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Background: Although the basic pathophysiology is the same in both cervical and thoracolumbar intervertebral disk (IVD) extrusions, there are considerable clinical differences that have only been partially explained. Hypothesis/Objectives: The epidural inflammatory response differs between cervical and thoracolumbar IVD extrusions. Animals: Fifty‐five dogs with cervical and 80 dogs with thoracolumbar IVD extrusions. Methods: Clinical data and histopathologic variables were investigated. Associations between severity of epidural inflammation and clinical and pathologic variables, impact of chondrodystrophic phenotype, and localization (cervical versus thoracolumbar) were evaluated statistically. Results: Dogs with cervical IVD extrusion were significantly older (P < 0.001), had less severe and longer duration of neurologic signs (both P < 0.001), were more painful (P = 0.038), and had a better outcome (P = 0.005) than dogs with a thoracolumbar IVD extrusion. On histopathology, cervical epidural material had less severe calcification (P = 0.002) and inflammation (P < 0.001). No significant differences regarding chondrodystrophic phenotype were found. Conclusion and Clinical Importance: There was significantly less intensive inflammatory response in the cervical epidural space. This observation correlated positively with less nucleus pulposus calcification in cervical extrusions indicating biochemical, metabolic, and biomechanical differences between the 2 locations, which remain to be characterized in future studies. [ABSTRACT FROM AUTHOR]

Background The pathophysiology of ascending/descending myelomalacia ( ADMM) after canine intervertebral disk ( IVD) extrusion remains poorly understood. Vasoactive molecules might contribute. Hypothesis/Objectives To investigate the immunoreactivity of endothelin-1 ( ET-1) in the uninjured and injured spinal cord of dogs and its potential association with intramedullary hemorrhage and extension of myelomalacia. Animals Eleven normal control and 34 dogs with thoracolumbar IVD extrusion. Methods Spinal cord tissue of dogs retrospectively selected from our histopathologic database was examined histologically at the level of the extrusion (center) and in segments remote from the center. Endothelin-1 immunoreactivity was examined immunohistochemically and by in situ hybridization. Associations between the immunoreactivity for ET-1 and the severity of intramedullary hemorrhage or the extension of myelomalacia were examined. Results Endothelin-1 was expressed by astrocytes, macrophages, and neurons and only rarely by endothelial cells in all dogs. At the center, ET-1 immunoreactivity was significantly higher in astrocytes (median score 4.02) and lower in neurons (3.21) than in control dogs (3.0 and 4.54) ( P < .001; P = .004) irrespective of the grade of hemorrhage or myelomalacia. In both astrocytes and neurons, there was a higher ET-1 immunoreactivity in spinal cord regions remote from the center (4.58 and 4.15) than in the center itself ( P = .013; P = .001). ET-1 mRNA was present in nearly all neurons with variable intensity, but not in astrocytes. Conclusion and Clinical Importance Enhanced ET-1 immunoreactivity over multiple spinal cord segments after IVD extrusion might play a role in the pathogenesis of ADMM. More effective quantitative techniques are required. [ABSTRACT FROM AUTHOR]

Background: Brain dysfunction is common in sepsis. We aimed to assess whether cerebral perfusion, oxygenation, and/or metabolism are abnormal during early endotoxemia, and how they may relate to potential neurohistological changes. Methods: In this prospective animal study, we included 12 pigs (weight: 42 ± 4 kg; mean ± SD) that were exposed to Escherichia coli lipopolysaccharide (E. coli LPS B0111 : B4, 0.4 μg/kg/h) or saline infusion (n = 6, each) for 10 h. Systemic hemodynamics, cerebral blood flow, intracranial pressure, and brain tissue oxygen tension were continuously measured. At the end of the experiment, formalin-fixed brains were cut in coronal sections and embedded in paraffin. Afterwards, the sections were cut at 5 microns and stained with hematoxylin and eosin. Results: Stable systemic hemodynamics in both groups were associated with higher carotid arterial blood flow after 10 h of endotoxemia (9.0 ± 2.2 ml/kg/min) compared to controls (6.6 ± 1.2 ml/kg/ min; time-group interaction: P = 0.014). Intracranial pressure, cerebral perfusion pressure, brain oxygen consumption, and brain tissue oxygen tension were similar in both groups. In four of the six endotoxemic animals but in none of the controls, cerebral tissue lesions were found (encephalomalacia with spongy degeneration of white matter, axonal swelling, and ischemic neuronal thalamic necrosis), including significant venous vascular alterations, predominantly in the brainstem, in three of the four animals. Conclusions: Early endotoxemia seems to be associated with histological signs of brain damage unrelated to systemic or cerebral hemodynamics or oxygenation. [ABSTRACT FROM AUTHOR]

