<?xml version="1.0" encoding="UTF-8"?><xml><records><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Campisciano, Giuseppina</style></author><author><style face="normal" font="default" size="100%">Cason, Carolina</style></author><author><style face="normal" font="default" size="100%">Palmisano, Silvia</style></author><author><style face="normal" font="default" size="100%">Giuricin, Michela</style></author><author><style face="normal" font="default" size="100%">Rizzardi, Alessia</style></author><author><style face="normal" font="default" size="100%">Croce, Lory Saveria</style></author><author><style face="normal" font="default" size="100%">De Manzini, Nicolo</style></author><author><style face="normal" font="default" size="100%">Comar, Manola</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Bariatric surgery drives major rearrangements of the intestinal microbiota including the biofilm composition.</style></title><secondary-title><style face="normal" font="default" size="100%">Front Biosci (Elite Ed)</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Front Biosci (Elite Ed)</style></alt-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Biofilms</style></keyword><keyword><style  face="normal" font="default" size="100%">Case-Control Studies</style></keyword><keyword><style  face="normal" font="default" size="100%">Gastric Bypass</style></keyword><keyword><style  face="normal" font="default" size="100%">Gastrointestinal Microbiome</style></keyword><keyword><style  face="normal" font="default" size="100%">Humans</style></keyword><keyword><style  face="normal" font="default" size="100%">Intestinal Mucosa</style></keyword><keyword><style  face="normal" font="default" size="100%">Obesity</style></keyword><keyword><style  face="normal" font="default" size="100%">Prospective Studies</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2018</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2018 06 01</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">10</style></volume><pages><style face="normal" font="default" size="100%">495-505</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;The intestinal microbiota disequilibrium has been associated with obesity, while the role of the gut mucosal biofilms in this pathology is still unknown. We analysed the changes in the intestinal microbiota of obese patients after bariatric surgery with the aim of disclosing the rearrangement of the biofilm configuration. Although the bariatric surgery drives major rearrangements of the gut microbiota, obese patients maintain the  enterotype before and after surgery, as shown by normal weight patients, with an increase of  and . The  enterotype guarantees the strong ability to form a biofilm which allows a more efficient digestion of polysaccharides than planktonic communities and leads to the production of acetate which is a key player to inhibit enteropathogens. Additionally, the laparoscopic gastric bypass induces an increase of , a facultative anaerobic bacterium involved in intestinal and inflammatory disorders. Bariatric surgery influences the microbial composition of gut biofilm. Further studies are needed to elucidate the impact of this variation on recovery after surgery and on weight loss.&lt;/p&gt;</style></abstract><custom1><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/29772522?dopt=Abstract</style></custom1></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Tricarico, Paola Maura</style></author><author><style face="normal" font="default" size="100%">Kleiner, Giulio</style></author><author><style face="normal" font="default" size="100%">Valencic, Erica</style></author><author><style face="normal" font="default" size="100%">Campisciano, Giuseppina</style></author><author><style face="normal" font="default" size="100%">Girardelli, Martina</style></author><author><style face="normal" font="default" size="100%">Crovella, Sergio</style></author><author><style face="normal" font="default" size="100%">Knowles, Alessandra</style></author><author><style face="normal" font="default" size="100%">Marcuzzi, Annalisa</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Block of the mevalonate pathway triggers oxidative and inflammatory molecular mechanisms modulated by exogenous isoprenoid compounds.</style></title><secondary-title><style face="normal" font="default" size="100%">Int J Mol Sci</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Int J Mol Sci</style></alt-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Animals</style></keyword><keyword><style  face="normal" font="default" size="100%">Apoptosis</style></keyword><keyword><style  face="normal" font="default" size="100%">Carotenoids</style></keyword><keyword><style  face="normal" font="default" size="100%">Carrier Proteins</style></keyword><keyword><style  face="normal" font="default" size="100%">Cell Line</style></keyword><keyword><style  face="normal" font="default" size="100%">Cytokines</style></keyword><keyword><style  face="normal" font="default" size="100%">Diterpenes</style></keyword><keyword><style  face="normal" font="default" size="100%">Humans</style></keyword><keyword><style  face="normal" font="default" size="100%">Mevalonate Kinase Deficiency</style></keyword><keyword><style  face="normal" font="default" size="100%">Mevalonic Acid</style></keyword><keyword><style  face="normal" font="default" size="100%">Mice</style></keyword><keyword><style  face="normal" font="default" size="100%">Mitochondria</style></keyword><keyword><style  face="normal" font="default" size="100%">Nitric Oxide</style></keyword><keyword><style  face="normal" font="default" size="100%">Phytol</style></keyword><keyword><style  face="normal" font="default" size="100%">Terpenes</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2014</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2014</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">15</style></volume><pages><style face="normal" font="default" size="100%">6843-56</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;Deregulation of the mevalonate pathway is known to be involved in a number of diseases that exhibit a systemic inflammatory phenotype and often neurological involvements, as seen in patients suffering from a rare disease called mevalonate kinase deficiency (MKD). One of the molecular mechanisms underlying this pathology could depend on the shortage of isoprenoid compounds and the subsequent mitochondrial damage, leading to oxidative stress and pro-inflammatory cytokines' release. Moreover, it has been demonstrated that cellular death results from the balance between apoptosis and pyroptosis, both driven by mitochondrial damage and the molecular platform inflammasome. In order to rescue the deregulated pathway and decrease inflammatory markers, exogenous isoprenoid compounds were administered to a biochemical model of MKD obtained treating a murine monocytic cell line with a compound able to block the mevalonate pathway, plus an inflammatory stimulus. Our results show that isoprenoids acted in different ways, mainly increasing the expression of the evaluated markers [apoptosis, mitochondrial dysfunction, nucleotide-binding oligomerization-domain protein-like receptors 3 (NALP3), cytokines and nitric oxide (NO)]. Our findings confirm the hypothesis that inflammation is triggered, at least partially, by the shortage of isoprenoids. Moreover, although further studies are necessary, the achieved results suggest a possible role for exogenous isoprenoids in the treatment of MKD.&lt;/p&gt;</style></abstract><issue><style face="normal" font="default" size="100%">4</style></issue><custom1><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/24758928?dopt=Abstract</style></custom1></record></records></xml>