3^rd World Congress on Pharmacology August 08-10, 2016 Birmingham, UK

Biography:

Walber Toma has completed his PhD from University of Campinas (Unicamp) from Brazil. He is the Researcher of the Department of Ecology from Santa Cecília University (Unisanta) and also from the Department of Pharmaceutical Sciences in São Camilo University (São Camilo). In Santa Cecília University, he is the main Researcher of a Laboratory of Natural Products that seeks ethnopharmacological informations from the south coast populations of São Paulo state. He is also the Director of a specialization course in Clinical Pharmacology at Unisanta. He has published more than 30 papers on the following subjects: ethnopharmacology, gastroprotective activity of plant extracts, toxicology and ecotoxicology assays from natural products.

Abstract:

Gastric ulcers are a significant medical problem and the development of complications lead to significant mortality rates worldwide. In Brazil, Carthamus tinctorius L., Asteraceae, seeds essential oil, the safflower oil, is currently used as a thermogenic compound and as treatment for problems related to the cardiovascular system. In this study, by Raman spectroscopy, it was shown that oleic and linoleic acids are the compounds present in higher concentrations in the safflower oil. We demonstrated that safflower oil (750 mg/kg, p.o.) decrease the ulcerogenic lesions in mice after the administration of hydrochloric acid-ethanol. The gastric ulcers induced by non-steroidal anti-inflammatory drug (NSAID) in mice treated with cholinomimetics were treated with four different doses of safflower oil, of which, the dose of 187.5 mg/kg (p.o.) showed significant antiulcerogenic properties (**p<0.01). Moreover, the safflower oil at doses of 187.5 mg/kg (i.d.) increased the pH levels, gastric volume (**p<0.01) and gastric mucus production (***p<0.001), and decreased the total gastric acid secretion (***p<0.001). The acute toxicity tests showed that safflower oil (5.000 mg/kg, p.o.) had no effect on mortality or any other physiological parameter. Ecotoxicological tests performed using Daphnia similis showed an EC50 at 223.17 mg/l, and therefore safflower oil can be considered “non-toxic” based on the directive 93/67/EEC on risk assessment for new notified substances by European legislation. These results indicate that the antiulcer activity of Safflower oil may be due to cytoprotective effects, which serve as support for new scientific studies related to this pathology.

Biography:

Elisabetta Radice has completed her degree in Medicine in 1983 and Specialization in Digestive Apparatus Surgery and Digestive Endoscopy in 1988 at Naples University School of Medicine, Italy. She did her Fellowship at Colorectal Surgery Department Mayo Clinic Rochester (MN, USA) 1995-1997. She worked as Assistant Professor from 2001 at Department of Surgical Sciences, University of Turin, Italy.

Abstract:

Dendritic cells (DCs), specialized antigen-presenting cells bridging innate and adaptive immunity, play a crucial role in determining specific immune response to tumors. Because of their potent immunoregulatory capacities, DCs have been exploited in anticancer vaccination, with limited success thus far. This pilot study compared low-dose interleukin (IL)-4 and IL-12 prepared by sequential kinetic activation (SKA) with standard doses of the same recombinant human cytokines on functional activity of ex vivo-generated monocyte-derived (Mo) DCs from colon carcinoma patients and normal subjects. MoDCs were exposed to medium alone, SKA-IL-4 (0.5 fg/ml), or SKA-IL-12 (2 fg/ml), alone or consecutively combined, in parallel with rhIL-4 (50 ng/ml) and rhIL-12 (1 ng/ml). Primary allogeneic one-way mixed lymphocyte reaction (MLR) was the end point to assess in vitro T-lymphocyte proliferation in response to MoDCs, and secreted IL-12p70 and interferon-γ in MLR supernatants measured by ELISA to assay for T-helper 1-promoting MoDC phenotype. No single agent enhanced the compromised allostimulatory activity of MoDCs from colon cancer patients, unlike healthy donors. However, MoDCs from nonmetastatic colon cancer patients, after sequential exposure to SKA-IL-4 (48 hours) and SKA-IL-12 (24 hours), displayed increased T-cell stimulatory capacity by MLR and acquired driving T-helper 1 polarization activity, although less markedly than the effects induced by recombinant human cytokines or found in normal subjects. These results point to an immunomodulatory capacity of low-dose SKA-IL-4 and SKA-IL-12 and encourage further investigation to provide clues for the rational development of new and more effective immunotherapeutic strategies against cancer.

Biography:

Alexander Kulikov has completed his PhD in 1983 and SD in 2005 from Institue of Cytology and Genetics (ICG). At present, he is the Head of Department of Collection of Neurophathologies. He has published more than 200 papers in reputed journals and participated at many international conferences. He is interested in the genetic and molecular mechanisms as well as the development of mouse models of  psychopathologies. Moreover, he is a well known expert in 5-HT system and tryptophan hydroxylase 2. He is coauthor of 6 new mouse models of psychopathologies. He supervised of 5 PhD students.

Abstract:

Mice with hereditary disturbances of the behavior and the brain are effective tools for preclinical study of the mechanisms of psychotropic drug action. Catalepsy or exagerated freezing is a sign of grave brain dysfunctions. The main gene determining of about 20% of genetic variation of catalepsy has been mapped at the terminal fragment of mouse chromosome 13. This fragment has been transferred from the catalepsy-prone CBA/Lac line to the genome of a catalepsy-resistant AKR/J line and the AKR.CBA-D13Mit76 (D13) recombinant line has been bred. About 50% of D13 mice are cataleptics. Mice of this line show elevated expression of the Il-6 gene, coding the pro-inflammation cytokine interleukine-6, in the cortex and hippocampus and sensitivity to lipopolysaccharide. MRI revealed a reduction of the pituitary gland in D13 mice. Unlike AKR mice, D13 mice show a spatial learning deficit in the Morris water maze (MWM). An acute ivc administration of 300 ng of brain derived neurotrophic factor (BDNF) normalized the performance and memory retention in the MWM in D13 mice. These results indicated a possible association between the hereditary catalepsy, MWM performance, pituitary gland reduction, BDNF and level of Il-6 mRNA in the brain, although the relation between these characteristics seems to be more complex. Thus, AKR.CBA-D13Mit76 recombinant mouse line with deficit of spatial learning, is a promising model for study of the genetic and molecular mechanisms of learning disorders as well as for screening potential cognitive enhancers.

