Scientific Program

Conference Series Ltd invites all the participants across the globe to attend 24th International Conference on Neuroscience and Neurochemistry Birmingham, UK.

Day 2 :

Keynote Forum

Linda Sage

Successful Mindset Ltd., England

Keynote: Overcome compassion fatigue and burnout
Conference Series Neurochemistry 2018 International Conference Keynote Speaker Linda Sage photo
Biography:

Linda Sage has her expertise and passion in improving personal psychological health and wellbeing. Her significant list of global clients, range from hospitals, educational institutions, prisons and corporate entities; throughout UK, US, Europe & Middle East. In all caring environments the professionals are less likely to care for themselves; changing that mindset is at the core of author’s message. It is possible to be, done and have everything you want, by helping others and looking after yourself. An international speaker, author, trainer and mentor, with decades of experience and knowledge, energize any event and attendees. Her simplified message of self-worth, instantly effects all levels of personnel, to achieve, do and be more with a positive frame of mind; demolishing the irrational fears, phobias, beliefs and habits that compassion fatigue can compound. Building a more resilient person provides the individual, employer and patient/client a much more competent and confident professional.

 

Abstract:

Compassion fatigue puts healthcare workers and patients at risk. Everyday care workers struggle to function in care giving environments that present heart wrenching emotional challenges. Compassion fatigue (CF) the profound emotional and physical erosion takes place when helpers cannot refuel and regenerate. Helping professionals open their hearts and minds to clients/patients. This empathy makes helpers vulnerable to be profoundly affected and possibly damaged. Burnout physical and emotional exhaustion is experienced when there is low job satisfaction, feeling powerless and overwhelmed. Signs of CF and burnout: overtaxed by work, showing similar symptoms to traumatized clients; difficulty in concentrating, intrusive imagery, feeling discouraged, hopelessness, exhaustion, irritability, high attrition (helpers leaving) and negative, dispirited, cynical workers remaining in the field, boundary violations which affect the workplace and create a toxic environment. Factors in CF and burnout of the individual: Life circumstances, coping style, personality type. Life stressors i.e. taking care of both young children and aging parents, in addition to managing a heavy and complex workload. Helpers are not immune to pain in their own lives; they can be vulnerable to life changes such as divorce and addictions. Helpers often do work, others don’t want to hear about; spend time caring for people who are not valued or understood in society, homeless, abused, incarcerated or chronically ill. The working environment is often stressful and fraught. The work is very stressful, clients/patients who are experiencing chronic crises, difficulty in controlling their emotions, or who may not get better. What can be done? Working in a healthy organization; access to supportive; flexible management; reduction of trauma exposure; ongoing staff education; timely and good quality supervision and; reducing hours of working directly with traumatized individuals. Personal strategies are strong social support, home and work; increased self-awareness regular self-care. Making life changes, prioritize personal health/wellness develop stress resiliency skills.

 

Keynote Forum

Mourad Tayebi

Western Sydney University, Australia

Keynote: Proteinopathies: A tale of human, dogs and kangaroos
Conference Series Neurochemistry 2018 International Conference Keynote Speaker Mourad Tayebi photo
Biography:

Mourad Tayebi is an Associate Professor in Biomedical Sciences in the School of Medicine at Western Sydney University, Australia. He is an international expert in the field of protein misfolding diseases, with specific focus on investigating the molecular mechanisms underlying pathogenic protein misfolding and characterizing the misfolding associated with these disorders. His team is very active in the development of early blood diagnostic test screen for Alzheimer and effective therapies for neurodegenerative diseases.

 

Abstract:

Proteinopathies such as Alzheimer’s disease (AD) and Parkinson’s disease (PD) are a group of disorders thought to be caused by abnormal folding or misfolding of beta amyloid (Ab) and alpha-synuclein respectively. Their pathogenesis is not well understood due to unresolved molecular mechanisms. This is further complicated by the lack of proper natural disease models that might be effective in aiding in the investigation of the molecular mechanisms underlying these disorders. Dogs spontaneously deposit human-type Ab as they age and thus are a natural higher mammalian model of aging. The canine Aβ precursor protein (APP) is virtually identical to human APP. Previous studies demonstrated that aging dogs spontaneously accumulate human-type Aβ and parallel declines in cognition. Further, the outcomes of immunotherapy studies in aged dogs has predicted human clinical trial outcomes; clearance of Aβ plaques with little cognitive benefits. In more recent work, we show that canine-derived Aβ was toxic to human neuronal cell lines and led to aggregation of human Aβ. Eastern Grey Kangaroos (EGK) display a typical movement disorder presentation associated with grass phalaris poisoning. We show that this disorder, known as Phalaris Staggers displays a Parkinsonian type syndrome with associated Parkinson’s-like signs and neuropathology, including synucleiopathy and neuromyelopathy. Studies of proteinopathies have typically used transgenic mouse models, and subsequently translated to human clinical trials. However, the success rate of these translational studies have been limited and unfortunately resulted in negative outcomes and some with adverse events. It is critical to identify and validate natural higher mammalian models of proteinopathies to investigate the molecular mechanisms underlying these disorders and test therapeutic outcomes prior to translation to human clinical trials.

