bluuebunny/crossref_metadata_2025_split huggingface dataset:
NF‐κB in inflammatory bowel disease
Authors: Atreya I. , Atreya R. , Neurath M. F. 
Published: May 2008

Abstract.Apart from genetic and environmental factors, the mucosal immune system of the gut plays a central role in the pathogenesis of inflammatory bowel disease (IBD). In the healthy gut, the mucosal immune system ensures the balance between pro‐ and anti‐inflammatory mediators and thereby allows an effective defence against luminal pathogens but at the same time prevents an overwhelming immune reaction directed against the huge amount of harmless luminal antigens (for example, components of food or nonpathological bacteria). In both entities of IBD (Crohn’s disease and ulcerative colitis) this immunological balance is severely impaired and shifted towards the pro‐inflammatory side. The chronic mucosal inflammation in IBD is caused by hyperactivation of effector immune cells, which produce high levels of pro‐inflammatory cytokines like tumour necrosis factor‐α, interleukin‐6 and interferon‐γ, resulting in colonic tissue damage. The nuclear transcription factor kappaB (NF‐κB) was identified as one of the key regulators in this immunological setting. Its activation is markedly induced in IBD patients and through its ability to promote the expression of various pro‐inflammatory genes, NF‐κB strongly influences the course of mucosal inflammation. Considering the different cell‐type specific effects which are mediated by NF‐κB, this review aims at describing the complex role of NF‐κB in IBD and discusses existing pharmacological attempts to block the activation of NF‐κB to develop new therapeutic strategies in IBD.
Interplay of commensal and pathogenic bacteria, genetic mutations, and immunoregulatory defects in the pathogenesis of inflammatory bowel diseases
Authors: Packey C. D. , Sartor R. B. 
Published: May 2008

AbstractEnteric microbiota can contribute to Crohn’s disease and ulcerative colitis in several ways. Pathogenic or functionally altered commensal bacteria with increased mucosal adherence, invasion and intracellular persistence can activate pathogenic T cells and chronic intestinal inflammation. Compositional changes in intestinal microbiota can lead to decreased protective and increased aggressive species. Genetic polymorphisms resulting in increased mucosal permeability, decreased microbial killing, ineffective clearance of bacteria, biased TH1 and TH17 immune responses and loss of immunological tolerance are probably key contributors to IBD. Future therapies for these heterogeneous diseases should be individualized based on the patient‐specific subset.
ULTRASTRUCTURAL CHANGES IN THE DORSAL ROOT AND TRIGEMINAL GANGLIA OF RATS POISONED WITH METHYL MERCURY
Authors: JACOBS JEAN M. , CARMICHAEL N. , CAVANAGH J. B. 
Published: May 2008

Ultrastructural changes in the dorsal root and trigeminal ganglia of rats poisoned with methyl mercuryRats have been dosed with methyl mercury chloride (7.5 mg/kg/day) for 8 days. The dorsal root and trigeminal ganglion cells have been studied by light and electron microscopy from 24 hours after the first dose to the 10th day. Earliest changes were found certainly at day 2 and possibly at day 1 and were confined to focal areas in the periphery of certain Type A cells in which ribosomes were lost from the rough endoplasmic reticulum (RER). Accumulations of dispersed granular material accompanied these earliest changes. After 4 days, changes in nuclear and perinuclear structures occurred just before or at the onset of axon degeneration, and may not be reactive to this event. These findings can be correlated with the defect in amino acid incorporation that occurs before axon degeneration.
VARIATIONS IN THE HUMAN PURKINJE CELL POPULATION ACCORDING TO AGE AND SEX
Authors: HALL T. C. , MILLER A. K. H. , CORSELLIS J. A. N. 
Published: May 2008

Systematic measurements and Purkinje cell counts have been made on ninety ‘normal’ cerebella. Forty‐eight were male, forty‐two were female. Both hemispheres were sampled in thirty‐eight cases, giving a total of 128 hemispheres. The fresh volume of the cerebellum was measured in each specimen and corrections were made for changes in size during fixation and processing. The methods used and their rationale are described and discussed in detail. A mean of 6318 nucleolated Purkinje cells was counted in each of the 128 hemispheres. The mean length of the Purkinje cell line along which they lay was 1–5 m. Twenty‐seven binucleated Purkinje cells were seen out of the 811769 cells that were counted (about 1 per 30000); they appeared to be unrelated to age, sex or disease.The number of Purkinje cells per unit length of the Purkinje cell line and the number per unit area of the Purkinje cell sheet were found to be similar at all ages in the two sexes. Since, however, the male cerebellum tends to be larger than the female, the total number of Purkinje cells in the male is 6–8% higher than in the female. Wide individual variations were found in the same sex at all ages but a mean reduction of 2.5% per decade or of 25% over 100 years was identified. The figures suggested, however, that the reduction was curvilinear with the fall first becoming apparent at about the sixtieth year. No evidence was found that the drop was related to vascular degeneration or to any other identifiable pathological process.
HEXACHLOROPHENE‐INDUCED LESIONS IN THE DEVELOPING PERIPHERAL NERVOUS SYSTEM OF MICE
Authors: PERSSON L. , WINGREN U. , KRISTENSSON K. 
Published: May 2008