Biography:

T G Borovskaya has graduated from the Tomsk State Medical University and received MD degree and completed her Post-doctoral studies from the Goldberg Research Institute of Pharmacology. She is the Head of Laboratory of Pharmacology. She has published 3 monographs, more than 190 papers in reputed journals and is the author of 17 patents. The field of interests covers Toxicology, Andrology and Embryology. 

Abstract:

Studies of the last decade show a degradation of reproductive health of men. At the same time great attention is paid to oxidative stress as a factor that negatively affects the organs of reproduction. The purpose of this work is to evaluate the effectiveness of antioxidants from the group of 8-hydroxy-pyridine, flavonoids, sterically hindered phenols in experimental models of pathospermia and benign prostatic hyperplasia (BPH). The experiments were performed on Wistar rats. Pathospermia was induced by a single administration of the cytostatic drug Etoposide in the maximum tolerated dose. BPH was induced by long-time administration (during 2 months) of Sulpiride. The both models gave a significant decrease in the redox potential, which is estimated by chemiluminescence. In the case of pathospermia was the only antioxidant from the group of sterically hindered phenols was found to be effective. This redox-potential of the male germ cells was not different from that of intact animals. The model of BPH showed statistically significant decrease of the area of epithelial acini under the introduction of all the studied antioxidants. But significant increase of the stromal-epithelial rate was found only on the background of the antioxidants from the group of hindered phenols. Redox-potential of prostate in this group of animals did not differ from the baseline values.

Biography:

Ali Sheikh Md Sayed has completed his MD and PhD in Cardiology from Xiangya School of Medicine, Central South University. He is the Visiting Professor of Hunan Traditional Medical University. He has published more than 13 papers in reputed journals.

Abstract:

Acute myocardial infarction (AMI) is the leading cause of sudden cardiac death (SCD) in the world and remains a significant unsolved clinical issue. Prevalence of AMI event will increase ≈18% by 2030. Though, in 20^th century, enormous progress has been made in the diagnosis, treatment, and prognosis of AMI but still there is a clinical demand for a novel diagnostic, prognostic biomarker and new therapeutic interventions to decrease the AMI incidence. The purpose of this study was to evaluate the diagnostic and prognostic value of circulating miRNAs as a biomarker for AMI patients, and therapeutic effect of miR-208b or miR-378 in cardiac cell during hypoxia-reoxygenation (HR) injury. In our study, we enrolled AMI patients, 12 week-old C57BL/6 mice AMI and H9c2 cells. Total RNA was isolated from plasma and H9c2 cells by using TRIZOL reagent. Circulating miRNAs levels were measured by quantitative real-time polymerase chain reaction. We found that circulating miR-208b, miR-499 and miR-765 levels were significantly up-regulated, whereas miR-149, miR-378 and miR-424 levels were markedly down-regulated both in AMI patients and Mice model of AMI compared with controls, (p<0.01). Plasma levels of these miRNAs were returned towards normal at 96 h after PCI (p<0.01). However, inhibition of miR-208b and over expression of miR-378 were dramatically increased cell survival through negative regulation of their targets in HR-induced cardiomyocyte injury cell. Our study demonstrated that circulating miRNAs represent as novel diagnostic and prognostic biomarkers for AMI patients, and also represents a new therapeutic approach for ischemic heart disease.

Biography:

Fleisher-Berkovich S has completed her PhD from Ben-Gurion University of the Negev. She is an Associate Professor in the Department of Clinical Biochemistry and Pharmacology. She has published papers and book chapters in reputed journals and serves as a reviewer of repute journals. She also received highly competitive national and international grants.

Abstract:

The pathology of Alzheimer's disease (AD) is associated with brain inflammation, which includes the involvement of glial cells e.g., microglia and astrocytes. Microglial activation by amyloid β (Aβ) (component of AD plaque) results in the production of various inflammatory mediators, oxidative radicals, and neurotoxic cytokines, which contribute to synaptic impairment and neuronal damage. Accumulating evidence indicate that the renin-angiotensin system (RAS) may contribute to the brain inflammation associated with AD pathology. Angiotensin II (Ang II) is considered as the major RAS effector, and acts mainly via stimulation of the angiotensin type 1 receptor (AT1R). Specific inhibition of brain RAS has been suggested as a potential therapeutic strategy for AD. The overall aim of the present study was to elucidate the role of RAS in the modulation of glial functions and to understand the possible implications for brain inflammation and AD in vitro and in vivo. Long term exposure of BV2 microglia to telmisartan (1-5 mM) decreased by about 50% the lipopolysaccharide (LPS)-induced nitric oxide (NO), inducible NO synthase (iNOS) and tumor necrosis factor  a (TNF- a) synthesis. Telmisartan did not affect the basal synthesis of these pro-inflammatory mediators in non-stimulated BV2 cells. Cell  viability was not altered following telmisartan treatment. Intranasal administration of telmisartan (1 mg/kg/day) for up to two months significantly reduced amyloid burden and microglia/macrophages activation in the cortex and hippocampus of five familial Alzheimer’s disease (5XFAD) mouse model. Based on these results, it is suggested that telmisartan act as an anti-inflammatory and a neuroprotective agent in the brain through modulation of microglial activation and of amyloid pathology.

This research was supported by the Israel Science Foundation (grant 101/11-16).

Biography:

Myung Koo Lee,  Professor of College of Pharmacy, Chungbuk National University (CNU), has received his PhD degree from the Faculty of Pharmaceutical Sciences, Kyushu University in 1988 and Post-doctoral studies from the Lab of Molecular Neurobiology, Cornell University Medical School in 1991-1992. He has served as a Dean at the College of Pharmacy, CNU in 2002-2004, and as a President at the Society of Korean College of Clinical Pharmacy in 2010-2012. He has also served as the Director at the Research Center for Bioresource and Health, CNU in 2001-present. He has published more than 190 papers in journals.

