E Adeghate

United Arab Emirates University, Al Ain, Abu Dhabi, United Arab Emirates

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Publications (171)365.55 Total impact

  • Acta Chromatographica 12/2014; 26(4):649–656. · 0.64 Impact Factor
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    ABSTRACT: Neuroinflammation (NI) contributes to the pathogenesis of several neurodegenerative disorders. Epidemiological and a few animal studies have shown that chronic exposure of organophosphorus compounds (OPC) may cause neuronal injury and predispose to neuro- as well as psychotic disorders in conjunction with NI. However, in vivo studies are meager and do not represent the entire toxicologically diversified OPC. The present study aimed to investigate the effect of a highly toxic OPC, terbufos sulfone (TBS), on the status of proinflammatory cytokinesinterleukin-1β, interleukin-6 and tumor necrosis factor-α in adult's rats' brain. In addition, lactate dehydrogenase, nitric oxide and reduced glutathione were determined in brain homogenates. Red blood cell acetylcholinesterase was measured weekly. Sub-chronic, no-observable adverse effect level dose was employed. Four groups were setup - saline control, diabetes control, non-diabetes TBS and diabetes treated groups. Control groups received saline and the experimental groups were injected with TBS intraperitonealy for fifteen days daily. Twenty four hours after the last injection, the animals were euthanized to collect brain and serum samples. The study showed significant elevation of interleukin-6,tumor necrosis factor-α and lactate dehydrogenase in brain homogenates of TBS treated groups, while the presence of interleukin-1βwas significantly greater in the non-diabetes TBS treated group when compared with saline control. The increase was observed to be independent of acetylcholinesterase level and diabetes condition. The change in reduced glutathione was modest as compared with control. Based on the findings, the study concludes that the no-observable adverse effect level dose of TBS has potential to cause NI and subsequent neurodegeneration, a remarkable sign of many chronic neuronal and psychotic disorders. Further studies with prolonged exposure and other neurodegenerative parameters are warranted.
    CNS & Neurological Disorders - Drug Targets (Formerly Current Drug Targets - CNS & Neurological Disorders) 10/2014; · 3.77 Impact Factor
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    ABSTRACT: This paper reviews the blood–brain barrier (BBB) penetration of newly developed pyridinium aldoximes. Pyridinium aldoximes are highly charged hydrophilic compounds used in the treatment of subjects exposed to organophosphonates because they are effective as acetylcholinesterase reactivators. Pyridinium aldoximes have antidotal effects against poisoning with cholinesterase inhibitors, a frequent problem affecting people working with organophosphate-based insecticides and pesticides. Toxic organophosphonate products such as sarin and tabun can be used by terrorists as chemical warfare agents. This poses a severe challenge to all innocent and peace-loving people worldwide. This review gives a brief summary of BBB transporters and description of the current in vitro and in vivo methods for the characterization of BBB penetration of established and novel pyridinium aldoximes. The authors provide a putative mechanism of penetration, outline some future ways of formulation and discuss the possible advantages and disadvantages of increasing BBB penetration. Copyright © 2014 John Wiley & Sons, Ltd.
    Journal of Applied Toxicology 09/2014; · 2.60 Impact Factor
  • Ernest Adeghate, Erzsébet Fehér, Huba Kalász
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    ABSTRACT: Introduction: The worldwide number of patients suffering from diabetes mellitus (DM) is projected to approach 552 million by the year 2030. As diabetic neuropathy (DN) is present in 8% of new diabetic patients at the time of diagnosis and occurs in ∼ 50% of all patients with established DM, the number of patients who will develop painful DN will also increase. The suboptimal efficacies of currently approved drugs have prompted investigators to develop new therapeutic agents for the management of painful DN.Areas covered: In this review, the authors present and elucidate the current status of drugs under investigation for the treatment of painful DN. A short synopsis of currently approved drugs is also given. Literature information and data analysis were retrieved from PubMed, the American Diabetes and Neurological Associations Websites and ClinicalTrials.gov. The keywords used in the search included: DM, DN, painful diabetic neuropathy.Expert opinion: In addition to treating the pain associated with DN, the actual causes of the disease should also be targeted for improved management. It is hoped that drugs which improve vascular blood flow, induce neural regeneration, reduce hyperglycemia, oxidative stress and inflammation can be more effective for the overall treatment of painful DN.