Hexachlorophene‐induced lesions in the developing peripheral nervous system of miceHexachlorophene (HCP) locally applied to the sciatic nerve of mice less than 2 weeks old caused a marked sponginess of the myelin. Ultrastructurally, this was due to a splitting of the minor dense lines of the myelin lamellae with the formation of vacuoles. The changes were reversed after discontinuing the treatment. Unexpectedly, this sponginess in the peripheral nerves was much less and failed almost completely to occur when the HCP application was continued after the second week of life. HCP treatment given to mice older than two weeks caused no sponginess of peripheral nerves, but status spongiosus instead developed in the white matter of the central nervous system. The only change in the peripheral nervous system (PNS) in the older mice was a Wallerian type of degeneration of nerve fibres at and distal to the site of HCP injection. It is therefore concluded that the response of the myelin of mouse PNS to HCP is age dependent and differs from the responses of CNS myelin.
EXPERIMENTAL LEAD ENCEPHALOPATHY OF CALVES. HISTOLOGICAL OBSERVATIONS ON THE NATURE AND DISTRIBUTION OF THE LESIONS
Authors: WELLS G. A. H. , HOWELL J. MCC. , GOPINATH C. 
Published: May 2008

Experimental lead encephalopathy of calves. Histological observations on the nature and distribution of the lesionsNeurological signs were induced in four calves by the daily administration of 20 mg/kg body weight lead acetate. The time of onset and duration of symptoms varied, and the severity progressed to an acute neurological episode in three calves. Histological lesions in the brains of three calves consisted of focal vacuolation of the neuropil, neuronal necrosis and changes in capillary walls. These changes occurred in the cerebral cortex and in certain grey centres of the brain stem. The encephalopathy was associated with elevated blood and tissue lead levels, but could not be correlated with pathological effects in other organs. The nature of the lesions suggests a basic change in transport mechanisms between the blood and brain.
DEFICIENT VASCULAR INNERVATION IN FAMILIAL DYSAUTONOMIA, AN EXPLANATION FOR VASOMOTOR INSTABILITY
Authors: GROVER‐JOHNSON NICOLA , PEARSON J. 
Published: May 2008

Deficient vascular innervation in familial dysautonomia, an explanation for vasomotor instabilityAn ultrastructural study of peripheral blood vessels in familial dysautonomia demonstrates the absence of autonomic nerve terminals. In control subjects both sympathetic terminals containing dense‐cored vesicles and presumptive cholinergic terminals containing agranular vesicles are readily shown. Lack of autonomic innervation of blood vessels in familial dysautonomia accounts for postural hypotension and other abnormalities of vasomotor reflexes. It also explains exaggerated responses to sympathomimetic and parasympathomimetic agents in terms of denervation hypersensitivity. Ultrastructural analysis of vascular nerve terminals may be of general value in the study of many diseases which show vasomotor instability.
AN ELECTRON MICROSCOPIC STUDY OF CELL DEGENERATION IN CHICK EMBRYO SPINAL GANGLIA
Authors: PANNESE E. 
Published: May 2008

An electron microscopic study of cell degeneration in chick embryo spinal gangliaCell degeneration which normally occurs during development was studied under the electron microscope in thoracic spinal ganglia of chicken embryos. Cells undergoing degeneration were often identified as primitive neuroblasts or transitional cells between the primitive and intermediate neuroblast, and sometimes as intermediate neuroblasts. Degeneration seems to begin with nuclear alterations (chromatin condensation and segregation of the nucleolar components) and ribosomal changes (polysomal disaggregation, and displacement of many membrane‐associated ribosomes). Soon the Golgi complex is no longer recognizable. Successively, large masses of finely granular material become prominent in the nucleus, the nuclear envelope breaks down, many mitochondria appear altered, many vacuoles with clear contents become evident, and ribosome crystals appear. At the end of the process the degenerated cell appears as a shrunken mass of granular debris and membrane fragments. Some neuroblastic processes contain clumped filaments and microtubules and/or polymorphic dense bodies. These structural changes are not unique to this degenerative process, but closely resemble those following other types of injuries of the nerve cell. A drastic reduction in the nuclear synthesis of RNA, and a profound impairment in protein synthesis are probably the main biochemical events which occur in these degenerating cells. Degeneration, which probably affects the neuroblasts which fail to establish appropriate connections with the periphery, seems to be one of the major factors controlling cell number in the spinal ganglia.
THE EFFECTS OF CARBON MONOXIDE ON NEURONS OF THE CEREBELLUM*
Authors: CHAN‐PALAY VICTORIA , MCCROSKEY L. 
Published: May 2008