Abstract:

Parkinson’s disease (PD) causes by the degeneration of dopamine neurons in the substantia nigra. L-3,4-Dihydroxyphenylalanine (L-DOPA) is the most frequently prescribed drug for controlling the symptoms of PD. However, the high levels of L-DOPA lead to cell death by generating reactive oxygen species in dopamine neurons and PC12 cells. The intracellular levels of cyclic AMP (cAMP) increase in response to cytotoxic concentrations of L-DOPA in PC12 cells, and multiple treatments with non-toxic L-DOPA (MT-LD) reduce dopamine biosynthesis in PC12 cells. We therfore investigated the effects of L-DOPA on ERK1/2 and JNK1/2-c-Jun systems. MT-LD (10 and 20 µM) induced cell survival via PKA-transient ERK1/2 activation in PC12 cells. MT-LD also induced differentiation via the Epac-sustained ERK1/2-c-Jun system, which subsequently led to the activation of the cell death process. In addition, SE and GP-EX enhanced dopamine biosynthesis and L-DOPA-induced increase in dopamine levels by inducing TH activity and TH gene expression in PC12 cells. SE and GP-EX protected L-DOPA-induced cytotoxicity through the modulation of the oxidative stress-induced cell death signaling pathways in PC12 cells. SE and GP-EX also showed the prophylactic and adjuvant therapeutic effects on long-term L-DOPA therapy in 6-hydroxydopamine-lesioned rat model of PD, suggesting that SE and GP-EX might serve as an adjuvant phytonutrient for PD. Taken together, it has been proposed that chronic treatment of L-DOPA led to the neurotoxic process via the cAMP-sustained ERK-c-Jun system and the modulation of ERK activity might be applied for screening the anti-neurodegenerative agents. 

Biography:

P Brindha has completed her PhD from University of Madras and Post-doctoral research in Traditional Ayurveda and Siddha Herbal Drugs at Captain Srinivasamurthi Drug Research Institute, Chennai under the Ministry of Health and Family Welfare, Govt. of India. Presently, she is the Associate Dean and Co-ordinator for Centre for Advanced Research in Indian System of Medicine (CARISM), School of Chemical and Biotechnology, SASTRA University, Thanjavur, Tamilnadu, India. She has published more than 240 papers in reputed journals and has guided 25 PhDs in Herbal Science.

Abstract:

Peptic ulcer disease (PUD) develops when the defensive mechanisms of the gastrointestinal mucosa are devastated by the aggressive effects of gastric acid and pepsin. The transformation to plant derived drugs from synthetic modern drugs is mainly due to their side effects. Hence, in the present study attempts were made to develop an eco-friendly herbal drug taking leads from traditional herbal medicine practitioners. Based on the literature survey and interviews with local traditional healers, Caesalpinia sappan L., Cyclea peltata (Lam.) and Gmelina arborea Roxb. were selected and evaluated for their antiulcer potential.  Hydro-alcoholic extracts of the selected plants were used for the present study. C. peltata showed significant proton pump inhibitory activity. It was observed that C. sappan had better antioxidant activity in DPPH assay. In vitro acid neutralizing capacity was not observed for the three plants, which indicated that the plants cannot act as antacids. Acute oral toxicity studies on C. sappan, C. peltata and G. arborea extract showed no mortality in rats at doses up to 2 g/kg. In ethanol induced ulcer model, screening of cytoptotective activity revealed that C. sappan at the dose level of 500 mg/kg showed 92% ulcer protective index, whereas G. arborea and C. peltata showed 58% and 47% ulcer protective index respectively when compared with standard sucralfate (53%). In Pylorus ligation induced model, the maximum ulcer protection was observed in C. peltata and the probable antiulcer mechanism must be mediation through gastric secretion inhibition. Cysteamine induced duodenal ulcer model showed no activity. In NSAID induced gastric ulcer model, C. sappan (86%) showed maximum ulcer protection followed by C. peltata (75%) and G. arborea (66%) when compared with standard (74%). The bioactive extracts were subjected to LC-MS/MS analysis to detect the major phytoconstituents. Findings from in silico molecular docking studies further provided supporting evidences for their mechanisms of actions. It is concluded from the present study that C.sappan showed potent antiulcer effect mediated by increasing PGE₂ level and promoting antioxidant status, thereby acting as a cytoprotective agent. C.peltata revealed significant antiulcer activity mediated through gastric juice inhibition and acting as an anti-secretory agent against gastric juice. G.arborea promoted ulcer healing through mucus secretions and protected the gastric mucosal damage against gastric acid secretions. A suitable combination of these three extracts can be used to formulate an antiulcer drug that could be useful in the management of any type of ulcers.

Biography:

Aline Diogo Marinho has completed her Bachelor's in Pharmacy from Federal University of Ceara- UFC (2011) and Master's in Pharmacology from School of Medicine, UFC (2013). She is a Scholarship student of CAPES (Coordenação de Aperfeiçoamento de Pessoal de Nível Superior) and Doctoral student in Pharmacology from UFC since 2014. She has experience in Pharmacology, with emphasis on Renal Pharmacology, focusing in the following topics: toxinology, venoms and renal alterations. She is a member of Laboratory of Pharmacology of Venoms, Toxins and Lectins (LAFAVET). Her related publications are: Bothropoides pauloensis venom effects on isolated perfused kidney and cultured renal tubular epithelial cells and Solanidane and iminosolanidane alkaloids from Solanum campaniforme.

Abstract:

Acute renal failure (ARF) is one of the most serious complications of Bothrops snake bites. Pathogenesis of ARF in snakebite envenomation may involve hemodynamic disturbances, immunologic reactions and direct nephrotoxicity, however, its pathogenesis remains obscure. Bothrops pauloensis is found in the State of São Paulo, Southeast region of Brazil. The aim of the work was to study Bothropos pauloensis venom (BpV) in rat isolated perfused kidneysand cytotoxicity on renal tubular cells Mardin-Darby Canine Kidney (MDCK). The renal effects were compared to a control group perfused with modified Krebs–Henseleit solution alone. BpV decreased the perfusion pressure (PP), renal vascular resistance (RVR),urinary flow (UF), glomerular filtration rate (GFR) and the percent sodium, potassium and chloride tubular transport (%TNa⁺, %TK⁺, %TCl⁻). The treatment with BpV caused decrease in cell viability to the lowest concentration tested with an IC (50) of 7.5 μg/mL. Flow cytometry with annexin V and propidium iodide showed that cell death, suggesting the participation of apoptosis and late apoptosis on BpV-induced cell death. Through caspases 3 and 7 activation, mitochondrial membrane potential collapse and ROS overproduction. These findings demonstrated that BpV cytotoxicity on renal epithelial cells might be responsible for the nephrotoxicity observed in isolated kidney. The characterization of the effects in the isolated kidney and renaltubular cells gives strong evidences that the acute renal failure induced by this venom is a result of the direct nephrotoxicity which may involve the cell death mechanism.

