The Retail FX Trader: Random Trading and the Negative Sum Game

With the internet boom of early 2000 making access to trading the Foreign Exchange (FX) market far simpler for members of the general public, the growth of 'retail' FX trading continues, with daily transaction volumes as high as $200 billion. Potential new entrants to the retail FX trading world may come from the recent UK pension deregulations, further increasing the volumes. The attraction of FX trading is that it offers high returns and whilst it has been understood that it is high-risk in nature, the rewards are seen as being commensurately high for the 'skilled and knowledgeable' trader who has an edge over other market participants. This paper analyses a number of independent sources of data and previous research, to examine the profitability of the Retail FX trader and compares the results with that of a simulated random trading models. This paper finds evidence to suggest that whilst approximately 20% of traders can expect to end up with a profitable account, around 40% might expect their account to be subject to a margin call. This paper finds a strong correlation between the overall profitability of traders and impact of the cost of the bid-ask spread, whilst finding little if any evidence that retail FX traders, when viewed as a group, are achieving results better than that from random trading

Bi-allelic JAM2 Variants Lead to Early-Onset Recessive Primary Familial Brain Calcification.

Primary familial brain calcification (PFBC) is a rare neurodegenerative disorder characterized by a combination of neurological, psychiatric, and cognitive decline associated with calcium deposition on brain imaging. To date, mutations in five genes have been linked to PFBC. However, more than 50% of individuals affected by PFBC have no molecular diagnosis. We report four unrelated families presenting with initial learning difficulties and seizures and later psychiatric symptoms, cerebellar ataxia, extrapyramidal signs, and extensive calcifications on brain imaging. Through a combination of homozygosity mapping and exome sequencing, we mapped this phenotype to chromosome 21q21.3 and identified bi-allelic variants in JAM2. JAM2 encodes for the junctional-adhesion-molecule-2, a key tight-junction protein in blood-brain-barrier permeability. We show that JAM2 variants lead to reduction of JAM2 mRNA expression and absence of JAM2 protein in patient's fibroblasts, consistent with a loss-of-function mechanism. We show that the human phenotype is replicated in the jam2 complete knockout mouse (jam2 KO). Furthermore, neuropathology of jam2 KO mouse showed prominent vacuolation in the cerebral cortex, thalamus, and cerebellum and particularly widespread vacuolation in the midbrain with reactive astrogliosis and neuronal density reduction. The regions of the human brain affected on neuroimaging are similar to the affected brain areas in the myorg PFBC null mouse. Along with JAM3 and OCLN, JAM2 is the third tight-junction gene in which bi-allelic variants are associated with brain calcification, suggesting that defective cell-to-cell adhesion and dysfunction of the movement of solutes through the paracellular spaces in the neurovascular unit is a key mechanism in CNS calcification

НЕ СВЯЗАННЫE С ВИЧ-ИНФЕКЦИЕЙ ЗАБОЛЕВАНИЯ И ПРИЧИНЫ СМЕРТИ СРЕДИ ВИЧ-ПОЗИТИВНЫХ ПАЦИЕНТОВ В САНКТ-ПЕТЕРБУРГЕ И ЛЕНИНГРАДСКОЙ ОБЛАСТИ

With the aim of an evaluation of the prevalence of non-AIDS-defining illnesses and causes of death in HIVinfected patients 111 medical records of subjects admitted to the specialized hospitals in St. Petersburg in 2001–2008,were analyzed retrospectively. The most frequent non-AIDSdefining illnesses in HIV-infected patients in the era of the absence of the systematical antiretroviral therapy are gastrointestinal diseases. HIV-infected patients mostly die from generalized tuberculosis and chronic viral hepatitis at the End-Stage liver cirrhosis. To properly evaluate the preavalnce of Non-HIV-related diseases and causes of death in HIV-infected people in St. Petersburg and Leningrad region we need to conduct prospective cohort study in comparison with general population.С целью изучения распространенности не связанных с ВИЧ-инфекцией заболеваний и определения основных причин смерти среди больных ВИЧ-инфекцией были ретроспективно оценены 111 историй болезни пациентов, поступивших в специализированные стационары в Санкт-Петербурге за 2001–2008 гг. Наиболее частой сопутствующей патологией среди больных ВИЧ-инфекцией в эру отсутствия широкого применения антиретровирусной терапии являются заболевания желудочно-кишечного тракта. Больные ВИЧ-инфекцией умирают преимущественно от генерализованного туберкулеза и хронических вирусных гепатитов в цирротической стадии. Для полноценной оценки распространенности и спектра не связанных с ВИЧ-инфекцией заболеваний и изучения причин смерти среди ВИЧ-позитивных лиц в Санкт-Петербурге и Ленинградской области необходимо проведение проспективного когортного исследования в сравнении с общей популяцией

Spectrum of Phenotypic, Genetic, and Functional Characteristics in Patients With Epilepsy With KCNC2 Pathogenic Variants

Background and ObjectivesKCNC2 encodes Kv3.2, a member of the Shaw-related (Kv3) voltage-gated potassium channel subfamily, which is important for sustained high-frequency firing and optimized energy efficiency of action potentials in the brain. The objective of this study was to analyze the clinical phenotype, genetic background, and biophysical function of disease-associated Kv3.2 variants.MethodsIndividuals with KCNC2 variants detected by exome sequencing were selected for clinical, further genetic, and functional analysis. Cases were referred through clinical and research collaborations. Selected de novo variants were examined electrophysiologically in Xenopus laevis oocytes.ResultsWe identified novel KCNC2 variants in 18 patients with various forms of epilepsy, including genetic generalized epilepsy (GGE), developmental and epileptic encephalopathy (DEE) including early-onset absence epilepsy, focal epilepsy, and myoclonic-atonic epilepsy. Of the 18 variants, 10 were de novo and 8 were classified as modifying variants. Eight drug-responsive patients became seizure-free using valproic acid as monotherapy or in combination, including severe DEE cases. Functional analysis of 4 variants demonstrated gain of function in 3 severely affected DEE cases and loss of function in 1 case with a milder phenotype (GGE) as the underlying pathomechanisms.DiscussionThese findings implicate KCNC2 as a novel causative gene for epilepsy and emphasize the critical role of KV3.2 in the regulation of brain excitability