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Biomedical subjects

K Kienast

Publications and source records attributed to K Kienast.

42 records · Page 3Linked to original sources
PubMed1992

[Primary pulmonary nodular amyloidosis and multiple emphysematous bullae in Sjögren syndrome].

The authors report on a very rare case of an isolated primary nodular pulmonary amyloidosis with multiple emphysematous bullae in Sjögren's syndrome. The circular foci present in both lungs in disseminated form were immunohistochemically speaking amyloid deposits of the AL-lambda type. There were no pointers to other organ manifestations or monoclonal immunoglobulins in the serum and/or urine.

Amyloid↗
PubMed1984

[Comparative protein chemistry studies on Factor VIII concentrates].

Large amounts of Factor VIII concentrates are required for the treatment of haemophiliacs. Two batches each of nine commercial preparations were examined for their in vitro properties. The parameters studied were Factor VIII coagulation activity (F VIII: C), ristocetin cofactor activity (F VIII R: CoF), the Factor VIII antigen content (F VIII R: Ag), fibrinogen, fibronectin and immunoglobulins. The preparations were also tested to determine their hepatitis A and B marker content. In none of the investigated concentrates compared to the data given by the manufacturers was a marked F VIII: C deficit. All the preparations showed higher values for F VIII R: Ag than for F VIII: C. Factor VIII concentrate HS was the only concentrate in which the fibrinogen concentration was below the detection limit and only small amounts of fibronectin and immunoglobulins were detected. In two of the nine preparations tested possible contamination with hepatitis B viruses was more or less ruled out by means of hepatitis serology.

Antibodies, Viral↗
PubMedDate not supplied

Nitrogen dioxide-induced reactive oxygen intermediates production by human alveolar macrophages and peripheral blood mononuclear cells.

Alveolar macrophages located on the alveolar surface have contact with air pollutants. We evaluated the dose-dependent effect of nitrogen dioxide exposure on the oxidative metabolism of alveolar macrophages and peripheral blood mononuclear cells by measuring the spontaneous and stimulated reactive oxygen intermediates production. Alveolar macrophages or peripheral blood mononuclear cells were placed on a polycarbonate membrane, which was in direct contact with the surface of a nutrient reservoir. The cells were exposed to nitrogen dioxide during different periods of time, varying between 30 and 120 min at concentrations ranging from 0.1 to 0.5 ppm. Exposure of alveolar macrophages to nitrogen dioxide for 30 min yielded a dose-dependent stimulation of reactive oxygen intermediates generation of 1.7- to 2.9-fold of control. An 120-min exposure to nitrogen dioxide at concentrations between 0.1 and 0.5 ppm resulted in a similar reactive oxygen intermediates production of about 1.9- to 2.2-fold of control at all concentrations tested. The nitrogen dioxide exposure to peripheral blood mononuclear cells yielded identical results. These experiments demonstrate that alveolar macrophages and peripheral blood mononuclear cells become activated by nitrogen dioxide and that concentrations up to 0.5 ppm nitrogen dioxide induce an increase in reactive oxygen intermediates production after 30 to 120 min exposure of the cells.

Aged↗
PubMedDate not supplied

Effect of sulfur dioxide on cytokine production of human alveolar macrophages in vitro.

Tumor necrosis factor-alpha, interleukin-1beta, interleukin-6, and transforming growth factor-beta are cytokines synthesized by alveolar macrophages. We investigated the effect of sulfur dioxide, a major air pollutant, on the production of these cytokines by alveolar macrophages. The cells were layered on a polycarbonate membrane and exposed for 30 min to 0.0, 1.0, 2.5, and 5.0 ppm sulfur dioxide at 37 degrees C and 100% air humidity. The cells were incubated for 24 h after exposure, thus allowing cytokine release. Cytotoxic effects of sulfur dioxide were evaluated by trypan blue exclusion. Cytokines were measured with enzyme-linked immunosorbent assays (i.e., tumor necrosis factor-alpha, interleukin-1beta, and interleukin-6) or by use of a specific bioassay (i.e., transforming growth factor-beta). The toxicity of sulfur dioxide for alveolar macrophages ranged from 3.1 % to 9.5 %. A 30-min exposure to sulfur dioxide induced a significant decrease in spontaneous and lipopolysaccharide-stimulated tumor necrosis factor-alpha (p < .001) and lipopolysaccharide-stimulated interleukin-1beta release (p < .05). The release of interleukin-6 and transforming growth factor-beta was not affected significantly by sulfur dioxide exposure. Our results demonstrated a functional impairment of alveolar macrophages after sulfur dioxide exposure (i.e., release of tumor necrosis factor-alpha and interleukin-1beta). Neither spontaneous nor stimulated release of interleukin-6 and transforming growth factors were influenced by exposure to sulfur dioxide.

Air Pollutants↗
PubMedDate not supplied

Phenotypic analysis of bronchoalveolar lavage lymphocytes from acquired immunodeficiency patients with and without Pneumocystis carinii pneumonia.

A study was performed to reveal possible differences in lymphocyte subpopulations from bronchoalveolar lavage (BAL) of acquired immunodeficiency patients with and without Pneumocystis carinii pneumonia. Forty-one consecutive human immunodeficiency virus-seropositive patients were studied. Pneumocystis carinii infection was detected in the BAL fluid from 18 patients. The BAL lymphocyte subpopulations were determined by surface marker analysis with the immunoperoxidase slide assay. No significant differences in the percentage of CD4+ and CD8+ lymphocytes were found between the two groups. The percentage of CD57+ natural killer (NK) cells was significantly higher in the Pneumocystis carinii-negative group than in the -positive group. Since NK cells protect from microbial infections, it is conceivable that the loss of CD57+ NK cells may be one of the phenomena leading to the immunodeficiency state that underlies the pulmonary complications characteristic of the acquired immunodeficiency syndrome.

AIDS-Related Opportunistic Infections↗