    Expert Opinion on Investigational Drugs 08/2014; · 4.74 Impact Factor
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    ABSTRACT: Incretins, such as glucagon-like peptide-1 (GLP)-1, have been shown to elevate plasma insulin concentration. The purpose of this study is to investigate the cellular and molecular basis of the beneficial effects of GLP-1. Normal and diabetic male Wistar rats were treated with GLP-1 (50 ng/kg body weight) for 10 weeks. At the end of the experiment, pancreatic tissues were taken for immunohistochemistry, immunoelectron microscopy and real-time polymerase chain reaction studies. Samples of blood were retrieved from the animals for the measurement of enzymes and insulin. The results show that treatment of diabetic rats with GLP-1 caused significant (P < 0.05) reduction in body weight gain and blood glucose level. GLP-1 (10(-12)-10(-6) M) induced significant (P < 0.01) dose-dependent increases in insulin release from the pancreas of normal and diabetic rats compared to basal. Diabetes-induced abnormal liver (aspartate aminotransferase and alanine aminotransferase) and kidney (blood urea nitrogen and uric acid) parameters were corrected in GLP-1-treated rats compared to controls. GLP-1 treatment induced significant (P < 0.05) elevation in the expression of pancreatic duodenal homeobox-1, heat shock protein-70, glutathione peroxidase, insulin receptor and GLP-1-receptor genes in diabetic animals compared to controls. GLP-1 is present in pancreatic beta cells and significantly (P < 0.05) increased the number of insulin-, glutathione reductase- and catalase-immunoreactive islet cells. The results of this study show that GLP-1 is co-localized with insulin and seems to exert its beneficial effects by increasing cellular concentrations of endogenous antioxidant genes and other genes involved in the maintenance of pancreatic beta cell structure and function.
    Cell and Tissue Research 08/2014; · 3.68 Impact Factor
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    ABSTRACT: Glucagon-like peptide 1 (GLP-1) agonists are promising therapeutic agents in the treatment of diabetes mellitus. This study examines the mechanism of the protective effects of exenatide in experimental diabetes employing four groups of 10 rats each, in which two groups were streptozotocin-induced diabetic and two were control groups. One control and one diabetic group were treated with exenatide (1 µg/kg body weight) for 10 weeks. Blood plasma was taken for biochemical analyses while pancreatic tissue was taken for immunofluorescence and immunoelectron microscopy studies and real-time polymerase chain reaction for the expression of genes. The results show that exenatide improved body weight gain and reduced blood glucose in diabetic rats compared to control. Similarly, exenatide enhanced insulin release from pancreatic fragments and improved liver and kidney functions and lipid profile in diabetic rats compared to control. Exenatide not only induced significant increases in serum insulin level, but it also elevated the number of insulin-, GLP-1- and exenatide-positive cells compared to untreated control. Exenatide also elevated the number of catalase- and glutathione reductase-positive cells in diabetic rat pancreas compared to control. Exenatide caused significant elevation in the gene expressions of pancreatic duodenal homeobox-1, heat shock protein-70, glutathione peroxidase, insulin receptor and glucagon-like peptide-1 receptor in the pancreas of both control and diabetic rats compared to untreated animals. The results have demonstrated that exenatide can exert its beneficial and protective effects by elevating the levels of endogenous antioxidants and genes responsible for the survival, regeneration and proliferation of pancreatic beta cell.
    Journal of Endocrinology 12/2013; · 4.06 Impact Factor
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    ABSTRACT: Selegiline [(-)-deprenyl] is used to treat patients with Parkinson's disease. Nevertheless, in much higher doses it has beneficial effects in depression, and dementia of the aged patients. Selegiline undergoes a complex metabolic pathway. Its major metabolites include desmethylselegiline, (-)-methamphetamine and (-)-amphetamine, selegiline-N-oxide and formaldehyde as a small metabolic fragment in animal experiments. In addition, more than 40 minor metabolites of selegiline have also been either detected or proposed by investigators and researchers. This review analyses the pharmacological activity, generation pathway and the detection method of the major metabolites of selegiline.
