Risk for human tick-borne encephalitis, borrelioses, and double infection in the pre-Ural region of Russia.

We assessed the risk for human tick-borne encephalitis (TBE), ixodid tick-borne borrelioses, and double infection from 1994 to 1998 in Perm, which has among the highest rates of reported cases in Russia. We studied 3,473 unfed adult Ixodes persulcatus ticks collected from vegetation in natural foci and 62,816 ticks removed from humans. TBE virus and Borrelia may coexist in ticks

ИММУНОФЕРМЕНТНЫЙ АНАЛИЗ И ПОЛИМЕРАЗНАЯ ЦЕПНАЯ РЕАКЦИЯ В ЛАБОРАТОРНОЙ ДИАГНОСТИКЕ ГРАНУЛОЦИТАРНОГО АНАПЛАЗМОЗА ЧЕЛОВЕКА

With the help of enzyme-linked immunosorbent assay (ELISA) and polymerase chain reaction (PCR) in 332 patients with acute feverish illness after a tick bite, treated at the Perm Regional Hospital of Infectious Diseases in the spring-summer period of 2010, the diagnostics of human granulocytic anaplasmosis was performed. By Omnix’s testsystems HGA-ELISA-IgM and HGA-ELISA-IgG 845 serum, as well as by «nested» PCR, using primers ge3a1-ge10r2 and ge9f3-ge2r4 for A. phagocytophilum genetic material amplification, 952 samples of dried blood spots were studied in the dynamics of the disease. The optimal period for the use of ELISA and PCR was determined. Anaplasmosis was confirmed by both methods in 79 patients (ELISA – in 68, PCR –in 25). In general, serodiagnosis, particularly ELISA, and PCR should be regarded not as alternative but as complementary to each other’s methods of laboratory diagnosis of anaplasmosis.Проведена диагностика гранулоцитарного анаплазмоза человека с помощью иммуноферментного анализа (ИФА) и полимеразной цепной реакции (ПЦР) у 332 пациентов, находившихся на лечении в краевой клинической инфекционной больнице г. Перми в весенне-летний период 2010 г. с острыми лихорадочными заболеваниями после присасывания клещей. В динамике болезни исследовано 845 сывороток крови тест-системами ООО «Омникс» ГАЧ-ИФА-IgM и ГАЧ-ИФА-IgG, а также 952 пробы сухих пятен крови методом «nested» ПЦР с использованием праймеров ge3a1-ge10r2 и ge9f3-ge2r4 для амплификации генетического материала A. phagocytophilum. Определены оптимальные сроки использования ИФА и ПЦР. Обоими методами анаплазмоз подтвержден у 79 пациентов (ИФА – у 68, ПЦР – у 25). В целом, серодиагностику, в частности ИФА, и ПЦР следует рассматривать не как альтернативные, а как взаимодополняющие друг друга методы лабораторной диагностики анаплазмоза

Alzheimer's Disease Amyloid-β Links Lens and Brain Pathology in Down Syndrome

Down syndrome (DS, trisomy 21) is the most common chromosomal disorder and the leading genetic cause of intellectual disability in humans. In DS, triplication of chromosome 21 invariably includes the APP gene (21q21) encoding the Alzheimer's disease (AD) amyloid precursor protein (APP). Triplication of the APP gene accelerates APP expression leading to cerebral accumulation of APP-derived amyloid-β peptides (Aβ), early-onset AD neuropathology, and age-dependent cognitive sequelae. The DS phenotype complex also includes distinctive early-onset cerulean cataracts of unknown etiology. Previously, we reported increased Aβ accumulation, co-localizing amyloid pathology, and disease-linked supranuclear cataracts in the ocular lenses of subjects with AD. Here, we investigate the hypothesis that related AD-linked Aβ pathology underlies the distinctive lens phenotype associated with DS. Ophthalmological examinations of DS subjects were correlated with phenotypic, histochemical, and biochemical analyses of lenses obtained from DS, AD, and normal control subjects. Evaluation of DS lenses revealed a characteristic pattern of supranuclear opacification accompanied by accelerated supranuclear Aβ accumulation, co-localizing amyloid pathology, and fiber cell cytoplasmic Aβ aggregates (∼5 to 50 nm) identical to the lens pathology identified in AD. Peptide sequencing, immunoblot analysis, and ELISA confirmed the identity and increased accumulation of Aβ in DS lenses. Incubation of synthetic Aβ with human lens protein promoted protein aggregation, amyloid formation, and light scattering that recapitulated the molecular pathology and clinical features observed in DS lenses. These results establish the genetic etiology of the distinctive lens phenotype in DS and identify the molecular origin and pathogenic mechanism by which lens pathology is expressed in this common chromosomal disorder. Moreover, these findings confirm increased Aβ accumulation as a key pathogenic determinant linking lens and brain pathology in both DS and AD

