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PubMed1991

Identification of the viroid-induced tomato pathogenesis-related (PR) protein P23 as the thaumatin-like tomato protein NP24 associated with osmotic stress.

P23, a 23 kDa pathogenesis-related (PR) protein, was purified from citrus exocortis viroid (CEVd)-infected tomato leaves. Partial amino acid sequencing of this protein including the N-terminal and nine additional tryptic fragments covering about 50% of its primary structure revealed extensive homologies to the members of the family of plant thaumatin-like proteins. Sequence alignment revealed that tomato P23 is the previously described NP24 protein found to be associated to osmotic stress in tomato. In view of this fact the possible role of pathogenesis-related P23 protein as a component of a general mechanism of response of the plant is discussed.

Amino Acid Sequence↗

PubMed1990

Tobacco genes encoding acidic and basic isoforms of pathogenesis-related proteins display different expression patterns.

The induction by cytokinin stress and ethylene of nine different tobacco mosaic virus-inducible mRNA classes (termed A-I) encoding pathogenesis-related (PR) proteins was studied. The induced mRNA levels were compared to basal levels in healthy tobacco plants grown in tissue culture and in a greenhouse. Cytokinin stress and ethylene were found to induce different subsets of the mRNAs, indicating that ethylene is not the primary inducing signal in cytokinin-stressed shoots. mRNAs F, H and G encoding the basic hydrolytic enzymes chitinase, beta-1,3-glucanase and a basic equivalent of PR-1, respectively, were found to be expressed at high levels in roots of healthy plants. mRNAs D, I and B encoding the acidic equivalents of the proteins proved to be present at low levels in healthy plants. These results indicate that genes encoding basic and acidic isoforms of pathogenesis-related proteins are differentially regulated.

Cloning, Molecular↗

PubMed1995

Dark induction and subcellular localization of the pathogenesis-related PRB-1b protein.

The PRB-1b gene codes for a basic-type pathogenesis-related protein of the PR-1 family of tobacco. PRB-1b mRNA accumulation is induced in response to biotic and abiotic elicitors, such as TMV, ethylene, salicylic acid, alpha-amino butyric acid and darkness. In order to determine the location of elements that control dark-regulated PRB-1b gene expression, we tested promoter, transcribed regions and 3'-downstream regions of the gene for their ability to respond to dark induction in transgenic tobacco plants. An ethylene-inducible promoter region of 863 bp was not able to confer dark induction to a beta-glucuronidase reporter gene, while a construct containing the transcribed region of the gene and 3'-downstream sequences, driven by the cauliflower mosaic virus 35S promoter, was correctly dark-regulated. The results indicate that dark-induction of the PRB-1b gene can be controlled by 3'-downstream elements at the transcriptional level or by transcribed sequences at the post-transcriptional level. A circadian clock regulation of the PRB-1b gene was excluded, as fluctuations of PRB-1b transcript levels were not observed in plants placed in constant light or darkness. Subcellular localization of the PRB-1b protein was also determined, in tobacco protoplasts preparations and in cell cultures. The PRB-1b polypeptide was predominantly detected in protoplast vacuoles and was not secreted to the media in cell cultures. These results support an intracellular localization for the PRB-1b protein, as reported for other basic-type components of the pathogenesis-related proteins family.

Cells, Cultured↗

PubMed1992

Dark-induced accumulation of a basic pathogenesis-related (PR-1) transcript and a light requirement for its induction by ethylene.

A gene encoding a basic-type pathogenesis-related protein from Nicotiana tabacum (prb-1b) was cloned, sequenced and characterized. It contains an open reading frame of 179 amino acids that is ca. 65% homologous with the acidic PR-1 class of pathogenesis-related proteins and 87% homologous with a different basic-type PR-1 gene. In the light, physiological levels of ethylene rapidly (1 h) induced basic, but not acidic-type, PR-1 transcript. Additional elicitors acting via ethylene, such as alpha-aminobutyric acid, were shown to induce basic- and acidic-type PR-1 transcript accumulation in a light-dependent manner. In contrast, xylanase, an ethylene-independent elicitor, induced transcript accumulation of basic- and acidic-type PR-1 in a light-independent manner. Dark-induced accumulation of basic PR-1 transcript occurred at night in greenhouse-grown plants and, to a greater extent, in continuously dark-treated plants. The novel dark regulation may point to additional nonpathogenesis-related roles for these genes in plant-environment interactions.