    Current Medicinal Chemistry 12/2013; · 3.72 Impact Factor
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    ABSTRACT: Authorities of Drug Administration in the United States of America approved about 5000 drugs for use in the therapy or management of several diseases. About two hundred of these drugs have active metabolites and the knowledge of their medicinal chemistry is important both in medical practice and pharmaceutical research. This review gives a detailed description of the medicinal chemistry of drugs with active metabolites generated after conjugation. This review focused on glucuronide-, acetyl-, sulphate- and phosphate-conjugation of drugs, converting the drug into an active metabolite. This conversion essentially changed the lipophilicity of the drug.
    Mini Reviews in Medicinal Chemistry 10/2013; 13(11):1550-63. · 2.87 Impact Factor
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    ABSTRACT: Water-pipe smoking (WPS) is a common practice in the Middle East, and is now gaining popularity in Europe and USA. However, there is a limited number of studies on the respiratory effects of WPS. More specifically, the underlying pulmonary pathophysiologic mechanisms related to WPS exposure are not understood. Presently, we assessed the respiratory effects of nose-only exposure to mainstream WPS generated by commercially available honey flavored ``moasel`` tobacco. The duration of the session was 30 min/day and 5days/week for 1 month. Control mice were exposed to air only. Here, we measured in BALB/c mice the airway resistance using forced oscillation technique. Lung inflammation was assessed histopathologically and by biochemical analysis of bronchoalveolar lavage (BAL) fluid and oxidative stress was evaluated biochemically by measuring Lipid peroxidation, reduced glutathione and several antioxidant enzymes. Pulmonary inflammation assessment showed an increase in neutrophil and lymphocyte numbers. Likewise, airway resistance was significantly increased in WPS group compared to controls. Tumour necrosis factor α and interleukin 6 concentrations were significantly increased in BAL fluid. Lipid peroxidation in lung tissue was significantly increased whereas the level and activity of antioxidants including reduced glutathione, glutathione S transferase and superoxide dismutase were all significantly decreased following WPS exposure, indicating the occurrence of oxidative stress. Moreover, carboxyhemoglobin levels were significantly increased in the WPS group. We conclude that one-month nose-only exposure to WPS significantly increased airway resistance, inflammation and oxidative stress. Our results provide mechanistic explanation for the limited clinical studies which reported the detrimental respiratory effects of WPS.
    Journal of Applied Physiology 07/2013; · 3.48 Impact Factor
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    ABSTRACT: Nociceptinergic system has become an important target for drug development since the identification of the "orphan", opioid-like-1 receptor and the isolation of its endogenous agonist nociceptin. Involvement of nociceptinergic system has been verified in a wide range of pathophysiological processes. A large number of nociceptinergic agonists and antagonists with peptide and non-peptide structures were developed. Several non- peptide nociceptinergic antagonists were recently shown effective in different animal models of parkinsonism. Neuropharmacological background for antiparkinsonian effect of nociceptinergic antagonists, experimental models with high predictive value, nociceptinergic antagonists shown to have potential effect in Parkinson's disease are summarized. Medicinal chemistry data (logP and TPSA) of the NOP receptor antagonists found effective in animal models of Parkinson's disease are provided.
    Mini Reviews in Medicinal Chemistry 05/2013; · 2.87 Impact Factor
  • Ernest Adeghate, Tibor Donath, Abdu Adem
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    ABSTRACT: The prevalence of diabetes mellitus (DM) continues to increase because of sedentary life style and inappropriate diet. DM is one of the most common metabolic diseases, affecting more than 240 million people worldwide. It is projected that the number of people with DM will continue to increase in the next decade. Alzheimer disease (AD) is the most common cause of dementia, and affects over 24 million people globally, mostly senior citizens. The worldwide prevalence of AD is estimated to double in the next 20 years. How are these two chronic and debilitating diseases similar? Do they have common denominators? AD is similar to DM in many ways, in that both are associated with defective insulin release and/or signalling, impaired glucose uptake, amyloidosis, increased oxidative stress, stimulation of the apoptotic pathway, angiopathy, abnormal lipid peroxidation, ageing (in type 2 DM), brain atrophy, increased formation of advanced glycation end products and tau phosphorylation, impaired lipid metabolism and mitochondrial pathology. The pathogenesis of both AD and DM has genetic as well as environmental components. Both can also cause impaired cognition and dementia. All of these common denominators indicate that AD and DM share a lot of factors in terms of pathophysiology, histopathology and clinical outcome. These similarities can be used in the search for and design of effective pharmacotherapy for AD, since potent therapeutic agents such as insulin, incretins, oral hypoglycaemic agents and antioxidants used in the management of DM may play a key role in the treatment of patients with AD.
