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. It also examines the prevalence of this type of anorexia, its associated comorbidities and mortality rates. We have reviewed 27 studies, with a total of 6208 patients. These reported changes in the secretion and response of both central and peripheral hormones that regulate appetite. Anorexia, very prevalent among hospitalized and institutionalized elderly people, is associated with comorbidity and represents a predictive factor for mortality. No treatment for it has been proved to be effective. The mechanism regulating ingestion in elderly people is complex and difficult to resolve. Comorbidity as a cause or a consequence of anorexia of ageing has become a research field of great interest in geriatrics. A correct nutritional evaluation is a fundamental part of an integrated geriatric assessment.     

The Smartphone in Medicine: A Review of Current and Potential Use Among Physicians and Students

Background

Advancements in technology have always had major impacts in medicine. The smartphone is one of the most ubiquitous and dynamic trends in communication, in which one’s mobile phone can also be used for communicating via email, performing Internet searches, and using specific applications. The smartphone is one of the fastest growing sectors in the technology industry, and its impact in medicine has already been significant.

Objective

To provide a comprehensive and up-to-date summary of the role of the smartphone in medicine by highlighting the ways in which it can enhance continuing medical education, patient care, and communication. We also examine the evidence base for this technology.

Methods

We conducted a review of all published uses of the smartphone that could be applicable to the field of medicine and medical education with the exclusion of only surgical-related uses.

Results

In the 60 studies that were identified, we found many uses for the smartphone in medicine; however, we also found that very few high-quality studies exist to help us understand how best to use this technology.

Conclusions

While the smartphone’s role in medicine and education appears promising and exciting, more high-quality studies are needed to better understand the role it will have in this field. We recommend popular smartphone applications for physicians that are lacking in evidence and discuss future studies to support their use.     

Physicians, historians, and the history of medicine.

For American medical historiography, to borrow from Dickens, these are the best of times and the worst of times. These are the times when rigorous scholarship has been brought to bear on the field (with great improvement in the quality of research) and when medicine is disappearing from its own history. These are the times when, in general, historians know only their field of specialization and physicians know only how to treat diseases. These are the times of focused competence and general ignorance. The history of medicine has become a field where historians write for other historians who, limited by their ignorance of medicine, cultivate mainly its sociological and political aspects. Physicians, on the other hand, are taught that only what is 'relevant' counts, and practise medicine in ignorance of their past because the history of medicine does not seem to have any immediate utility (1). The few among them who attempt to do something in what is, after all, the history of their profession, are often considered, by historians, naive dabblers who lack knowledge and capacity for the task. This state of affairs came to be fairly recently. It began with a positive development in medical historiography: the realization that the history of medicine was not a discipline that helped to treat diseases but the history of one of man's endeavours, in other words, that it was not a branch of medicine but of history.     

Physiopathology of natural auto-antibodies: The case for regulation

The cause of autoimmune diseases remains unknown and, as a consequence, disease prediction and prophylaxis are not part of current clinical practice. Many autoimmune syndromes are accompanied by serological evidence of autoimmunity in the form of circulating auto-antibodies (AAb). As normal individuals produce large amounts of AAb, exploring the main differences between such physiologic AAb and those classified as pathogenic may provide the clues needed for new clinical approaches to this group of disorders. Reviewing the differential characteristics of normal and disease-associated autoantibodies, we conclude that the problem will be best tackled if we understand how the organism normally ensures that autoantigen-driven B cell activation does not lead to high titers of autoantibodies and severe autoimmunity. As natural activation of autoreactive B cells occur by both T cell dependent and T cell independent mechanisms, we argue that absence of clonal expansion in normal autoreactive B cells upon activation does not result from lack of appropriate stimulation but, rather, from the presence of negative regulation and suppressive mechanisms.     

Physiopathology and molecular diagnosis for prion diseases

Prion diseases, including Creutzfeldt-Jakob disease (CJD), are infectious neurodegenerative disorders. The etiological agent, prion, is postulated to consist mainly of a proteinase K-resistant isoform of prion protein (PrPSc) which is generated by post-translational conversion from the proteinase K-sensitive normal version (PrPC) physiologically expressed on the surface of neuronal and glial cells. The constitutive conversion results in the tremendous accumulation of PrPSc in the prion-infected brain. Homozygous disruption of the Prnp gene encoding PrPC renders mice resistant to prion, and the animals are no longer capable of generating PrPSc, indicating an essential role for PrPSc in the pathogenesis of prion diseases. The PrP-null mice (Ngsk Prnp0/0) revealed progressive ataxia due to the degeneration of cellebellar Purkinje cells at old ages. Successful rescue of Ngsk Prnp0/0 mice from neurodegeneration by a transgene encoding the normal mouse PrPC has indicated that the functional loss of PrPC is essential for this phenotype. Moreover, we detected aberrant mRNAs chimeric between Prnp exon 1-2 and a novel gene encoding PrP-like protein (PrPLP). These results suggested that, in addition to the functional loss of PrPC, ectopic expression of the PrPLP in the brain of Ngsk Prnp0/0 mice could be associated with Purkinje cell degeneration.