Amino Acid Sequence↗

PubMed1992

Pathogenesis of Purtscher's retinopathy. An experimental study.

Laboratory and clinical observations have implicated microparticles in the pathogenesis of Purtscher's retinopathy, which leads to the occlusion of small arterioles. These microparticles may be caused by aggregated leukocyte platelets or fibrin clots. The phenomenon of intravascular coagulation is well known following trauma or acute pancreatitis. Purtscher's retinopathy is linked with both diseases. To support this presumed pathogenesis of Purtscher's retinopathy, fibrin clots ranging in size from 0.15 to 1.0 mm were injected into the ophthalmic artery of the pig. They resulted in superficial and deep retinal infarctions. In addition, flame-shaped and spotted hemorrhages occurred. These retinal changes are characteristic of Purtscher's retinopathy.

Animals↗

PubMed1992

Endothelial heterogeneity and the acquired immunodeficiency syndrome: a paradigm for the pathogenesis of vascular disorders.

Vascular disorders comprise a wide range of diverse disease entities. Correspondingly, vessels, and even more so the endothelial which line them, show a remarkable extent of heterogeneous differentiation, e.g. between the blood vascular and lymphatic systems, along the length of the vascular trees, and in the microvascular beds of various organs. The most important morphologic criterion to discriminate between endothelia is continuity (continuous endothelial cell layer and well-formed basement membrane) versus discontinuity (intra- or intercellular gaps and/or reduced or missing basement membrane). Most blood vascular endothelia are of the continuous type, while most sinusoidal and lymphatic endothelia are discontinuous by these criteria. Antigen expression corroborates these morphologic data in that CD31, CD34, and 1F10 antigen are exclusively expressed in continuous endothelia, while MS-1 antigen is preferentially expressed in non-continuous sinusoidal endothelia. In contrast, no specific marker has as yet been described for lymphatic endothelia. Endothelial heterogeneity substantially contributes to the pathogenesis of vascular disorders. For example, in patients with acquired immunodeficiency syndrome the same infectious agent may cause either bacillary angiomatosis (a lobular capillary proliferation) or peliosis (sinusoidal dilatation, endothelial denudation, and development of blood-filled cysts) depending on whether the affected organs have predominantly continuous endothelia or noncontinuous sinusoidal endothelia. Moreover, in Kaposi's sarcoma, it is still an open question of whether the lesion is derived from blood vascular or lymphatic endothelia (Kaposi's sarcoma cells in situ do not express the von Willebrand factor+, PAL-E+, 1F10+ phenotype of mature, resting blood vascular endothelia). It is also unresolved how endothelia of either type may be differentially induced to dedifferentiate and how they are recruited into the lesion. Clearly, knowledge about endothelial heterogeneity is still too incomplete to identify the actual mechanisms and molecules that govern the pathogenesis of vascular disorders (including still others than those mentioned here such as atherosclerosis, diabetic angiopathy, and rheumatoid arthritis) affecting distinct endothelia. Further efforts in antigenic phenotyping and in cell and molecular biology of heterogeneously differentiated endothelia should be made to improve this state of affairs.

Angiomatosis, Bacillary↗

PubMed1986

The pathology and pathogenesis of tuberculous encephalopathy and myeloradiculopathy: a comparison with allergic encephalomyelitis.

The pathology and pathogenesis of tuberculous encephalopathy are reviewed. They confirm the findings in a smaller series previously published. The main features were: diffuse brain edema and myelin pallor in the majority of specimens; microvascular distension or necrosis with perivascular macrophage reaction and greater demyelination; focal glial nodules in the white matter; less frequently, hemorrhagic lesions in the presence of mild-to-moderate tuberculous meningitis (TM), but in the virtual absence of the commoner brain-damaging mechanisms. Focal demyelinating lesions in the nerve roots are now added to the above pathology in the brain in some of the cases of spinal tuberculous meningitis. In addition, a picture similar to that in human postinfectious allergic or experimental allergic encephalomyelitis (EAE) has emerged. The spinal cords from one case of the former condition and from four animals with EAE are described to illustrate this similarity. The pathogenesis of tuberculous encephalopathy and myeloradiculopathy is believed, as before, to be due to delayed hypersensitivity, i.e., cell-mediated immunity (CMI) to tuberculoprotein. Experimental confirmation of this demyelination as a nonspecific consequence of CMI to various forms of tubercle bacillus proteins has recently been published. In a proportion of our cases, where two episodes of TM had occurred, the possibility of a hypersensitivity reaction to the brain's own myelin protein is also considered.

