Guglielmina Chimienti
University of Bari
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Featured researches published by Guglielmina Chimienti.
Nutrition Research | 2012
Francesco Russo; Michele Linsalata; Caterina Clemente; Marisa Chiloiro; Antonella Orlando; Emanuele Marconi; Guglielmina Chimienti; Giuseppe Riezzo
Apart from the intestinal environment, inulin induces physiological effects, which includes a reduction in glucose and lipid concentrations and modulation of gastrointestinal motility through the release of different peptides. We hypothesized that inulin-enriched pasta may also improve small intestine permeability in relation to zonulin and glucagon-like peptide 2 (GLP-2) levels in healthy young subjects. Twenty healthy, young male volunteers completed a randomized, double-blind crossover study consisting of a 2-week run-in period and two 5-week study periods (11% inulin-enriched or control pasta), with an 8-week washout period in between. The intestinal barrier function was assessed by lactulose-mannitol excretion in urine. Zonulin values and GLP-2 release were evaluated by enzyme-linked immunosorbent assay. In the inulin group, the urinary lactulose recovery was significantly lower than the other 2 groups. There were no significant differences in urinary mannitol levels between groups. Accordingly, the lactulose-mannitol excretion ratio was significantly decreased in the inulin-enriched pasta group compared with the other 2 groups. The inulin-enriched pasta group had significantly lower zonulin serum values and significantly higher GLP-2 basal values when compared with the baseline and control pasta groups. The dietary use of inulin-enriched pasta preserves intestinal mucosal barrier functioning and modulates circulating levels of zonulin and GLP-2, suggesting that prebiotics could be used in the prevention of gastrointestinal diseases and metabolic disorders.
Scandinavian Journal of Gastroenterology | 2013
Francesco Russo; Guglielmina Chimienti; Caterina Clemente; Benedetta D’Attoma; Michele Linsalata; Antonella Orlando; Massimo De Carne; Filomena Cariola; Francesco P. Semeraro; Gabriella Pepe; Giuseppe Riezzo
Abstract Objective. The role of adipokines such as resistin, leptin, and adiponectin could be pivotal in the molecular crosstalk between the inflamed intestine and the surrounding mesenteric adipose tissue. Our aims were to a) evaluate their circulating concentrations in patients with active celiac disease (ACD) and compare them to those in patients with diarrhea-predominant irritable bowel syndrome (IBS-d) and healthy subjects; b) establish the impact of genetic variability in resistin; and c) evaluate whether a 1-year gluten-free diet (GFD) modifies circulating concentrations of resistin, leptin, and adiponectin in celiac patients. Material and methods. The study included 34 ACD patients, 29 IBS-d patients, and 27 healthy controls. Circulating concentrations of resistin, leptin, adiponectin, IL-6, and IL-8 were evaluated at the time of enrollment. Resistin +299 G/A polymorphism was also analysed. In CD patients, biochemical measurements were repeated after a 1-year GFD. Results. Along with higher IL-6 and IL-8 plasma levels, higher resistin and adiponectin concentrations were found in ACD and IBS-d patients compared with controls (p: 0.0351 and p: 0.0020, respectively). Resistin values proved to be predictable from a linear combination of IL-8 and +299 polymorphism. GFD affected resistin (p: 0.0009), but not leptin and adiponectin concentrations. Conclusions. Our data suggest that these adipokines are involved in modulating inflammatory processes in both CD and IBS-d patients. Alterations in the adipokine profile as well as the higher prevalence of the resistin +299 G/A SNP A allele compared to controls support the hypothesis that, at least in well-defined cases of IBS, a genetic component may also be supposed.
Biochemical and Biophysical Research Communications | 1992
Guglielmina Chimienti; Antonio Capurso; Francesco Resta; Gabriella Pepe
We describe a new case of lipoprotein lipase deficiency in a proband from a Southern-Italian family. Enzyme activity and mass were absent. Amplification and sequencing of individual exons, intron boundaries and the regulatory region revealed only one homozygous G----C transversion at the first nucleotide of intron 1. The single strand conformation polymorphism analysis proved to be a helpful tool for the identification of the single base mutation. Northern hybridization failed to reveal the presence of mature lipoprotein lipase mRNA. The mutation, which destroys the conserved dinucleotide at the junction site of intron 1, causes defective mRNA splicing and it is responsible for the deficiency.