    Current Alzheimer research 04/2013; · 4.97 Impact Factor
  • Ernest Adeghate, Jaipaul Singh
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    ABSTRACT: Diabetes mellitus (DM) is a major metabolic disorder currently affecting over 250 million people globally. It costs the worldwide health services almost £800 billion annually to diagnose, treat and care for patients with diabetes. DM is predicted to rise to 350 million by 2030. If left unmanaged, DM can lead to numerous long-term complications including micro- and macro-angiopathy and heart failure (HF). Most diabetics usually die as a result of HF resulting from diabetes-induced coronary artery disease and cardiomyopathy. Coronary artery disease and cardiomyopathy are normally preceded by hyperglycaemia (HG). This review examines the structural changes, which occur within the myocardium and cardiomyocytes during exposure of the heart to diabetes-induced HG and HG-induced oxidative stress. HG and the resulting oxidative stress are associated with marked myocardial hypertrophy and fibrosis compared to control heart. At the ultrastructural level, cardiomyocytes subjected to chronic HG and subsequent oxidative stress display swollen mitochondria, reduced mitochondrial number and defective myofibrils and intercalated discs. Evidence from many studies shows that both type 1 and type 2 diabetes-induced HG can cause myocardial fibrosis, mitochondriopathy, myocyte hypertrophy and deranged myofibrils. All of these structural changes may eventually result in HF if left untreated.
    Heart Failure Reviews 03/2013; · 4.45 Impact Factor
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    ABSTRACT: Nociceptin and nocistatin are endogenous ligands of G protein coupled receptor family. Numerous techniques have been used to study the diverse parameters including, localization, distribution and ultrastructure of these peptides. The majority of the studies parameters are based on their physiological roles in different organ systems. The present study presents an overview of the different methods used for the study of nociceptin, nocistatin and their receptors. Nociceptin has been implicated in many physiological functions including, nociception, locomotion, stressed-induced analgesia, learning and memory, neurotransmitter and hormone release, renal function, neuronal differentiation, sexual and reproductive behavior, uterine contraction, feeding, anxiety, gastrointestinal motility, cardiovascular function, micturition, cough, hypoxic-ischemic brain injury, diuresis and sodium balance, temperature regulation, vestibular function, and mucosal transport. It has been noted that the use of light and electron microscopy was less frequent, though it may be one of the most promising tools to studying the intracellular localization of these neuropeptides. In addition, more studies on the level of circulating nociceptin and nocistatin are also necessary for investigating their clinical roles in health and disease. A variety of modern tools including physiological, light and electron microscopy (EM) are needed to decipher the extent of intracellular localization, tissue distribution and function of these peptides. The intracellular localization of nociceptin and nocistatin will require a high resolution transmission EM capable of identifying these peptides and other supporting molecules that co-localize with them. A tracing technique could also elucidate a possible migratory ability of nociceptin and nocistatin from one cellular compartment to the other.
    Peptides 02/2013; · 2.52 Impact Factor
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    ABSTRACT: Heart failure in chronic type 2 diabetes mellitus is partly attributable to adverse structural remodelling of the left ventricle (LV), but the contribution of hyperglycaemia (HG) per se in remodelling processes is debated. In this study, we examined the molecular signature of LV remodelling in 18-month-old spontaneously diabetic male Goto-Kakizaki (GK) rats that represent a long-term mildly diabetic phenotype, using histological, immunoblotting and quantitative gene expression approaches. Relative to age-matched Wistar controls, mildly diabetic GK rats presented with LV hypertrophy, increased expression of natriuretic peptides and phosphorylation of pro-hypertrophic Akt. Fibrosis proliferation in the GK LV paralleled increased transcriptional and biologically active pro-fibrogenic transforming growth factor-β1 (TGFβ1) in the LV with upregulated mRNA abundance for key extracellular matrix (ECM) components such as fibronectin, collagen type(s) 1 and 3α and regulators including matrix metalloproteinases 2 and 9, and their tissue inhibitor (TIMP) 4, connexin 43 and α5-integrin. GK rats also presented with altered mRNA expression for cardiac sarcoplasmic reticulum Ca(2+)ATPase, Na(+)/Ca(2+) exchanger and the L-type Ca(2+) channels which may contribute to the altered Ca(2+) transient kinetics previously observed in this model at 18 months of age (t test, p < 0.05 vs. age-matched Wistar control for all parameters). The results indicate that chronic mild HG can produce the molecular and structural correlates of a hypertrophic myopathy. Diffuse ECM proliferation in this model is possibly a product of HG-induced TGFβ1 upregulation and altered transcriptional profile of the ECM.
