Hospital Universitario Central Of Asturias

Hospital de Órbigo, Spain

Hospital Universitario Central Of Asturias

Hospital de Órbigo, Spain

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Pascual J.,Hospital Universitario Central Of Asturias
Revista de neurologia | Year: 2012

We define chronic migraine as that clinical situation in which migraine attacks appear 15 or more days per month. Until recently, and in spite of its negative impact, patients with chronic migraine were excluded of the clinical trials. This manuscript revises the current treatment of chronic migraine. The first step should include the avoidance of potential precipitating/aggravating factors for chronic migraine, mainly analgesic overuse and the treatment of comorbid disorders, such as anxiety and depression. The symptomatic treatment should be based on the use of nonsteroidal anti-inflammatory agents and triptans (in this case < 10 days per month). It is necessary to avoid the use of combined analgesics, opioids and ergotamine-containing medications. Preventive treatment includes a 'transitional' treatment with nonsteroidal anti-inflammatory agents or steroids, while preventive treatment exerts its actions. Even though those medications efficacious in episodic migraine prevention are used, the only drugs with demonstrated efficacy in the preventive treatment of chronic migraine are topiramate and pericranial infiltrations of Onabotulinumtoxin A.

Moro-Garcia M.A.,Hospital Universitario Central Of Asturias | Alonso-Arias R.,Hospital Universitario Central Of Asturias | Lopez-Larrea C.,Hospital Universitario Central Of Asturias
Frontiers in Immunology | Year: 2013

Beyond midlife, the immune system shows aging features and its defensive capability becomes impaired, by a process known as immunosenescence that involves many changes in the innate and adaptive responses. Innate immunity seems to be better preserved globally, while the adaptive immune response exhibits profound age-dependent modifications. Elderly people display a decline in numbers of naïve T-cells in peripheral blood and lymphoid tissues, while, in contrast, their proportion of highly differentiated effector and memory T-cells, such as the CD28null T-cells, increases markedly. Naïve and memory CD4+ T-cells constitute a highly dynamic system with constant homeostatic and antigen-driven proliferation, influx, and loss of T-cells. Thymic activity dwindles with age and essentially ceases in the later decades of life, severely constraining the generation of new T-cells. Homeostatic control mechanisms are very effective at maintaining a large and diverse subset of naïve CD4+ T-cells throughout life, but although later than in CD8 + T-cell compartment, these mechanisms ultimately fail with age. © 2013 Moro-García, Alonso-Arias and López-Larrea.

Martinez-Borra J.,Hospital Universitario Central Of Asturias | Lopez-Larrea C.,Hospital Universitario Central Of Asturias
Advances in Experimental Medicine and Biology | Year: 2012

Autophagy is a highly conserved mechanism which is essential for the maintenance of cellular homeostasis in response to cellular stress. Autophagy has been conserved from yeast to humans as a quality control process that is involved in the recognition and turnover of damaged proteins and organelles. It is also a response mechanism to nutrient starvation. In mammals, autophagy is involved in antigen presentation, tolerance, inflammation and protection against neurodegenerative diseases. The decrease of autophagy during aging reduces the removal of damaged organelles and increases the accumulation of waste products in the cells. In this chapter, we review these aspects of autophagy along with their role in self-nonself distinction, their implication in innate and adaptive immune response, and its dysregulation in the pathology of certain inflammatory and autoimmune diseases. © 2012 Landes Bioscience and Springer Science+Business Media.

Ortega F.,Hospital Universitario Central Of Asturias
Advances in Experimental Medicine and Biology | Year: 2012

Mankind has always been interested in investigating and searching for solutions regarding the body deterioration due to factors such as disease, damage caused by trauma, toxins or radiation or just the process of ageing. Here, we summarize the history of scientific advances in solid organ transplantation, in the areas strictly linked to transplantation. The period between the end of the 19th and beginning of the 20th century has been called by some authors the "Era of allografting". This was a muddled period with many studies and publications on very diverse transplants, from Kocher's (Nobel Prize in 1909) who transplanted thyroid extracts, to Brown-Sequard who tried to rejuvenate people by using grafts of guinea pig testicle extracts. In the midst of the 20th century, Sir Medawar pointed out that the rejection of transplant organs by the recipient body was mediated by an immunological reaction, which should be modified. Since then, there has been an open period of discovery of new immunosuppressive drugs which have revolutionised the outcomes of solid organ transplantations. New challenges have appeared over the last few years, these efforts have focused on the search to extend graft durability and with it recipient patient survival times, as well as improve their quality of life. © 2012 Landes Bioscience and Springer Science+Business Media.

