of survival of these animals was evident with the same protocol. Boric acid treatment resulted in a decrease in NP-SH contents with a concomitant increase in MDA levels in EAC cells as revealed by the results of the biochemical analysis. These data are supported by our results on histopathological investigations, which apparently showed fast growth, in addition to several mitotic figures and mixed inflammatory reaction, after treatment with boric acid. It seems likely that a particular combination of properties of boric acid, rather than a single characteristic alone, will provide useful information on the use of this boron carrier in neutron capture therapy.
Animals↗
Long-term alteration of calcium homeostatic mechanisms in the pilocarpine model of temporal lobe epilepsy.
The pilocarpine model of temporal lobe epilepsy is an animal model that shares many of the clinical and pathophysiological characteristics of temporal lobe or limbic epilepsy in humans. This model of acquired epilepsy produces spontaneous recurrent seizure discharges following an initial brain injury produced by pilocarpine-induced status epilepticus. Understanding the molecular mechanisms mediating these long lasting changes in neuronal excitability would provide an important insight into developing new strategies for the treatment and possible prevention of this condition. Our laboratory has been studying the role of alterations in calcium and calcium-dependent systems in mediating some of the long-term neuroplasticity changes associated with epileptogenesis. In this study, [Ca(2+)](i) imaging fluorescence microscopy was performed on CA1 hippocampal neurons acutely isolated from control and chronically epileptic animals at 1 year after the induction of epileptogenesis with two different fluorescent dyes (Fura-2 and Fura-FF) having high and low affinities for [Ca(2+)](i). The high affinity Ca(2+) indicator Fura-2 was utilized to evaluate [Ca(2+)](i) levels up to 900 nM and the low affinity indicator Fura-FF was employed for evaluating [Ca(2+)](i) levels above this range. Baseline [Ca(2+)](i) levels and the ability to restore resting [Ca(2+)](i) levels after a brief exposure to several glutamate concentrations in control and epileptic neurons were evaluated. Epileptic neurons demonstrated a statistically significantly higher baseline [Ca(2+)](i) level in comparison to age-matched control animals. This alteration in basal [Ca(2+)](i) levels persisted up to 1 year after the induction of epileptogenesis. In addition, the epileptic neurons were unable to rapidly restore [Ca(2+)](i) levels to baseline following the glutamate-induced [Ca(2+)](i) loads. These changes in Ca(2+) regulation were not produced by a single seizure and were not normalized by controlling the seizures in the epileptic animals with anticonvulsant treatment. Peak [Ca(2+)](i) levels in response to different concentrations of glutamate were the same in both epileptic and control neurons. Thus, glutamate produced the same initial [Ca(2+)](i) load in both epileptic and control neurons. Characterization of the viability of acutely isolated neurons from control and epileptic animals utilizing standard techniques to identify apoptotic or necrotic neurons demonstrated that epileptic neurons had no statistically significant difference in viability compared to age-matched controls. These results provide the first direct measurement of [Ca(2+)](i) levels in an intact model of epilepsy and indicate that epileptogenesis in this model produced long-lasting alterations in [Ca(2+)](i) homeostatic mechanisms that persist for up to 1 year after induction of epileptogenesis. These observations suggest that altered [Ca(2+)](i) homeostatic mechanisms may underlie some aspects of the epileptic phenotype and contribute to the persistent neuroplasticity changes associated with epilepsy.
Animals↗
Anticonvulsant activities of the FS-1 subfraction isolated from roots of Delphinium denudatum.
Delphinium denudatum Wall. (Ranunculaceae) is a medicinal herb used for the treatment of epilepsy in the subcontinent. The present study reports the anticonvulsant activities in the maximal electroshock test (MEST) and subcutaneous pentylenetetrazole (PTZ), bicuculline (BIC), picrotoxin (PIC)-induced seizures of the FS-1 subfraction (FS-1) that was obtained by purification of an aqueous fraction isolated from the roots of D. denudatum. In CF 1 mice, FS-1 (600 mg/kg i.p.) exhibited very potent anticonvulsant activity that was comparable to the effects of the well-known antiepileptic drug phenytoin (20 mg/kg) in MEST and protected 100% animals from hind limb tonic extension phase of this model. FS-1 also suppressed PTZ-induced threshold seizure and the loss of the righting reflex with tonic fore and hind limb extension by 100%, similar to the antiepileptic drug valproic acid (350 mg/kg). BIC-induced seizures were suppressed in 80% of the animals. FS-1 exhibited weak anticonvulsant effect on PIC-induced seizures, however, it significantly reduced mortality and delayed the onset of seizures. FS-1 had no effect on strychnine (STN)-induced extensor seizures. The results demonstrate the broad and potent anticonvulsant activity of the compounds in FS-1 of D. denudatum.