The effects of carbon monoxide on neurons of the cerebellumAcute CO exposure in rats produces multifocal edema and neuroglial swelling in cerebellar cortex and nuclei. Chronic multiple daily exposures to CO produce degenerative changes in neurons–shrinkage of cell somata and dendrites, enlargement of nuclei and nucleoli, vacuolation in neuronal cytoplasm, pyknosis and ultimate engulfment by microglia. Focal areas of Purkinje cell loss are typical; individual basket cells and their axons, stellate cells and the deep nuclear neurons are severely affected. Counts of Purkinje cells and their dendritic thorns show reductions of 30% and 31% respectively in affected regions. In foci of severe Purkinje cell loss, dendritic thorns of the neighboring cells which remain assume a greater number of synapses with unusual presynaptic partners, e. g. both parallel fibers and climbing fibers in a single thorn. An increase of 4.2% more synapses per thorn was measured when compared to the normal. Thus, the stress of chronic CO exposure stimulates synaptic plasticity or a compensatory remodelling of neuronal elements in the central nervous system. A scheme is proposed to summarize these changing relationships caused by the loss of some dendritic thorns and the migration of the presynaptic partners to other surviving thorns.
MYELINATION OF THE OVINE CNS WITH SPECIAL REFERENCE TO BORDER DISEASE. II. QUANTITATIVE ASPECTS*
Authors: BARLOW R. M. , STOREY I. JANICE 
Published: May 2008

Myelination of the ovine CNS with special reference to Border disease. II. Quantitative aspectsSemithin Araldite sections and electron micrographs of the dorsal funiculus of spinal cord of sheep fetuses have been examined by methods devised to quantitate certain aspects of myelination. The data relating to axon size and shape, numbers of myelin lamellae, numbers and types of glial cells in normal fetuses have been compared with similar data obtained from an age‐matched series of fetuses affected with Border disease (BD). It was found that the enlargement of axons normally associated with the initial phases of myelination was greater in affected fetuses and, together with the accompanying irregularities of profile, tended to persist throughout gestation. In BD fetuses the rate and degree of myelination was reduced and the high periodicity which characterizes early myelin persisted into late gestation. Mature oligodendrocytes in BD fetuses were reduced by up to 40%, the normal total complement of glial cells being made up by cells with the morphology of multipotential (Type III) glial cells. It is tentatively concluded that Border disease affects the differentiation of oligodendrocytes from their precursors and thus leads to reduced myelin formation. Border disease is compared with relevant experimental and natural conditions and some similarities with Quaking in the mouse are indicated.
LONGTERM INFECTION OF CULTURED HAMSTER DORSAL ROOT GANGLIA WITH HALLÉ SSPE VIRUS
Authors: ECOB‐JOHNSTON MARION S. , BORNSTEIN M. B. , RAINE C. S. 
Published: May 2008

Longterm infection of cultured hamster dorsal root ganglia with Hallé SSPE virusThe morphogenesis of Hallé SSPE virus in cultures of hamster dorsal root ganglia (DRG) over a period of 60 days was followed by light and electron microscopy and by immunoperoxidase techniques. The Hallé virus was originally isolated from the lymph node of a patient with SSPE, and had been passaged only in non‐neural cell lines. In organotypic cultures of hamster DRG, all cells except the neurons became infected. Large intracytoplasmic and intranuclear inclusions were commonly found in fibroblasts, but never in Schwann cells. The latter cells rounded up and were lost from the culture by 20 days post‐infection (PI). Cell‐free virus was detected by 7 days PI, reached a maximum at 30–40 days PI, and even at 60 days PI, substantial amounts of virus were still recorded. Budding virus particles were seen throughout the course of the infection. The formation of syncytia was rare. The present results are compared with previous data on the growth of measles virus in hamster DRG, and the growth of measles and SSPE viruses in cultures of hamster cerebellum. It was concluded that among the available strains of SSPE and measles virus, the Hallé strain is unique in its failure to infect nerve cells.
THE DISTRIBUTION AND ROLE OF MICROTUBULES AND FILAMENTS IN THE NEOPLASTIC ASTROCYTES OF EXPERIMENTAL GLIOMAS
Authors: LANTOS P. L. 
Published: May 2008

