Estudio de la asociación de genotipos del virus del papiloma humano con Chlamydia trachomatis y otros gérmenes en pacientes con fallo reproductivo

Tesis doctoral inédita leída en la Universidad Autónoma de Madrid, Facultad de Medicina, Departamento de Anatomía Patológica. Fecha de lectura: 7-10-2016Esta tesis tiene embargado el acceso al texto completo hasta el 7-04-201

Infection by Human Papillomavirus (HPV), Chlamydia trachomatis and Ureaplasma urealyticum, in Relation with Reproductive Failure

Recent studies suggest that besides oncogenic capacity, HPV could have etiological role on infertility, but more evidence is necessary to confirm these results. We present in this chapter the microbiological and clinical outcome of 104 infertile women aleatory selected, from northeast of Mexico: 84.6%, with genital infection (GI) by multiple germs: Chlamydia trachomatis (Ct) [86.5%], HPV [49%], Ureaplasma urealyticum (Uu) [47.11%] and Mycoplasma hominis [35.57%]. Significant association (P ≤ 0, 05) was observed between the HPV presence and Uu diagnosis, assisted‐reproduction unsuccessful like previous treatment, cervical cytology with inflammatory process, multiple sexual partners, white‐dense‐mucous, secretion into the vagina, and HPV diagnosed in early years. The more frequent genotypes of HPV present in the infertile women studied were 6/18/16/58/11 and 68. In 60% of them, more than two genotypes were founded. The most frequent associations of high‐risk HPV (HPVhr) were 16/18, 16/58, 16/33, 16/52 and 18/58. Considering the isolate or combined presentation of HPVhr, 79.5% of these women would have a potential to develop cervix carcinoma. GI by HPV/Uu/Ct affects the fertility. Infertile women with GI that include these microorganisms with probed (HPV/Ct) or suspicious carcinogenic effect (Uu) would be considered a group of high risk for cervical cancer

Chondrocyte Turnover in Lung Cartilage

Cartilage is a highly differentiated connective tissue that forms mechanical support to soft tissues and is important for bone development from fetal period to puberty. It is conformed by chondrocytes and extracellular matrix. It is generally believed that adult cartilage has no capacity to renewal. A delicate balance between cell proliferation and cell death ensures the maintenance of normal tissue morphology and function. Stem cells play essential roles in this process. Mesenchymal stem cells (MSCs) can give rise to multiple lineages including bone, adipose and cartilage. Nestin protein was initially identified as a marker for neural stem cells, but its expression has also been detected in many types of cells, including MSCs. In vivo, chondrocyte turnover has been almost exclusively studied in articular cartilage. In this chapter we will review the findings about the chondrocyte turnover in lung cartilage. We have presented evidence that there exist nestin-positive MSCs in healthy adulthood that participates in the turnover of lung cartilage and in lung airway epithelium renewal. These findings may improve our knowledge about the biology of the cartilage and of the stem cells, and could provide new cell candidates for cartilage tissue engineering and for therapy for devastating pulmonary diseases

Nestin-Expressing Cells in the Lung: The Bad and the Good Parts

Nestin is a member of the intermediate filament family, which is expressed in a variety of stem or progenitor cells as well as in several types of malignancies. Nestin might be involved in tissue homeostasis or repair, but its expression has also been associated with processes that lead to a poor prognosis in various types of cancer. In this article, we review the literature related to the effect of nestin expression in the lung. According to most of the reports in the literature, nestin expression in lung cancer leads to an aggressive phenotype and resistance to chemotherapy as well as radiation treatments due to the upregulation of phenomena such as cell proliferation, angiogenesis, and metastasis. Furthermore, nestin may be involved in the pathogenesis of some non-cancer-related lung diseases. On the other hand, evidence also indicates that nestin-positive cells may have a role in lung homeostasis and be capable of generating various types of lung tissues. More research is necessary to establish the true value of nestin expression as a prognostic factor and therapeutic target in lung cancer in addition to its usefulness in therapeutic approaches for pulmonary diseases

Cell Proliferation and Apoptosis—Key Players in the Lung Aging Process

Currently, the global lifespan has increased, resulting in a higher proportion of the population over 65 years. Changes that occur in the lung during aging increase the risk of developing acute and chronic lung diseases, such as acute respiratory distress syndrome, chronic obstructive pulmonary disease, idiopathic pulmonary fibrosis, and lung cancer. During normal tissue homeostasis, cell proliferation and apoptosis create a dynamic balance that constitutes the physiological cell turnover. In basal conditions, the lungs have a low rate of cell turnover compared to other organs. During aging, changes in the rate of cell turnover in the lung are observed. In this work, we review the literature that evaluates the role of molecules involved in cell proliferation and apoptosis in lung aging and in the development of age-related lung diseases. The list of molecules that regulate cell proliferation, apoptosis, or both processes in lung aging includes TNC, FOXM1, DNA-PKcs, MicroRNAs, BCL-W, BCL-XL, TCF21, p16, NOX4, NRF2, MDM4, RPIA, DHEA, and MMP28. However, despite the studies carried out to date, the complete signaling pathways that regulate cell turnover in lung aging are still unknown. More research is needed to understand the changes that lead to the development of age-related lung diseases

Schwann Cell Precursor Transplant in a Rat Spinal Cord Injury Model

Background: Differentiation of mesenchymal stem cells into Schwann cell precursors could reverse established lesions and sequelae of medullary transection. Objective: The objective of this study was to study the clinical response of mesenchymal stem cell transplantation with Schwann precursor cell transplantation in a rat spinal cord injury model, using motor function and histopathologic studies. Materials and methods: A total of 28 Sprague-Dawley rats were randomly divided among four groups (n = 7 in each): sham group, control group, mesenchymal stem cell transplant group, and Schwann cell precursor transplant group. The surgical procedure was a laminectomy with transection of the spinal cord at the T11 level in the transplant groups and the injury control group. After 1 week, the transplant groups received stem cells directly in the injury site. Hind limb motor function was assessed using the locomotive scale of Basso, Beattie, and Bresnahan. 1 month after transplantation, all specimens were sacrificed to make a histopathologic description of sections taken from the site of injury and where stem cells were transplanted. Mean scores of mobility were compared using analysis of variance (ANOVA) of one factor with 95% reliability between groups and ANOVA of repetitive measures to evaluate evolution in the same group. Results: We observed that the control group had statistically greater mobility than the other groups (p < 0.0001) and that the group with spinal injury without treatment had the lowest mean mobility. The mobility score values from the Schwann cell precursor group were statistically higher than the group treated with mesenchymal stem cells (p < 0.0001). Conclusion: Schwann precursor cells had a greater effect on locomotive function than mesenchymal stem cells