Suarez-Alvarez B.,Hospital Universitario Central Of Asturias | Rodriguez R.M.,University of Oviedo | Fraga M.F.,University of Oviedo | Lopez-Larrea C.,Hospital Universitario Central Of Asturias
Trends in Genetics | Year: 2012

During hematopoiesis, a unique hematopoietic stem cell (HSC) from the bone marrow gives rise to a subset of mature blood cells that directs all the immune responses. Recent studies have shown that this well-defined, hierarchical process is regulated in part by epigenetic mechanisms. Changes in the DNA methylation profile have a critical role in the division of these stem cells into the myeloid and lymphoid lineages and in the establishment of a specific phenotype and functionality in each terminally differentiated cell type. In this review, we describe how the DNA methylation patterns are modified during hematopoietic differentiation and what their role is in cell plasticity and immune function. An in-depth knowledge of these epigenetic mechanisms will help clarify how cell type-specific gene programs are established, and how they can be leveraged in the development of novel strategies for treating immune system-related pathologies. © 2012 Elsevier Ltd.

Delgado E.,Hospital Universitario Central Of Asturias
International Journal of Clinical Practice | Year: 2012

Aim: We evaluated the effectiveness of insulin glargine (glargine)-based regimens in patients with type 2 diabetes mellitus (T2DM) in clinical practice in Spain. Methods: This was a retrospective, registry-based study of 1482 patients treated with neutral protamine Hagedorn (NPH) who were either switched to glargine or maintained on NPH at investigators' discretion. The primary outcomes were HbA 1c change over a period of 4-9 months follow-up and incidence of hypoglycaemia. Results: Prior to switching treatment, mean ± standard deviation HbA 1c was worse in the glargine vs. the NPH group (8.3 ± 1.2% vs. 7.9 ± 1.1% respectively; p < 0.0001). After 4-9 months of treatment, mean reductions in HbA 1c were greater with glargine vs. NPH (-1.0 ± 1.0% vs. -0.2 ± 0.8% respectively; p < 0.0001) and the incidence of hypoglycaemia in the month prior to the study visit was lower (21.8% vs. 47.6% respectively; p < 0.0001). An expected reduction in dosing frequency, as well as in the basal insulin dose was reported for glargine vs. NPH, with 97.3% of glargine-treated patients on once-daily injections and 81.2% on NPH receiving twice-daily therapy. Improvements in treatment satisfaction were significantly higher with glargine (p < 0.0001). Conclusions: In a Spanish clinical practice setting, patients with T2DM who switched to glargine from NPH experienced significantly greater reductions in mean HbA 1c and a lower incidence of hypoglycaemia than patients maintained on NPH. © 2012 Blackwell Publishing Ltd.

Rodriguez-Rodero S.,Hospital Universitario Central Of Asturias
Discovery medicine | Year: 2010

Aging is one of the most challenging and unresolved problems in biology owing to its highly complex nature. Public interest in aging has increased not only because all of us can expect to live to a ripe old age but also because we wish to avoid those age-related changes that lead to physical invalidity or other diseases (cancer, depression) and may ultimately cause social isolation. Aging is a process of genetic and epigenetic interactions at all biological levels, where epigenetics has an important function in determining the phenotypic differences that arise. Epigenetics also plays a key role in the development of diseases associated with aging and explains the relationship between an individual's genetic background, the environment, aging, and disease. DNA plasticity is mediated in part by the epigenetic changes that lead the role of a cell, and can be passed on to future generations. Epigenetics establishes the idea that our health can be affected not only by the interplay of our genes and environment but also by the inherited effects of our ancestors' genes and environment.