  • Workshop
Location: Norfolk
Speaker
Biography:

Sheena Vella, MSc. is a social and cultural psychologist and has worked in the field of migration for the past 7 years in Malta and the U.K. Her photovoice research on the social representations of asylum seeking and the future in Malta was awarded a distinction from the Institute of Social & Cultural Psychology at the London School of Economics & Political Science. She has worked at the University of Malta, within government open centres for asylum seekers, and the NGO and voluntary sector. She is currently co-ordinator of the Integration and Community Development activities at Migrants Resource Centre in London. She is particularly interested in empowerment and development models of migrant and refugee women, development of transcultural competencies and social justice.

Abstract:

Migratory experiences often exacerbate the mental health care needs of vulnerable migrants and refugees. Mental health services access and provision, therefore, need to be adaptive to the specific needs of these populations. Thus, development and promotion of these types of services require that migrants be not only at the heart of physical and mental health delivery models but also be able to influence them. My Health project, a thirty-six months initiative oriented to identify health needs of newly arrived migrants – women and children in various European cities, is implementing innovative participatory methodological strategies. The aim is to move from a consultative process to a more participatory and inclusive one in the access/provision of health services. Preliminary findings regarding the innovative strategies used by My Health, namely community participation activities, visual expressions of people’s stories and a stakeholder learning alliance, show that professionals involved are increasingly aware of a) the need to develop better networks with diverse communities, b) the importance of conscious participatory design that moves beyond consultation with migrants through research, and c) the need to recognise and bolster the role of migrant professionals. Furthermore, by using pictograms health and mental health professionals are mastering new ways to communicate effectively using images, reducing a high reliance on verbal language. Lastly through the learning alliance, professionals and researchers are becoming aware of how involving a more comprehensive network can increase the impact of their work on a broader range of stakeholders. Overall both the intended and unintended results of the innovative strategies used by My Health—an initiative supported by the European Commission, so far are demonstrating creative ways to be used when engaging with mental and physical service delivery for newly arrived migrants.

  • Neuroscience and Neurological Disorders | Clinical Psychology | Advances in Neurological Disorders | Clinical Neuropsychology | Psychotherapy | Humanistic Psychology | Developmental Psychology | Abnormal Psychology | Occupational Psychology
Location: Norfolk
Speaker

Chair

Courtland C Lee

The Chicago School of Professional Psychology, USA

Speaker

Co-Chair

Vivian V Lee

Johns Hopkins University, USA

Session Introduction

Sharron Dolan

Glasgow Caledonian University, UK

Title: Role of adipokines in enhanced pain and inflammation in a rodent model of obesity
Speaker
Biography:

Sharron Dolan is a Senior Lecturer in Pharmacology and Assistant Head of the Department of Life Sciences at Glasgow Caledonian University. After completing her PhD in Neuropharmacology at University of Stirling with Dr Peter Cahusac, she took up a BBSRC funded Post-Doctoral position with Professor Andrea Nolan at Glasgow University’s Veterinary School, working to characterize the spinal mechanisms of inflammatory pain and analgesia. She took up a tenured post as lecturer at GCU in 2004. Her research over the past 20 years has focused on understanding the neuronal mechanisms of pain and inflammation and more recently focused on mechanisms underlying co-morbid pain with diabetes and obesity.

