Aplastic anemia is a rare disease caused by destruction of pluripotent stem cells in bone marrow. The occurrence of aplastic anemia during pregnancy is rare and can be fatal for both mother and child. The association is not well explained and there is no consensus on optimal management. We report the case of 30 years-old women treated for aplastic anemia during pregnancy, the evolution is favorable.

Polyclonal CD8(+)/CD57(+)T cell lymphocytosis can be observed in various conditions such as chronic viral infections, autoimmune cytopenias, connective tissue diseases, chronic graft-versus-host disease and primary or secondary immune deficiencies. This population results from the chronic stimulation of CD8(+)/CD28(+)/CD57(-)lymphocytes by exogenous (mostly infection-related), autologous or allogeneic antigens. Paralleling chronic antigen stimulation, these CD8(+) T cells acquire a poor capacity to proliferate in standard conditions in relation with the loss of CD28, whereas CD57 antigen becomes expressed at their surface. CD8(+)/CD57(+)T cells represent activated cytotoxic T lymphocytes at a terminal stage of their differentiation with evidence of immunological senescence, which have usually lost their cytotoxic properties to become "regulatory" T cells. Patients with a CD8(+)/CD57(+)T cell lymphocytes expansion can display features of organ infiltration, as well as chronic idiopathic neutropenia. The search of this population has therefore a diagnostic value in clinical practice. A CD8(+)/CD57(+)T cell lymphocytes expansion must be suggested in patients with an organomegaly or organ(s) infiltration, particularly in patients infected by the human immunodeficiency virus or in the setting of allogeneic hematopoietic stem cell transplantation, as well as in patients with a neutropenia of unexplained origin. The identification of a CD8(+)/CD57(+)T cell lymphocytes expansion also has therapeutical consequences since patients with an organ infiltration or a neutropenia may respond remarkably to immunomodulatory therapies. The search of a CD8(+)/CD57(+) T cell expansion thus represents a useful and still poorly known diagnostic tool which clinical interest deserves further evaluation.

Gap junctions are specialized plasma membrane structures consisting of transmembrane channels that directly link the cytoplasms of adjoining cells and mediate the reciprocal exchange of ions and low molecular weight molecules (<1200 Da). Structural studies have demonstrated that each gap junctional channel is formed by the extracellular interaction of two hemi-channels (connexons). Each connexon is a hexameric assembly of protein subunits (connexins), which delineate an aqueous pore. Connexins are homologous proteins encoded by a multigene family and are named according to their predicted molecular weight. Connexin 43, widely distributed in different cell types, is the main gap junction protein expressed in human bone cells, although Cx45 and Cx46 have been reported to be expressed as well. Bone remodeling requires coordinated activity among osteoblasts and osteoclasts. Osteoblasts (bone forming cells) are derived from mesenchymal stem cells, and osteoclasts (bone resorbing cells), are multinucleated cells of monocyte/macrophage origin. Here, we review what is known regarding the structure of gap junctions and the mechanisms regulating bone remodeling, and discuss the evidence suggesting that gap junctional intercellular communication contributes to the bone remodeling.

The objective of the current study was to perform a review of literature concerning stem cells therapy (preclinical and clinical studies) applied to the treatment of stress urinary incontinence (SUI).

The long-term outlook for adult patients with acute myeloid leukemia (AML) remains dismal. The main reason for this state of affairs lies in the fact that the majority of AML patients will eventually relapse, even after obtaining complete remission following front-line chemotherapy. Relapses are generally attributed to the persistence of a small number of chemotherapy-resistant leukemic (stem) cells, a condition known as minimal residual disease (MRD). The eradication of MRD, with the eventual aim of reducing the risk of relapse, therefore represents a high-priority goal of modern AML therapy. It is now well established that the immune system plays a crucial role in the defense against AML. This knowledge has fuelled the development of immune-based approaches to control MRD and, ultimately, to prevent relapse. One of the promising strategies that have emerged in this regard involves the use of dendritic cells for therapeutic vaccination. This review article aims to introduce the reader into the conceptual and practical aspects of DC-based vaccination for AML. Next, we will review the first clinical results obtained with this immunotherapeutic approach in AML patients. Finally, we will briefly reflect on the potential place of DC vaccination in the future therapy of AML.

