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Gut microbiota play a critical role in the development of metabolic diseases such as non-alcoholic fatty liver disease (NAFLD), which is a critical public health issue worldwide. This mini review provides new insights in the association between gut microbiota and liver disease, in order to gain better grasp of microbiota-related metabolic pathways and try to establish the key microbes that are implicated in NAFLD progression. It gives better knowledge to understand a possible cause of this disease and to be closer on the development of new diagnosis and therapies.

The aim of the study was to analyse the presence of several metabolites related to atherosclerosis in the plasma of patients with unstable carotid plaque and in the plasma of healthy subjects. Materials and methods We included 20 patients who had undergone carotid endarterectomy and 20 healthy subjects as a control group. All the subjects recruited were male. We used a metabolomic approach with liquid chromatography coupled to mass spectrometry to evaluate plasma metabolite levels in the metabolic pathway involved in the progression of atherosclerotic plaque. Results We observed that circulating levels of 20-HETE were significantly higher in patients with atheroma plaque than in healthy subjects (p = 0.018). No differences were found with regard to the other metabolites analysed. We also conducted a random forest analysis and found that 20-HETE was the main differentiator in the list of selected metabolites. In addition, plasma levels of 20-HETE correlated positively with body mass index (r = 0.427, p = 0.007) and diastolic blood pressure (r = 0.365, p = 0.028). Conclusion This study confirms that of all the molecules studied only 20-HETE is related to carotid plaque. Further studies are needed to compare patients with stable carotid plaque vs. patients with unstable carotid plaque in order to confirm that 20-HETE could be a potential factor related to carotid plaque.

Cryptococcosis is a major fungal disease caused by members of the Cryptococcus gattii and Cryptococcus neoformans species complexes. After more than 15 years of molecular genetic and phenotypic studies and much debate, a proposal for a taxonomic revision was made. The two varieties within C. neoformans were raised to species level, and the same was done for five genotypes within C. gattii. In a recent perspective (K. J. Kwon-Chung et al., mSphere 2:e00357-16, 2017, https://doi.org/10.1128/mSphere.00357-16), it was argued that this taxonomic proposal was premature and without consensus in the community. Although the authors of the perspective recognized the existence of genetic diversity, they preferred the use of the informal nomenclature "C. neoformans species complex" and "C. gattii species complex." Here we highlight the advantage of recognizing these seven species, as ignoring these species will impede deciphering further biologically and clinically relevant differences between them, which may in turn delay future clinical advances.

© 2017 Hagen et al. Cryptococcosis is a major fungal disease caused by members of the Cryptococcus gattii and Cryptococcus neoformans species complexes. After more than 15 years of molecular genetic and phenotypic studies and much debate, a proposal for a taxonomic revision was made. The two varieties within C. neoformans were raised to species level, and the same was done for five genotypes within C. gattii. In a recent perspective (K. J. Kwon-Chung et al., mSphere 2:e00357-16, 2017, https://doi .org/10.1128/mSphere.00357-16), it was argued that this taxonomic proposal was premature and without consensus in the community. Although the authors of the perspective recognized the existence of genetic diversity, they preferred the use of the informal nomenclature C. neoformans species complex and C. gattii species complex. Here we highlight the advantage of recognizing these seven species, as ignoring these species will impede deciphering further biologically and clinically relevant differences between them, which may in turn delay future clinical advances.

Familial hypercholesterolemia (FH) is the best known monogenic disorder from the fat metabolism. This disease is characterized by xanthomas , increased serum levels of cLDL and premature cardiovascular disease. We carry out the genetical diagnosis from the DNA study, from selected patients who present clinical symptomps for FH in Mallorca Island. Thanks to molecular tecnics applied to this study we can have unequivocal results in those patients, we are able to start a treatment as soon as posible in order to delay the complications from this illness such as atherosclerosis. The objetives we persue are: study prevalence of mutaciones on coronary LRDR gene, on those patients with clinical criteria for FH in Mallorca population. To know the typus and characteristic from the different mutations of gen LRDR resulting on FH. Detect the effects on the different mutations. To study the frecuency of clinical symptoms (xanthomas tendinosos, arco corneal, xanthelasma, Achilles tendinitis , Hypertension and DM) in order to start correct and early treatment on patients with FH. We collect 212 cases with clinical criteria for FH, 65 cases (CI) were selected by Med Ped holandes for FH. 23% develop premature cardiovascular disease. Those results compared to the rest of the mainland were smaller. First complication was ischaemic heart disease, twice in number on males and middle age population. Coronary disease (17%) was first followed by brain disease (4.6%). We found 24 mutations, 4 of them were new finding on this study. We found that HF prevalence is 1/474 and HF by genetical diagnosis is 1/780. Resulting from this study we have realized a proposal for the diagnosis for FH., La hipercolesterolemia familiar (HF) es la enfermedad monogénica del metabolismo lipídico mejor conocida. La enfermedad se caracteriza por la presencia de xantomas, elevados niveles plasmáticos de cLDL y cardiopatía isquémica prematura debida al desarrollo de arteriosclerosis coronaria. En este trabajo realizamos el diagnóstico genético, a través de estudio del DNA, de los pacientes que presentaban características clínicas de HF de la Isla de Mallorca. La aplicación de las técnicas de biología molecular al estudio de la HF permite realizar un diagnóstico inequívoco en estos pacientes, iniciar un tratamiento precoz para intentar evitar las complicaciones ateroscleróticas de la enfermedad. Los objetivos que se plantean son: estudiar la prevalencia de mutaciones en el gen del LDLR, en los pacientes con criterios clínicos de HF en la población de Mallorca. Conocer el tipo y características de las distintas mutaciones en el gen LDLR responsables de HF en la Isla. Evaluar la repercusión de las distintas mutaciones. Conocer la frecuencia de manifestaciones clínicas (xantomas tendinosos, arco corneal, xantelasmas, tendinitis aquilea, HTA y DM) y conseguir el tratamiento adecuado y precoz de los individuos con HF. De la población de Mallorca se recogieron 212 casos con criterios clínicos de HF, de éstos se seleccionaron 65 casos índices (CI) que cumplían los criterios del MedPed holandés para HF. Un 23% presentaron enfermedad cardiovascular prematura (ECVP) ( 11 varones y 3 mujeres) resultados inferiores a los descritos en otras provincias españolas. La primera manifestación fue la cardiopatía isquémica (CI) que fue el doble en varones y más frecuente en las edades medias de la vida. El territorio más afectado fue el conorario (17%) seguido del cerebral (4,6%). Se han encontrado 24 mutaciones y de éstas 4 han sido descritas por primera vez en este trabajo. Del mismo, se deduce una prevalencia de HF clínica de 1/474 y de HF con diagnostico genético de 1/780. De este estudio h