Study protocol: High-protein nutritional intervention based on β-hydroxy-β-methylbutirate, vitamin D3 and calcium on obese and lean aged patients with hip fractures and sarcopenia. The HIPERPROT-GER study.

Introduction: Loss of muscle strength is associated with falls, which, in turn, are the main cause of hip fractures in elderly people. The factors that most influence loss of strength in elderly people are a decrease in muscle mass, i.e.

The anorexia of ageing: physiopathology, prevalence, associated comorbidity and mortality. A systematic review.

The physiological processes of ageing and factors prevalent in the elderly such as comorbidities and polypharmacy often cause loss of appetite in the elderly, which we call anorexia of ageing. Social factors, together with changes in the sensory organs, can be important causes of a reduction in both appetite and ingestion. This review assesses the regulation of appetite in the elderly and the development of anorexia of ageing.

Effectiveness of nutritional supplementation on muscle mass in treatment of sarcopenia in old age: a systematic review.

Background: Much interest has been focused on nutritional treatment of sarcopenia, loss of muscle mass and performance associated to aging; however, its benefits are unclear.

Objective: To analyze the relevance of nutritional treatment of sarcopenia and assess the effects of supplementation on muscle mass and function within the aged population.

Methods: We searched Medline and the Cochrane Library for controlled trials published between 1991 and 2012.

Sarcopenia in the elderly: diagnosis, physiopathology and treatment.

Sarcopenia, defined as a syndrome rather than as a pathology, is the loss of muscle mass and function associated with age. Sarcopenia is an enigma for medicine, and despite the numerous publications available in the literature and the number of papers currently being published, there is no agreement about its definition, and even less about its root causes. One salient aspect that proves the lack of consensus is the fact that different working groups are still debating about the right name for this syndrome (which is associated with the loss of muscle mass and strength in the elderly).

In vitro and in vivo down-regulation of regulatory T cell activity with a peptide inhibitor of TGF-beta1.

Down-regulation of CD4+CD25+ regulatory T (Treg) cell function might be beneficial to enhance the immunogenicity of viral and tumor vaccines or to induce breakdown of immunotolerance. Although the mechanism of suppression used by Treg cells remains controversial, it has been postulated that TGF-beta1 mediates their immunosuppressive activity. In this study, we show that P17, a short synthetic peptide that inhibits TGF-beta1 and TGF-beta2 developed in our laboratory, is able to inhibit Treg activity in vitro and in vivo.

Upregulation of indoleamine 2,3-dioxygenase in hepatitis C virus infection.

Indoleamine 2,3-dioxygenase (IDO) is induced by proinflammatory cytokines and by CTLA-4-expressing T cells and constitutes an important mediator of peripheral immune tolerance. In chronic hepatitis C, we found upregulation of IDO expression in the liver and an increased serum kynurenine/tryptophan ratio (a reflection of IDO activity). Huh7 cells supporting hepatitis C virus (HCV) replication expressed higher levels of IDO mRNA than noninfected cells when stimulated with gamma interferon or when cocultured with activated T cells.

[New therapies for hepatitis C].

Hepatitis C virus is an important public health threat, not only because of the high prevalence of this infection in western and third world countries, but also because of the high rate of resistance to the available antiviral therapy that consists on the use of pegylated interferon plus ribavirin. Currently, new forms of therapy are being developed based on a more precise knowledge of the structure and function of the viral proteins and of the strategies used by the virus to escape the immune and interferon systems. The new therapeutic approaches aim at different objectives: a) the inhibition of viral replication by blocking the viral protease and/or replicase; b) the use of other types of interferon with more potent antiviral effect, c) the induction of a specific anti-viral immune response by means of immunomodulatory compounds or therapeutic vaccination, d) the blockade of "de novo" infection of other cells with neutralizing antibodies, e) the induction of a antiviral state in the liver by transferring to this organ the gene of interferon and/or immunostimulating cytokines.