studies of serum and egg yolk cholesterol level of hens immunized against newcastle disease

Abstract In studies of biochemical patterns in blood, Agarwal (1956) observed an increase in plasma iron and a reduction of blood cholesterol, but little change in the end products of protein metabolism following experimentally induced rabies in sheep. Similar results were reported by Mondini (1955) in horses hyperimmunized against tetanus toxin. Contrary to these reports, Puntigam and Berger (1955), investigating serum cholesterol levels of healthy heifers used for the production of smallpox vaccine, observed that, within four days following inoculation, the esterified cholesterol rose by approximately 16 percent in two-thirds of the animals. Then a gradual drop in cholesterol level occurred and, between the 10th and 14th day after inoculation, a minimum value of 40 percent of the initial level was reached. Free cholesterol was affected similarly. Owing to the importance of cholesterol in many body functions and, in view of the frequency with which vaccination is used in modern prophylaxis

An artificial neural network approach for modelling the ward atmosphere in a medical unit

Artificial neural networks (ANNs) have been developed, implemented and tested on the basis of a four-year-long experimental data set, with the aim of analyzing the performance and clinical outcome of an existing medical ward, and predicting the effects that possible readjustments and/or interventions on the structure may produce on it. Advantages of the ANN technique over more traditional mathematical models are twofold: on one hand, this approach deals quite naturally with a large number of parameters/variables, and also allows to identify those variables which do not play a crucial role in the system dynamics; on the other hand, the implemented ANN can be more easily used by a staff of non-mathematicians in the unit, as an on-site predictive tool. As such, the ANN model is particularly suitable for the case study. The predictions from the ANN technique are then compared and contrasted with those obtained from a generalized kinetic approach previously proposed and tested by the authors. The comparison on the two case periods shows the ANN predictions to be somewhat closer to the experimental values. However, the mean deviations and the analysis of the statistical coefficients over a span of multiple years suggest the kinetic model to be more reliable in the long run, i.e., its predictions can be considered as acceptable even on periods that are quite far away from the two case periods over which the many parameters of the model had been optimized. The approach under study, referring to paradigms and methods of physical and mathematical models integrated with psychosocial sciences, has good chances of gaining the attention of the scientific community in both areas, and hence of eventually obtaining wider diffusion and generalization.

Post-Mortem Examination of the International Financial Network

As the recent crisis has forcefully suggested, understanding financial-market interconnectedness is of a paramount importance to explain systemic risk, stability and economic dynamics. In this paper, we address these issues along two related perspectives. First, we explore the statistical properties of the International Financial Network (IFN), defined as the weighted-directed multigraph where nodes are world countries and links represent debtor-creditor relationships in equities and short/long-run debt. We investigate whether the 2008 financial crisis has resulted in a significant change in the topological properties of the IFN. Our findings suggest that the crisis caused not only a reduction in the amount of securities traded, but also induced changes in the topology of the network and in the time evolution of its statistical properties. This has happened, however, without changing the disassortative, core-periphery structure of the IFN architecture. Second, we perform an econometric study to examine the ability of network-based measures to explain crosscountry differences in crisis intensity. We investigate whether the conclusion of previous studies showing that international connectedness is not a relevant predictor of crisis intensity may be reversed, once one explicitly accounts for the position of each country within the IFN. We show that higher interconnectedness reduces the severity of the crisis, as it allows adverse shocks to dissipate quicker. However, the systemic risk hypothesis cannot be completely dismissed and being central in the network, if the node is not a member of a rich club, puts the country in an adverse and risky position in times of crises. Finally, we find strong evidence of nonlinear effects, once the high degree of heterogeneity that characterizes the IFN is taken into accountfinancial networks, crisis, early warning systems

Post-Mortem Examination of the International Financial Network

As the recent crisis has forcefully suggested, understanding financial-market interconnectedness is of a paramount importance to explain systemic risk, stability and economic dynamics. In this paper, we address these issues along two related perspectives. First, we explore the statistical properties of the International Financial Network (IFN), defined as the weighted-directed multigraph where nodes are world countries and links represent debtor-creditor relationships in equities and short/long-run debt. We investigate whether the 2008 financial crisis has resulted in a significant change in the topological properties of the IFN. Our findings suggest that the crisis caused not only a reduction in the amount of securities traded, but also induced changes in the topology of the network and in the time evolution of its statistical properties. This has happened, however, without changing the disassortative, core-periphery structure of the IFN architecture. Second, we perform an econometric study to examine the ability of network-based measures to explain cross-country differences in crisis intensity. We investigate whether the conclusion of previous studies showing that international connectedness is not a relevant predictor of crisis intensity may be reversed, once one explicitly accounts for the position of each country within the IFN. We show that higher interconnectedness reduces the severity of the crisis, as it allows adverse shocks to dissipate quicker. However, the systemic risk hypothesis cannot be completely dismissed and being central in the network, if the node is not a member of a rich club, puts the country in an adverse and risky position in times of crises. Finally, we find strong evidence of nonlinear effects, once the high degree of heterogeneity that characterizes the IFN is taken into account.financial networks, crisis, early warning systems

Methodological advances in imaging intravital axonal transport

Axonal transport is the active process whereby neurons transport cargoes such as organelles and proteins anterogradely from the cell body to the axon terminal and retrogradely in the opposite direction. Bi-directional transport in axons is absolutely essential for the functioning and survival of neurons and appears to be negatively impacted by both aging and diseases of the nervous system, such as Alzheimer's disease and amyotrophic lateral sclerosis. The movement of individual cargoes along axons has been studied in vitro in live neurons and tissue explants for a number of years; however, it is currently unclear as to whether these systems faithfully and consistently replicate the in vivo situation. A number of intravital techniques originally developed for studying diverse biological events have recently been adapted to monitor axonal transport in real-time in a range of live organisms and are providing novel insight into this dynamic process. Here, we highlight these methodological advances in intravital imaging of axonal transport, outlining key strengths and limitations while discussing findings, possible improvements, and outstanding questions