Tuca A.,University of Barcelona | Jimenez-Fonseca P.,Hospital Universitario Central Of Asturias | Gascon P.,University of Barcelona
Critical Reviews in Oncology/Hematology | Year: 2013

Cancer anorexia-cachexia syndrome (CACS) is a complex metabolic syndrome, different from malnutrition and sarcopenia, which is very common in cancer patients. Treatment for CACS is based on nutritional support and CACS pathophysiology-modulating drugs. The most commonly used are megestrol acetate (MA) and corticosteroids. The efficacy of MA has been confirmed by multiple clinical trials and meta-analyses. Glucocorticoids are also effective but should only be used for short periods and in selected cases. Future strategies should include intensified research into potentially effective drugs (ω-3 fatty acids, thalidomide, cannabinoids, ghrelin, bortezomib, and COX-2 inhibitors), combined treatment and new drugs (anti-IL-6 monoclonal antibodies, melanocortin, β-2 antagonists, and androgen receptor-modulating analogues). We propose a review based on the literature on the pathophysiology of CACS, the diagnostic criteria and treatment, and future strategies. © 2013 Elsevier Ireland Ltd.

Paz Aparicio J.,Hospital Universitario Central Of Asturias
European spine journal : official publication of the European Spine Society, the European Spinal Deformity Society, and the European Section of the Cervical Spine Research Society | Year: 2011

To determine whether polymorphisms (SNPs) in the genes encoding cytokines and nitric oxide synthase (NOS) might play some role in lumbar disc herniation (LDH). Case-control study in which 179 patients were retrospectively reviewed. The case group was made of 50 patients with symptomatic LDH diagnosed by MRI while the control group was made of 129 individuals undergoing routine hip or knee arthroplasty with a lifetime lack of low back pain. SNPs in the cytokine genes of IL-1 [IL-1α (-889 C/T), IL-1β (+3953 T/C)], TNF-α (-308 G/A and -238 G/A) and NOS genes [eNOS (r 27 bp, intron 4 and -786 T/C) and iNOS (22 G/A)]. The CC genotype and C allele of the IL-1β (+3953 T/C) SNP were significantly more frequent among LDH patients compared to controls. On the other hand, eNOS (-768 T/C) and iNOS (22 G/A) SNPs were significantly more common in the control group. Carriers of the CC genotype of the IL-1β (+3953 T/C) SNP were more frequent among LDH patients suggesting some potential role of the IL-1β SNP on LDH pathogenesis. The eNOS (-786 T/C) and iNOS (22 G/A) SNPs were more frequent among the control subjects, suggesting their possible protective role against LDH. Genotyping these SNPs could be useful to identify persons with an increased lifetime risk of disc herniation in whom measures to avoid LDH could be implemented.

Lopez F.,Hospital Universitario Central Of Asturias
European archives of oto-rhino-laryngology : official journal of the European Federation of Oto-Rhino-Laryngological Societies (EUFOS) : affiliated with the German Society for Oto-Rhino-Laryngology - Head and Neck Surgery | Year: 2013

Novel markers to accurately predict the risk of malignant transformation in laryngeal epithelial precursor lesions (EPL) are needed. We tried to identify some molecular alterations occurring in laryngeal tumorigenesis. In this study, 60 paraffin-embedded EPL and 17 metachronous invasive carcinomas were immunostained for markers associated with proliferation (Ki67), cell cycle control (p53, p21, p16, p27, cyclin D1), and cell adhesion and invasion (laminin and β-catenin). Aberrant expression of p16 and p53 and positivity at cytoplasm for β-catenin and cyclin D1 were detected significantly in EPL with progression to invasive laryngeal carcinoma. All cases with basal and suprabasal reactivity of p53 showed β-catenin overexpression. We found that β-catenin protein expression increased significantly with the grade of dysplasia. This is one of the studies with the largest number of laryngeal EPL and invasive carcinoma studied sequentially. Our data confirm the role of some cell cycle regulatory proteins in the development of laryngeal carcinoma. Cytoplasmic retention of β-catenin in EPL seems to be related with more aggressive biological behavior. Combined increased p53 and cytoplasmic β-catenin protein expression could be biologically important in laryngeal tumorigenesis. Further research is required to clarify the involvement of β-catenin in the mechanism associated with malignant transformation in laryngeal tissues.

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