Veterinary Science Collected Works - Research Publications
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ItemInput-to-state stability analysis via averaging for parameterized discrete-time systems(Watam Press, 2010-12-15)The paper studies semi-global practical input-to-state stability (SGP-ISS) of a parameterized family of discrete-time systems that may arise when an approximate discrete-time model of a sampled-data system with disturbances is used for controller design. It is shown under appropriate conditions that if the solutions of the time varying family of discrete-time systems with disturbances converge uniformly on compact time intervals to the solutions of the average family of discrete-time systems, then ISS of the average family of systems implies SGP-ISS of the original family of systems. A trajectory based approach is utilized to establish the main result.
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ItemIdentification, distribution and molecular evolution of the pacifastin gene family in Metazoa.(Springer Science and Business Media LLC, 2009-05-12)BACKGROUND: Members of the pacifastin family are serine peptidase inhibitors, most of which are produced as multi domain precursor proteins. Structural and biochemical characteristics of insect pacifastin-like peptides have been studied intensively, but only one inhibitor has been functionally characterised. Recent sequencing projects of metazoan genomes have created an unprecedented opportunity to explore the distribution, evolution and functional diversification of pacifastin genes in the animal kingdom. RESULTS: A large scale in silico data mining search led to the identification of 83 pacifastin members with 284 inhibitor domains, distributed over 55 species from three metazoan phyla. In contrast to previous assumptions, members of this family were also found in other phyla than Arthropoda, including the sister phylum Onychophora and the 'primitive', non-bilaterian Placozoa. In Arthropoda, pacifastin members were found to be distributed among insect families of nearly all insect orders and for the first time also among crustacean species other than crayfish and the Chinese mitten crab. Contrary to precursors from Crustacea, the majority of insect pacifastin members contain dibasic cleavage sites, indicative for posttranslational processing into numerous inhibitor peptides. Whereas some insect species have lost the pacifastin gene, others were found to have several (often clustered) paralogous genes. Amino acids corresponding to the reactive site or involved in the folding of the inhibitor domain were analysed as a basis for the biochemical properties. CONCLUSION: The absence of the pacifastin gene in some insect genomes and the extensive gene expansion in other insects are indicative for the rapid (adaptive) evolution of this gene family. In addition, differential processing mechanisms and a high variability in the reactive site residues and the inner core interactions contribute to a broad functional diversification of inhibitor peptides, indicating wide ranging roles in different physiological processes. Based on the observation of a pacifastin gene in Placozoa, it can be hypothesized that the ancestral pacifastin gene has occurred before the divergence of bilaterian animals. However, considering differences in gene structure between the placozoan and other pacifastin genes and the existence of a 'pacifastin gene gap' between Placozoa and Onychophora/Arthropoda, it cannot be excluded that the pacifastin signature originated twice by convergent evolution.
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ItemEvolution of female carotenoid coloration by sexual constraint in Carduelis finches.(Springer Science and Business Media LLC, 2010-03-25)BACKGROUND: Females often express the same ornaments as males to a similar or lesser degree. Female ornaments can be adaptive, but little is known regarding their origins and mode of evolution. Current utility does not imply evolutionary causation, and therefore it is possible that female ornamentation evolved due to selection on females, as a correlated response to selection on males (sexual constraint), or a combination of both. We tested these ideas simulating simple models for the evolution of male and female correlated traits, and compared their predictions against the coloration of finches in the genus Carduelis. RESULTS: For carotenoid-based ornamental coloration, a model of sexual constraint on females fits the Carduelis data well. The two alternative models (sexual constraint on males, and mutual constraint) were rejected as causing the similarities in carotenoid coloration between males and females. For melanin coloration, the correlation between the sexes was weaker, indicating that males and females evolved independently to a greater extent. CONCLUSIONS: This indicates that sexual constraint on females was an important mechanism for the evolution of ornamental carotenoid coloration in females, but less so for melanin coloration. This does not mean that female carotenoid coloration is non-adaptive or maladaptive, because sexual dichromatism could evolve if it were maladaptive. It suggests, however, that most evolution of female carotenoid coloration was male-driven and, when adaptive, may not be an adaptation stricto sensu.