    Heart Failure Reviews 02/2013; · 4.45 Impact Factor
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    ABSTRACT: In vivo and in vitro systems were employed to investigate the biocompatibility of two forms of calcined mesoporous silica microparticles, MCM41-cal and SBA15-cal, with ventricular myocytes. These particles have potential clinical use in delivering bioactive compounds to the heart. Ventricular myocytes were isolated from 6 to 8 week male Wistar rats. The distribution of the particles in ventricular myocytes was investigated by transmission electron microscopy and scanning electron microscopy. The distribution of particles was also examined in cardiac muscle 10 min after intravenous injection of 2.0 mg/mL MCM41-cal. Myocyte shortening and the Ca(2+) transient were determined following exposure to 200 μg/mL MCM41-cal or SBA15-cal for 10 min. Within 10 min of incubation at 25 °C, both MCM41-cal and SBA15-cal were found attached to the plasma membrane, and some particles were observed inside ventricular myocytes. MCM41-cal was more abundant inside the myocytes than SBA15-cal. The particles had a notable affinity to mitochondrial membranes, where they eventually settled. Within 10 min of intravenous injection (2.0 mg/mL), MCM41-cal traversed the perivascular space, and some particles entered ventricular myocytes and localized around the mitochondrial membranes. The amplitude of shortening was slightly reduced in myocytes superperfused with MCM41-cal or SBA15-cal. The amplitude of the Ca(2+) transient was significantly reduced in myocytes superperfused with MCM41-cal but was only slightly reduced with SBA15-cal. Overall, the results show reasonable bioavailability and biocompatibility of MCM41-cal and SBA15-cal with ventricular myocytes.
    Chemical Research in Toxicology 12/2012; · 3.67 Impact Factor
  • Mohamed A Fahim, Saeed Tariq, Ernest Adeghate
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    ABSTRACT: Lead (Pb) is known to cause abnormal function of several systems including the male reproductive system, where it has been shown to reduce sperm count. In order to examine the morphological basis of the reduction in sperm count and a possible effect of vitamin E, lead acetate (1mg/kg body weight) was given to control and vitamin E-treated mice daily, intraperitoneally for 3 weeks. The testis and body of epididymis of the mice were subjected to electron microscopy study. Pb caused degenerative changes in spermatids inducing vacuolization and a reduction in the number of cytoplasmic organelles in Leydig cells. Pb also destroyed the stereocilia of epididymal epithelium. The addition of vitamin E ameliorated the severity of these morphological changes. In conclusion, Pb-induced reduction in sperm count may be due to changes in the ultrastructure of spermatids, epididymal epithelia and Leydig cells. These changes can be reduced by vitamin E.
    Annals of anatomy = Anatomischer Anzeiger: official organ of the Anatomische Gesellschaft 12/2012; · 1.96 Impact Factor
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    ABSTRACT: Much is known about the chronic effects of cigarette smoke (CS) on lung function and inflammation and development of chronic obstructive pulmonary disease. However, the underlying pathophysiological mechanisms related to the short-term exposure to CS are not fully understood. Here, we assessed the effect of CS generated by nine consecutive cigarettes per day for four days in a nose-only exposure system on airway resistance measured using forced oscillation technique, lung inflammation and oxidative stress in BALB/c mice. Control mice were exposed to air. Mice exposed to CS showed a significant increase of neutrophils and lymphocytes numbers in bronchoalveolar lavage (BAL). The total protein and endothelin levels in BAL fluid were significantly augmented suggesting an increase of alveolar-capillary barrier permeability. Similarly, airway resistance was significantly increased in the CS group compared with controls. Furthermore, reactive oxygen species and lipid peroxidation levels in lung tissue were significantly increased. The antioxidant activities of reduced glutathione, glutathione S transferase and superoxide dismutase were all significantly increased following CS exposure, indicating that CS could trigger adaptive responses that counterbalance the potentially damaging activity of oxygen radicals induced by CS exposure. In conclusion, our data indicate that short-term nose-only exposure to CS causes lung inflammation and increase of airway resistance mediated at least partly through the oxidative stress.