Abstract:

Obese individuals are more likely to be affected by chronic pain, however, the biological mechanisms underpinning this comorbidity are not known. A causal link may be dysregulated secretion of inflammatory adipokines both from expanding adipose tissue and centrally. The aim of this study was to characterize altered pain processing and changes in inflammatory cytokine expression in spinal cord in rodent models of obesity. Responses to thermal and mechanical stimulation of the hind paw were assessed in adult male Wistar rats fed a high fat diet (HFD; 22%) or normal diet for 16 weeks (n=6/group) in absence of inflammation, and then in response to intradermal hind paw injection of carrageenan (3%; 50μl), a model of acute inflammation. Spinal cord was collected and adipokine mRNA expression, cholesterol and triglycerides (TAGs) measured using real-time PCR and ELISA. Rats fed a HFD gained significantly more weight than controls (502 ± 12g vs. 444 ± 7g; P<0.01), and displayed plasma hyperinsulaemia and hypercholesterolaemia (both P<0.05 vs. controls) but normoglycaemia. Acute nociceptive responses were unchanged in obese rats but they displayed potentiated mechanical and thermal hyperalgesia and increased paw edema (all P<0.05 vs. lean controls) in response to carrageenan. Significant changes in levels of resistin C reactive protein, TGFβ and visfatin (but not IL1β or TNFβ) were detected in obese rat spinal cord. The increased pain and inflammation in obese rats fits with the hypothesis that obesity is a chronic low-grade inflammatory disorder, producing a state where responses to inflammatory challenge are potentiated. The altered adipokine profile observed suggests adipokines may be useful biomarkers for monitoring initiation and progression of pain with obesity, or even be involved in the development of co-morbid pain in obese individuals.

Speaker
Biography:

Joyceline Ntoh Yuh is a Feminist and Doctoral candidate in the University of Oldenburg, Germany. She holds an MA in Women & Gender Studies from the ISS Erasmus University Netherlands. Her research interest includes HIV/AIDS related issues, Psychology, Gender, Sexual and Reproductive health. Since 2006, she took keen interest in the field of HIV/AIDS were she researched on the impact of HIV on agriculture affecting mostly women with the UN FAO gender unit (Italy), mainstreaming HIV policies in UNFFE Uganda, HIV stigma & child bearing in Africa and currently facilitates workshops with MA students in the area of gender, sexuality & HIV/AIDS. She is also a Reviewer in the Journal of AIDS Clinical Research & STD (USA) and works as a counseling volunteer in the AIDS Help NGO, Germany.

 

Abstract:

Reports from Germany (2012-13) points a 70% increase in heterosexual transmission with about 40-50% from Sub Saharan Africa marking new diagnosis especially in women. HIV-related stigma among African women is rather complex using the intersectionality framework for analysis, which distinguishes the subjective experiences and realities of women's lives, not just as a single category stemming from a gender-based research critique. Meanwhile, HIV-stigma denotes the link between sero-status and negative behaviors toward people who are seropositive. Stigma thus reflects guilt, shame, denial, prejudice, discrediting, discrimination, stereotypes, denial, rejection and self-blame. African women are particularly vulnerable to stigma due to various factors often undermined or neglected. It is imperative to mention that women are generally susceptible to infection due to biological and other socio-cultural reasons, which eventually positions them into a high risk category. Furthermore, women tend to be negatively perceived when infected and labeled promiscuous for transmitting the virus to their partners, without knowing the transmission dynamic. Stigma further constrains relationships within families and communities. This in the long term results into secrecy affects infection status disclosure and seeking of the much needed support services. This highlights the link between HIV and mental health because people living with HIV are prone to mental problems compared to the others. Thus, their psychological and social wellbeing becomes essential just as their physical health. HIV-related stigma further complicates the overall wellbeing of these women in realizing their potentials in life, which tends to hamper their productivity and sense of purpose. The in-depth study of six women shows the dilemmas and challenges faced by seropositive women in the face of HIV, dealing with disclosure issues, anxiety, depression, social isolation, stress, fear and rejection. This convenient sample examines how psychological impact continues to affect sero-positive women negatively in living fulfilled lives while impacting on their unfulfilled sexual satisfactions due to continuous use of condoms and other related anxieties. At times, such insecurities become overwhelming, pushing them to neglect their self-esteem as women. Interpretative phenomenological analysis here aims to gain deeper understanding from participants’ perspectives on how they manage to make opinions and viewpoints of their own experiences, events and social world. It is then vital to provide lived experiences and interpretations in own terms, than simply attributing to pre-existing theoretical preconceptions, by getting details of each case than general claims (ibid).