Receptive Field Inference with Localized Priors

The linear receptive field describes a mapping from sensory stimuli to a one-dimensional variable governing a neuron's spike response. However, traditional receptive field estimators such as the spike-triggered average converge slowly and often require large amounts of data. Bayesian methods seek to overcome this problem by biasing estimates towards solutions that are more likely a priori, typically those with small, smooth, or sparse coefficients. Here we introduce a novel Bayesian receptive field estimator designed to incorporate locality, a powerful form of prior information about receptive field structure. The key to our approach is a hierarchical receptive field model that flexibly adapts to localized structure in both spacetime and spatiotemporal frequency, using an inference method known as empirical Bayes. We refer to our method as automatic locality determination (ALD), and show that it can accurately recover various types of smooth, sparse, and localized receptive fields. We apply ALD to neural data from retinal ganglion cells and V1 simple cells, and find it achieves error rates several times lower than standard estimators. Thus, estimates of comparable accuracy can be achieved with substantially less data. Finally, we introduce a computationally efficient Markov Chain Monte Carlo (MCMC) algorithm for fully Bayesian inference under the ALD prior, yielding accurate Bayesian confidence intervals for small or noisy datasets

Tick-borne encephalitis virus in dogs - is this an issue?

The last review on Tick-borne encephalitis (TBE) in dogs was published almost ten years ago. Since then, this zoonotic tick-borne arbovirus has been geographically spreading and emerging in many regions in Eurasia and continues to do so. Dogs become readily infected with TBE virus but they are accidental hosts not capable to further spread the virus. They seroconvert upon infection but they seem to be much more resistant to the clinical disease than humans. Apart from their use as sentinels in endemic areas, however, an increasing number of case reports appeared during the last decade thus mirroring the rising public health concerns. Owing to the increased mobility of people travelling to endemic areas with their companion dogs, this consequently leads to problems in recognizing and diagnosing this severe infection in a yet non-endemic area, simply because the veterinarians are not considering TBE. This situation warrants an update on the epidemiology, clinical presentation and possible preventions of TBE in the dog

Theories of schizophrenia: a genetic-inflammatory-vascular synthesis

BACKGROUND: Schizophrenia, a relatively common psychiatric syndrome, affects virtually all brain functions yet has eluded explanation for more than 100 years. Whether by developmental and/or degenerative processes, abnormalities of neurons and their synaptic connections have been the recent focus of attention. However, our inability to fathom the pathophysiology of schizophrenia forces us to challenge our theoretical models and beliefs. A search for a more satisfying model to explain aspects of schizophrenia uncovers clues pointing to genetically mediated CNS microvascular inflammatory disease. DISCUSSION: A vascular component to a theory of schizophrenia posits that the physiologic abnormalities leading to illness involve disruption of the exquisitely precise regulation of the delivery of energy and oxygen required for normal brain function. The theory further proposes that abnormalities of CNS metabolism arise because genetically modulated inflammatory reactions damage the microvascular system of the brain in reaction to environmental agents, including infections, hypoxia, and physical trauma. Damage may accumulate with repeated exposure to triggering agents resulting in exacerbation and deterioration, or healing with their removal. There are clear examples of genetic polymorphisms in inflammatory regulators leading to exaggerated inflammatory responses. There is also ample evidence that inflammatory vascular disease of the brain can lead to psychosis, often waxing and waning, and exhibiting a fluctuating course, as seen in schizophrenia. Disturbances of CNS blood flow have repeatedly been observed in people with schizophrenia using old and new technologies. To account for the myriad of behavioral and other curious findings in schizophrenia such as minor physical anomalies, or reported decreased rates of rheumatoid arthritis and highly visible nail fold capillaries, we would have to evoke a process that is systemic such as the vascular and immune/inflammatory systems. SUMMARY: A vascular-inflammatory theory of schizophrenia brings together environmental and genetic factors in a way that can explain the diversity of symptoms and outcomes observed. If these ideas are confirmed, they would lead in new directions for treatments or preventions by avoiding inducers of inflammation or by way of inflammatory modulating agents, thus preventing exaggerated inflammation and consequent triggering of a psychotic episode in genetically predisposed persons

Neurobiology of social behavior abnormalities in autism and Williams syndrome

Social behavior is a basic behavior mediated by multiple brain regions and neural circuits, and is crucial for the survival and development of animals and humans. Two neuropsychiatric disorders that have prominent social behavior abnormalities are autism spectrum disorders (ASD), which is characterized mainly by hyposociability, and Williams syndrome (WS), whose subjects exhibit hypersociability. Here we review the unique properties of social behavior in ASD and WS, and discuss the major theories in social behavior in the context of these disorders. We conclude with a discussion of the research questions needing further exploration to enhance our understanding of social behavior abnormalities