Biography:

Hui-Hui Xiao is a Scientific Officer in The Hong Kong Polytechnic University. She received her PhD in Natural Product Chemistry from Shenyang Pharmaceutical University, China in 2011 and finished Post-doctoral studies from Jinan University in 2014. She has published more than 10 papers in reputed journals and obtained one authorized patent of invention. Her research interests are in the areas of preclinical study about the therapeutic effects of Traditional Chinese Medicine (TCM) on Osteoporosis, the chemical components of TCM and the involved mechanism in anti osteoporosis.

Abstract:

Sambucus williamsii Hance, as a fork herbal medicine has been used in China on treatment of bone and joint diseases for thousands of years. Our previous studies clearly demonstrated that a fraction composed of 50% and 95% ethanol eluate from S. williamsii exerted protective effects on trabecular bone and cortical bone without side effects on uterus in ovariectomized mice and rats. The fraction is rich in lignans and 55 lignans were isolated and identified in this fraction. Among them, 44 lignans were characterized as bioactive components by in vitro activity screening. In the present study, PPD, a typical norlignan was selected for mechanism investigation involved in the anabolic effects of S. williamsii. The results showed that PPD exerted beneficial effects in osteoblasts and its effects were abolished by co-incubation with ICI 182,780 or U0126. It failed to bind to either ERα or ERβ at the concentration up to 10^-6 M and did not activate estrogen response element (ERE)-ludiferase activities via ER. PPD induced the phosphorylation of ERK and ERα at serine 118. The data indicated that PPD exerts oestrogen-like actions in ostoblast-like cells via ligand-independent, ERE-independent and mitogen-activated protein (MAP) Kinase-mediated rapid nongenomic ER signalling pathway. In order to elucidate the real bioactive components in body, we further study the metabolites of DDA, a major norlignan in the bioactive fraction. In rats model, 14 metabolites were identified in the plasma, urine and feces administrated with DDA. The final metabolite was enterodiol. However, the metabolic pathway was still in study.

Biography:

Jiyoung Kim has completed her Ph.D from University of Georgia, GA, USA and postdoctoral studies from University of Wisconsin-Madison, WI, USA. She is the research assistant professor at Seoul National University, Seoul, Korea.  She has published more than 33 papers in reputed journals and 3 book chapters. Her papers “Naturally occurring phytochemicals for the prevention of Alzheimer's disease, Journal of Neurochemistry 2010 Mar: 112(6): 1415–1430” and “A protective role of nuclear factor-erythroid 2-related factor-2 (Nrf2) in inflammatory disorders. Mutation Research/Fundamental and Molecular Mechanisms of Mutagenesis 2010 Aug 7: 690(1-2): 12-23” have been noted by more than 120 citation records.

Abstract:

Sulforaphane, an organosulfur compound present in cruciferous vegetables, has been shown to exert neuroprotective effects in experimental in vitro and in vivo models of neurodegeneration. To determine whether sulforaphane can preserve cognitive function, we examined its effects on scopolamine-induced memory impairment in mice using the Morris water maze test. Sulforaphane (10 or 50 mg/kg) was administered to C57BL/6 mice by oral gavage for 14 days (days 1–14), and memory impairment was induced by intraperitoneal injection of scopolamine (1 mg/kg) for 7 days (days 8–14). Mice that received scopolamine alone showed impaired learning and memory retention and considerably decreased cholinergic system reactivity in the hippocampus and frontal cortex, as indicated by a decreased acetylcholine (ACh) level and an increased acetylcholinesterase (AChE) activity. Sulforaphane significantly attenuated the scopolamine-induced memory impairment and improved cholinergic system reactivity, as indicated by an increased ACh level, decreased AChE activity, and increased choline acetyltransferase (ChAT) expression in the hippocampus and frontal cortex. These effects of sulforaphane on cholinergic system reactivity were confirmed in vitro. Sulforaphane (10 or 20 µM) increased the ACh level, decreased the AChE activity, and increased ChAT expression in scopolamine-treated primary cortical neurons. These observations suggest that sulforaphane might exert a significant neuroprotective effect on cholinergic deficit and cognitive impairment.

Biography:

Chia-Wen Tsai received her PhD degree (2006) in Department of Nutrition from Chung Shan Medical University. She has been working as a Associate Professor at the Department of Nutrition, China Medical University in Taiwan. Her research interests include the herbs in prevention of neurodegenerative diseases, the modulations of glucose and lipid metabolism in herbs, and the functional foods in cancer chemoprevention.

Abstract:

Understanding the neuroprotective effects of carnosic acid (CA) from rosemary has attracted increasing attention in recent years. Parkin promotes the degradation of mitochondria pro-apoptotic ARTS (apoptosis-related protein in the TGF-β signaling pathway) protein and prevents it antagonizes XIAP (X-linked inhibitors of apoptosis proteins) leading to caspase activation. In this present study, we explored whether CA could prevent 6-hydroxydopamine (6-OHDA)-induced apoptosis via modulation of ARTS  and XIAP by parkin in SH-SY5Y cells. The results showed that pretreatment cells with CA reduced 6-OHDA-induced the nuclear condensation and apoptotic proteins. Treatment cells with 6-OHDA increased ARTS protein and decreased XIAP protein as well as parkin protein. However, CA pretreatment reversed the effect by 6-OHDA. Performing immunoprecipitation using an anti-ARTS antibody, 6-OHDA increased the XIAP protein. In contrast, CA pretreatment reduced XIAP protein and increased ubiquitin protein in 6-OHDA treated cells. Silencing of XIAP reduced the CA inhibited 6-OHDA-increased the cleavage of caspase 9, 3, 7 and PARP. With parkin siRNA, CA reversed the 6-OHDA-induced ARTS and reduced XIAP was inhibited, which resulted in increasing apoptotic related proteins. In conclusion, CA protects SH-SY5Y cells against 6-OHDA-stimulated apoptosis via induction of parkin by enhancing the ubiquitination of ARTS, leading to induction of XIAP.

