Tissue repair in a poikilothermic vertebrate, Carassius auratus (L.): a preliminary study

The effects of mechanical injury on the skin, connective tissue, muscle and bone of the goldfish is described 28 days following the injury. There is evidence of a dynamic response but the apparent inability of muscle regeneration to any degree is noted.     

Lipid changes during development of Blastocladiella emersonii

The lipid composition of swimming spores, cysts and five hour germlings was established. Spores utilized triglycerides first, then phospholipids. Upon encystment all glycolipid components decreased, while in germlings the phospholipids, monoglycerides and sterol esters exhibited a marked increase.     

Ontogeny of the proventitious epicormic buds in Quercus petraea.

In the present work, we described the fate of proventitious epicormic buds on the trunks of 40-year-old Quercus petraea trees and in parallel the vascular trace they produced in the wood. Our results show that small and large individual epicormic buds can survive as buds for 40 years and that both are composed of a terminal meristem and scales. Meristematic areas are detected in the scale axils of small buds; in addition to these meristems the large buds also have secondary bud primordia. The small buds are connected to the pith of the main stem by a unique trace, whereas the large buds are connected by one or multiple traces. A single trace might imply that the whole bud is still alive and multiple traces might indicate that the terminal meristem has died. In the latter case, each trace is connected to a secondary bud of the large bud. The buds found in a cluster are composed of a terminal meristem and scales with axillary meristems in the scale axils. A cluster is connected to the pith of a stem either by a unique trace when it seems to be the result of partial abscission of an epicormic shoot or multiple traces when it might have originated from an epicormic bud in which the terminal meristem has died. Whatever the type of the bud, the vascular trace in the bark is composed of a cambium, secondary xylem and parenchyma cells and the trace present in the wood had parenchyma cells with vestiges of secondary xylem. Each year, the vascular trace should be produced in the bark by the cambium of the tree but not by the bud itself. On 40-year-old Q. petraea, we observed a proliferation of epicormic buds and in parallel a multiplication of the number of vascular traces in the trunk, but the knots caused by the traces of epicormic buds in the wood, either as individuals or in clusters, are minor since their colours are only slightly darker than those of woody rays and they are less than 2 mm in diameter. The knots will appear when epicormic buds develop into shoots. Received: 30 March 1999 / Accepted: 09 June 1999     

Environmental Particulate (PM2.5) Augments Stiffness-Induced Alveolar Epithelial Cell Mechanoactivation of Transforming Growth Factor Beta

Dysfunctional pulmonary homeostasis and repair, including diseases such as pulmonary fibrosis (PF), chronic obstructive pulmonary disease (COPD), and tumorigenesis have been increasing over the past decade, a fact that heavily implicates environmental influences. Several investigations have suggested that in response to increased transforming growth factor - beta (TGFβ) signaling, the alveolar type II (ATII) epithelial cell undergoes phenotypic changes that may contribute to the complex pathobiology of PF. We have previously demonstrated that increased tissue stiffness associated with PF is a potent extracellular matrix (ECM) signal for epithelial cell activation of TGFβ. The work reported here explores the relationship between tissue stiffness and exposure to environmental stimuli in the activation of TGFβ. We hypothesized that exposure of ATII cells to fine particulate matter (PM2.5) will result in enhanced cell contractility, TGFβ activation, and subsequent changes to ATII cell phenotype. ATII cells were cultured on increasingly stiff substrates with or without addition of PM2.5. Exposure to PM2.5 resulted in increased activation of TGFβ, increased cell contractility, and elongation of ATII cells. Most notably, on 8 kPa substrates, a stiffness greater than normal but less than established fibrotic lung, addition of PM2.5 resulted in increased cortical cell stiffness, enhanced actin staining and cell elongation; a result not seen in the absence of PM2.5. Our work suggests that PM2.5 exposure additionally enhances the existing interaction between ECM stiffness and TGFβ that has been previously reported. Furthermore, we show that this additional enhancement is likely a consequence of intracellular reactive oxygen species (ROS) leading to increased TGFβ signaling events. These results highlight the importance of both the micromechanical and biochemical environment in lung disease initiation and suggest that individuals in early stages of lung remodeling during fibrosis may be more susceptible than healthy individuals when exposed to environmental injury adjuvants.