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Biomedical subjects

J W Mills

Publications and source records attributed to J W Mills.

At least 19 recordsLinked to original sources
PubMed1995

Preventing a fall.

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Pennsylvania↗
PubMed1994

The cytoskeleton and membrane transport.

This review summarizes recent studies demonstrating that the actin-based cytoskeleton regulates the activity of many ion channels and transport proteins. Stretch-activated ion channels; channels conductive to chloride, to sodium, and to potassium; electroneutral transport proteins, including the Na(+)-K(+)-2Cl-cotransporter, the Na+/H+ exchanger, and the organic osmolyte transporter; as well as water channels are all regulated by the actin cytoskeleton. Several potential mechanisms whereby the actin cytoskeleton and microtubules regulate transport protein activity are discussed.

Animals↗
PubMed1992

Zinc alters actin filaments in Madin-Darby canine kidney cells.

Exposure of semiconfluent cultures of Madin-Darby canine kidney cells to 10 microM zinc leads to a change in the organization of the actin filament system. Most of the stress fibers at the basal end of the cell are lost and the actin associated with the lateral membrane and junctional regions appears to retract into the cytoplasm. In addition, at the base of the cell in regions of cell-substratum contact, dense, actin-rich plaques appear. These alterations in actin filaments are associated with a change in cell shape. Microtubules were unaffected by exposure to 10 microM zinc. At zinc concentrations greater than or equal to 50 microM the microtubules depolymerized. Exposure to cadmium alters the actin filaments as well but the effect is different from the change seen with zinc. When the cells are exposed simultaneously to zinc and cadmium the cells appear the same as they would if exposed to zinc alone. Exposure of MDCK cells to either metal, individually or in combination, results in a significant and similar increase in F-actin content as determined spectrofluorometrically. The changes in organization and amount of F-actin are associated with a reduction in the ability of the cells to remain attached to the substrate, a toxic effect of these metals with regard to epithelial function. The results indicate that zinc, an essential metal, and cadmium, a highly toxic metal, interact with the actin cytoskeleton in intact cells.

Actins↗
PubMed1992

Hypotonicity and cell volume regulation in shark rectal gland: role of organic osmolytes and F-actin.

Hypotonic stress (reduction of external tonicity from approximately 900 mosM and 295 mM NaCl to approximately 600 mosM and 135 mM NaCl) produced a relatively slow regulatory volume decrease (RVD) in dogfish shark (Squalus acanthias) rectal gland cells. During the 5-h experiment, cell K+ content remained unchanged; cell content of Na+ and Cl- dropped in the initial swelling phase by some 50% (reflecting the corresponding reduction in medium NaCl), and then remained unchanged during volume recovery phase. Also, cellular fluxes of 86Rb+ and urea were not affected by hypotonic stress. However, hypotonicity enhanced 10- to 20-fold the efflux of organic cell osmolytes taurine, betaine, and trimethyloxamine, and this accounted for the loss of osmotically obliged water during RVD. Enhancement of osmolyte efflux by hypotonic stress was abolished by readjusting the low-Na+ saline to isotonicity (approximately 900 mosM) with innocuous cations (choline+, Li+, or N-methylglucamine+). The results suggest that reduction of medium tonicity may be the determinant for the RVD response to hypotonic stress. The above properties of the observed RVD were also displayed when studying changes on cell F-actin at the basolateral cell face; hypotonic stress (medium with 135 mM NaCl) produced a rapid disappearance of fluorescence related to this cytoskeletal component, whereas no such changes were seen in low-Na+ salines made isotonic with choline or N-methylglucamine chloride nor in a saline made hyposmolar by omitting urea. Hence, hypotonicity is required to affect F-actin organization (depolymerization?). These changes of F-actin fluorescence are transient; they were completed within 5-10 min of hypotonic stress, and afterwards a gradual reconstitution of cell F-actin organization was seen. The above observations are consistent with the assumption that, in shark rectal gland cells, transient loss of cytoskeleton (F-actin) organization at the basolateral cell face, induced by hypotonicity, brings about a selective efflux of organic osmolytes, thus producing the observed RVD.

Actins↗
PubMed1992

Phagocytosis and ATP levels in alveolar macrophages during acute hypoxia.

Pulmonary alveolar macrophages (PAM) function as phagocytes of inhaled particulate matter and microorganisms at the air-tissue interface of lung alveoli. Changes in cellular ATP concentrations ([ATP]) and phagocytic function during acute hypoxia may be important in conditions associated with low alveolar O2. We proposed that acute hypoxia would decrease phagocytosis and reduce [ATP] in freshly isolated PAM. Phagocytic function (fluorescent microscopic technique determining percent phagocytosis in live cells) was monitored by recording uptake and retention of glutaraldehyde-fixed red blood cells (GRBC) in isolated rabbit PAM during acute incubations in air (20% O2) or hypoxia (1.7% O2). Macrophage [ATP] were determined spectrophotometrically. Acute hypoxia for 30 to 150 min decreased phagocytic function 30 to 56% in PAM without significantly affecting cell adherence and viability. Pre-exposure of PAM to hypoxia before addition of GRBC resulted in an even greater reduction in phagocytosis (97% decrease by 30 min), and recovery of phagocytic function occurred 60 to 90 min after returning PAM to air. The cellular retention of phagocytosed GRBC (percentage of PAM with GRBC and number of GRBC/PAM) was reduced 30% by 1 h of hypoxia. Compared with [ATP] of PAM in air, [ATP] of PAM exposed to hypoxia were reduced 55 and 35% at 30 and 60 min, respectively. Compared with [ATP] of cells with GRBC in air at 0 and 30 min, PAM with GRBC in hypoxia for 30 min had, respectively, 61 and 40% lower [ATP]. By 60 min with GRBC, PAM [ATP] in air and hypoxia were similar but were 50% lower than [ATP] at time 0.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosine Triphosphate↗
PubMed1992

Development and resolution of Pneumocystis carinii pneumonia in severe combined immunodeficient mice: a morphological study of host inflammatory responses.

The development and resolution of naturally-acquired Pneumocystis carinii pneumonia was studied in a severe combined immunodeficient (SCID) mouse model by light and electron microscopies. Initial infection was evident in 3-week-old SCID mice and started as focal alveolar colonization in the areas near terminal airways. Pronounced pulmonary inflammation occurred in animals of 10 weeks or older and the infection intensity reached a plateau in animals 12 weeks of age. At this stage of disease, the histopathological features of P. carinii infection in SCID mice were similar to those of immunodeficient man. Reconstitution of SCID mice with immunocompetent spleen cells at day 0 induced substantial pulmonary inflammation that was evident already by day 7 and most severe and extensive by day 12. The clearance of P. carinii did not begin until after day 12 and was almost completed by day 17. Alveolar macrophages in mice killed between days 12 and 15, at the time when P. carinii are being rapidly cleared, appeared active but phagocytosis of P. carinii was not commonly observed by either light or electron microscopy. These results suggest that (1) the presence of non-lymphoid inflammatory cells in SCID mice is not sufficient to control P. carinii infection; (2) the clearance of P. carinii from the lungs of reconstituted SCID mice requires local recruitment of large numbers of inflammatory cells with an active appearance; and (3) intracellular killing of P. carinii by phagocytosis does not appear to be a major mechanism in host defences against P. carinii infection in this model.

Age Factors↗