Loose connective tissue | EPFL Graph Search

Loose connective tissue, also known as areolar tissue, is a cellular connective tissue with thin and relatively sparse collagen fibers. Its ground substance occupies more volume than the fibers do. It has a viscous to gel-like consistency and plays an important role in the diffusion of oxygen and nutrients from the capillaries that course through this connective tissue as well as in the diffusion of carbon dioxide and metabolic wastes back to the vessels. Moreover, loose connective tissue is primarily located beneath the epithelia that cover the body surfaces and line the internal surfaces of the body. It is also associated with the epithelium of glands and surrounds the smallest blood vessels. This tissue is thus the initial site where pathogenic agents, such as bacteria that have breached an epithelial surface, are challenged and destroyed by cells of the immune system. In the past, the designations areolar tissue, adipose tissue, and reticular tissue have been listed as subsets of

Kinetics of collagen denaturation in tendon

Collagen is constituted of three polypeptides forming a triple helix maintained by numerous weak chemical interactions, such as hydrogen bonds. In connective tissue it further packs into very long cylinders of few nanometers of diameter, called fibrils. Once heated sufficiently, the molecules loose their original structure and take more random conformations (denaturation). The kinetics at which this reaction occurs is strongly dependent upon temperature, because of its co-operative nature. Although the reaction at the molecular level is likely complex and multiple, modelling the kinetics can be simplified considering a single reaction from the native to the denatured state. The rate limiting step of the reaction involves an activated state to which an activation enthalpy and entropy are attributed. The first part of this work is concerned with the characterisation of this activated state. Rates of denaturation are measured under isothermal conditions by monitoring the shrinkage of native bovine tendon. These measurements permit the extraction of the enthalpy and entropy of the molecular state limiting the kinetics. It is shown here that the model considering the activated state as the denatured state of the co-operative fraction of the molecule also permits a modelling of the effect of tension on the rate of reaction. Based upon the theory of rubber elasticity, we derive a quadratic dependence of the kinetics with linear tension applied to denaturing sample. This quadratic behaviour is verified experimentally. The effect of stress is also suspected to be responsible for the heterogeneous form of denatured tissue. By performing isothermal shrinkage measurements on rat tail tendons, the activation parameters of this tissue are also extracted. Additional cross-linking is realised by Glutaraldehyde fixation. It is found experimentally that additional cross-linking leads to a reduction of the entropy of the activated state. In the second part of this work, we are mainly interested in the kinetics of high temperature denaturation as induced by pulsed infrared lasers during surgical procedures. New tools are developed to monitor the reaction during and after CTH:YAG laser pulses on rat tail tendon. For this purpose, an imaging setup is built to generate images of the phase shift between two orthogonal polarisation directions of a probe beam passing through the sample. By careful analysis of the images obtained, the instantaneous local state of birefringence of the sample is derived. This very sensitive method is first used to analyse reversible structural changes of the tissue below the threshold of laser radiant exposure leading to denaturation. Surprisingly, we measured a totally reversible increase of birefringence with temperature. This mechanism is shown to be of different origin than the denaturation process and is suspected to be linked to a variation of the fibril diameter with temperature. The same optical method permits the observation of the state of denaturation of rat tail tendons that are heated by laser pulses of higher energy. Local sites of denaturation are detected by the irreversible modification of birefringence. The method allows one to determine the pulse threshold radiant exposure for rat tail tendon denaturation. Comparison is then made between the threshold radiant exposures determined experimentally with predictions made using the kinetic model whose parameters were obtained previously with isothermal measurements. This is our first successful attempt to validate the model for higher temperatures in a time scale of 10 ms, ruled by the heat diffusion. In order to characterise even higher rates of denaturation, the optical setup is slightly modified to permit a follow up of the reaction during the laser pulse. A streak imaging principle is added to the phase shift detection. The time scales probed by this technique are in the range of 50 μs. By applying higher power laser pulses on the samples, the method reveals a total denaturation in a fraction of a millisecond. The starting point of denaturation during a laser pulse is compared to the computations realised assuming a first order kinetic model. A good agreement between theory and experiments is observed. These experiments realised under high heating rates validate the use of the phenomenological first order kinetic model up to the 50 μs time scale.

EPFL2000

Determination of the identity of the derivatives of the cephalic neural crest: incompatibility between Hox gene expression and lower jaw development

Anne Grapin-Botton

In addition to pigment cells, and neural and endocrine derivatives, the neural crest is characterized by its ability to yield mesenchymal cells. In amniotes, this property is restricted to the cephalic region from the mid-diencephalon to the end of rhombomere 8 (level of somites 4/5), The cephalic neural crest is divided into two domains: an anterior region corresponding to the diencephalon, mesencephalon and metencephalon (r1, r2) in which expression of Hox genes is never observed, and a posterior domain in which neural crest cells exhibit (with a few exceptions) the same Hox code as the rhombomeres from which they originate. By altering the normal distribution of neural crest cells in the branchial arches through appropriate embryonic manipulations, we have investigated the relationships between Hox gene expression and the level of plasticity that neural crest cells display when they are led to migrate to an ectopic environment. We made the following observations. (i) Hox gene expression is not altered in neural crest cells by their transposition to ectopic sites. (ii) Expression of Hox genes by the I)A ectoderm does not depend upon an induction by the neural crest. This second finding further supports the concept of segmentation of the cephalic ectoderm into ectomeres (Couly and Le Douarin, 1990), According to this concept, metameres can be defined in large bands of ectoderm including not only the CNS and the neural crest but also the corresponding superficial ectoderm fated to cover craniofacial primordia, (iii) The construction of a lower jaw requires the environment provided by the ectomesodermal components of BA1 or BA2 associated with the Hox gene non-expressing neural crest cells. Hox gene-expressing neural crest cells are unable to yield the lower jaw apparatus including the entoglossum and basihyal even in the BA1 environment. In contrast, the posterior part of the hyoid bone can be constructed by any region of the neural crest cells whether or not they are under the regulatory control of Hox genes. Such is also the case for the neural and connective tissues (including those comprising the cardiovascular system) of neural crest origin, upon which no segmental restriction is imposed. The latter finding confirms the plasticity observed 24 years ago (Le Douarin and Teillet, 1974) for the precursors of the PNS.

1998

Mechanisms of T Cell Development and Transformation

Ute Koch, Freddy Radtke

T cells are the key mediators in cell-mediated immunity. Their development and maturation involve a complex variety of interactions with nonlymphoid cell products and receptors. Highly specialized to defend against bacterial and viral infections, T cells also mediate immune surveillance against tumor cells and react to foreign tissues. T cell progenitors originate in the bone marrow and, through a series of defined and coordinated developmental stages, enter the thymus, differentiate, undergo selection, and eventually mature into functional T cells. The steps in this process are regulated through a complex transcriptional network, specific receptor-ligand pair interactions, and sensitization to trophic factors, which mediate the homing, proliferation, survival, and differentiation of developing T cells. This review examines the processes and pathways involved in the highly orchestrated development of T cell fate specification under physiological as well as pathological conditions.

2011

Kinetics of collagen denaturation in tendon

EPFL2000

Determination of the identity of the derivatives of the cephalic neural crest: incompatibility between Hox gene expression and lower jaw development

Anne Grapin-Botton

1998