The article presents a case study of a 6-year-old male Chihuahua which experienced a single generalized seizure. It says that findings of the magnetic resonance imaging (MRI) of the brain showed a multifocal, acute, ischemic infarction. In addition, histopathologic examination of the brain revealed areas of pale-staining tissue in thalamus, cerebellar vermis, and medial parts of the brainstem and the central cerebellar nuclei.

Ozone decomposition in real water is often empirically modeled due to the system complexity. Mechanistic models, however, can be of great value in view of engineering applications. The high number of model parameters often restricts their applicability. In this study, sensitivity analyses were used to determine the most important elementary reactions from a kinetic model and to understand the reaction mechanism. Only seven of the 28 rate constants showed to impact ozone and hydroxyl radical concentrations. Mass-transfer related parameters were of major importance. Ozone decomposition was extremely sensitive to parameters involving dissolved organic matter (DOM) at very low scavenger levels implying that even in "ultrapure " water systems impurities should be considered. To increase the applicability of mechanistic ozonation models, simplification of the elementary radical scheme combined with a more detailed description of reactions involving DOM is needed. [ABSTRACT FROM AUTHOR]

Background Little is known about the pathologic changes in the epidural space after intervertebral disk ( IVD) extrusion in the dog. Objectives To analyze the pathology of the epidural inflammatory response, and to search for correlations between this process and clinical findings. Methods Clinical data from 105 chondrodystrophic ( CD) and nonchondrodystrophic ( NCD) dogs with IVD extrusion were recorded. Epidural material from these dogs was examined histopathologically and immunohistochemically. Using statistical analysis, we searched for correlations between severity of epidural inflammation and various clinical and pathologic variables. Results Most dogs exhibited an epidural inflammatory response, ranging from acute invasion of neutrophils to formation of chronic granulation tissue. The mononuclear inflammatory infiltrates consisted mostly of monocytes and macrophages and only few T and B cells. Surprisingly, chronic inflammatory patterns also were found in animals with an acute clinical history. Severity of the epidural inflammation correlated with degree of the epidural hemorrhage and nucleus pulposus calcification ( P = .003 and .040), but not with age, chondrodystrophic phenotype, neurologic grade, back pain, pretreatment, or duration. The degree of inflammation was statistically ( P = .021) inversely correlated with the ability to regain ambulation. Conclusion and Clinical Importance Epidural inflammation occurs in the majority of dogs with IVD extrusion and may develop long before the onset of clinical signs. Presence of calcified IVD material and hemorrhage in the epidural space may be the triggers of this lesion rather than an adaptive immune response to the nucleus pulposus as suggested in previous studies. Because epidural inflammation may affect outcome, further research is warranted. [ABSTRACT FROM AUTHOR]

