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Biomedical subjects

J Appel

Publications and source records attributed to J Appel.

At least 37 records · Page 2Linked to original sources
PubMed1994

Transforming growth factor beta 1 is an inducer of erythroid differentiation.

Normal human bone marrow cells, highly enriched for burst-forming units-erythroid (BFU-E), were cultured in serum-free medium, in the presence and absence of various factors, to investigate the mechanisms involved in regulating erythroid differentiation. In cultures containing interleukin 3 (IL-3), Steel factor (SF), and erythropoietin (Ep), benzidine-positive erythroblasts first became detectable on day 6. Their numbers then rapidly increased until, by day 16, > 99% of the cells, which were 20,000-fold amplified over input numbers, were benzidine-positive. It is interesting to note that omission of either SF or Ep from this assay markedly enhanced the rate of differentiation and reduced total cell numbers, whereas omission of IL-3 had no effect on the rate of differentiation and only slightly reduced cell numbers. Of various agents tested, the most potent erythroid differentiation inducer (and inhibitor of cell proliferation) was found to be transforming growth factor beta 1 (TGF-beta 1). This cytokine stimulated both the rapid appearance of hemoglobin-positive cells and an early cessation of cell proliferation. Using fluorescently tagged antibodies to glycophorin A and fluorescence-activated cell sorter (FACS) analysis, this phenomenon was shown to be due to an early induction of erythroid differentiation rather than an aberrant production of hemoglobin. Methylcellulose assays indicated that the well-documented reduction of BFU-E colony numbers observed with TGF-beta 1 may actually be due to a TGF-beta 1-induced "conversion" of BFU-E into colony-forming units-erythroid (CFU-E). Thus, in vivo, TGF-beta 1 might serve, in part, to decrease the number of mature erythrocytes by stimulating BFU-E to skip a number of cell divisions and differentiate early.

Animals↗
PubMed1993

[Needle biopsy of the pleura].

A total of 171 pleural needle biopsies were carried out in 123 patients with pleural effusion. The sensitivity of the method proved to be 51% for malignant diseases and 75% for tuberculotic pleurisy, respectively. Performing biopsy simultaneously with the cytological examination of the pleural fluid, malignancy was proved only by needle biopsy in 20% of the patients, while cytology was found negative in these cases. Simultaneously performed thoracocentesis and pleural needle biopsy is suggested.

Adenocarcinoma↗
PubMed1992

[Electron microscopic structure of mastocytes of the airways and changes in the clinical status during steroid inhalation therapy].

The structure of epithelial mast cells obtained by bronchial biopsy from asthmatic patients reveals characteristic qualitative and quantitative features. Great amount of partly or completely depleted mast cells can be observed in active asthmatic patients, indicating the liberation of bronchoconstrictive mediators. After a two months treatment with inhalative steroid (budesonide) the process of degranulation slows down, the number of depleted mast cells decreases. Parallel with the above described phenomenon, the number of dyspneic attacks, as well as the necessity of other antiasthmatic drugs show a significant decrease. However, in this patient material, during the treatment period, airway hyperreactivity, detected by bronchial provocation, failed to show any remarkable change.

Asthma↗
PubMed1991

Heparin-induced thrombocytopenia and thrombosis: reversal with streptokinase. A case report and review of literature.

Heparin-induced thrombocytopenia and thrombosis is associated with a significant incidence of morbidity and mortality. Prompt recognition of this complication and immediate withdrawal of heparin therapy are imperative. This report describes a case of heparin-induced thrombosis and thrombocytopenia with major vascular insufficiency of the extremities. This is the first reported instance of the use of intravenous streptokinase for the treatment of heparin-induced venous thrombosis.

Aged↗
PubMed1990

Vancomycin-resistant Pediococcus acidilactici: nine cases of bacteremia.

Pediococci, vancomycin-resistant gram-positive cocci, have been isolated from human specimens, but an association with clinical illness has not been established. Clinical and epidemiologic data were obtained on nine patients who had Pediococcus acidilactici isolated from blood. Patients were eight elderly adults with complicated medical problems and one infant with congenital jejunoileal atresia. Seven patients were hospitalized before P. acidilactici was isolated. Eight had received multiple antibiotics; however, only two had received vancomycin. In all cases there was a delay in correct bacterial identification, and the significance of the isolate was uncertain. There was no clearly identified syndrome associated with P. acidilactici bacteremia. All eight adults had fever and six had pneumonia potentially attributable to other causes. The findings underscore the importance of proper identification of vancomycin-resistant gram-positive cocci. P. acidilactici may be an opportunistic pathogen in severely compromised hosts; however, further observations are necessary to clarify its role in human disease.

Aged↗
PubMed1989

The effects of noncollagenous matrix proteins on hydroxyapatite formation and proliferation in a collagen gel system.

The effects of several noncollagenous matrix proteins on hydroxyapatite formation and growth were studied in a dynamic collagen gel system. In this system growth plate proteoglycan aggregates at concentrations of 1-10 micrograms/ml were effective inhibitors, desulfated aggregates from brachymorphic mice were less effective. Phosphophoryn at 1-100 micrograms/ml had no effect on formation; 60-120 micrograms/ml retarded mineral growth. Type X collagen at concentrations of 50-300 micrograms/ml had no effect on formation or growth.

Calcification, Physiologic↗
PubMed1989

[Pneumothorax caused by histiocytic pneumonitis].

Specimens from the lung obtained during the treatment of spontaneous pneumothorax revealed a hitherto unknown histological phenomenon characterised by a histiocytic, inflammatory interstitial pulmonary tissue containing gas. By following the course of the gas an intracellular pathogen could be identified in the macrophages. Its shape resembled that of micrococci, ist size was between 2-4 microns. The ultrastructure within the pathogen suggested gas formation. In these cases the origin of the pneumothorax was attributed to the aerogenous microorganism that had induced a phagocytic inflammation in the pulmonary tissue.

Adult↗
PubMed1987

The molecular basis of inhibitor resistance in a mammalian mitochondrial cytochrome b mutant.

The mitochondrial gene for the cytochrome b of Complex III has been cloned from a mouse L-cell mutant with increased resistance to 2-n-heptyl-4-hydroxyquinoline-N-oxide and other inhibitors which block reactions at the b562 heme group. Nucleotide sequencing revealed that this gene contained a G:A transition on the coding strand at position 14,830. At the amino acid level, this mutation results in the substitution of an aspartic acid residue for a conserved glycine at position 231 of cytochrome b. Based upon current models for the secondary structure of cytochrome b, the altered amino acid lies in close proximity to one of the invariant histidine residues involved in binding the heme groups. Combining this result with the previous biochemical studies of this mutant, we hypothesize that the insertion of this highly charged side chain alters the conformation around the b562 heme group such that 2-n-heptyl-4-hydroxyquinoline-N-oxide and the other inhibitors of this group have reduced access to the inhibitor binding domain.

Amino Acid Sequence↗