Biography:

Syed Arman Rabbani has completed his PhD in Clinical Pharmacology from the Clinical Pharmacology Unit, Ranbaxy Research Laboratories in collaboration with Jamia Hamdard University, New Delhi, India. He is a University Gold Medalist. Currently, he is working as an Assistant Professor in Department of Clinical Pharmacy and Pharmacology, RAK College of Pharmaceutical Sciences, RAK Medical and Health Sciences University. He has a rich blend of experience in both industry as well as academics. In industry, he was involved in the conceptualization and conduct of Phase III and Phase IV Clinical Trials.

Abstract:

The objective of the study was to assessthe prevalence of hyperphosphatemia in End Stage Renal Disease patients (ESRD) undergoing maintenance hemodialysis at a tertiary care hospital in Ras Al Khaimah, UAE. The study also aimed to describe the characteristics of the ESRD patients with hyperphosphatemia. The study was a prospective, observational study including all the patients undergoing hemodialysis at the nephrology unit of the hospital. Patients who were on hemodialysis for less than six months, with less than thrice weekly hemodialysis and with acute kidney injury were excluded from the study. Patient’s characteristics were compared according to phosphatemia level, between patients with or without hyperphosphatemia of the 80 patients included (mean age, 61.1 ± 9.4 years), 73.8% had hyperphosphatemia, defined by a mean serum phosphate > 1.45 mmol/L. Patients with hyperphosphatemia are younger and have a higher BMI than those with normal phosphate levels, and more often women. They were more likely to have hypertensive and diabetic nephropathy, and had less comorbidity. The study showed that ESRD patients with hyperphosphatemia differ from those with normal phosphate levels.

Biography:

Lihua Sun, Associate Professor of Pharmacology, has completed her PhD at the age of 29 years from Harbin Medical University and postdoctoral studies from Harbin Medical University. She is working on the research and teaching of Pharmacology, the research interest focuses on Cardio-Cerebral Vascular pharmacology. She has published more than 35 papers in international peer-reviewed journals and has been supported by series of national scientific foundations and has been serving as a Reviewer for PLOS ONE and Gene. She obtained the rewards from Ministry of Education of China due to her success in researches.

Abstract:

Previous studies have demonstrated that the trafficking defects of Nav1.1/Nav1.2 are involved in the dementia pathophysiology. However, the detailed mechanisms are not fully understood. Moreover, whether the impaired miRNAs regulation linked to dementia is a key player in sodium channel trafficking disturbance remains unclear. The cognitive impairment induced by chronic cerebral ischemia through chronic brain hypoperfusion (CBH) by bilateral common carotid artery occlusion (2VO) is likely reason to precede dementia. Our results found the impairment of Nav1.1/Nav1.2 trafficking and decreased expression of Navβ2 and increased miR-9 in the hippocampus and cortex of rats following CBH generated by bilateral 2VO. Intriguingly, MiR-9 suppressed, while AMO-miR-9 enhanced, the trafficking of Nav1.1/Nav1.2 from cytoplasm to cell membrane. Further study showed that overexpression of miR-9 inhibited the expression of Navβ2 by targeting on its coding sequence (CDS) domain by dual luciferase assay. However, binding-site mutation or miR-masks failed to influence Navβ2 expression as well as Nav1.1/Nav1.2 trafficking process, indicating that Navβ2 is a potential target for miR-9. Lentivirus-mediated miR-9 overexpression also inhibited Navβ2 expression and elicited translocation deficits to cell membrane of Nav1.1/Nav1.2 in rats, whereas injection of lentivirus-mediated miR-9 knockdown could reverse the impaired trafficking of Nav1.1/Nav1.2 triggered by 2VO. We conclude that miR-9 may play a key role in regulating the process of Nav1.1/Nav1.2 trafficking via targeting on Navβ2 protein in 2VO rats at post-transcriptional level, and inhibition of miR-9 level may be a potentially valuable approach to prevent Nav1.1/Nav1.2 trafficking disturbance induced by CBH.

Biography:

Jing Ai has completed her PhD from Department of Pharmacology, Harbin Medical University and Post-doctoral studies from College of Bioinformatics Science and Technology and Bio-pharmaceutical Key Laboratory of Heilongjiang Province, Harbin Medical University. She has published more than 40 papers in reputed journals and has been serving as an Editorial Board Member of PloS One.

Abstract:

Large cohort studies have revealed a close relationship between cognitive impairment and cardiovascular diseases, although the mechanism underlying this relationship remains incompletely understood. In this study, using a transgenic (Tg) mouse model of cardiac-specific over-expression of microRNA-1-2 (miR-1-2), we observed that microRNA-1 (miR-1) levels were increased not only in the heart but also in the hippocampus and blood, whereas its levels did not change in the skeletal muscle of Tg mice compared with age-matched wild type (WT) mice. Six-month-old Tg mice showed cognitive impairment compared with age-matched WT mice, as assessed using the Morris Water Maze test. The brain-derived neurotrophic factor (BDNF) level and cyclic AMP-responsive element-binding protein (CREB) phosphorylation were also significantly reduced in the hippocampi of the Tg mice, as evaluated by western blot. Further examination showed that BDNF proteins expression was down- or up-regulated by miR-1 over-expression or inhibition, respectively, and was unchanged by binding site mutations or miRNA-masks for the 3’UTR of Bdnf, indicating that this gene is a potential target of miR-1. Knockdown of miR-1 by hippocampal stereotaxic injection of an anti-miR-1 oligonucleotide fragment carried by a lentivirus vector (lenti-pre-AMO-miR-1) led to up-regulation of BDNF expression and prevented the reduction in cognitive performance in the Tg mice without affecting cardiac function. Our findings demonstrate that cardiac over-expression of miR-1 also induces behavioral abnormalities that may be associated, at least in part, with the down-regulation of BDNF expression in the hippocampus. This study definitely contributes to the understanding of the relationship between cardiovascular disease and cognitive impairment.