Molecular Aspects of Secretory Granule Exocytosis by Neurons and Endocrine Cells

Neuronal communication and endocrine signaling are fundamental for integrating the function of tissues and cells in the body. Hormones released by endocrine cells are transported to the target cells through the circulation. By contrast, transmitter release from neurons occurs at specialized intercellular junctions, the synapses. Nevertheless, the mechanisms by which signal molecules are synthesized, stored, and eventually secreted by neurons and endocrine cells are very similar. Neurons and endocrine cells have in common two different types of secretory organelles, indicating the presence of two distinct secretory pathways. The synaptic vesicles of neurons contain excitatory or inhibitory neurotransmitters, whereas the secretory granules (also referred to as dense core vesicles, because of their electron dense content) are filled with neuropeptides and amines. In endocrine cells, peptide hormones and amines predominate in secretory granules. The function and content of vesicles, which share antigens with synaptic vesicles, are unknown for most endocrine cells. However, in B cells of the pancreatic islet, these vesicles contain GABA, which may be involved in intrainsular signaling.' Exocytosis of both synaptic vesicles and secretory granules is controlled by cytoplasmic calcium. However, the precise mechanisms of the subsequent steps, such as docking of vesicles and fusion of their membranes with the plasma membrane, are still incompletely understood. This contribution summarizes recent observations that elucidate components in neurons and endocrine cells involved in exocytosis. Emphasis is put on the intracellular aspects of the release of secretory granules that recently have been analyzed in detail

Travelling Together: A Unifying Pathomechanism for ALS

Axonal transport is critical for neuronal homeostasis and relies on motor complexes bound to cargoes via specific adaptors. However, the mechanisms responsible for the spatiotemporal regulation of axonal transport are not completely understood. A recent study by Liao et al. contributes to filling this gap by reporting that RNA granules ‘hitchhike’ on LAMP1-positive organelles using annexin A11 as a tether

Model predictive control using MISO approach for drug co-administration in anesthesia

In this paper, a model predictive control system for the depth of hypnosis is proposed and analyzed. This approach considers simultaneous co-administration of the hypnotic and analgesic drugs and their effect on the Bispectral Index Scale (BIS). The control scheme uses the nonlinear multiple-input–single-output (MISO) model to predict the remifentanil influence over the propofol hypnotic effect. Then, it exploits a generalized model predictive control algorithm and a ratio between the two drugs in order to provide the optimal dosage for the desired BIS level, taking into account the typical constraints of the process. The proposed approach has been extensively tested in simulation, using a set of patients described by realistic nonlinear pharmacokinetic/pharmacodynamic models, which are representative of a wide population. Additionally, an exhaustive robustness evaluation considering inter- and intra-patient variability has been included, which demonstrates the effectiveness of the analyzed control structure

Expanding the Toolkit for In Vivo Imaging of Axonal Transport

Axonal transport maintains neuronal homeostasis by enabling the bidirectional trafficking of diverse organelles and cargoes. Disruptions in axonal transport have devastating consequences for individual neurons and their networks, and contribute to a plethora of neurological disorders. As many of these conditions involve both cell autonomous and non-autonomous mechanisms, and often display a spectrum of pathology across neuronal subtypes, methods to accurately identify and analyze neuronal subsets are imperative. This paper details protocols to assess in vivo axonal transport of signaling endosomes and mitochondria in sciatic nerves of anesthetized mice. Stepwise instructions are provided to 1) distinguish motor from sensory neurons in vivo, in situ, and ex vivo by using mice that selectively express fluorescent proteins within cholinergic motor neurons; and 2) separately or concurrently assess in vivo axonal transport of signaling endosomes and mitochondria. These complementary intravital approaches facilitate the simultaneous imaging of different cargoes in distinct peripheral nerve axons to quantitatively monitor axonal transport in health and disease

Altered sensory neuron development in CMT2D mice is site-specific and linked to increased GlyRS levels

Dominant, missense mutations in the widely and constitutively expressed GARS1 gene cause a peripheral neuropathy that usually begins in adolescence and principally impacts the upper limbs. Caused by a toxic gain-of-function in the encoded glycyl-tRNA synthetase (GlyRS) enzyme, the neuropathology appears to be independent of the canonical role of GlyRS in aminoacylation. Patients display progressive, life-long weakness and wasting of muscles in hands followed by feet, with frequently associated deficits in sensation. When dysfunction is observed in motor and sensory nerves, there is a diagnosis of Charcot-Marie-Tooth disease type 2D (CMT2D), or distal hereditary motor neuropathy type V if the symptoms are purely motor. The cause of this varied sensory involvement remains unresolved, as are the pathomechanisms underlying the selective neurodegeneration characteristic of the disease. We have previously identified in CMT2D mice that neuropathy-causing Gars mutations perturb sensory neuron fate and permit mutant GlyRS to aberrantly interact with neurotrophin receptors (Trks). Here, we extend this work by interrogating further the anatomy and function of the CMT2D sensory nervous system in mutant Gars mice, obtaining several key results: 1) sensory pathology is restricted to neurons innervating the hindlimbs; 2) perturbation of sensory development is not common to all mouse models of neuromuscular disease; 3) in vitro axonal transport of signalling endosomes is not impaired in afferent neurons of all CMT2D mouse models; and 4) Gars expression is selectively elevated in a subset of sensory neurons and linked to sensory developmental defects. These findings highlight the importance of comparative neurological assessment in mouse models of disease and shed light on key proposed neuropathogenic mechanisms in GARS1-linked neuropathy