The distribution and role of microtubules and filaments in the neoplastic astrocytes of experimental gliomasNeoplasms of the nervous system were induced transplacentally by giving N‐ethyl‐N‐nitrosourea (ENU) to pregnant rats on the 15th day of gestation. Astrocytomas and mixed gliomas with a significant astrocytic component were selected in order to study the distribution of microtubules and filaments in neoplastic fibrillary astrocytes. Electron microscopy of these gliomas revealed a population of pleomorphic astrocytes at various stages of differentiation. Poorly differentiated neoplastic astrocytes showed many microtubules but few filaments. In moderately differentiated cells there was a decrease in the number of microtubules with a concurrent increase of filaments. In well differentiated neoplastic astrocytes filaments dominated the cytoplasm forming thick, tightly packed bundles at the periphery of the cells and in the large processes, while occasional microtubules were intermingled with shorter and looser bundles of filaments. Thus, neoplastic fibrillary astrocytes in ENU‐induced gliomas simulate the various stages in the differentiation of normal fibrillary astrocytes. This suggests that the ratio of microtubules to filaments may be one of the more discriminating criteria by which the degree of differentiation of neoplastic astrocytes can be established.
A LIGHT AND ELECTRON MICROSCOPIC STUDY OF AXON REACTION IN THE RED NUCLEUS OF THE RAT FOLLOWING CERVICAL AND THORACIC LESIONS
Authors: EGAN D. A. , FLUMERFELT B.A. , GWYN D. G. 
Published: May 2008

Egan D.A., Flumerfelt B.A. & Gwyn D.G. (1977) Neuropathology and Applied Neurobiology 3, 423–439A light and electron microscopic study of axon reaction in the red nucleus of the rat following cervical and thoracic lesionsAxon reaction in neurons of the caudal 200 pm of the red nucleus was studied by light and electron microscopy from 1–250 days after axotomy at cervical and at thoracic levels. Following cervical lesions, severe chromatolysis occurred on the third day and by 55 days all of the neurons were atrophic. After thoracic lesions, the reaction was less intense and by 55 days the neurons had returned to normal. The initial morphological changes suggested a regenerative response which was characterized by early dissolution of the ER followed by an increase in its elaboration from the nuclear envelope, and the formation of a nuclear cap. Dilated cisternae of ER were observed in both groups and were seen to contain material similar to that in the ER cisternae generally. Neurofilamentous hyperplasia was most prominent at day 7 in both groups. Neurons of those operated at the cervical level became atrophic at the later stages and signs of autophagy were seen. Evidence of neuronal degeneration, characterized by densely packed whorls, vacuoles and dense bodies, was also seen. The fate of the neuron, i.e. regeneration, atrophy or death, appeared to be determined by the percentage of cytoplasm lost.
PROTEIN AND NUCLEIC ACID CONTENT IN THE AGING HUMAN BRAIN*
Authors: NABER D. , DAHNKE H. G. 
Published: May 2008

Naber D. & Dahnke H.G. (1979) Neuropathology and Applied Neurobiology5, 17–24Protein and nucleic acid content in the aging human brainThe frontal cortex, white matter, cerebellum, caudate nucleus, thalamus and putamen of human brains, ranging from 16 to 91 years, were assayed for protein and nucleic acids. In all these areas the protein content decreased by 5–15% between 30 years and 90 years‐of‐age. The nucleic acid content, however, did not show any significant change. During a post‐mortem interval of 6–25 hours there was no significant decrease found in either the protein or the nucleic acid content of brain tissue.
PERIPHERAL NERVOUS SYSTEM IN A CASE OF CANINE GIANT AXONAL NEUROPATHY
Authors: DUNCAN I. D. , GRIFFITHS I. R. 
Published: May 2008

Duncan I.D. & Griffiths I.R. (1979) Neuropathology and Applied Neurobiology5, 25–39Peripheral nervous system in a case of canine giant axonal neuropathyThe pathology of the peripheral nerves in a dog with naturally occurring giant axonal neuropathy (GAN) is described. Axonal swellings were found predominantly in the distal portions of the tibial and recurrent laryngeal nerves. Excess neuro‐filaments, often arranged in whorls, were present in the swellings which were found in both myelinated and non‐myelinated fibres. Other axonal organelles tended to be isolated in small pockets and on occasions adaxonal Schwann cell processes partially separated these organelles from the axoplasm. The myelin sheath was attenuated over the swellings and short lengths of demyelinated axon were often seen adjacent to the enlargements. Some Schwann cells also contained excessive microfilaments. The peripheral nerve pathology in the dog appears closely similar to that of human GAN and to certain experimental toxic neuropathies, particularly those produced by n‐hexane and methyl‐butyl ketone.
ULTRASTRUCTURAL CHANGES OF OLIGODENDROGLIA AND MYELIN SHEATHS INDUCED BY ETHIDIUM BROMIDE
Authors: YAJIMA KUNIO , SUZUKI KINUKO 
Published: May 2008