Biography:

Cherine A Ismail has completed her PhD at the age of 26 years from Alexandria University and postdoctoral studies from Alexandria University School of Medicine. She is a lecturer in Clinical Pharmacology Department, Alexandria University School of Medicine. She has published 8 papers in reputed journals.

Abstract:

Sporadic dementia of Alzheimer’s type is a progressive neurodegenerative disorder. While, Alzheimer’s disease (AD) patients have an increased risk of developing seizures, epileptic activity triggers a variety of inhibitory compensatory responses in hippocampal circuits to counteract imbalances in network activity, interfering with normal neuronal/synaptic functions required for learning and memory. Since, antiepileptic drugs (AEDs) have been claimed to variably modulate cognition, a concern is raised about the most favorable AEDs member in such indication. The study compared the impact of relatively newer AEDs (gabapentin/levetiracetam) versus an old one (carbamazepine) on cognitive impairment-induced by intracerebroventricular (icv) colchicine injection in rats. Fifty-six male Wistar rats were equally assigned into control (normal, aCSF-injected, and vehicle-treated AD) and treated groups. Following icv colchicine injection (15μg/5μl/bilaterally), rats (8-rat/group) randomly received gabapentin (60mg/kg/day), levetiracetam (100mg/kg/day), carbamazepine (100mg/kg/day), donepezil (2mg/kg/day), or vehicle orally once daily for 26 days. Behavioral assessment was done using Morris water maze (days 13, 14 and 21 post-surgery), and passive avoidance (days 25/26) tasks. Biochemically, oxidative stress (malondialdehyde and reduced-glutathione), cholinergic deficit (acetylcholinesterase (AChE) activity), and neurotrophic (Brain-derived neurotrophic factor (BDNF)) parameters were measured in hippocampus and prefrontal cortex. Gabapentin, and levetiracetam significantly improved colchicine-induced cognitive impairment, oxidative stress, and reduced BDNF level. Gabapentin increased AChE activity, while levetiracetam decreased it, in both tissues. Despite the increase in BDNF, carbamazepine didn’t significantly improve colchicine-induced cognitive impairment, oxidative stress, or cholinergic deficit. New AEDs, particularly levetiracetam, improved cognitive function and obviously protected both hippocampus and prefrontal cortex from colchicine deleterious effects. Based on its significant neuroprotection, levetiracetam might be the most favorable AEDs to be used in Alzheimer’s-like dementia.

Biography:

Xin Liang received her PhD degree in Biochemical Engineering from East China University of Science and Technology in 2012, studying antineoplastic agents and pharmacology. Did her postdoctoral research in Renhao Li Lab in Department of Pediatrics, Emory University, USA in 2015; she became a lecturer in School of Pharmacy, East China University of Science and Technology.

Abstract:

With the development of colorectal tumor, it gradually formed the hypoxic tumor microenvironment, and infiltration of a large number of inflammatory cells. The mast cell is a kind of immune cells which can secrete a variety of effector molecules, and plays an important role in the angiogenesis of tumor. But whether MC in colorectal cancer is to promote tumor growth or inhibition of tumor growth is not clear, the role of mast cell-derived HIF-1α in the regulation of mast cell function itself in the lack source of oxygen conditions remains to be elucidated. Here, we analysis of the clinical samples of colorectal cancer, immunohistochemical detection observed that carcinoma tissues and tissues adjacent to colorectal carcinoma were infiltrated with large numbers of mast cells, and the mast cell infiltration quantity increased with the Duke’s stage. The survival time of mast cell deficient mice which bearing colorectal carcinoma was remarkably longer than wild type C57BL/6 mice bearing colorectal carcinoma, the growth of tumor was the same. And this weakens recovered in mast cell reconstruction mice. Further in vitro experiments show that when inhibit the expression of HIF-1α through HIF-1α siRNA in mast cells, the release of inflammatory factors in mast cells reduced and also the degranulation degree of mast cells. This suggested that mast-cell derived hypoxia-inducible 1α(HIF-1α) play an important role in regulating the function of mast cells. According to phenomenon observed, we think that the mast cells promote the development of colorectal cancer, and mast-cell derived hypoxia-inducible 1α (HIF-1α) play an important role in regulating the function of mast cells. Therefore, our study revealed a novel role for mast cell-derived HIF-1α in the colorectal carcinoma microenvironment and has important implications for the design of therapeutic strategies.

Biography:

Ke Xu received his PhD degree in Medicinal Chemistry from East China University of Science and Technology in 2013. After that, he worked in Winship cancer center of Emory University as a post-doctor fellow in the United State. At June 2015, he became a Research Associate of Putuo Hospital and Cancer Institute, Shanghai University of Traditional Chinese Medicine, study on pharmacology of traditional Chinese Medicine and the mechanism of miRNA in the gastrointestinal carcinoma.

Abstract:

Colorectal carcinoma is a frequent cause of cancer-related death in men and women. miRNAs (microRNAs) are endogenous small non-coding RNAs that regulate gene expression negatively at the post-transcriptional level. In the present study we investigated the possible role of microRNAs in the development of MDR (multidrug resistance) in colorectal carcinoma cells. We analysed miRNA expression levels between MDR colorectal carcinoma cell line HCT116/L-OHP cells and their parent cell line HCT116 using a miRNA microarray. miR-297 showed lower expression in HCT116/L-OHP cells compared with its parental cells. MRP-2 (MDR-associated protein 2) is an important MDR protein in platinum-drug-resistance cells and is a predicted target of miR-297. Additionally miR-297 was down-regulated in a panel of human colorectal carcinoma tissues and negatively correlated with expression levels of MRP-2. Furthermore, we found that ectopic expression of miR-297 in MDR colorectal carcinoma cells reduced MRP-2 protein level and sensitized these cells to anticancer drugs in vitro and in vivo. Taken together, our findings suggest that miR-297 could play a role in the development of MDR in colorectal carcinoma cells, at least in part by modulation of MRP-2.

Biography:

Songul Cetik_­­­ has successfully completed her Master’s and PhD from Eskisehir Osmangazi University in 2011 & 2014 respectively. She studies on topic: Phytotherapy on Side Effects of Chemotherapy (Toxicology). She is working as Assistant Professor in the Vocational Higher of Health Services unit.