H. Madarame, T. Seuberlich, C. Abril, A. Zurbriggen, M. Vandevelde and A. Oevermann (2011) Neuropathology and Applied Neurobiology 37, 753-767 The distribution of E-cadherin expression in listeric rhombencephalitis of ruminants indicates its involvement in Listeria monocytogenes neuroinvasion Aim: To investigate the expression of E-cadherin, a major host cell receptor for Listeria monocytogenes (LM) internalin A, in the ruminant nervous system and its putative role in brainstem invasion and intracerebral spread of LM in the natural disease. Methods: Immunohistochemistry and double immunofluorescence was performed on brains, cranial nerves and ganglia of ruminants with and without natural LM rhombencephalitis using antibodies against E-cadherin, protein gene product 9.5, myelin-associated glycoprotein and LM. Results: In the ruminant brain, E-cadherin is expressed in choroid plexus epithelium, meningothelium and restricted neuropil areas of the medulla, but not in the endothelium. In cranial nerves and ganglia, E-cadherin is expressed in satellite cells and myelinating Schwann cells. Expression does not differ between ruminants with or without listeriosis and does not overlap with the presence of microabscesses in the medulla. LM is observed in phagocytes, axons, Schwann cells, satellite cells and ganglionic neurones. Conclusion: Our results support the view that the specific ligand-receptor interaction between LM and host E-cadherin is involved in the neuropathogenesis of ruminant listeriosis. They suggest that oral epithelium and Schwann cells expressing E-cadherin provide a port of entry for free bacteria offering a site of primary intracellular replication, from where the bacterium may invade the axonal compartment by cell-to-cell spread. As E-cadherin expression in the ruminant central nervous system is weak, only very locally restricted and not related to the presence of microabscesses, it is likely that further intracerebral spread is independent of E-cadherin and relies primarily on axonal spread. [ABSTRACT FROM AUTHOR]

The article describes the clinical cases of two cats diagnosed with segmental myelitis caused by Toxoplasma gondii. The first case involves a four-year-old neutered female domestic shorthair cat that was presented with a one-month history of progressive gait abnormalities, while the other is a six-year-old intact male domestic shorthair cat with three-month history of progressive gait abnormalities in the pelvic limbs. The pathological, immunocytochemical, serological and magnetic resonance imaging (MRI) findings on each cat are also described.

An 18-month-old European shorthair cat was presented with a two week history of progressive decrease in consciousness, ambulatory tetraparesis, moderate ataxia and generalised decreased-to-absent postural reactions. Bilateral facial and nasal hypalgesia, absent menace response and anisocoria were found, and segmental spinal reflexes were normal. Neurological signs progressed to non-ambulatory tetraparesis, tremor and spinal hyperalgesia. Histopathological examination revealed a mild-to-moderate lymphoplasmacytic and histiocytic infiltration, predominantly in the dorsal spinal roots, cranial nerves and ganglia in association with marked demyelination and proliferation of Schwann cells. Neurons and axons were preserved. Lesions were multi-focal and varied in severity. A predominantly sensory polyganglioradiculoneuritis was diagnosed. This lesion has not been reported previously in cats. Rabies, herpesviruses, feline infectious peritonitis, feline immunodeficiency virus, Toxoplasma gondii and feline leukaemia virus were excluded as possible aetiologies. Infections by other viruses or an autoimmune disease are discussed. [ABSTRACT FROM AUTHOR]

The article describes the cases of eosinophilic granulomatous encephalitis in two unrelated youg Belgian Tervueren and Shepherd dogs. It explains that the cases do not resemble reported description of eosinophilic meningitis adn meningoencephalitis as protozoal infections and as an idiopathic condition. The details of the diagnoses conducted on the dogs are presented along with the clinical manifestation of the disease in the dogs.

The article describes the case of a 2.5-year-old female Leonberger dog with a 1-year history of intermittent and spontaneous knuckling in the thoracic limbs. The dog showed generalized ataxia and a hypermetric gait of the thoracic limbs with a proprioceptive deficits in all limbs. This article describes other clinical signs, magnetic resonance imaging (MRI) findings and neuropathology of a novel neurogenerative disorder affecting the white matter of brain and spinal cord in dogs.