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ItemNo Preview AvailableCAN VIRAL ENVELOPE GLYCOLIPIDS PRODUCE AUTOIMMUNITY, WITH REFERENCE TO THE CNS AND MULTIPLE-SCLEROSIS(BLACKWELL SCIENCE LTD, 1984)Many viruses, with lipid envelopes derived from the host cell membranes, have been implicated in the aetiology of multiple sclerosis (MS), and epidemiological studies support an infectious agent. Alternatively the disease is thought by other workers to be auto-immune in nature, and recently much attention has been focused on immunological sensitivity to glycolipids in MS patients. In this paper it is proposed that CNS demyelination could arise in susceptible individuals (HLA type) from an immune response to glycolipids, triggered by the carrier effect of one or more enveloped neurotropic viruses.
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ItemNo Preview AvailableDO HUMAN T-LYMPHOTROPHIC VIRUSES (HTLVS) AND OTHER ENVELOPED VIRUSES INDUCE AUTOIMMUNITY IN MULTIPLE-SCLEROSIS(WILEY, 1987)A virally induced autoimmune reaction may be important in the pathogenesis of multiple sclerosis. The role that glycolipids and myelin basic protein presented to the virus may play in this process is considered. The most likely cells to be the source of autoantigens are neurons, myelin and oligodendrocytes. Viral infection of class II-expressing cells and association of the viral envelope autoantigens and the class II molecules could trigger an autoimmune reaction. It is suggested that for MS to develop following a virus infection the virus will need to cause expression of class II antigens on brain cells as well as fulfill the same role as an antigen presenting cell. The part which T-lymphotrophic viruses (HTLVs) and other enveloped viruses may play in this phenomenon is discussed.
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ItemNo Preview AvailablePATHOGENESIS OF VIRUS-INDUCED DEMYELINATION(ELSEVIER ACADEMIC PRESS INC, 1993)Demyelination is a component of several viral diseases of humans. The best known of these are subacute sclerosing panencephalitis (SSPE) and progressive multifocal leukoencephalopathy (PML). There are a number of naturally occurring virus infections of animals that involve demyelination and many of these serve as instructive models for human demyelinating diseases. In addition to the naturally occurring diseases, many viruses have been shown to be capable of producing demyelination in experimental situations. In discussing virus-associated demyelinating disease, the chapter reviews the architecture and functional organization of the CNS and considers what is known of the interaction of viruses with CNS cells. It also discusses the immunology of the CNS that differs in several important aspects from that of the rest of the body. Experimental models of viral-induced demyelination have also been considered. Viruses capable of producing demyelinating disease have no common taxonomic features; they include both DNA and RNA viruses, enveloped and nonenveloped viruses. The chapter attempts to summarize the important factors influencing viral demyelination, their common features, and possible mechanisms.
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ItemNo Preview AvailableVirus demyelination(SPRINGER, 2003-04)A number of viruses can initiate central nervous system (CNS) diseases that include demyelination as a major feature of neuropathology. In humans, the most prominent demyelinating diseases are progressive multifocal leukoencephalopathy, caused by JC papovirus destruction of oligodendrocytes, and subacute sclerosing panencephalitis, an invariably fatal childhood disease caused by persistent measles virus. The most common neurological disease of young adults in the developed world, multiple sclerosis, is also characterized by lesions of inflammatory demyelination; however, the etiology of this disease remains an enigma. A viral etiology is possible, because most demyelinating diseases of known etiology in both man and animals are viral. Understanding of the pathogenesis of virus-induced demyelination derives for the most part from the study of animal models. Studies with neurotropic strains of mouse hepatitis virus, Theiler's virus, and Semliki Forest virus have been at the forefront of this research. These models demonstrate how viruses enter the brain, spread, persist, and interact with immune responses. Common features are an ability to infect and persist in glial cells, generation of predominantly CD8(+) responses, which control and clear the early phase of virus replication but which fail to eradicate the infection, and lesions of inflammatory demyelination. In most cases demyelination is to a limited extent the result of direct virus destruction of oligodendrocytes, but for the most part is the consequence of immune and inflammatory responses. These models illustrate the roles of age and genetic susceptibility and establish the concept that persistent CNS infection can lead to the generation of CNS autoimmune responses.