Adolescent↗

PubMed1989

Lessons from the NOD mouse for the pathogenesis and immunotherapy of human type 1 (insulin-dependent) diabetes mellitus.

Suitable animal models of human Type 1 (insulin-dependent) diabetes mellitus have long been sought, in particular a model that would permit detailed histological and immunological investigation of changes in the islet preceding the metabolic disorder. This would allow hypotheses as to pathogenesis of the condition to be examined and interventions such as immunotherapy to be tested. The most widely studied models include the low-dose streptozotocin induced diabetic mouse and the BB rat, but both differ in important respects from the human disease. In this review we describe one highly successful model, the non obese diabetic mouse. Selected aspects of pathogenesis and immunotherapy are presented and analogies with human Type 1 diabetes discussed.

Animals↗

PubMed1991

Pathogenesis of SLE: immunopathology in man.

Antibodies against native DNA are not only a disease-specific marker for systemic lupus erythematosus (SLE); in addition, there is good direct evidence that these antibodies also play a major part in pathogenic mechanisms leading to systemic and organ-specific disease manifestations. The origin of anti-dsDNA antibodies is still poorly understood, especially as dsDNA per se is not immunogenic. As recently shown, evidence is now accumulating that anti-dsDNA antibodies are not germline-encoded but antigen-driven, as demonstrated by the establishment of human anti-dsDNA antibody clones from SLE patients and sequence analysis. In sera of SLE patients there is an elevated level of nucleic acids, which indicates that defective clearance mechanisms for nucleic acids are present. The question as to whether these nucleic acids could serve as an antigen has been recently addressed by studies of plasma nucleic acids isolated from circulating immune complexes from SLE patients. These studies indicate that plasma nucleic acids in SLE patients have structures of amino acid sequences which have a striking homology with the gag-pol overlap region of HIV-1. Whether these nucleic acids play a role in the pathogenesis of SLE, indicating the involvement of a retrovirus in the pathogenesis, or whether they rather reflect an amino acid homology with an endogenous human retrovirus family is not yet known.

Antibodies, Antinuclear↗

PubMed1985

Direct evidence of hypertension and the possible role of post-menopause oestrogen deficiency in the pathogenesis of berry aneurysms.

To determine the significance of hypertension in the pathogenesis of berry aneurysms, 113 patients with subarachnoid haemorrhage (SAH) and verified aneurysm and 63 patients with SAH without aneurysm were compared. Of those patients with angiographically verified aneurysms, 61.9% were found to have elevated blood pressure (greater than 160/95 mmHg) and 19.5% showed electrocardiographic signs of left ventricular hypertrophy (SV1 + RV5 (6) greater than 3.5 mV). The percentages for patients without aneurysm were 36.5% and 6.4% respectively. A significant correlation was found between anterior aneurysms and left ventricular hypertrophy (P less than 0.01). The mean Sokolow index values were also significantly elevated in cases of aneurysm (P less than 0.01). There was a complementary relationship between the extent of left ventricular hypertrophy and the percentage of females with regard to localization of an aneurysm and age group. The predominance of females in the total aneurysm population, in the 50- to 59-year-old age group, and among patients with internal carotid aneurysms indicates that a sex-specific hormonal factor may also play a role in the pathogenesis of aneurysms in addition to hypertension. The collagen wasting commonly observed in bone and skin in the post-menopausal period due to decreased oestrogen levels could possibly be responsible for the formation of aneurysms in the proximal segments of the cerebral arteries, as occurs in various connective tissue diseases.

Adult↗

PubMed1977

The mechanism of palatal shelf elevation and the pathogenesis of cleft palate.