Yajima K. & Suzuki K. (1979) Neurobiology and Applied Neuropathology5, 49–62Ultrastructural changes of oligodendroglia and myelin sheaths induced by ethidium bromideIntracisternal injection of ethidium bromide, an inhibitor of mitochondria associated RNA, DNA and protein synthesis, produced status spongiosus in the subpial surface of the CNS of rats. Ultrastructurally, numerous intra‐myelink vacuoles and prominent degenerative changes of oligodendroglia were observed. The vacuoles were formed between the myelin lamellae by splitting of the intraperiod lines, between the axolemma and the innermost myelin lamellae, and/or between the inner tongue of oligodendroglia and myelin lamellae. In the degenerating oligodendroglia, proliferation and alteration of the endoplasmic reticulum were prominent. In places, altered membranes of the endoplasmic reticulum formed concentrical scroll‐like structures. These ultrastructural changes in ethidium bromide treated rats were compared with other similar previously described changes in animals treated with TET, cuprizone, hexachlorophene, hypocholesterolaemic drugs and actino‐mycin D.
A QUANTITATIVE STUDY OF THE GLIA OF THE PURKINJE CELL LAYER OF THE CEREBELLUM IN MAMMALS
Authors: MANN D. M. A. , YATES P. O. 
Published: May 2008

Mann D.M.A. & Yates P.O. (1979) Neuropathology and Applied Neurobiology5, 71–76A quantitative study of the glia of the Purkinje cell layer of the cerebellum in mammalsThe cerebella of fourteen mammals have been examined and the number of each DNA class of glial cell, within the Purkinje cell layer, counted. Diploid glial cells were present in all species and related in number to the surface area of the Purkinje cell. It is likely that they assist in the maintenance of the physiology of this latter cell type. Tetraploid glial cells, however, occur in significant numbers only in the human and chimpanzee and possibly play a part in the establishment of certain learned patterns of co‐ordinated movement peculiar to these species.
SPINAL CORD TRANSECTION: A QUANTITATIVE ANALYSIS OF ELEMENTS OF THE CONNECTIVE TISSUE MATRIX FORMED WITHIN THE SITE OF LESION FOLLOWING ADMINISTRATION OF PIROMEN, CYTOXAN OR TRYPSIN
Authors: MATTHEWS M. A. , ONGE M. F. ST. , FACIANE C. L. , GELDERD J. B. 
Published: May 2008

Spinal cord transection: a quantitative analysis of elements of the connective tissue matrix formed within the site of lesion following administration of piromen, cytoxan or trypsinLong‐Evans hooded rats were cordotomized at the T‐5 level and given either (1) cyclophosphamide (cytoxan), an immunosuppressive, (2) piromen, a bacterial polysaccharide‐nucleic acid complex, (3) topical and systemic trypsin, or (4) no further specific treatment. Because of past and present controversy surrounding the proposed ability of these agents to promote spinal cord regeneration, a systematic study, employing light and electron microscopy, and quantitative methods in a single animal model, was done in order to re‐evaluate the effects of each treatment upon the connective tissue matrix which forms in the defect left by transection. After an initial inflammatory reaction during the first week after surgery, the lesion zone is characterized either by areas of dense collagenous connective tissue with occasional fibroblasts and macrophages, or a loose areolar tissue with numerous sheets and cords of mesodermal cellular elements but minimal collagen. By 45 days postoperatively (dpo), axons supported by Schwann cells invade and become entangled in the loose connective tissue matrix. With longer postoperative survival, cysts appear craniad and caudad to the lesion and erode much of the scar together with viable neural tissue. Giving cytoxan or piromen did not result in any qualitative alteration of the scar matrix as evidenced by electron microscopy. Quantitative analysis revealed a slight reduction in the fibrous connective tissue component of the scar at 45–90 dpo, but this was transient when longer postoperative periods were studied. Trypsin caused a significant reduction in the amount of fibrous connective tissue with a concomitant increase in loose connective tissue and the appearance of a few distinctive, compact bundles of unmyelinated axons lacking Schwann cells.