Applied Microbiology and Biotechnology | 2016
Guglielmina Chimienti; Roberta Piredda; Gabriella Pepe; Inez Dorothé van der Werf; Luigia Sabbatini; Carmine Crecchio; Patrizia Ricciuti; Anna Maria D’Erchia; Caterina Manzari
Comprehensive studies of the biodiversity of the microbial epilithic community on monuments may provide critical insights for clarifying factors involved in the colonization processes. We carried out a high-throughput investigation of the communities colonizing the medieval church of San Leonardo di Siponto (Italy) by Illumina-based deep sequencing. The metagenomic analysis of sequences revealed the presence of Archaea, Bacteria, and Eukarya. Bacteria were Actinobacteria, Proteobacteria, Bacteroidetes, Cyanobacteria, Chloroflexi, Firmicutes and Candidatus Saccharibacteria. The predominant phylum was Actinobacteria, with the orders Actynomycetales and Rubrobacteriales, represented by the genera Pseudokineococcus, Sporichthya, Blastococcus, Arthrobacter, Geodermatophilus, Friedmanniella, Modestobacter, and Rubrobacter, respectively. Cyanobacteria sequences showing strong similarity with an uncultured bacterium sequence were identified. The presence of the green algae Oocystaceae and Trebuxiaceae was revealed. The microbial diversity was explored at qualitative and quantitative levels, evaluating the richness (the number of operational taxonomic units (OTUs)) and the abundance of reads associated with each OTU. The rarefaction curves approached saturation, suggesting that the majority of OTUs were recovered. The results highlighted a structured community, showing low diversity, made up of extremophile organisms adapted to desiccation and UV radiation. Notably, the microbiome appeared to be composed not only of microorganisms possibly involved in biodeterioration but also of carbonatogenic bacteria, such as those belonging to the genus Arthrobacter, which could be useful in bioconservation. Our investigation demonstrated that molecular tools, and in particular the easy-to-run next-generation sequencing, are powerful to perform a microbiological diagnosis in order to plan restoration and protection strategies.
Journal of Clinical Gastroenterology | 2017
Francesco Russo; Guglielmina Chimienti; Caterina Clemente; Giuseppe Riezzo; Benedetta D'Attoma; Manuela Martulli
Goals: The goals of the study were to investigate in both postprandial distress syndrome (PDS) and epigastric pain syndrome (EPS) the gastric electrical activity and the gastric emptying (GE) time together with the circulating concentrations of motilin, somatostatin, corticotrophin-releasing factor, and neurotensin, and to establish whether the genetic variability in the neurotensin system genes differs between these 2 categories of functional dyspepsia (FD). Background: The current FD classification is based on symptoms and it has been proven not to be completely satisfying because of a high degree of symptom overlap between subgroups. Study: Gastric electrical activity was evaluated by cutaneous electrogastrography: the GE time by 13C-octanoic acid breast test. Circulating concentrations of gut peptides were measured by a radioimmunoassay. NTS 479 A/G and NTSR1 rs6090453 SNPs were evaluated by PCR and endonuclease digestion. Results: Fifty-four FD patients (50 female/4 male) were studied. Using a symptom questionnaire, 42 patients were classified as PDS and 12 as EPS, although an overlap between the symptom profiles of the 2 subgroups was recorded. The electrogastrographic parameters (the postprandial instability coefficient of dominant frequency, the dominant power, and the power ratio) were significantly different between the subgroups, whereas the GE time did not differ significantly. In addition, EPS was characterized by a different gut peptide profile compared with PDS. Finally, neurotensin polymorphism was shown to be associated with neurotensin levels. This evidence deserves further studies in consideration of an analgesic role of neurotensin. Conclusions: Analysis of gut peptide profiles could represent an interesting tool to enhance FD diagnosis and overcome limitations due to a distinction based solely on symptoms.