Speaker
Biography:

Parasuraman Basker had been awarded Doctoral degree in zoology from Annamalai University, Tamil Nadu, India. Following it he was Research Associate in ICAR and UGC research projects on the fauna of Carabids (Coleopteran Insect) in South India and mosquito cytogenetics in the University of Agricultural Sciences, Bangalore and Bangalore University respectively. Subsequently, he was posted as Senior Entomologist in 1995 in the Department of public Health and Preventive Medicine through Tamil Nadu Public Service Commission (TNPSC). In his credit 33 Research Abstracts presented in 8 International and 25 National Conferences since 1983. 21 research papers have been published in reputed national and international journals. He visited Canada, Malaysia, Morocco, Singapore and Spain as presenters with the Government of India Travel Grants (CSIR, INSA, ICMR and NRHM).

Abstract:

The neuroendocrine complex of adult insects consists of neurosecretory cells (NSC) of the brain, corpora cardiaca (CC), and corpora allata (CA). Following the pioneering work of Weyer (1935) in honeybees, several investigators have been explored on the histomorphology of NSC, CC and CA in many orders of insects including in hemipteran insects. The present study is dealt the regulatory mechanism of the male accessory reproductive glands (MARG) of a hemipteran cotton pest Serinetha augur. Histological and electrophoretic studies were made to understand the interrelationship of the neuroendocrine complex (NEC) and the MARG of the insect. The brain of Serinetha augur is divisible into three regions, namely proto-deuto and tritocerebrum. Protocerebrum lies at the anterior region, deutocerebrum is in the latero mid region and tritocerebrum is in the latero posterior region of the brain. The neurosecretory cells (NSC) in the brain complex have been arbitrarily classified into four types (A, B, C and D) and are connected by pars intercerebralis. NSC in this region is distinguished as median neuro secretory cells (MNC). Among NSC identified in three regions of the brain of Serinetha augur A is found larger (13- 18 microns) which is located in tritocerebrum with weak reaction of chrom alum haematoxylin and phloxin (CAHP) due to lower concentration of neurosecretory materials. The type B are 10-12 microns situated in protocerebral region with higher concentration of neurosecretory materials. C and D are moderate and weak reaction respectively with aldehyde fuchsin (AF) and CAHP indicate lesser amounts of neurosecretion. On the regulation of the MARG, it was understood that CA took part directly for its maturation and function. It was proved by the experiments of gonadectomy and extirpation of the MARG. Besides, electropherogram of brain complex in pre and post mating insects showed the quantitative changes of protein. This observation further supports the view that NSC in brain complex has a regulatory role in the MARG which has varieties of vital functions in sperm transfer activities.

 

Wafaa Ramadan

King Faisal Specialist Hospital and Research Center, Saudi Arabia

Title: Confirming the recessive inheritance of SCN1B mutations in developmental epileptic encephalopathy
Speaker
Biography:

Wafaa Ramadan has completed her MBBS degree this June at the age of 24 years from AlFaisal University, Riyadh, KSA. She has a diploma in clinical research activities and a certificate for one year training in developmental genetic department. Dr. Wafaa graduated with first honor degree and has the award of being best intern of the year. She has three papers published, she is the first author in the one she's presenting. Her field of interest is neurology and neuroscience and her work is dedicated towards it.

Abstract:

Introduction: Dominant SCN1B mutations are known to cause several epilepsy syndromes in humans. Only two epilepsy patients to date have been reported to have recessive mutations in SCN1B as the likely cause of their phenotype. Here, we confirm the recessive inheritance of two novel SCN1B mutations in five children from three families with developmental epileptic encephalopathy. The negative clinical exome in one of these families highlight the need to consider recessive mutations in the interpretation of variants in typically dominant genes.

Materials & Methods: We conducted autozygosity mapping and a multi-gene panel in five children with epileptic encephalopathy from three unrelated consanguineous families with normal parents.

Mutation Analysis: In family one and three the same splicing variant was identified (NM_001037.4:c.449-2A>G). In family two a missense homozygous SCN1B variant (NM_001037.4:c.355T>G:p.Y119D) was identified with high pathogenicity scores using in silico prediction tools (PolyPhen (0.997), SIFT (0) and CADD (27)). These variants were completely absent in >7,000 Saudis screened for these genes using exome sequencing and gene panel testing. They were also absent in ExAC.

Conclusion: Although dominant mutations are the typical class of mutations in SCN1B in the context of epilepsy, recessive mutations in this gene have also been reported, albeit very rarely (two patients to date). The negative clinical exome in one of these families highlight the need to consider recessive mutations in the interpretation of variants in typically dominant genes.