Both normal Wistar rat fetuses and those with cleft palate induced by 5-Fluoro-2-Desoxyuridine were studied with a view to elucidating the mechanism of palatal shelf elevation and the pathogenesis of cleft palate. It was postulated that normal shelf elevation is brought about rapidly by an intrinsic turgor shelf force generated by binding of water to mucopolysaccharides. Interference with mucopolysaccharide synthesis would seem to be an important factor in the pathogenesis of some types of cleft palate.

Animals↗

PubMed1981

A contribution to the pathogenesis of cholesteatoma. A histochemical and ultrastructural study.

In a histochemical and ultrastructural study the pathogenesis of cholesteatoma ostitis is analysed on human tissue. In the subepithelial layer there is evidence of an inflammatory reaction leading to proliferation of granulation tissue with bony invasion. Bony destruction is initiated by osteocytic osteolysis. In the case of cholesteatoma there is a combined action of extraosseous and osseous lysosomal enzymes. The pathological changes of the fibrillar elements suggest that the self-perpetuation of degeneration is maintained by a disturbance of fibrillogenesis. The causal pathogenesis of cholesteatoma formation is discussed as a function of a disturbance between cellular activity, extracellular matrix, and cellular surface.

Cholesteatoma↗

PubMed1988

The clinical features and pathogenesis of myringitis granulosa.

Myringitis granulosa is not a rare pathologic condition of the tympanic membrane. However, the condition can be misdiagnosed as chronic suppurative otitis media, since intermittent purulent discharge is the commonest symptom in both disorders. Although the clinical features of myringitis granulosa have been well described by several authors, its pathogenesis is still obscure. In this study, 40 cases of myringitis granulosa were examined in detail to clarify the clinical features and the pathogenesis present. No drum perforations, no hearing impairments and normal X-ray findings indicated that myringitis granulosa had no relation to chronic suppurative otitis media. The other areas of the affected tympanic membrane, except for the site of granulation, showed such pathologic conditions as atrophy, clouding and calcifications. In these pathologic tympanic membranes, epithelial migration was disturbed to a high degree. We suggest that the granulation process on the tympanic membrane should be divided into two stages: (1) injury reaching the lamina propria of the tympanic membrane; and (2) disturbed epithelization of the tympanic membrane. The disturbance of epithelial migration of the tympanic membrane occurs with both stages.

Diagnosis, Differential↗

PubMed1986

Experimental study on pathogenesis of the fetal brain damage by acute carbon monoxide intoxication of the pregnant mother.

The pathogenesis of fetal brain damage caused by acute maternal carbon monoxide (CO) intoxication was experimentally investigated in cats; 11 pregnant cats in various gestational stages were exposed to 0.2-0.3% CO/air gas for 76-150 min; thereafter, 29 live and stillborn neonates and 14 fetuses removed by cesarean section were observed pathologically. In the full-term or late-gestational-stage fetuses and neonates, the most vulnerable areas were the cerebral white matter and brain stem, followed by the basal ganglia and thalamus, and then the cerebral cortex. No changes were found in the cerebellum. From the distribution and nature of the brain changes, a hypoxic-ischemic mechanism was proposed as the pathogenesis of fetal brain damage. In the fetuses or neonates in middle and early gestational stages, the frequency and severity of the brain changes were generally lower than in those in the late gestational stage, and the cerebral white matter and basal ganglia were most often involved, but the thalamus, brain stem and the cerebral cortex were spared. The severity and extent of the brain changes were not the same among all littermates, but varied from normal to severely damaged animals. Among the maternal physiological factors measured during the CO exposure, only the severity of acidosis was correlated with the grade of fetal brain damage.

Animals↗

PubMed1982

Comparative study on pathogenesis of selective cerebral lesions in carbon monoxide poisoning and nitrogen hypoxia in cats.