European Journal of Gastroenterology & Hepatology | 2017
Francesco Russo; Guglielmina Chimienti; Michele Linsalata; Caterina Clemente; Antonella Orlando; Giuseppe Riezzo
Background Ghrelin levels and obestatin/ghrelin ratio have been proposed as activity markers in ulcerative colitis, but no data are available in celiac disease (CD) and irritable bowel syndrome (IBS). Our aims were as follows: (a) to assess obestatin and ghrelin concentrations in adult active CD patients, diarrhea-predominant IBS (IBS-d), and healthy controls (HC) in relation to intestinal permeability; (b) to evaluate the ghrelin–obestatin profile in CD patients after a 1-year gluten-free diet (GFD); and (c) to establish the impact of ghrelin genetics. Methods The study included 31 CD patients, 28 IBS-d patients, and 19 HC. Intestinal permeability, assayed by high-performance liquid chromatography determination of urinary lactulose (La)/mannitol (Ma), and circulating concentrations of obestatin, ghrelin, and their ratio were evaluated at enrollment and after GFD. The ghrelin single nucleotide polymorphisms Arg51Gln (rs34911341), Leu72Met (rs696217), and Gln90Leu (rs4684677) were analyzed. Results Intestinal permeability was impaired in CD patients and ameliorated after GFD. Ghrelin was significantly (P=0.048) higher and the obestatin/ghrelin ratio was significantly (P=0.034) lower in CD patients compared with both IBS-d and HC, and GFD reduced the peptide levels, but without reaching the concentrations in HC. Significant differences (P<0.05) were found in the Leu72Met polymorphism among groups, with the reduction of the GT genotype and the T allele in both CD and IBS-d patients compared with HC. Conclusion Intestinal permeability is altered in CD, but not in IBS-d patients, and ghrelin levels increase in CD patients as observed in other inflammatory conditions. Moreover, a role for ghrelin genetics is hypothesized in sustaining the many pathogenetic components of these different pathologies, but with a similar symptom profile.
Journal of Neuroinflammation | 2014
Anna Mezzapesa; Cyrille Orset; Laurent Plawinski; Loïc Doeuvre; Sara Martinez de Lizarrondo; Guglielmina Chimienti; Denis Vivien; Alexandre Mansour; Sabrina Matà; Gabriella Pepe; Eduardo Anglés-Cano
BackgroundPlasminogen activation is a ubiquitous source of fibrinolytic and proteolytic activity. Besides its role in prevention of thrombosis, plasminogen is involved in inflammatory reactions in the central nervous system. Plasminogen has been detected in the cerebrospinal fluid (CSF) of patients with inflammatory diseases; however, its origin remains controversial, as the blood-CSF barrier may restrict its diffusion from blood.MethodsWe investigated the origin of plasminogen in CSF using Alexa Fluor 488-labelled rat plasminogen injected into rats with systemic inflammation and blood-CSF barrier dysfunction provoked by lipopolysaccharide (LPS). Near-infrared fluorescence imaging and immunohistochemistry fluorescence microscopy were used to identify plasminogen in brain structures, its concentration and functionality were determined by Western blotting and a chromogenic substrate assay, respectively. In parallel, plasminogen was investigated in CSF from patients with Guillain-Barré syndrome (n = 15), multiple sclerosis (n = 19) and noninflammatory neurological diseases (n = 8).ResultsEndogenous rat plasminogen was detected in higher amounts in the CSF and urine of LPS-treated animals as compared to controls. In LPS-primed rats, circulating Alexa Fluor 488-labelled rat plasminogen was abundantly localized in the choroid plexus, CSF and urine. Plasminogen in human CSF was higher in Guillain-Barré syndrome (median = 1.28 ng/μl (interquartile range (IQR) = 0.66 to 1.59)) as compared to multiple sclerosis (median = 0.3 ng/μl (IQR = 0.16 to 0.61)) and to noninflammatory neurological diseases (median = 0.27 ng/μl (IQR = 0.18 to 0.35)).ConclusionsOur findings demonstrate that plasminogen is transported from circulating blood into the CSF of rats via the choroid plexus during inflammation. Our data suggest that a similar mechanism may explain the high CSF concentrations of plasminogen detected in patients with inflammation-derived CSF barrier impairment.
BioMed Research International | 2017
Giuseppe Riezzo; Guglielmina Chimienti; Caterina Clemente; Benedetta D’Attoma; Antonella Orlando; Caterina Mammone Rinaldi; Francesco Russo
Purpose To investigate whether pathophysiological differences exist among healthy controls (HC) and patients with slow and normal transit constipation (STC and NTC), we evaluated (1) gastrointestinal (GI) symptoms using validated questionnaires; (2) circulating concentrations of neurotensin, motilin, corticotrophin-releasing factor (CRF), and somatostatin; and (3) possible differences in frequency distribution of the neurotensin rs1800832 A/G and Neurotensin Receptor 1 rs6090453 C/G SNPs. Methods Fifty-one patients with severe functional constipation and 20 HC completed the study. Symptoms were evaluated by GSRS and Constipaq scoring system. Plasma concentrations of GI peptides were evaluated by ELISA on fasting and six sequential blood samples after a standard meal. Genotyping was performed by PCR and endonuclease digestion. Results Symptom profiles largely overlapped between NTC and STC patients. As for peptide profiles, neurotensin showed lower concentrations at 60 and 90 min in STC versus HC, and motilin showed throughout the curve 85% and 82% lower levels in STC than HC and NTC, respectively. Finally, neurotensin polymorphism resulted in being associated with the peptide levels. Conclusions Symptom profile is not a reliable tool to discriminate STC, whilst the GI peptide profiles might help in identifying it.