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ItemNo Preview AvailableComputer analysis suggests a role for signal sequences in processing polyproteins of enveloped RNA viruses and as a mechanism of viral fusion.(Springer Science and Business Media LLC, 1989-05)We have used a computer program to scan the entire sequence of viral polyproteins for eucaryotic signal sequences. The method is based on that of von Heijne (1). The program calculates a score for each residue in a polyprotein. The score indicates the resemblance of each residue to that at the cleavage site of a typical N-terminal eucaryotic signal sequence. The program correctly predicts the known N-terminal signal sequence cleavage sites of several cellular and viral proteins. The analysis demonstrates that the polyproteins of enveloped RNA viruses--including the alphaviruses, flaviviruses, and bunyaviruses--contain several internal signal-sequence-like regions. The predicted cleavage site in these internal sequences are often known cleavage sites for processing of the polyprotein and are amongst the highest scoring residues with this algorithm. These results indicate a role for the cellular enzyme signal peptidase in the processing of several viral polyproteins. Not all high-scoring residues are sites of cleavage, suggesting a difference between N-terminal and internal signal sequences. This may reflect the secondary structure of the latter. Signal sequences were also found at the N-termini of the fusion proteins of the paramyxoviruses and the retroviruses. This suggests a mechanism of viral fusion analogous to that by which proteins are translocated through the membranes of the endoplasmic reticulum at synthesis.
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ItemNo Preview AvailableTHE V5A13.1 ENVELOPE GLYCOPROTEIN DELETION MUTANT OF MOUSE HEPATITIS-VIRUS TYPE-4 IS NEUROATTENUATED BY ITS REDUCED RATE OF SPREAD IN THE CENTRAL-NERVOUS-SYSTEM(ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS, 1992-03)Following intracerebral inoculation of adult Balb/c Byj mice, the MHV-4 strain of mouse hepatitis virus (MHV) had an LD50 of less than 0.1 PFU, whereas its monoclonal antibody resistant variant V5A13.1 had an LD50 of 10(4.2) PFU. To determine the basis for this difference in neurovirulence we have studied the acute central nervous system (CNS) infection of these two viruses by in situ hybridization. Both viruses infected the same, specific neuroanatomical areas, predominantly neurons, and spread via the cerebrospinal fluid, along neuronal pathways and between adjacent cells. The neuronal nuclei infected and the spread of virus within the brain are described. The main difference between the parental and variant viruses was the rate at which the infection spread. MHV-4 spread rapidly, destroying large numbers of neurons and the animals died within 4 days of infection. The variant virus spread to the same areas of the brain but at a slower rate. This difference in the rate of virus spread was also apparent from the brain virus titers. The slower rate of spread of the variant virus appears to allow intervention by the immune response. Consistent with this, the variant virus spread slowly in athymic nu/nu mice, but in the absence of an intact immune response, infection and destruction of neurons eventually reached the same extent as that of the parental virus and the mice died within 6 days of infection. We conclude that the V5A13.1 variant of MHV-4 is neuroattenuated by its slower rate of spread in the CNS.
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ItemNo Preview AvailableA bioreactor model of mouse tumor progression(HINDAWI PUBLISHING CORPORATION, 2007)The present study represents an investigation of a novel stirred bioreactor for culture of a transformed cell line under defined hydrodynamic conditions in vitro. Cell colonies of the EL-4 mouse lymphoma cell line grown for the first time in a rotating disc bioreactor (RDB), were observed to undergo changes in phenotype in comparison to standard, static flask cultures. RDB cultures, with or without agitation, promoted the formation of adherent EL-4 cell plaques that merged to form contiguous tumor-like masses in longer-term cultures, unlike the unattached spheroid aggregates of flask cultures. Plaques grown under agitated conditions were further altered in morphology and distribution in direct response to fluid mechanical stimuli. Plaque colonies growth in RDBs with or without agitation also exhibited significant increases in production of interleukin-4 (IL-4) and lactate, suggesting an inducible "Warburg effect." Increases in cell biomass in RDB cultures were no different to flask cultures, though a trend toward a marginal increase was observed at specific rotational speeds. The RDB may therefore be a suitable alternative method to study mechanisms of tumor progression and invasiveness in vitro, under more complex physicochemical conditions that may approximate natural tissue environments.