Since in a previous study hypoxia and subsequent hypotension were considered to be essential for the pathogenesis of carbon monoxide encephalopathy (CO-encephalopathy), experiments were conducted to see whether a combination of nitrogen hypoxia and subsequent systemic hypotension of similar degree and duration as in the previous experimental CO poisoning could induce the same lesion in the CNS of cats. The partial pressure of blood oxygen was reduced to less then 26 mm Hg by increasing the concentration of nitrogen in N2/O2 gas to be inhaled in 1.5h and then the aortic blood pressure (BP) was reduced to 60-80 mm Hg by blood depletion and ganglion-blockage for 1h. In 11 of the 15 cats, lesions were produced in the CNS which were similar by light and electron microscopy to those in CO-encephalopathy. In control groups which were treated by hypoxemia only, hypotension only or a combination CO2-gas inhalation and hypotension without hypoxemia, such lesions were not found in the cerebral white matter. Considering the pathogenesis of lesions in the cerebral white matter in both nitrogen hypoxia and CO-poisoning, two factors i.e., hypoxemia and subsequent systemic hypotension, are common and essential. Further, the enormous vasodilatation in the cerebral white matter induced by hypoxemia and subsequent drop in BP seem to cause a more severe circulatory disturbance in the cerebral white matter than in the cortex.

Animals↗

PubMed1978

Heterotopic brain tissue in the submandibular region and lung. Report of two cases and comments about pathogenesis.

Two cases of extracranial heterotopia of the brain are reported. Case 1, in an otherwise normal female baby, had a brain heterotopia in the submandibular region. Case 2, in a still-born female baby with anencephaly, had the heterotopia in the lung. The lesion in case 1 is believed to be an encephalocele that has been pinched off through a cleft in the bone or through a foramen of the skull; the pathogenesis is similar to that of the so-called "nasal glioma". Concerning the pathogenesis of case 2, contrary to the generally supported embolism theory, observation of serial sections of the tumor in the lung favors the aspiration theory according to which amniotic brain tissue fragments, which are dislocated into the amnion because of nonclosure of the ventricle or following destruction of the fetal brain, are aspirated by fetal respiratory movements in the 4th to 6th month of intra-uterine life.

Anencephaly↗

PubMed1994

Lectin domains in the toxin of Bordetella pertussis: selectin mimicry linked to microbial pathogenesis.

The pathogenesis of many infectious diseases is critically determined by prokaryotic lectins which enable differential recognition and activation of targeted eukaryotic cells. Some bacterial adhesins mimic and co-opt eukaryotic cell-cell adhesion motifs. This is illustrated by the toxin of Bordetella pertussis. Pertussis toxin mediates intoxication of eukaryotic cells by elevation of cAMP and it serves as an adhesin binding the bacteria to ciliated cells and respiratory macrophages. These activities are mediated by the lectin-like properties of the binding oligomer of the toxin. A comparison of pertussis toxin and the selectins involved in leukocyte trafficking indicates that these prokaryotic and eukaryotic C-type lectins share some element of primary sequence similarity, three dimensional structure, and biological activities. Such mimicry suggests a link between eukaryotic cell-cell adhesion motifs and microbial pathogenesis.

Amino Acid Sequence↗

PubMed1993

Pathogenesis of idiopathic IgA nephropathy.

Despite a prodigious amount of work on the physiology of IgA production in man, and many studies on the immunopathology of IgA nephropathy, ranging from the immunogenetics to the immune response to chemical characteristics of the IgA, we are hardly any nearer to defining the pathogenesis of this disease. One of the main changes in our understanding has been to recognise that the bone marrow, now known to produce normally one-third of the body's IgA, overproduces this immunoglobulin in IgA nephropathy. This alters the previous notion that IgA nephropathy was due simply to IgA production in the mucosa, although a mucosal component is not excluded. Certain characteristics of the IgA in the diseased kidney and the circulation have been defined: it is of subclass IgA1 and has a higher proportion of lambda light chains and negative charge than in normal subjects. The specificities of the IgA, either in the kidney or in complexes, have not helped to clarify the pathogenesis. They have been found for a wide range of endogenous and exogenous antigens, suggesting that the antibody activity represents polyclonal B cell activation. These findings have not helped to confirm the prevailing theory that IgA nephropathy is an immune complex disease. Other theories put forward are that IgA nephropathy is an autoimmune disease, glomerular components or IgA itself being among the candidate antigens, or that there is primary dysregulation of the IgA immune system. At this stage of development in our understanding of this common nephropathy, it is important to guard against the assumption that idiopathic IgA nephropathy is one disease and is the result of a single pathogenetic mechanism.

Glomerulonephritis, IGA↗