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J T van Dissel

Publications and source records attributed to J T van Dissel.

94 records · Page 6Linked to original sources

A teflon culture dish for high-magnification microscopy and measurements in single cells.

A simple tissue culture dish is described which permits the use of oil immersion optics (X 100) while maintaining access to cells in culture. In combination with a micro-CO2-incubator (Ince et al. 1983) long-term as well as short-term experiments can be performed under microscopical control. The teflon dish is re-usable, resistant to sterilization procedures, and easy to assemble. Standard glass coverslips with adherent cells are secured to the dish by an aluminium ring with a bayonet fitting. Both phase-contrast and interference-contrast microscopy with high magnification can be used. The dish is of particular use in electrophysiological investigations where the patch-clamp technique is used and frequent exchange of cultures is required. With this unit, single ion channel activity in cultured human monocytes was measured. The dish has also been used in studies in which membrane potential measurements were performed with glass microelectrodes in small cells under culture conditions. The applications described include video time-lapse sequences of phagocytosis with micro-organisms presented to mouse peritoneal macrophages with broken-tipped pipettes. This easy to use, multi-purpose dish offers the cell physiologist a valuable aid for the manipulation and observation of single cells in culture.

Animals↗

Effects of halothane on the ventilatory response to hypoxia and hypercapnia in cats.

The influence of halothane 0.8-1.2% inspired on the peripheral hypoxic chemoreflex was investigated in 13 cats subjected to artificial brain stem perfusion (ABP). This technique allows for an independent control of blood gas tensions and halothane concentration between blood perfusing the brain stem (central) and the systemic circulation (peripheral). In six cats the ventilatory response to isocapnic hypoxia was assessed during overall halothane anesthesia (HO) before and during ABP. Before ABP, systemic and brain stem circulations both were rendered hypoxic. During ABP, hypoxia was induced systemically while the brain stem was maintained hyperoxic. The ventilatory response in non-ABP cats (mean 698 ml . min-1 at PaO2 6.6 kPa; 50 mmHg) was about half the response in ABP cats (mean 1,194 ml . min-1 at PaO2 6.5 kPa; 49 mmHg), indicating that in the presence of halothane, central hypoxia depressed ventilation appreciably. Compared with chloralose-urethane anesthesia (CU), halothane reduced the ventilatory response to hypoxia in both perfusion conditions but never abolished it. To assess the influence of halothane on peripheral and central mediation of the CO2 response during hypoxia, each was assessed during CU anesthesia, during HO, and with halothane applied exclusively peripherally against a background of CU (CUHP). In all drug states, the periphery was kept hypoxic and brain stem hyperoxic. Compared with CU anesthesia, HO and CUHP anesthesia reduced both peripheral (Sp) and central (Sc) CO2 sensitivity but not the Sp/Sc ratio. Similarly, the extrapolated PaCO2 at zero ventilation was not detectably different among these three states.(ABSTRACT TRUNCATED AT 250 WORDS)

Anesthesia, General↗

The characterization, origin, and kinetics of skin macrophages during inflammation.

This report deals with the characterization, origin, and kinetics of exudate skin macrophages. The inflammatory stimulus used was a subcutaneously inserted glass coverslip. The macrophages adhering to the glass surface have many characteristics in common with circulating monocytes. During this kind of inflammation there is little differentiation into a more mature or activated type of mononuclear phagocyte. The kinetic studies with [3H]thymidine as cell marker and calculation of local production at the site of inflammation as well as the influx of cells to that site led to the conclusion that greater than or equal to 99% of the exudate skin macrophages were monocyte derived and less than or equal to 1% originated by local division of macrophages.

Animals↗

Differences in initial rate of intracellular killing of Salmonella typhimurium by resident peritoneal macrophages from various mouse strains.

To determine the underlining mechanism of the difference in innate susceptibility of mouse strains to infection by Salmonella typhimurium, the ingestion and in vitro intracellular killing of S. typhimurium by resident peritoneal macrophages of mouse strains that differ in natural resistance to this microorganism has been studied. The results revealed that the rate constants of in vitro phagocytosis (Kph) in the presence of inactivated rabbit immune serum did not differ between macrophages of susceptible C57BL/10 and resistant CBA mice (for both strains: Kph = 0.021 min-1). The rate constant of in vitro intracellular killing (Kk) was determined 1) after in vivo phagocytosis (CBA, Kk = 0.055 min-1; C57BL/10, Kk = 0.031 min-1), 2) after in vitro phagocytosis of preopsonized bacteria (CBA, Kk = 0.020 min-1; C57BL/10, Kk = 0.012 min-1), and 3) during continuous phagocytosis in vitro (CBA, Kk = 0.029 min-1; C57BL/10, Kk = 0.013 min-1). With all three approaches, the initial rate of intracellular killing by normal macrophages of Salmonella-resistant CBA mice amounted to about 1.7 times the value found for macrophages of susceptible C57BL/10 mice (p less than 0.01). This trait difference was independent of the previous way of ingestion of the bacteria, unaffected by the kind of opsonization, and specific for S. typhimurium, because Staphylococcus aureus and Listeria monocytogenes were killed by macrophages of these mouse strains with equal efficiency (p greater than 0.50). These findings indicate that a difference in genetic background expressed in the efficacy of intracellular killing by resident peritoneal macrophages immediately upon ingestion of S. typhimurium is relevant for the innate resistance of mice against S. typhimurium.

Animals↗