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At least 289 records · Page 16Linked to original sources
PubMed1979

Advanced stage and early relapse of breast carcinomas associated with high thymidine labeling indices.

The thymidine labeling index (TLI) showed a lognormal distribution for 133 primary breast carcinomas with a median of 2.21 and a range of 0.04 to 18.6/100. High TLI's were associated significantly with nuclear anaplasia, pushing tumor border, necrosis, cellular inflammation, and total replacement of lymph nodes involved by tumor, and the data suggested an association of high TLI with large primary tumor and the presence of axillary metastasis. Five patients who initially had local or distant spread all had above median TLI's. They and the 38 patients who developed recurrent tumor during a mean interval of 3.2 years of observation after mastectomy showed a higher geometric mean TLI than those who remained tumor-free (2.93 versus 1.85; p less than 0.05). The rate of early relapse for operable patients with above-median TLI's was significantly greater than that for patients with below-median TLI's (p = 0.0018). High TLI appears to be associated with rapid evolution of breast carcinoma both prior to and following diagnosis and treatment.

Age Factors↗
PubMed1983

[Pathogenesis of acrokeratosis Bazex].

A 67-year-old male patient with typical signs of acrokeratosis Bazex is presented. The psoriasiform skin lesions appeared 9 months after diagnosis of an oesophagus neoplasm. Clinically there was a marked hepatopathy but no signs of metastases. Histological, immunofluorescence-histological, and ultrastructural findings revealed a capillaritis with humoral as well as cellular inflammation. With treatment of the neoplasm the paraneoplasia regressed under additional treatment with topical steroids. The vitamin A deficit could not be normalized by oral or parenteral vitamin A substitution. We discuss some mechanisms in formal pathogenesis.

Aged↗
PubMed1978

[Granulomatous angiitis of the central nervous system].

It is reported on 3 observations of isolated granulomatous angiitis of the central nervous system. The case in question was in two 42-year-old men a granulomatous giant cell arteriitis with exclusive affection of the intracranial arteries. In a 33-year-old woman (case 3) there existed a granulomatous angiitis in generalised cerebrospinal granulomatous epitheloid-cellular inflammation (sarcoidosis) of the central nervous system with participation of bifurcal lymph nodes and of the lung. In all the three reports the diagnosis could be made only by autopsy. Clinic, pathomorphology, and diagnostic difficulties are described.

Adult↗
PubMed1994

The significance of tubulointerstitial nephritis in IgA nephritis.

The occurrence of significant tubulointerstitial nephritis (TIN) was observed in 6 (18.3%) of 32 patients with IgA nephritis registered in 1991. T lymphocytes and macrophages in the interstitium were seen to invade the tubulus through injured tubular basement membrane (TBM), then were seen in the intercellular spaces of tubular cells which showed degeneration, single cell necrosis or detachment. Thus some tubular components were seen destroyed and had disappeared resulting in interstitial fibrosis, and others showed a regeneration process forming a renewed TBM on the innerside of the original TBM. However the recurrence of cellular inflammation was again observed in these regenerated tubuli. Thus the progression of nephron loss by TIN was seen to be independent of the glomerular changes and TIN is considered to be one of the important factors in predicting the prognosis of IgA nephritis.

Adolescent↗
PubMed1994

[The problems of collagen formation in chronic liver diseases].

With employment of radioimmunoassay, the level of procollagen-III-peptide was measured in the blood of 71 patients with chronic hepatic diseases versus 20 healthy controls. This level was examined for correlation with characteristics of the etiological factor, the degree of hepatic-cellular inflammation and immune reactions. Procollagen-III-peptide concentrations were directly correlated with transaminases and reversely with activity of antibody formation. Collagenopoiesis gained intensity in the range from chronic persistent hepatitis to hepatic cirrhosis. Virus infection and alcohol are among the most potent etiological factors stimulating collagenopoiesis. The least procollagen levels occurred in hepatic diseases obscure in origin.

Adolescent↗
PubMed1996

Induction of E-selectin-dependent leukocyte recruitment by mast cell degranulation in human skin grafts transplanted on SCID mice.