Abstract:

Hypericum triquetrifolium Turra. (HT) is a phenolic component with anti-oxidative, analgesic and anti-carcinogenic properties. This study aimed to investigate the possible protective effect of HT on CP-induced hepatotoxicity. In order to determine the protective effect of HT upon the liver, the levels of Aspartate transaminase (AST), Alanine transaminase (ALT), Alkaline phosphatase (ALP) and Lactate dehydrogenase (LDH) as well as the total levels of Total Anti-oxidant Capacity (TAC) and Total Oxidant Capacity (TOC), were determined. Also, Oxidative Stress Index (OSI) was measured. Furthermore, the liver tissues were analyzed histologically. Albino rats (Wistar, 3-4 months old, male, weight 220 ± 20 g healthy) were randomly divided in 9 nine groups, each including 7 animals: Group 1 (control) treated with saline, Group 2 treated with 150 mg/kg CP, Group 3, 4 and 5 treated with 25, 50 and 100 mg/kg HT respectively, Groups 6, 7 and 8 treated with 25, 50 or 100 mg/kg HT+CP respectively, and Group 9 treated with 0.5 ml of %0.2 DMSO. The results were analyzed by One Way Analysis of Variance and Kruskal-Wallis One Way Analysis of Variance on Ranks Test. Our study demonstrated that in line with the rise in the dose of 150 mg CP, we determined an increase in the levels of serum ALT, AST, ALP, LDH, TOS and OSI, besides degeneration in the liver tissue. With 25, 50 and 100 mg/kg HT, there was an important decrease with respect to CP toxicity. In the groups given both CP plus HT, there was a rise in serum Total Anti-Oxidant Status (TAS) levels, while the levels of AST, ALT, ALP, LDH, TOS and OSI showed a remarkable decrease. The signs of recovery in the serum biochemical levels were also true for the histological findings of the liver. Our data suggest that HT is a highly effective antioxidant substance with a cell-protecting effect. Therefore, HT could serve as effective agent that could lessen the adverse effects of anti-cancer drugs in the course of chemotherapy protocols.

Biography:

Anna Morozova is working on her PhD project in the Department of Basic and Applied Neurobiology, V P Serbsky Federal Medical Research Center for Psychiatry and Narcology. She is also a Medical Doctor (Psychiatrist) in a mental hospital named Gilyarovskiy. She has published more than 10 papers. The last paper deals with a new approach in modeling of depressive-like behavior in rats and mice. She also studied the Ultrasound of alternating frequencies cause variable emotional impact which evokes depressive syndrome in mice and rats.

Abstract:

Emotional stress is primarily triggered by the cognitive processing of negative input; it is regarded as a serious pathogenetic factor of depression that is challenging to model in animals. While available stress paradigms achieve considerable face and construct validity in modeling depressive disorders, broader use of naturalistic stressors instead of the more prevalent models with artificial challenges inducing physical discomfort or pain may substantially contribute to the development of novel antidepressants. Here, we investigated whether a three-week exposure of Wistar rats and BALB/c mice to unpredictably alternating frequencies of ultrasound between the ranges of 20–25 and 25–45 kHz, which are known to correspond with an emotionally negative and with a neutral emotional state respectively, for small rodents in nature can induce behavioral and molecular depressive like changes. Both rats and mice displayed decreased sucrose preference, elevated despair behavior in a swim test, reduced locomotion and social exploration. Rats showed an increased expression of SERT and 5-HT2A receptor, a decreased expression of 5-HT1A receptor in the prefrontal cortex and hippocampus, diminished BDNF on gene and protein levels in the hippocampus. Fluoxetine, administered to rats at the dose of 10 mg/kg, largely precluded behavioral depressive-like changes. Thus, the applied paradigm of emotional stress is generating an experimental depressive state in rodents, which is not related to any physical stressors or pain. In essence, this ultrasound stress model, besides enhancing animal welfare, is likely to provide improved validity in the modeling of clinical depression and may help advance translational research and drug discovery for this disorder.

Biography:

Luciana Lopes Guimarães has completed her PhD from Federal University of São Paulo (Brazil) and Post-doctoral studies from the same Institution. She is an Adjunct Professor at Santa Cecília University (Brazil). She has published papers in reputed journals and has been serving as a Reviewer for Frontiers in Physiology, Frontiers in Microbiology and also for Medicine (Baltimore).

Abstract:

Special attention has been given to environmental contamination related to pharmaceuticals compounds because these pollutants, so-called emerging, may represent biological-ecological risk, especially in aquatic ecosystems. Antihypertensive drugs are used worldwide with evidence of their occurrence in environmental matrices and domestic effluents. This study aimed to investigate the occurrence of Losartan and Valsartan in a Brazilian coastal zone and also evaluated their adverse biological effects on sea urchin Lytechinus variegatus. Seawater samples were collected from six points surrounding the submarine outfall of Santos (São Paulo, Brazil) and the samples were analyzed by LC/MS/MS. The analysis revealed the presence of both Losartan and Valsartan with concentrations up to 0.024 µg.L-1. Acute toxicity assays were conducted according to U.S. Environmental Protection Agency protocol. Both Losartan and Valsartan exhibited IC₅₀ above 100 mg.L^-1 and these results classify these pharmaceuticals as "Non Toxic" according to directive 93/67/EEC, which classifies substances according to specific toxicity results. Chronic toxicity assays were performed according to Brazilian National Standards Organization protocol. Losartan exhibited values of NOEC (No Observed Effect Concentration) of 50 mg.L^-1 and CEO (Concentration Effect Observed) of 70 mg.L^-1. The results of NOEC and CEO for Valsartan were 9.37 mg. L^-1 and 18.75 mg L^-1, respectively. Differences of NOEC and CEO values for Losartan and Valsartan may be explained by the differences of Kow (octanol-water partition coefficient) values for these two molecules. Despite the occurrence of Losartan and Valsartan in seawater samples, it’s unlikely the occurrence of ecotoxicological effects, considering the environmental concentrations detected for these pharmaceuticals.