Animals↗
Anticonvulsant activities of ethanolic extract and aqueous fraction isolated from Delphinium denudatum.
Dried roots of Delphinium denudatum Wall. are a popular folk remedy for the treatment of epilepsy in the traditional Unani system of medicine in the sub-continent. We carried out anticonvulsant screening of the ethanolic extract (EE) and aqueous fraction (AF) of this plant utilising the maximal electroshock (MEST) and subcutaneous pentylenetetrazole (scPTZ), bicuculline (scBIC), picrotoxin (scPTX) and strychnine (scSTN) tests for anticonvulsant activity. EE had weak dose-dependent anticonvulsant effects on seizures induced by PTZ and BIC. AF exhibited dose-dependent activity against hind limb tonic extension phase (HLTE) of MEST and comparatively stronger anticonvulsant activity against seizures induced by PTZ and BIC. The results suggest the presence of potent anticonvulsant compounds in AF of D. denudatum and deserve further investigation for isolation of active compounds and elucidation of the mechanism of anticonvulsant action.
Animals↗
Effect of ninhydrin on the biochemical and histopathological changes induced by ethanol in gastric mucosa of rats.
Studies on the effect of ninhydrin in the normal gastric mucosa and against the ethanol induced gastric injury were undertaken in rats in view of the presence of a carbonyl function as well as hydroxyl groups in its chemical structure. In spite of its potentials to generate hydroxyl radicals, it is deemed to possess antioxidant property by virtue of its electrophilic nature. Recent studies have shown gastro-protection to mediate through a reaction between the electrophilic compounds and sulfhydryl groups of the mucosa. Hence it was found worthwhile to evaluate the interaction between the oxidant and antioxidant functions in the structure of the same compound. The effects of ninhydrin pretreatment on gastric mucosal injuries caused by 80% ethanol, 25% NaCl and 0.2M NaOH were investigated in rats. The gastric tissue in ethanol-treated rats was analyzed for different histopathological lesions. In addition, the effects on ethanol-induced changes in the gastric levels of proteins, nucleic acids, non-protein sulfhydryl (NP-SH) and malondialdehyde (MDA) were also evaluated. Ninhydrin, as such, failed to induce any significant changes in normal gastric mucosa, while its pretreatment at oral doses of 5, 10 and 20 mg/kg was found to provide a dose-dependent protection against the ulcers induced by ethanol, NaOH and NaCl. The results of histopathological evaluation revealed a protective effect of ninhydrin on congestion, hemorrhage, edema, erosions and necrosis caused by ethanol. Furthermore, the pretreatment afforded a dose-dependent inhibition of the ethanol-induced depletion of proteins, nucleic acids, NP-SH and increase of MDA in the gastric tissue. The results obtained clearly demonstrate the anti-ulcerogenic activity of ninhydrin. The exact mechanism of action is not known. However, the carbonyl function in ninhydrin appears to achieve antioxidant balance and protect the gastric mucosa from the ethanol-induced gastric injury. Further studies are warranted to investigate the toxicity and detailed mechanism of action of this potent compound before any clinical trials, especially at the effective lower doses.
Animals↗
Inhibition of gastric mucosal damage by methylglyoxal pretreatment in rats.
The effect of methylglyoxal pretreatment on gastric mucosal injuries caused by 80% ethanol, 25% NaCl and 0.2 M NaOH, was investigated in rats. The effects caused by pylorous ligation accumulated gastric acid secretions and ethanol-induced changes in gastric mucus secretions, levels of proteins, nucleic acid, malondialdehyde (MDA) and non-protein sulfhydryl groups were also investigated. Methylglyoxal pretreatment at oral doses of 50, 100 and 200 mg/kg body weight was found to provide a dose-dependent protection against the ulcerogenic effects of different necrotizing agents used. With the same dose regimen methylglyoxal offered significant protection against ethanol-induced damage on the parameters evaluated for histopathology. Furthermore, the pretreatment afforded a dose-dependent inhibition of pylorous ligated accumulation of gastric acid secretions and ethanol-induced depletion of stomach wall mucus, proteins, nucleic acids, NP-SH contents and an increase in the MDA levels in gastric tissue. The protective effect of methylglyoxal against ethanol-induced damage to the gastric wall mucosa may be mediated through its effect on mucous production, proteins, nucleic acids, NP-SH groups and its free-radical scavenging property under the influence of polyamines stimulated by ornithine decarboxylase activity (ODC).
Animals↗