Previous in vitro data indicate that degranulation of human mast cells triggers the induction of endothelial molecules important in leukocyte adhesion. In vivo experimental systems have not previously existed, however, to determine whether human mast cell degranulation is sufficient stimulus for leukocyte recruitment. To study this question, neonatal foreskins were transplanted onto immunodeficient mice. The grafts contained physiological numbers of human dermal mast cells that could be degranulated by a number of secretagogues that activate mast cells by different mechanisms. Degranulation was associated with an inflammatory response characterized by edema, up-regulation primarily of microvessel E-selectin, and influx of neutrophils. Leukocyte emigration associated with mast cell degranulation was inhibited by a monoclonal antibody against human E-selectin. These data indicate that degranulation of human mast cells in the human/SCID mouse model provokes cellular inflammation in skin. The ability to significantly inhibit early leukocyte infiltration with an antibody against E-selectin in this model supports the hypothesis that this molecule plays an important role in mast-cell-induced inflammation.

Animals↗
PubMed1997

[Enhanced lymphocyte proliferative response to house dust mite in the older but not in the younger asthmatic children].

Allergen-specific lymphocyte proliferation was measured by flow cytometry in 16 children with atopic dermatitis (AD). 26 with bronchial asthma (BA) and 13 non-atopic controls. Although the level of mite-S.I.F. (stimulation index measured by flow cytometry) in the younger AD children (2-7 y) was significantly higher than that in the non-atopic subjects (189.6 +/- 70.7 vs 113.9 +/- 11.0, p < 0.02), there was no elevation in the younger BA children (122.6 +/- 23.4). It is therefore likely that the elevated mite-S.I.F. level is related to the development of the allergic cellular inflammation representing the pathology of AD, rather than the IgE-mediated allergic reaction as a mechanism of childhood BA. Because the level of mite-specific IgE antibody in the younger BA children is elevated (93.6 +/- 41.2 PRU/ml), the result also indicates that mite-specific peripheral T lymphocytes do not play a critical role in stimulating the mite-specific IgE synthesis. On the contrary, the older BA children (8-15 y) showed an elevated mite-S.I.F. level (176.0 +/- 54.6) significantly higher than that in the non-atopic subjects (114.6 +/- 13.9, p < 0.05) as well as that in the younger BA children (p < 0.05). Because other investigators have reported that the level of mite-specific lymphocyte proliferation is increased in the adult BA patients, the transition from childhood BA to adult-type BA may start at the age of about 8 y.

Adolescent↗
PubMed1977

Tyzzer's disease in Syrian hamsters.

Tyzzer's disease was diagnosed in 18 Syrian hamsters. The clinical signs included sudden onset of diarrhea, dehydration, and lethargy; all affected hamsters died within 48 hours. Gross lesions consisted of multiple white nodules in the heart; dilated cecum and colon containing semiliquid feces, sometimes bearing necrotic plaques on the mucosa; and occasionally, a few small scattered white spots in the liver. Microscopic study of those lesions revealed areas of necrosis and mixed cellular inflammation. The causative agent, Bacillus piliformis, was demonstrated within myocardial fibers, hepatocytes, and colonic epithelial cells. Inoculation of chicken embryos and a clinically normal hamster with a homogenate of cecal wall prepared from affected hamsters resulted in reproduction of the agent and transmission of the disease.

Animals↗
PubMed1997

[Cutaneous innervation: anatomy and physiology. Neuropeptides].

The skin is involved in the tactile sensations and hydric and thermic regulation. This structure contains immunological cells with inflammatory activity in addition to several bioactive molecules. This review will focus primarily on the relation of cutaneous innervation in these processes and its capacity to release neuropeptides as functional molecules. This paper will discuss the organization of the motor and sensitive fibres, the biosynthesis, molecular modifications, regulation and the functions of the best well known neuropeptides. The specific function of these molecules in the neurogenic inflammation and how the nervous system can influence in several skin diseases is explained. In conclusion, the cutaneous innervation can affect processes such as inflammation, cellular proliferation and healing. This possibility is likely to be mediated by neuropeptides. In the future, a growing list of neuropeptides will be compiled and the precise role in cutaneous physiology will be known, but the most important of this knowledge is probably the repercussion in the therapies of some cutaneous diseases.

Humans↗
PubMed1998

[Role of cytokines in acute coronary syndrome].

Cytokines modulate immunologic processes, inflammation, proliferative responses and apoptosis. Recent studies focused on the role of proinflammatory cytokines in cardiovascular diseases. Proinflammatory cytokines, such as interleukin (IL)-6, IL-8, IL-1 beta and tumor necrosis factor-alpha play important roles in acute coronary syndrome by regulating inflammation, cellular adhesion and production of growth factors and various vasoactive substances. Reperfusion after myocardial infarction and transient myocardial ischemia are supposed to induce these proinflammatory cytokines. We reviewed the mechanisms and clinical significance of proinflammatory cytokine expression in acute coronary syndrome. In addition we recently found out that an interaction between monocytes and vascular endothelial cells induces matrix metallo-proteinase expression by these cytokine-mediated mechanisms.