CD45, also called leucocyte common antigen is a transmembrane protein tyrosine phosphatase on the surface of nearly all white blood cells and has a functional role in signal transduction. In the brain, the expression of CD45 can be used to distinguish microglial cells with a characteristic phenotype of CD11b/c+ and CD45low from other central nervous system (CNS) macrophages which show an expression of CD11b/c+ and CD45high. In the course of pathological changes in the CNS, microglia in rodents is known to readily upregulate expression of various surface molecules, such as CD45. Understanding the mechanisms that regulate expression of surface molecules is essential to study the pathogenesis of CNS diseases. In the present study, the expression of CD45 on microglia of 42 dogs was examined ex vivo by means of flow cytometry. The dogs were classified in two groups according to the histopathological diagnosis in the CNS. All dogs without changes in the CNS (group I; n = 22) only showed low percentages of CD45+ microglial cells. In group II consisting of 20 dogs with different intracranial diseases varying results were obtained. Thirteen dogs showed a low percentage of CD45+ microglial cells whereas seven dogs exhibited high percentages of microglial cells expressing CD45. Evaluation of expression intensity in these seven dogs revealed two subpopulations of CD45+ microglial cells: a large subpopulation with CD45low and a small subpopulation with CD45high. The expression intensity of CD45high was comparable with that of canine monocytes. It was attempted to correlate these findings to age of the animals, underlying disease, duration of clinical signs, medical treatment, occurrence of seizure activity and the expression of other surface molecules. It appeared that dogs with high percentages of CD45+ suffered from long-lasting CNS disease with seizures. In future studies, the reason and consequences for upregulated CD45 in long-lasting CNS diseases has to be further evaluated. [ABSTRACT FROM AUTHOR]

A 20-month-old, female French bulldog was presented with a three-month history of generalised seizures and progressive ataxia with occasional falling over on either side. Neurological examination revealed signs, suggesting a multifocal intracranial lesion. Magnetic resonance imaging of the brain revealed two connected lesions on the left side of the caudal brainstem and a further lesion in the cerebrum. The dog was euthanased, and histopathological examination revealed lesions which closely resembled those of necrotising encephalitis in Yorkshire terriers. This is the first case describing this type of necrotising encephalitis in a French bulldog. [ABSTRACT FROM AUTHOR]

Late onset of hereditary cerebellar cortical abiotrophy has been described in a large variety of canine breeds. In some reported conditions, the cerebellar lesion is combined with degeneration of other systems. Here we describe a new hereditary cerebellar cortical degeneration in eight adult American Staffordshire and Pit Bull Terriers. The neuronal degeneration in these animals not only affects Purkinje cells of the cerebellum but also certain thalamic nuclei. In addition, nerve cell loss appears to be associated with a lysosomal storage disease, which is restricted to the affected cell populations. The stored material was histologically and ultrastructurally identified as fluorescent lipopigment. Since animals were euthanized at various stages of the disease, it could be shown that lysosomal storage preceded neuronal loss. Selective involvement of restricted neuronal populations is highly unusual in ceroid lipofuscinoses. It remains to be determined if the present neurodegenerative disease is caused by a primary or secondary neuronal ceroid lipofuscinosis. [ABSTRACT FROM AUTHOR]

Canine distemper virus (CDV), a negative-stranded RNA morbillivirus, causes a persistent infection within the central nervous system resulting in a progressive, multifocal demyelinating disease. Demyelination is thought to be caused by a selective alteration of the myelin-producing oligodendrocytes. Metabolic impairment and morphological changes of the oligodendrocytes after CDV infection have previously been observed in vitro as well as in vivo. Until now it has been suggested that the oligodendrocytes completely disappear from CDV-induced demyelinating lesions. However, ultrastructural analysis in brain tissue sections and immunohistochemical examination of oligodendrocytes in dog brain cell cultures contradicted these observations. In this study oligodendrocytes from different categories of CDV-induced lesions were examined by in situ hybridization for proteolipid protein mRNA and – as a new tool employed on canine brain tissue sections – by immunohistochemistry using a monoclonal antibody against 2',3'-cyclic nucleotide 3'-phosphodiesterase, a myelin-specific enzyme. A down-regulation in the myelin gene transcription was detected already before demyelination occurred. However, a decrease in the number of oligodendrocytes was not observed until demyelination became evident. Although there was further depletion of oligodendrocytes in plaques with progressive demyelination, we demonstrated for the first time that these cells were still present in a significant amount even in chronic, completely demyelinated distemper lesions. [ABSTRACT FROM AUTHOR]

