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Background: Psychological trauma is considered to be a risk factor for the development of a number of psychiatric disorders. Although 40-90% of the population is exposed to a traumatic event in their lifetime, only a small fraction of individuals will develop a disorder. In recent years, numerous studies described epigenetic changes, such as DNA methylation, histone modifications and non-coding RNA as potential biological mechanisms by which the environment can have long-term effects on an organism., Methods and Results: This article reviews the accumulating evidence for the involvement of epigenetic factors in the development of psychiatric disorders associated with psychological trauma. Clinically the review focuses on posttraumatic stress disorder (PTSD) for which trauma is a diagnostic criterion. In this context, we specifically focus on studies that show trauma and disease-associated epigenetic changes in humans and animal models. Both tissue-specific as well as cross-tissue effects have been described and underline the global consequences of psychological trauma on the whole organism. In addition, possible epigenetic mechanisms are presented which could be responsible for the long-lasting effects of gene-environment interactions in psychiatric disorders. Finally, the review addresses how a better understanding of these epigenetic mechanisms could suggest avenues for possible future pharmacological and psychotherapeutic treatment approaches.

Psoriasin (S100 A7) was discovered two decades ago as a protein abundantly expressed in psoriatic keratinocytes. Even though much scientific research has been carried out on the characterization of psoriasin, only recent studies point to an important role of psoriasin as an antimicrobial and immunomodulatory protein in skin and other epithelia. In this review, we provide an overview of the major findings in psoriasin research and discuss novel studies highlighting the role of psoriasin as an important effector molecule of the cutaneous barrier., (© The Authors • Journal compilation © Blackwell Verlag GmbH, Berlin.)

Chronic leg ulcers affect about 1% of the German population. The intense search for the underlying cause of impaired wound healing is an essential requirement for successful therapy. The most common causes comprise chronic venous insufficiency (70%), peripheral arterial occlusive disease (10%) and diabetes mellitus. Besides vasculitis, infectious diseases and tumors, genetic diseases may constitute the underlying cause for impaired wound healing. In this review various rare genetic diseases causing chronic wounds like the Klinefelter-Syndrome, immunological diseases including the TAP-deficiency-syndrome and the leukocyte adhesion deficiency-syndromes, red blood cell disorders, thalassemia, thrombotic diseases, progeroid syndromes and inherited connective tissue disorders are presented.

Underlying disease may impair normal wound healing, leading to chronic, poorly healing wounds. Efficient treatment strategies require identification and treatment of the underlying disease as well as directed correction of the wound healing defect. A thorough knowledge of tissue repair mechanisms at the cellular and molecular level will help to achieve these goals. This review focuses on new developments in wound healing research and the resulting non-operative therapeutic implications.

Acute inflammation and the innate immune response to severe tissue trauma continue to pose a critical pathophysiological challenge in the intensive care regimen. Advances in the development of improved gene therapeutics and their application in diverse animal models of acute inflammation have shown promising results in reducing both morbidity and mortality. The introduction of inflammatory antagonists, by either viral or non-viral vectors, has thereby proven to play a significant role in determining the overall outcome. Recent findings of utilizing the functional characteristics of immunocompetent cells (e.g. dendritic cells) in combination with the gene therapy-induced overexpression of anti-inflammatory target proteins have significantly expanded this gene therapeutic spectrum. The results from diverse experiments in our own murine model of sepsis, in connection with findings from various other analogous international studies, have demonstrated great potential to revolutionize the clinical treatment concept and prevention of acute inflammatory diseases.

Modern molecular and genetic technologies enable the modification of a cellular genome through transfer of specific genes. The various procedures alter specific cell functions, which allow the transfected cell to produce any encoded transgene information. The transfected cell then synthesizes proteins that are normally not produced or only in very small amounts. Numerous animal studies have demonstrated that gene therapy may support and accelerate the healing and regeneration of specific tissues such as skin, tendons, cartilage, and bones. Currently, further animal studies are evaluating new vectors with reduced immunogenicity in the continuous effort to improve the efficacy and safety of gene transfer. In the forthcoming decade we expect gene therapy to have an important influence on the treatment of fractures, cartilage lesions, and infection.

Growth factors are important players in orchestrating all stages of wound healing. They are mitogen, chemotactic, they regulate cell-cell interactions and influence synthesis and composition of extra-cellular matrix components. The use of growth factors to stimulate wound healing is a promising new therapeutic approach to repair chronic tissue defects. The delivery of genetic material offers an attractive treatment modality to produce an appropriate amount of growth factor proteins within the wound site. This review discusses several methods of growth factor gene transfer into wound tissue and presents recent experimental results of gene therapy approaches in stimulating wound repair.