Acute Disease↗
PubMed1998

Neurochemical imaging of Alzheimer's disease and other degenerative dementias.

A wide variety of neurochemical and functional imaging approaches have been applied to the study of progressive dementias, particularly Alzheimer's disease (AD) and related disorders. Despite considerable progress in the past decade, the cause(s) of most cases of AD remain undetermined and preventive or protective therapies are lacking. Specifically-designed imaging procedures have permitted the testing of pathophysiological hypotheses of the etiology and progression of AD, and have yielded important insights in several areas including the potential roles of cerebral cortical cholinergic lesions, cellular inflammation, and losses of cortical synapses. From the perspective of clinical diagnosis, PET glucose metabolism imaging with use of [18F]2-fluorodeoxyglucose (FDG) is the most sensitive and specific imaging modality yet identified. The overall performance of PET FDG is favorable for routine clinical evaluation of suspected AD, and will likely gain increasing utilization in the near future. Assessments of glucose metabolism and other, specific aspects of neurochemistry in AD will provide direct measures of therapeutic drug actions and may permit distinction of symptomatic versus disease-modifying therapies as they are developed and introduced in clinical trials.

Acetylcholinesterase↗
PubMedDate not supplied

Cellular kinetics of inflammation in the pleural space of mice in response to the injection of exogenous particles.

CD-1 mice were used to study the cellular kinetics of the inflammatory response of the pleural space to the injection of 250 micrograms of silica or of tungsten microparticles. The pleural exudates were collected by lavage of the serous cavity of mice that were sacrificed at 30 min and up to 7 days after the intrapleural instillation of the particles. The samples were studied by light and electron microscopy (transmission and scanning modes); the quantitative cellular kinetics of the inflammation was determined by leukocyte counting in exudates using cytocentrifuge preparations. The normal resident population of cells of CD-1 mice was made up of (2.47 +/- 0.37) x 10(6) cells. It consisted mostly of macrophage-like cells ((2.03 +/- 0.26) x 10(6) cells, 82% of total cells), some lymphocytes ((0.37 +/- 0.07) x 10(6) cells, 15% of total cells), a few mast cells and eosinophilic granulocytes (1-2% of total cells). The initial inflammatory reaction (30-60 min after injection) was characterized by a decrease in the number of cells harvested from the pleural space. This was followed by an intense recruitment of granulocytes and monocytes that resulted in a peak of intrapleural cells at 24 h ((16.8 +/- 4.0) x 10(6) cells induced by silica particles and (18.3 +/- 4.2) x 10(6) cells induced by tungsten particles). In tungsten-injected mice (but not in silica-treated animals) the enhancement in the number of intrapleural macrophages continued up to 72 h after particle injection. The highest percentage of macrophages with ingested tungsten (50% of total macrophages) was found early (6 h) and decreased thereafter; at day 7 it encompassed just 17% of the macrophages. Injection of any of the two particulates led to the disappearance of mast cells from the pleural space of mice. Silica particles attracted a high number of eosinophils to the pleural cavity of mice. Light and electron microscopy documented that pleural macrophages underwent striking morphological changes during the inflammatory response: the phagocytes showed marked increase in size and in number of surface processes, and their cytoplasm often contained large amounts of the injected particles and also of cellular debris. This study establishes the mouse as a reliable animal model to study the dynamics of the pleural space and it offers a precise definition of the cellular kinetics of inflammation in this serous cavity. The data indicate that the kinetics of experimental pleural inflammation induced by particulates may depend on the nature of the injected particles.

Animals↗
PubMedDate not supplied

Cellular imaging of inflammation after experimental spinal cord injury.

