ABSTRACT After a century after the discovery of penicillin, the indiscriminate use of antibiotics in human and animal health has favored the emergence and spread of microbial resistance, thereby generating "superbugs" capable of resisting antibiotics. In this article, the origin of antibiotics, the concepts of superbugs and the generation of antimicrobial resistance (AMR), as well as the genomic analysis of antimicrobial resistance, as a new bioinformatics tool for its identification, will be addressed in a simple way.

RESUMEN A casi un siglo del descubrimiento de la penicilina, el uso indiscriminado de los antibióticos en la salud humana y animal, ha favorecido la aparición y propagación de la resistencia microbiana, generando con ello las “súper-bacterias”, capaces de resistir a los antibióticos. En este artículo se abordará de una manera sencilla el origen de los antibióticos, los conceptos de súper-bacterias y la generación de la resistencia antimicrobiana (AMR), así como el análisis genómico de la resistencia antimicrobiana, como una nueva herramienta bioinformática para su identificación.

Diabetes mellitus represents a serious public health problem owing to its global prevalence in the last decade. The causes of this metabolic disease include dysfunction and/or insufficient number of β cells. Existing diabetes mellitus treatments do not reverse or control the disease. Therefore, β-cell mass restoration might be a promising treatment. Several restoration approaches have been developed: inducing the proliferation of remaining insulin-producing cells, de novo islet formation from pancreatic progenitor cells (neogenesis), and converting non-β cells within the pancreas to β cells (transdifferentiation) are the most direct, simple, and least invasive ways to increase β-cell mass. However, their clinical significance is yet to be determined. Hypothetically, β cells or islet transplantation methods might be curative strategies for diabetes mellitus; however, the scarcity of donors limits the clinical application of these approaches. Thus, alternative cell sources for β-cell replacement could include embryonic stem cells, induced pluripotent stem cells, and mesenchymal stem cells. However, most differentiated cells obtained using these techniques are functionally immature and show poor glucose-stimulated insulin secretion compared with native β cells. Currently, their clinical use is still hampered by ethical issues and the risk of tumor development post transplantation. In this review, we briefly summarize the current knowledge of mouse pancreas organogenesis, morphogenesis, and maturation, including the molecular mechanisms involved. We then discuss two possible approaches of β-cell mass restoration for diabetes mellitus therapy: β-cell regeneration and β-cell replacement. We critically analyze each strategy with respect to the accessibility of the cells, potential risk to patients, and possible clinical outcomes.