Karolina Can is a Post-Doctoral Researcher, whose expertise focuses on Rett syndrome and oxidative stress. She performed her PhD at the Georg-August University in Göttingen in Germany, where she now continues running various projects towards mitochondrial dysfunction and potential molecular targets involved in this neurodevelopmental disorder. She strictly extended her proficiency already during her Master’s studies (MSc performed at Jagiellonian University in Krakow in Poland), when she took advantage on annual internship in the Institute of Human Genetics in Göttingen in Germany, and switched her gears from genetics

towards neurophysiology and live-cell imaging.

Statement of the Problem: Rett syndrome (RTT) is a neurodevelopmental disorder, which occurs almost exclusively in girls with a prevalence of 1:10.000-1:15.000 life births. The genetic causes of RTT are de novo mutations in the MECP2 gene. After a short normal development, developmental stagnation occurs with a neuronal and autonomic dysfunction, manifested as mental retardation, erratic breathing, epilepsy, loss of speech and stereotypical hand movements. Growing evidence indicates that RTT associates with mitochondrial dysfunction and oxidative stress. We previously showed that mitochondria of MeCP2-deficient (Mecp2-/y) mouse hippocampus are partly uncoupled and show a higher consumption of O2. To assess molecular events contributing to redox impairment, we intensified our analyses focusing specifically on neurons and their cytosolic and mitochondrial compartments. Methodology & Theoretical Orientation: Quantitative real-time imaging of redox dynamics was performed with the geneticallyencoded redox sensor roGFP1 in cytosol and mitochondrial matrix of dissociated neurons and organotypic hippocampal slices. Optimized expression was achieved by viral transduction. Findings: Detailed excitation ratiometric fluorescence microscopy confirmed that in Mecp2-/y hippocampal neurons, the redox imbalance affects the cytosolic and mitochondrial compartments. These changes were especially obvious for more complex organotypic slices. Redox challenge by H2O2 and severe hypoxia elicited intensified oxidizing and reducing transients in Mecp2-/y neurons, respectively. Inhibition of superoxide dismutase elicited only a dampened oxidation in Mecp2-/y cytosol and mitochondria, suggesting a decreased efficiency of this scavenging enzyme in Rett mice. More importantly, stimulation by neurotransmitters consistently evoked intensified oxidizing shifts in the cytosol of Mecp2-/y neurons. Conclusions & Significance: Redox imbalance associated with RTT clearly affects cytosol and mitochondria of central neurons. Even physiological events such as neurotransmitter stimulation are sufficient to provoke overshooting redox responses in Mecp2-/y neurons. As these changes are already evident in presymptomatic mice, they may promote the progression of RTT.

Xavier F Figueroa has completed his PhD from Pontificial Catholic University of Chile and Postdoctoral Studies from University of Virginia, Cardiovascular  esearch Center. Currently, he is Associate Professor at Pontificial Catholic University of Chile and is the Director of the Laboratory of Vascular Biology at the Department of Physiology. He has published more than 30 papers in reputed peer-reviewed journals, several of which have been highly cited. His lab combines cellular approaches with studies in intact and in vivo preparations to study the mechanisms involved in the control of microvascular function in peripheral tissues and in the brain.

Neuronal activity depends on the fine and timely regulation of cerebral blood flow by a mechanism known as neurovascular coupling. Neurotransmitters released during an increase in synaptic activity (e.g. glutamate) activate receptors in astrocytes located between neurons and parenchymal arterioles, which initiates a Ca2+ signaling that is propagated to the astrocytic-endfeet and