The ability to visualize the cellular inflammatory responses after experimental spinal cord injury (SCI) was investigated using a clinical 1.5-T magnetic resonance imaging scanner, a custom-built, high-strength gradient coil insert, a 3-D fast imaging employing steady-state acquisition (FIESTA) imaging sequence and a superparamagnetic iron oxide (SPIO) contrast agent. An "active labeling" approach was used, with SPIO administered intravenously at different time points following SCI. Our results show that this strategy can be used to visualize clusters of iron-labeled cells associated with the inflammatory response in SCI. Of particular importance for this application was the finding that in FIESTA images hemorrhage does not cause signal loss. In T2-weighted spin echo or T2*-weighted gradient-echo images, which are more commonly used to detect signal loss associated with SPIO, the signal loss associated with hemorrhage interferes with the detection of iron-induced signal loss. FIESTA, therefore, allowed us to discriminate between iron associated with blood products in hemorrhage that occurs in acute SCI and the iron associated with SPIO-labeled cells accumulating in the injured cord.

Animals↗
PubMed1987

Cellular aspects of inflammation. The Ciba-Geigy Prize for Research in Animal Health.

The migration of leucocytes to sites of acute and chronic inflammation is an event of central importance to the maintenance of inflammatory processes; extravascular leucocytes are responsible for generating chemical mediators of inflammation and the phagocytosis of particulate matter. They may also be involved in the conversion of acute to chronic inflammatory lesions. Leucocytes are attracted to sites of tissue injury by a range of chemoattractants. This paper describes the development of a method for separating on Percoll gradients purified populations of equine polymorphonuclear and mononuclear leucocytes and use of the isolated cells in vitro studies. Two independent assay methods, the agarose microdroplet and the Boyden chamber microfilter techniques, were used. The assays were utilised in three ways: (a) to investigate the sensitivity of polymorphonuclear and mononuclear leucocytes to two standard chemoattractants, zymosan activated plasma and n-formyl-methionyl-leucyl phenylalanine; (b) to study the chemoattractant properties of leukotriene B4 and prostaglandin E2 for equine leucocytes; and (c) to investigate the inhibitory actions of several nonsteroidal anti-inflammatory drugs (NSAIDs) on equine leucocyte movement.

Acute Disease↗
PubMed2004

Some lung cellular parameters reflecting inflammation after combined inhalation of amosite dust with cigarette smoke by rats.

Cellular changes were followed in lung cell suspensions after 175 day inhalation by rats of concentrations 30 mg/m3 or 60 mg/m3 of amosite asbestos every second day combined with daily exposure to cigarette smoke at 30 mg of total particulate matter (TPM)/m3 air. Concomitantly, lung inflammation was assessed by changes in the bronchoalveolar lavage fluid (BALF). A dose-dependent rise in the BALF inflammatory parameters was found. The rise of the proportion of binucleate (BNC) and multinucleate cells (MNC) in lung cell suspensions was also dose-dependent. It is concluded that, in the experimental assessment of effects of fibrogenic dusts, the number of BNC and of MNC in lung cell suspensions may serve as a useful semiquantitative biomarker of the inflammation.

Administration, Inhalation↗
PubMed1998

Nonspecific interstitial pneumonia. Individualization of a clinicopathologic entity in a series of 12 patients.

Nonspecific interstitial pneumonia/fibrosis (NSIP) has recently been individualized within the group of idiopathic interstitial pneumonias mainly based on a pathologic pattern of temporally uniform lesions distinct from usual, desquamative, and acute interstitial pneumonia. We studied 12 consecutive patients with NSIP at lung biopsy done as a diagnostic procedure for idiopathic interstitial lung disease. The patients were six males and six females, aged 52.5 +/- 11.8 yr. In 8 of 12 cases the pathologic lesions consisted of both cellular interstitial inflammation and fibrosis, whereas only cellular inflammation was present in three cases, and fibrosis in one. Dyspnea, cough, inspiratory crackles, and squeaks were the most common symptoms and signs. Six cases were cryptogenic. An associated disorder or a presumed cause was present in the other six patients, including underlying connective tissue disease (n = 3), organic dust exposure (n = 2), and prior acute lung injury (n = 1). Lung function tests found a restrictive ventilatory defect (11/12), impairment of TLCO (11/11), and hypoxemia at rest (7/12). Chest X-ray showed infiltrative opacities in all cases. Computed tomography of the chest in 11 cases mainly showed ground glass opacities (9/11), patchy areas of alveolar consolidation (6/ 11), and thickening of interlobular septas (5/11). All patients were treated with corticosteroids, and seven with immunosuppressive agents. All patients were alive at last follow-up, 50 +/- 40 mo after diagnosis. Ten patients (83%) were clinically improved or stabilized. Thus, despite its heterogeneity, NSIP deserves to be individualized as an original clinicopathologic entity and should be clearly distinguished from usual interstitial pneumonia, especially because of a better prognosis.

Acute Disease↗