    Experimental Biology and Medicine 12/2012; 237(12):1449-56. · 2.80 Impact Factor
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    ABSTRACT: Metabolic fate plays an important role in the elimination of drugs and other foreign compounds from the body. Metabolism through various enzyme systems, makes the parent compound more hydrophilic, thus, it can be readily excreted from the body. Some active metabolites of drugs are produced following N-, O-, and S-desalkylation. These metabolites are either more or less potent, or as potent as their parent drugs. The removal of alkyl groups from tertiary aliphatic and acyclic amines is carried out by hepatic cytochrome P450 mixed-function oxidase enzymes. Several drugs undergo this process, which yields free hydroxyl-, or amino-groups, in addition to aldehyde from the splitted alkyl group. Metabolism of drugs into clinically active compounds indicates an extra target of therapeutic drug monitoring. Numerical data of logP values show how lipophilicity changes through metabolism to facilitate excretion. The example of phenacetin paracetamol opened up a way for improving pharmacological effect by the use of a metabolite. This review gives a detailed description of these drugs, their active and major metabolites found in humans or animals, metabolizing cytochrome P450s, and the most recent analytical methods for their determination.
    Current Medicinal Chemistry 08/2012; · 3.72 Impact Factor
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    ABSTRACT: There is an increasing belief that organophosphorus compounds (OPCs) impair glucose homeostasis and cause hyperglycemia and diabetes mellitus. The present study was undertaken to investigate the putative diabetogenic effect of sub-lethal and sub-chronic exposure to paraoxon (POX), an extremely hazardous OPC used in pesticides. The effect of paraoxon on streptozotocin-induced diabetic rats was also examined. Each rat was injected with 100 nmol of POX 5 days per week for 6 weeks. Blood glucose levels and red blood cell acetylcholinesterase activity were measured weekly. Biochemical analysis and morphological studies were performed at the end of the experiment. The results revealed that POX neither induces nor exacerbates diabetes mellitus in experimental rats. Liver and kidney/body weight ratios revealed statistically insignificant differences when compared with controls. Biochemical analysis of urine samples showed a small but not significant increase in protein level in all groups. Urine bilirubin was significantly higher in the diabetes + POX group when compared with the control group. The number of blood cells in urine was significantly higher in the POX-treated group compared with the control group. Hyperglycemia was noted in the diabetes and diabetes + POX groups, but neither in the saline control nor in POX-treated normal rats. Electron microscopy of POX-treated pancreas did not show any morphological changes in beta cells. These results suggest that POX does not cause diabetes mellitus at sub-lethal sub-chronic exposure. Copyright © 2012 John Wiley & Sons, Ltd.
    Journal of Applied Toxicology 08/2012; · 2.60 Impact Factor
  • Source
    Ernest Adeghate
    Experimental physiology 08/2012; 97(8):906-7. · 3.17 Impact Factor

Publication Stats

1k Citations
365.55 Total Impact Points

Institutions

  • 1994–2014
    • United Arab Emirates University
      • • Department of Anatomy
      • • Department of Physiology
      • • Department of Pharmacology and Therapeutics
      • • College of Medicine and Health Sciences
      Al Ain, Abu Dhabi, United Arab Emirates
  • 2013
    • The University of Manchester
      Manchester, England, United Kingdom
  • 1996–2011
    • University of Central Lancashire
      • School of Forensic and Investigative Sciences
      Preston, ENG, United Kingdom
  • 1988–2011
    • Semmelweis University
      • • Department of Pharmacodynamics
      • • Department of Pharmacology and Pharmacotherapy
      • • Department of Anatomy, Histology and Embryology
      • • First Department of Internal Medicine
      Budapest, Budapest fovaros, Hungary
  • 2002
    • University of Granada
      • Departamento de Fisiología
      Granada, Andalusia, Spain
  • 1997–1998
    • Uzsoki Hospital
      Budapeŝto, Budapest, Hungary