evokes the release of vasodilator factors, leading to an increase in local blood flow. This process is coordinated among neighboring astrocytes, mainly, through gap junctions and ATP release via hemichannels. It has been proposed that release of NO, a potent vasodilator, from neurons, during an increase in synaptic activity, may be involved in neurovascular coupling. However, astrocytes express the Ca2+-dependent NO-synthetizing enzymes eNOS and nNOS and NO may be involved in the control of Ca2+ signals by direct S-nitrosylation of Ca2+ permeable channels such as connexins-based gap junction channels and hemichannels or pannexinformed channels. Then, the participation of NO in the neurovascular coupling initated by metabotropic glutamate receptor (mGluR) stimulation was assessed in primary cultures of astrocytes and rat brain slices. NO production, vasomotor response of brain cortex arterioles, changes in [Ca2+]i and ATP release were evaluated. In addition, the activity of connexin hemichannels, pannexin channels and Ca2+ homeostasis modulator 1 (CALHM1) channels was also analyzed. Interestingly, the results indicate that NO and CALHM1 channels play an essential role in the astrocyte signaling that mediates neurovascular coupling. Stimulation of astrocytes mGluRs leads to NO-mediated activation of CALHM1 channels by S-nitrosylation, which evokes ATP release. The subsequent ATP-dependent purinergic receptor stimulation induces the opening of Cx43 hemichannels and Panx-1 channels, which contributes to the astrocytic Ca2+ signaling. These findings may provide clues to the design of new therapeutic strategies for the treatment of neurodegenerative diseases.

Wang Liao is a first-year PhD candidate majoring in Neurology at Sun Yat-Sen Memorial Hospital, Sun Yat-Sen University. He mainly focused on regulation of adult neurogenesis, and development of new therapeutic targets for treatment of Alzheimer’s disease.

Adult neurogenesis, which is the generation of functional neurons from neural precursors, occurs throughout life in restricted anatomical regions among mammals. Numerous studies have demonstrated a correlation between the level of hippocampal neurogenesis and cognition, whereas dysfunction of neurogenesis contributes to some pathological processes including Alzheimer’s disease, Parkinson’s disease, and other degenerative diseases. Magnesium is the fourth most abundant ion in mammals, and its elevation in the brain has been shown to enhance memory and synaptic plasticity in vivo. The substantial synaptoprotective effects of magnesium elevation in the brain have also been demonstrated in a mouse model of Alzheimer’s disease. However, the effects of

magnesium on fate determination of aNPCs, which are vital processes in neurogenesis, remain unknown. NPCs isolated from the dentate gyrus of adult C57/BL6 mice were induced to differentiate in a medium with varying magnesium concentrations (0.6, 0.8 and 1.0 mM) and extracellular signal-regulated kinase (ERK) inhibitor PD0325901. The proportion of cells that differentiated into neurons and glial cells was evaluated using immunofluorescence. Quantitative real-time polymerase chain reaction and Western blot methods were used to determine the expression of β-III tubulin (Tuj1) and glial fibrillary acidic protein (GFAP). The activation of ERK and cAMP response element-binding protein (CREB) was examined by Western blot to reveal the underlying mechanism. Magnesium elevation increased the proportion of Tju1-positive cells and decreased the proportion of GFAP-positive cells. Also, the expression of Tuj1 was upregulated, whereas the expression of GFAP was downregulated. Moreover, magnesium elevation enhanced the activation of both ERK and CREB. Treatment with PD0325901 reversed these effects in a dose-dependent manner. This study showed that magnesium elevation effected fate determination of adult neural progenitor cells (aNPCs) and the possibly via ERKinduced CREB activation.

Christina Accordino has her expertise in operational accountability for the clinical and financial management of the utilization of intra-operative neuromonitoring (IONM) during surgical procedures that may put a surgical patient’s central nervous system at risk. Her passion is in providing superior patient care while meeting or exceeding clinical and quality metrics. Since 2007, she has held her Certification Examination in Neurophysiologic Intraoperative Monitoring (CNIM) through ABRET (American Board of Registration of Electroencephalographic and Evoked Potential Technologists). Her foundational skill-set includes SSEP, TceMEP, S/TEMG, EEG, BAER, and direct cortical mapping. She feels that the use of these combined modalities supports spinal cord continuity during cranial, spine, vascular, ENT, and cardio-thoracic procedures. Her experience both in the operating room as a clinician and out, as Director of Operations for SpecialtyCare, has helped her excel in providing direction in managing complex customer, physician, employee and patient related tasks regarding the use of neurophysiological monitoring in the healthcare field. 

Intraoperative neuromonitoring (IONM) can bring value to the operating suite. This presentation will review the expectations from adding this additional service to your practice. The talk will address the need for quality assurance processes and tell a story of the true purpose of IONM. A review of the benefit of utilizing a multi-modality approach, common signal changes, actions following changes, resolution of neuromonitoring changes, post-operative status, confound avoidance from a technical and anesthetic` standpoint, and the necessity of performing safety checklists will be addressed  uring this demonstration. Learn how to walk through the processes of the use of IONM and look for opportunities of internal and external improvement to ultimately improve patient outcomes.