Materials Science and Engineering: C | 2018
Paola Semeraro; Guglielmina Chimienti; Emiliano Altamura; P. Fini; Vito Rizzi; Pinalysa Cosma
Chlorophyll a (Chl a), an amphipathic porphyrin, was employed as natural photosensitizer for photodynamic therapy applications. Due to its lacking solubility in water and high tendency to aggregate, Chl a was included into different modified cyclodextrins (CDs) to form stable water-soluble supramolecular complexes. To achieve this aim, 2-Hydroxypropyl-β-cyclodextrin (2-HP-β-CD), 2-Hydroxypropyl-γ-cyclodextrin (2-HP-γ-CD), Heptakis(2,6-di-o-methyl)-β-cyclodextrin (DIMEB) and Heptakis(2,3,6-tri-o-methyl)-β-cyclodextrin (TRIMEB) were used. The chemical physical properties of Chl a/CD complexes in cellular medium were studied by means of UV-Vis absorption spectroscopy. Results demonstrated the good aptitude of 2-HP-γ-CD, and more particularly of 2-HP-β-CD, to solubilize the Chl a in cell culture medium in monomeric and photoactive form. Then, Chl a/2-HP-β-CD and Chl a/2-HP-γ-CD complexes were evaluated in vitro on human colorectal adenocarcinoma HT-29 cell line, and cytotoxicity and intracellular localization were respectively assessed. Further tests, such as phototoxicity, ROS generation, intracellular localization and mechanism of cell death were then focused exclusively on Chl a/2-HP-β-CD system. This complex exhibited no dark toxicity and a high phototoxicity toward HT-29 cells inducing cell death via necrotic mechanism. Therefore, it is possible to affirm that Chl a/2-HP-β-CD supramolecular complex could be a promising and potential formulation for applications in photodynamic therapy.
Free Radical Biology and Medicine | 2018
Guglielmina Chimienti; Anna Picca; Giuseppe Sirago; Flavio Fracasso; Riccardo Calvani; Roberto Bernabei; Francesco Russo; Christy S. Carter; Christiaan Leeuwenburgh; Vito Pesce; Emanuele Marzetti; Angela Maria Serena Lezza
Abstract The well‐known age‐related mitochondrial dysfunction deeply affects heart because of the tissues large dependence on mitochondrial ATP provision. Our study revealed in aged rat heart a significant 25% decrease in mtDNA relative content, a significant 29% increase in the 4.8 Kb mtDNA deletion relative content, and a significant inverse correlation between such contents as well as a significant 38% decrease in TFAM protein amount. The TFAM‐binding activity to specific mtDNA regions increased at those encompassing the mtDNA replication origins, D‐loop and Ori‐L. The same mtDNA regions were screened for different kinds of oxidative damage, namely Single Strand Breaks (SSBs), Double Strand Breaks (DSBs), abasic sites (AP sites) and oxidized bases as 7,8‐dihydro‐8‐oxoguanine (8oxoG). A marked increase in the relative content of mtDNA strand damage (SSBs, DSBs and AP sites) was found in the D‐loop and Ori‐L regions in the aged animals, unveiling for the first time in vivo an age‐related, non‐stochastic accumulation of oxidative lesions in these two regions that appear as hot spots of mtDNA damage. The use of Formamidopyrimidine glycosylase (Fpg) demonstrated also a significant age‐related accumulation of oxidized purines particularly in the D‐loop and Ori‐L regions. The detected increased binding of TFAM to the mtDNA damage hot spots in aged heart suggests a link between TFAM binding to mtDNA and loss of mitochondrial genome likely through hindrance of repair processes. Graphical abstract Figure. No Caption available. HighlightsMitochondrial dysfunction in aged heart involves a 25% decrease in mtDNA content.A 29% increase in 4.8 Kb mtDNA deletion and a 38% decrease in TFAM are age‐related.With aging TFAM‐binding increases at mtDNA replication origins, D‐loop and Ori‐L.In vivo mtDNA D‐loop and Ori‐L are hot spots of age‐related oxidative damage.TFAM‐binding might be linked to mtDNA loss through hindrance of repair processes.