The data from 20 dogs with histopathologically confirmed granulomatous meningoencephalomyelitis were reviewed in an attempt to identify clinical signs and morphological and cellular parameters, particularly the infiltration of mast cells, which might be associated with the clinical course of the disease. Thirteen of the dogs had the acute form of the disease and seven had the chronic form. Young to middle-aged, small breed female dogs were over-represented. Central vestibular signs were observed in six of the dogs with the acute disease. Analyses of cerebrospinal fluid revealed moderate to severe pleocytosis and high protein concentrations in all cases. Histopathological investigations revealed disseminated perivascular cuffs, large confluent granulomata, tissue necrosis, infiltration with neutrophils and a large number of mitotic cells in the dogs with either of the clinical forms of the disease. Tryptase-positive mast cells were observed in all the cases, but there were significantly larger numbers in the dogs with the acute form. [ABSTRACT FROM PUBLISHER]

Steroid responsive meningitis-arteriitis (SRMA) is a well-known disease in dogs, but the aetiology and pathogenesis are not yet understood. In the peripheral blood an overrepresentation of B cells was found. In the present study we therefore evaluated the distribution of lymphocyte subsets in SRMA in paraffin-embedded tissue sections directly at the lesion sites and compared the results to different canine encephalitides. An intriguing finding was that the B cell/T cell distribution varied depending on the aetiology of the disease: in viral encephalitides, T cells were the predominant cell population in perivascular cuffs, whereas in protozoal and bacterial diseases B cells prevailed. In SRMA an overrepresentation of B cells occurred in meningeal lesions, as already found in the peripheral blood. The distribution of lymphocyte subsets was similar to bacterial and protozoal diseases and was not a unique phenomenon for this specific inflammatory lesion in the canine central nervous system (CNS). Multiple mechanisms seem to be responsible for recruitment and activation of different leukocyte subsets after alteration of the CNS tissue by an environmental factor. A specific finding in SRMA was that the distribution of T and B cells depended also on the lesion site. In contrast to meningeal lesions, in inflamed arteries T cells were the only lymphocyte population found. In these vessels, diffuse infiltration with immunoglobulins was revealed. Inactivated or resting lymphocytes and large granular lymphocytes occurred in each of the diseases examined. These similarities between SRMA and infectious CNS diseases of the dog support earlier suggestions that the disease is somehow triggered by a hitherto unknown environmental factor which leads to the dysregulation of the immune system. [ABSTRACT FROM AUTHOR]

A dot-blot assay for the detection of IgM antibodies (ABs) against canine distemper virus (CDV) in canine serum is described. The diagnostic potential of this technique was evaluated by analysing sera from three test groups: (i) specific pathogen-free (SPF) beagle dogs experimentally infected with virulent CDV; (ii) SPF dogs immunized with a combined vaccine containing CDV, and (iii) SPF dogs immunized with a CDV-free vaccine. As antigen for the dot-blot assay we used the recombinant nucleocapsid protein (N protein) of the virulent A75/17 CDV strain. All 12 dogs of group 1, infected with virulent CDV, showed detectable CDV-specific IgM levels in their serum. All dogs of group 2 were also positive for anti-CDV IgM after the first immunization with the CDV-containing vaccine. The four dogs immunized with a CDV-free vaccine (group iii) remained negative throughout the course of the experiment. From these results, we conclude that the IgM detection test, which requires only a single serum sample, is a useful method for diagnosing current or recent CDV infection in CDV-infected or CDV-immunized dogs under experimental conditions. [ABSTRACT FROM AUTHOR]