Biography:

Melike Ertem is a Research Assisstant at Psychiatric Nursing Programme. She completed her Master’s education at Duzce University. Currently, she is studying her PhD at Dokuz Eylül University Psychiatric Nursing Department. She voluntarily gave psychological counselling services at Elder Health Center in Bolu. She studied at Europen Union Grundving Life Long Lerning Project which named "Training and Psyco-Social Therapy for Informal Caretakers of Bedridden Disabled Individuals".  She has been studying on motivational interviews with schizophrenia diagnosed patients. She has published papers in reputed journals and oral –poster presentations at conferences.   

Abstract:

Medication nonadherence decreases the success of clinical treatment and the efficient use of resources, thereby creating a barrier to effective health care. In this report, we describe the achievement of treatment collaboration through motivational interviews (MI) in a patient with treatment-resistant schizophrenia. MI interventions are based on individual-centered counseling, cognitive-behavioral therapy, social-cognitive theory, the health belief model and the trans-theoretical model. In this case study, we conducted six MIs during which we asked open-ended and reflective questions, established empathy with the patient, and developed discrepancies, leading to ambivalent feelings being revealed. Each interview was structured in accordance with the principles of MI.  In this context, The Morisky Medication Adherence Scale and a questionnaire were used to assess his medication adherence. We used the importance, confidence and self-efficacy ruler. The MI method can be used to ensure continued treatment effectiveness, to increase patient awareness about the disease and benefits of treatment, and to increase patients' self-efficacy. MI can be included during any of the patient visits to establish treatment collaboration with patients as long as the provider has experience with limiting the length of the interaction at psychiatric facilities, outpatient clinics and community mental health centers. It can take months or years for people to experience a behavior change. MI techniques can encourage patients to think about their medication-taking behaviors in a different way, and after each short session they may be able to improve awareness and self efficacy.

This study was published at Archives in Psychiatric Nursing

Biography:

Kecheng Lei is pursuing her Doctor's degree in Jianwen Liu’s Lab. She has published a paper in Tumor Biology in 2015.

Abstract:

Epigenetic mutations are closely associated with human diseases, especially cancers. Among them, dysregulations of histone deacetylases (HDACs) are commonly observed in human cancers. Recent years, HDAC inhibitors have been identified as promising anticancer agents; several HDAC inhibitors have been applied in clinical practice. In this study, we synthesized a novel N-hydroxyacrylamide-derived HDAC inhibitor, I-7ab, and examined its antitumor activity. Our investigations demonstrated that I-7ab exerted cytotoxicity toward and inhibited the growth of human cancer cell lines at micromolar concentrations. Among tested cells, HCT116 was the most sensitive one to the treatment of I-7ab. However, I-7ab displayed far less cytotoxicity in human normal cells. In HCT116 cells, I-7ab inhibited the expression of class I HDACs, especially that of HDAC3 and suppressed EGFR signaling pathway. With respect to the cytotoxic effect of I-7ab, it induced apoptosis via increasing the Bax/Bcl-2 ratio and suppressing the translocation of NF-kB. Other than inducing apoptosis, I-7ab inhibited the expression of cyclin B1 and thereby arrests cell cycle progression at G2/M phase. Further analyses revealed potential role of p53 and p21 in I-7ab-induced apoptosis and cell cycle arrest. According to our findings, I-7ab may serve as a lead compound for potential antitumor drugs.

Biography:

S Al-azzawi a 3^rd PhD Student from School of Pharmacy and Bimolecular Sciences at University of Brighton, UK

Abstract:

Alzheimer's disease (AD) is a neurodegenerative disease caused by plaque accumulation of abnormal deposits of Amyloid-β (Aβ) in the brain. AD is considered epidemic with 33.9 million people worldwide suffering from it. The development of drugs to combat AD is hampered due to the presence of the Blood-Brain Barrier (BBB). Receptor mediated transcytosis is one of the promising strategies to deliver molecules with low BBB permeability by utilizing natural transport route. This project focuses on the innovative combination of ApoE-derived peptide integrated to a dendronized-drug conjugate which has the potential for improved brain endothelial uptake and targeting. ApoE-derived peptide was found to act as a ligand that can be recognized by lipoprotein receptors which are widely expressed in brain endothelium. ApoE-derived peptide and dendron-based carrier system were synthesized using solid phase peptide method by microwave peptide synthesizer. This carrier system was loaded chemically with Flurbiprofen which is one of poorly permeable AD drugs that decrease Aβ. Immortalized brain endothelial cell has been used as a model for BBB. This study has demonstrated the successful designing, synthesis and functionalization of a biocompatible drug carrier system with the potential to act as novel carrier for improved targeting and crossing the BBB.

Biography:

Sopio Gokadze has graduated from Tbilisi State Medical University (TSMU). She has obtained her MS degree in Pharmacy in 2012. She worked at Scientific Research and Practical Skills Laboratory. Currently, she is a PhD Student at TSMU Department of Pharmaceutical Technology. She is also a co-author of 5 scientific publications and 3 presentations at international conferences. 

Abstract:

A high molecular (> 1000 KDa) water soluble biopolymer WSCP was obtained from the roots and stems of two Caucasian species of comfrey S. asperum and S. caucasicum. The biopolymer appeared to have diverse pharmacological activity including anti-inflammatory, antioxidant, anticancer and wound healing. The aim of present study was an attempt to choose optimal carriers and excipients for novel ointment on the basis of biopharmaceutical investigations. Eight compositions with various combinations of carriers and excipients (petroleum jelly, anhydrous lanoline, distilled water, sodium carboxymethylcellulose, polyethylene glycol -1000, glycerin, sodium alginate, askana clay, and Tween-80) were designed and studied for: Determination of optimal ointment base, establishment of ointment stability, and biopharmaceutical study. Stability of ointment was evaluated using centrifugation (6000 rpm for 5 min) and thermal assays. Compositions 1, 2, 3 and 6 passed the test, whereas in compositions 4, 5, 7 and 8 the stability was slightly affected by centrifugation. The biopharmaceutical study was carried out by using the agar diffusion assay. Based on the obtained results the optimal ointment formulation has been justified and formulated WSCP is with the combination from S. asperum, distilled water, and sodium alginate. Biopharmaceutical studies established that the maximal release of WSCP from the ointment was achieved when sodium alginate was used as ointment base.