Craniopagus parasiticus is a rare medical case and it is unique unlike other cases reported from different literature. In this case, the head of parasitic twins is protruding from the temporal area of cranium. Parasitic head has two deformed lower limbs; one is too rudimentary attached to the mass; long bones of bilateral lower limbs and some pelvic bones. After dissection of the mass, the intestine was seen but no chest organs and other abdominal organs are seen. There is also rudimentary labium but no vaginal opening.

Case presentation: A 38-years-old multigravida (Gravida V para IV) women from Amhara ethnicity referred from rural health center to Referral Hospital due to prolonged second state of labor at 42+1 weeks. Upon arrival she had contraction, term sized gravid uterus, and fetal heart beat was 112. On digital pelvic examination the cervix was fully diluted, station of the head was high and

the pulsating umbilical cord coming in front of the presenting part with ruptured membrane but yet in the vaginal canal. The team decided to emergency cesarean section and then a live female infant weighing 4200 g was delivered. The placenta was single and normal. The APGAR scores were 7 and 9 at 1 and 5 min, respectively. The infant appeared to be grossly normal except the parasitic

co-twin attached at the cranium. The neonate was investigated with the available investigations (CBC, X-Ray, Doppler ultrasound) and pediatric side consultation was made. After a week of counseling and investigations, successful separation operation was done. During post-operative time the neonate was comfortably suckling on breasts with no neurological deficit. The details of the surgery, post-operative condition and subsequent follow up will be discussed during the conference.

Conclusion: The possible etiologies craniopagus parasiticus is still unknown due to a rarity of cases. Doctors, Genetic Scientists, Epidemiologists and Researchers continue to investigate this case as the reasons that could give clue to birth defect and to provide answer for better prognosis of cases and to improve the life chances of the twins. This case will have some input in the effort to know the etiology and pathogenesis of this new born 

Statement of the problem: Research results in Cognitive and Psychology sciences in field of relationships between mind and body led a new subject to appeared in modern age medicine calling “Psychosomatic”. Despite of the new concept of Psychosomatic but it has an old background particularly in Islamic Medicine.

The purpose of this study: This study has tried to shed light on Islamic physicians studies about Psychosomatic diseased till end of 10th century and categorized their methods in this field of study.

Methodology & theoretical Orientation: This research used historical method. This study has aimed several famous Islamic medicine books mostly between 6 BC till 10 BC. It consisted of Canon of Medicine from Avicenna, Al-Hawi from Rhazes, and Abu Zayd al-Balkhi notes.

Findings: This study has classified physiology-psychology impacts, diseased, Problems and methods of their treatment based on medieval Islamic Physicians opinions

Robert L Tanguay completed his BSc from the University of Lethbridge, attended Medical School at University of Calgary and did his Residency in Psychiatry. He completed his Fellowship in Addiction Medicine under the guidance of Nady el-Guebaly. He is also a Pain Medicine Fellow in the Department of Anesthesia at University of Calgary. He is actively involved in education, teaching medical students and psychiatry residents at the University of Calgary.

We reviewed the literature that proposes the mechanisms of cannabis induced psychotic disorders and hence, increases the risk of early onset of schizophrenia. There have been recent studies showing psychosis as secondary to the THC levels in marijuana, and several studies were found showing CBD may be protective and actually have antipsychotic properties equal in efficacy to atypical antipsychotics such as amisulpride. The percentage of THC is much higher today than in the past and certain formulations have been able to even further concentrate THC such as shatter, wax, honey oil, etcetera. Complicating this is that CBD is almost nonexistent in illicit and legal marijuana around the world. Due to Mendelian genetics, as THC concentration is increased, CBD concentration seems to be inversely reduced. This eliminates the protective factors of CBD while increasing the risk of psychosis. THC and CBD seem to have opposite physiologic effects on endogenous anandamide levels and cannabinoid receptor binding, the mechanism likely leading to CBD’s antipsychotic effect.