The objective of this study was to model the expected numbers of cattle incubating bovine spongiform encephalopathy (BSE) and the numbers of clinical cases of BSE in the Swiss cattle population between 1984 encephalopathy (BSE) and the numbers of clinical cases of BSE in the Swiss cattle population between 1984 and 2005. The results were compared with the observed number of clinical BSE cases and with the results of a culling and testing scheme on herdmates of cattle with BSE. The age distribution of the Swiss cattle population, the age-at-death distribution of the first 235 BSE cases and exposure information were used to calculate the expected number of infected cattle in each birth cohort and the resulting numbers of clinical cases and survivors incubating the disease for each year. The model which did not assume any underreporting of cases fitted the observed epidemic curve of clinical cases reasonably well, and predicted that the Swiss BSE epidemic would come to an end between 2003 and 2005. The age of survivors incubating BSE iS increasing. The higher than expected incidence of subclinical cases observed in animals from the culling scheme is most probably the result of the heterogeneous distribution of infected animals and affected herds in the population. The results of the model need to be taken into account when designing surveillance and testing schemes for BSE. [ABSTRACT FROM PUBLISHER]

The monoclonal antibody (mAB) L1, which binds to the nucleocapsid protein of canine distemper virus (CDV), was shown to bind to avirulent CDV obtained after serial passages in Vero cells, but not to two different virulent demyelinating CDV-strains propagated in dog glial cell cultures. However, when both virulent CDV-strains were passaged through Vero cells they expressed, after a number of passages, an epitope recognized by mAB L1. The occurrence of the L1 epitope appeared to coincide with loss of virulence in animal inoculation experiments. [ABSTRACT FROM AUTHOR]

In 57% of 151 BSE positive brains of Swiss cattle, degenerating neurons were found in BSE predilection sites, either single scattered (34%) or involving large parts of brain stem nuclei (23%). The lesion consisted of central chromatolysis, shrinkage, karyolysis or nuclear pyknosis. In 43% of the BSE positive brains no neuronal changes besides vacuolation were present. Neuronal degeneration other than vacuolation alone is not pathognomonic for BSE but, according to our findings, seems to be of some importance together with the typical vacuolation of neuropil and neurons. There is no correlation between extent of these degenerative changes and accumulation of PrPSc protein, determined by immunohistochemistry. The significance remains obscure, yet as it had not been seen in cattle brains before the outbreak of BSE in Switzerland in 1990 it certainly is linked to the disease. Possible pathogenetic mechanisms are discussed. [ABSTRACT FROM AUTHOR]

In about 5% of the cows showing clinical signs of bovine spongiform encephalopathy (BSE) the histopathological examination is not conclusive. In order to rule out BSE in these cases, additional methods are necessary. For that reason, non-radioactive in situ hybridization (ISH) was performed using a riboprobe against the messenger RNA coding for the prion protein (PrP). In addition, a polyclonal antibody for immunohistochemistry (IHC) was generated against a synthetic peptide derived from bovine PrP. ISH and IHC were used to analyse brain sections of cattle suffering from BSE and various neurological diseases including four cows with clinically suspect but histologically unconfirmed BSE. ISH revealed no differences in localization, distribution and neuronal levels of PrP mRNA between BSE positive and negative cattle. However, there was a BSE-specific staining pattern in IHC allowing to exclude BSE the four suspected cases. Additionally, IHC for PrP is an elegant alternative to search for scrapie associated fibrils by electron microscopy. [ABSTRACT FROM AUTHOR]

Studies on the development of the canine central nervous system and on demyelinating diseases demand unequivocal identification of the glial cells. For that reason, nonradioactive in situ hybridization (ISH) was performed in primary dog brain cell cultures (DBCC) and in brain sections of neonatal dogs. Specific RNA probes were used to detect messenger RNA (mRNA) coding for proteolipid protein (PLP), myelin basic protein (MBP) and glial fibrillary acidic protein (GFAP). PLP and MBP are markers for oligodendrocytes, GFAP for astrocytes. Oligodendrocytes positive for PLP and MBP mRNA were found in both DBCC and brain sections of neonatal dogs. Astrocytes expressing GFAP specific mRNA were detected in DBCC and in brain sections. These cells were evenly distributed in the white matter with additional accumulation in the membrana limitans gliae superficialis, around the ventricles and blood vessels. ISH clearly improves the study of oligodendrocytes in brain sections as, in contrast to the immunohistochemical methods, this technique allows to identify individual cells. [ABSTRACT FROM AUTHOR]