Multipotent stem cells of adult skin are found in distinct biological locations identified as niches. These stem cell populations are defined by specific molecular and functional attributes. The epidermal stem cells are found in the interfollicular areas and in the bulge and isthmus of the hair follicles. Dermal stem cells are harbored in the peripilar connective tissue sheaths and in the hair papilla. Some skin stem cells are found in extracutaneous sites. Other stem cells are involved in pathology, such as neoplastic stem cells identified in malignant melanomas.

In a normal context, bone morphogenetic proteins (BMPs), members of the TGFβ superfamily, are key players in adult stem cell biology. They are involved in the control of the overall functional and phenotypic properties of the stem cell population (self-renewal, proliferation, differentiation, apoptosis, quiescence, etc.). They can act directly on the stem cell or through its microenvironment, contributing to the tight balance of this system. In the tumorigenic context, alterations of the BMP signalling are involved in the deregulation of the interaction between stem cells and their microenvironment and, as such, participate to the different steps of the transformation process.

The TP53 family member TP63 encodes two main isoforms TAp63 and ΔNp63 with distinct, often opposite functions during development and in the adult. ΔNp63 is crucial for the formation of the ectodermal derivatives and epidermis, while TAp63 is essential for heart development. In the adult, ΔNp63 behaves as a cell survival factor, controlling cell proliferation, adhesion and cell differentiation. In contrast, TAp63 is a proapoptotic factor that protects oocytes from genotoxic insults and prevents premature aging of dermal stem cells. In agreement with these activities, TAp63 is often lost and ΔNp63 overexpressed in cancer cells. Because of their opposite and competitive effects, p63 isoforms could be viewed as Janus two faces. The review focuses on the accumulating data on the p63 functions and regulation in the last decade.

Aging is a complex process that is accompanied by the onset of a series of age-related diseases, including Alzheimer's disease. Aging is controlled by a combination of genetic and environmental factors. Among the genes that regulate aging, the insulin-FOXO signaling pathway plays a central role, as this pathway regulates lifespan in multiple species, such as worms, flies, and mice. In humans, exceptional longevity - being a centenarian - is also associated with genetic variation in this insulin-FOXO pathway. Recent evidence indicates that the FOXO family of transcription factors plays a key role in the self-renewal of adult and embryonic stem cells, which could contribute to tissue regeneration. Understanding the mechanisms underlying aging should help better prevent and treat age-dependent diseases.

Most of the signalling pathways involved in aging regulation have been recently found well conserved at various levels throughout the evolution. Taking this into account, a diversity of model organisms, including worms, rodents, and lemurs as well, allows to address different questions: how to understand the interactions between genetic and environmental factors while challenging theories of aging, to preserve hearing integrity, to fight against senescence of neural stem cells, or to explore brain fitness from gene expression to cognitive and social behavior? Here are the main issues that can be considered, stressing the complementarities of the models. The differentiation of aging physiological aspects from those induced by age-related pathologies will also be specified. By emphasizing recent ability of technologies to promote new aging insights, we discuss towards a better understanding of mechanisms governing aging.

The experience accumulated in cardiac cell therapy suggests that regeneration of extensively necrotic myocardial areas is unlikely to be achieved by the sole paracrine effects of the grafted cells but rather requires the conversion of these cells into cardiomyocytes featuring the capacity to substitute for those which have been irreversibly lost. In this setting, the use of human pluripotent embryonic stem cells has a strong rationale. The experimental results obtained in animal models of myocardial infarction are encouraging. However, the switch to clinical applications still requires to address some critical issues, among which optimizing cardiac specification of the embryonic stem cells, purifying the resulting progenitor cells so as to graft a purified population devoid from any contamination by residual pluripotent cells which carry the risk of tumorigenesis and controlling the expected allogeneic rejection by clinically acceptable methods. If the solution to these problems is a pre-requisite, the therapeutic success of this approach will also depend on the capacity to efficiently transfer the cells to the target tissue, to keep them alive once engrafted and to allow them to spatially organize in such a way that they can contribute to the contractile function of the heart.