Contact-sensing or thigmotropism is the directional growth response of cells in relation to topographical guidance cues. Thigmotropism is thought to play a major role in the location of infectable sites on plants by phytopathogenic fungi and has recently been shown to be a property of hyphae in the human pathogenic fungus Candida albicans. Here we show that hyphae of the dermatophytes Epidermophyton floccosum, Microsporum canis and Trichophyton mentagrophytes reorientate their direction of growth in response to grooves and pores of membrane substrata as did hyphae of the saprophytes Mucor mucedo and Neurospora crassa. This suggests that the thigmotropic behaviour of hyphae is not a specific property of pathogens, but rather a general feature of the growth of fungal hyphae that must forage for nutrients on surfaces and within solid materials.

Arthrodermataceae↗

PubMedDate not supplied

Heat-induced damage to HeLa-S3 cells: correlation of viability, permeability, osmosensitivity, phase-contrast light-, scanning electron- and transmission electron-microscopical findings.

The responses of HeLa S-3 to mild hyperthermia for relatively critical times at 43 and 45 degrees C were analysed in detail, including growth and colony-forming ability, permeability, osmotic sensitivity and microscopical appearances. For comparative purposes lower temperatures (e.g. 41 degrees C) and higher temperatures (50 and 55 degrees C) were used in some experiments. The evidence from many different aspects, including scanning and transmission electron microscopy, suggests that critical heat exposures do not per se cause severe membrane damage and loss of cell integrity, but changes quickly become manifest when cells are 'recovered' by returning to 37 degrees C. Attention is drawn to the ability of heat-treated cells to show osmotic-like swelling and restoration towards normal volume in medium of 30 per cent normal strength, which would not be expected on the hypothesis that hyperthermia primarily disrupts membrane structure and functioning. Ultrastructural changes during and after hyperthermia--including nucleolar changes, the appearance of perichromatin granules, the formation of electron-dense cytoplasmic clusters, and the development of intranuclear actin rods--corroborate and extend other findings. However, mitochondrial changes were found to be particularly significant, appearing early and correlating well with the loss of viability and metabolic functioning found after heat treatment. These include the early development of intramitochondrial dense granules, followed by vesicularization of the cristae, swelling of the intracristal spaces, myelin degeneration and the formation of bodies which could otherwise be mistaken for secondary lysosomes. The findings indicate the need for more intensive investigations of mitochondria and mitochondrial functioning in hyperthermia-induced cell damage, and their careful correlation with the 'recovery' of energy-dependent process in cells subsequently returned to 37 degrees C.

Cell Division↗

PubMedDate not supplied

Combined effects of hyperthermia (to 45 degrees C) and ultrasound irradiation on the surface ultrastructure of HeLa cells.

Hyperthermic treatment of HeLa cells in suspension combined with ultrasound irradiation produced alterations to the cell surfaces. The changes induced were related to ultrasound intensity in the standing wave and to heat treatments between 37 and 45 degrees C. Two transducers were used, driven at resonant frequencies of 0.75 and 1.5 MHz, and producing peak intensities up to 7 W/cm2. These intensities produced a negligible rise in temperature of the cell suspension medium. Ultrastructural damage in standing wave fields, as seen by scanning electron microscopy, progressed through stages. The first stage was characterized by the loss of microvilli and smooth appearance of the cell surface, e.g. after insonation at 41.5 degrees C for 10 min; damage increased to a final stage where the surface appeared heavily pitted and porous, with the cells showing signs of disintegration, e.g. after insonation at 45 degrees C for 10 min. The monitoring of ultrasound-induced cavitation suggested that damage was caused by bubble oscillations, not collapse cavitation. Shearing stresses accentuated by hyperthermia were considered the probable cause of such damage. Coulter counter studies of cell size distribution showed that the extent of cell damage depended on the geometry of the vessel in which insonation was carried out.

Cell Membrane↗