Dissociated brain cell cultures derived from neonatal dogs were examined for the presence of neurons from 7 to 42 days after seeding. Two different antibodies were used: one commercial rabbit antiserum against neuron specific enolase (NSE) and a monoclonal antibody specifically binding to neurons and axons. Decreasing numbers of NSE+ cells were detected up to two weeks after seeding. The monoclonal antibody detected neurons throughout the duration of the experiment. Neurons usually occurred in small clusters and were also concentrated around undissociated tissue fragments. Since the number of neurons remained relatively small throughout the observation period, it was concluded that this type of canine brain culture is not an optimal system to study neuronal pathology. Zusammenfassung Neurone in dissoziierten Hirnzellkulturen des Hundes: Mittels einem polyklonalen Antikörper gegen spezifische Enolase (NSE) und einem monoklonalen Antikörpern der spezifisch an Nervenzellen und Axonen bindet, wurden dissoziierte Hirnzellkulturen von neugeborenen Hunden auf die Präsenz von Nervenzellen untersucht. Abnehmende Zahlen von NSE positiven Zellen wurden beobachtet bis zu 2 Wochen nach Ansetzen der Kulturen. Der monoklonale Antikörper erkannte Nervenzellen für die ganze Dauer des Experimentes (42 Tage). Die Nervenzellen traten meistens in kleinen Gruppen auf und waren vielfach konzentriert um undissoziierte Gewebefragmente. Da die Gesamtzahl der Nervenzellen in der Kultur verhältnismäßig gering blieb, scheint dieses Kultursystem wenig geeignet für das Studium der Nervenzellpathologie. [ABSTRACT FROM AUTHOR]

Sporadically occurring non-suppurative encephalitis appears to be a frequent condition of Swiss cattle. Fifty-one such cases diagnosed over a period of 10 years were examined retrospectively to investigate whether they constituted one or more distinct diseases, and to search for aetiological agents. Three cases were characterised by periventricular granulomatous encephalitis, and most probably represented a different disease, but the remaining 48 cases had disseminated non-suppurative encephalitis with widespread neuronal changes. Neuronal degeneration was very marked in the hippocampus of 10 cases and in the cerebellar Purkinje cells of 11. It was thought that the latter cases represented morphological variations of the same disease rather than a different disease because of their overlapping morphological features. The 48 cases had the following features in common: the disease had primarily neurological signs affecting mostly adult cattle, it was a sporadic condition, and there was a clear tendency for it to have a subacute to chronic course. Polymerase chain reaction (PCR) amplification for chlamydial DNA was negative except in one of 32 specimens, and immunohistochemistry did not demonstrate the presence of chlamydial antigens either in the one PCR-positive case or in the other cases examined. Immunohistochemistry for rabies virus, Borna disease virus, and central European tickborne encephalitis virus was negative. In four cases, immunolabelled cells were found in the lesions with antibodies against paramyxovirus antigens. [ABSTRACT FROM PUBLISHER]

The weight-average M and number-average M molecular weights of gum arabic are identical after a proteolysis treatment with pronase. The value (1.8×10) is closed from M early reported in the literature whereas M before treatment are dispersed for a large lot of samples up to more 10. This can be interpreted by the 'wattle blossom' model for which some homogeneous chains of molecular weight c.a. 2.10 are still linked to a protein core, the crude gum being a mixture of this complex and free chains. [ABSTRACT FROM AUTHOR]

Potentiometric data of arabic acid in salt-free aqueous Solutions can be interpreted by the Lifson-Katchalsky cell model. The best fit between experimental and theoretical titration curves is obtained using a spatial intercharge distance of 11 Å. This value is corroborated by equilibrium dialysis binding of Ethidium Bromide. When compared with already published results, the apparent charge density of arabic acid is four to six times higher than if it was a linear polyelectrolyte. [ABSTRACT FROM AUTHOR]