Paul Martin

Bio: Paul Martin is an academic researcher from University of Bristol. The author has contributed to research in topics: Wound healing & Migraine. The author has an hindex of 72, co-authored 237 publications receiving 26916 citations. Previous affiliations of Paul Martin include Robertson Centre for Biostatistics & Edinburgh Cancer Research Centre.

Wound Healing--Aiming for Perfect Skin Regeneration

Abstract: The healing of an adult skin wound is a complex process requiring the collaborative efforts of many different tissues and cell lineages. The behavior of each of the contributing cell types during the phases of proliferation, migration, matrix synthesis, and contraction, as well as the growth factor and matrix signals present at a wound site, are now roughly understood. Details of how these signals control wound cell activities are beginning to emerge, and studies of healing in embryos have begun to show how the normal adult repair process might be readjusted to make it less like patching up and more like regeneration.

Measuring Behaviour: An Introductory Guide

Abstract: Measuring Behaviour is a guide to the principles and methods of quantitative studies of behaviour, with an emphasis on techniques of direct observation, recording and analysis. Numerous textbooks describe and analyse human and animal behaviour, but none provides a comprehensive review of the principles and techniques of its measurement. Those undertaking this task for the first time are often bemused by the apparent difficulty of the job facing them - how will they accurately and systematically record all that is happening? The purpose of this book is to provide this basic knowledge in a succinct and easily understood form. This concise review of methodology includes a comprehensive annotated bibliography. Written with ,brevity and clarity, Measuring Behaviour is intended, above all, as a practical guide-book.

Wound repair and regeneration: Mechanisms, signaling, and translation

Abstract: The cellular and molecular mechanisms underpinning tissue repair and its failure to heal are still poorly understood, and current therapies are limited. Poor wound healing after trauma, surgery, acute illness, or chronic disease conditions affects millions of people worldwide each year and is the consequence of poorly regulated elements of the healthy tissue repair response, including inflammation, angiogenesis, matrix deposition, and cell recruitment. Failure of one or several of these cellular processes is generally linked to an underlying clinical condition, such as vascular disease, diabetes, or aging, which are all frequently associated with healing pathologies. The search for clinical strategies that might improve the body’s natural repair mechanisms will need to be based on a thorough understanding of the basic biology of repair and regeneration. In this review, we highlight emerging concepts in tissue regeneration and repair, and provide some perspectives on how to translate current knowledge into viable clinical approaches for treating patients with wound-healing pathologies.

Wound repair at a glance

Abstract: This article is part of a Minifocus on collective cell migration. For further reading, please see related articles: `Mechanisms of collective cell migration at a glance' by Olga Ilina and Peter Friedl ( J. Cell Sci. 122 , [3203-3208][1]) and `Collective cell migration in development' by Cornelis

Using Multivariate Statistics

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Re-epithelialization and immune cell behaviour in an ex vivo human skin model.

Abstract: A large body of literature is available on wound healing in humans. Nonetheless, a standardized ex vivo wound model without disruption of the dermal compartment has not been put forward with compelling justification. Here, we present a novel wound model based on application of negative pressure and its effects for epidermal regeneration and immune cell behaviour. Importantly, the basement membrane remained intact after blister roof removal and keratinocytes were absent in the wounded area. Upon six days of culture, the wound was covered with one to three-cell thick K14+Ki67+ keratinocyte layers, indicating that proliferation and migration were involved in wound closure. After eight to twelve days, a multi-layered epidermis was formed expressing epidermal differentiation markers (K10, filaggrin, DSG-1, CDSN). Investigations about immune cell-specific manners revealed more T cells in the blister roof epidermis compared to normal epidermis. We identified several cell populations in blister roof epidermis and suction blister fluid that are absent in normal epidermis which correlated with their decrease in the dermis, indicating a dermal efflux upon negative pressure. Together, our model recapitulates the main features of epithelial wound regeneration, and can be applied for testing wound healing therapies and investigating underlying mechanisms.

Ordinary magic. Resilience processes in development.

Abstract: The study of resilience in development has overturned many negative assumptions and deficit-focused models about children growing up under the threat of disadvantage and adversity. The most surprising conclusion emerging from studies of these children is the ordinariness of resilience. An examination of converging findings from variable-focused and person-focused investigations of these phenomena suggests that resilience is common and that it usually arises from the normative functions of human adaptational systems, with the greatest threats to human development being those that compromise these protective systems. The conclusion that resilience is made of ordinary rather than extraordinary processes offers a more positive outlook on human development and adaptation, as well as direction for policy and practice aimed at enhancing the development of children at risk for problems and psychopathology.

Cutaneous wound healing.

Abstract: The primary function of the skin is to serve as a protective barrier against the environment. Loss of the integrity of large portions of the skin as a result of injury or illness may lead to major disability or even death. Every year in the United States more than 1.25 million people have burns1 and 6.5 million have chronic skin ulcers caused by pressure, venous stasis, or diabetes mellitus.2 The primary goals of the treatment of wounds are rapid wound closure and a functional and aesthetically satisfactory scar. Recent advances in cellular and molecular biology have greatly expanded our understanding . . .