F Rosina

Presidio Sanitario San Camillo, Torino, Torino, Piedmont, Italy

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Publications (186)956.04 Total impact

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    ABSTRACT: MicroRNAs (miRNAs), a class of small non-coding RNAs, are fundamental for the post-transcriptional regulation of gene expression. Altered expression of miRNAs has been detected in cancers, not only in primary tissue but also in easily obtainable specimens like plasma and stools. miRNA expression is known to be modulated by diet (micro and macronutrients, phytochemicals) and possibly by other lifestyle factors; however, such influence has not yet been exhaustively explored in humans. In the present study, we analysed the expression levels of a panel of seven human miRNAs in plasma and stool samples of a group of 24 healthy individuals characterised by different dietary habits (eight vegans, eight vegetarians and eight subjects with omnivorous diet, all groups with similar age and sex distribution). The dual aim of the study was to identify possible differences in miRNA expression due to diet (or other lifestyle factors recorded from questionnaires) and to compare results in both types of specimens. miR-92a was differentially expressed in both plasma and stool samples and with the same trend, among the three groups with different diets (P = 0.0002 and P = 0.02, respectively, with expression levels of vegans>vegetarians>omnivores). miR-92a was also associated with low body mass index (P = 0.04 and P = 0.05, respectively) in both types of specimens, and with several dietary factors. Other analysed miRNAs (miR-16, miR-21, mir-34a and miR-222) were associated with dietary and lifestyle factors, but not consistently in both stool and plasma. Our pilot study provides the first evidence of miRNA modulation by diet and other factors, that can be detected consistently in both plasma and stools samples.
    Mutagenesis 09/2014; 29(5):385-91. · 3.50 Impact Factor
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    ABSTRACT: tBackground: Data on the efficacy of Peg-interferon/ribavirin therapy for chronic hepatitis C are mostlyderived from treatment of selected patients enrolled in clinical trials. This study aimed to assess theeffectiveness of Peg-interferon/ribavirin therapy in “real world” chronic hepatitis C patients in Italy.Methods: Independent observational multicentre study including consecutive patients receiving Peg-interferon/ribavirin in the 18 months before (retrospective phase) and after (prospective phase) the startof the study.Results: 4176 patients were eligible. The final study population consisted of 2051 patients in the retro-spective and 2073 in the prospective phase.Sustained virological response was achieved by 1036 patients (50.5%) during the retrospective phase:325 were genotypes 1/4 (34.1%) and 684 were genotypes 2/3 (67.2%) and by 800 patients (38.6%) duringthe prospective phase: 300 were genotypes 1/4 (28.4%) and 473 were genotypes 2/3 (51.5%).During multivariate analysis genotypes 2/3 were significantly associated with higher sustained viro-logical response rates; cirrhosis and �-glutamil-transpeptidase >2 times the normal limit were associatedwith poorer response.Conclusions: The response to Peg-interferon/ribavirin therapy in “real world” clinical practice is distinctlylower than in registration trials. The difference in response rates was more pronounced among easy-to-treat than among difficult-to-treat hepatitis C virus genotypes.© 2014 Editrice Gastroenterologica Italiana S.r.l. Published by Elsevier Ltd. All rights reserved
    Digestive and Liver Disease 09/2014; · 2.89 Impact Factor
  • G C Actis, R Pellicano, F Rosina
    Minerva gastroenterologica e dietologica. 09/2014; 60(3):201.
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    ABSTRACT: Current knowledge on inflammatory bowel disease (IBD) is mainly endorsed by controlled trials and epidemiologic studies. Yet, we seldom look at the messages from real-world practice. Among a patient population followed since 2008, we looked at an unselected sample of 64 IBD patients [26 Crohn's disease (CD) and 38 ulcerative colitis (UC)] who had been seen as out-patients in the last year. Inducing remission, mesalamines (86% for UC/69% for CD/33%-16% as MMX formulation) prevailed as prescriptions; steroids (55%/19% for UC/CD) ranked second. Prescription of third-party drugs (antibiotics, NSAIDs, biologics) and adherence, were issues in the maintenance. 34% of CD, and 23% of UC patients showed accompanying immunologic diseases: CD-associated familiar psoriasis (4:9) ranked first. Main Message. The association between IBD (CD mainly) and psoriasis, now found in our practice, matches current basic science gathering IBD together with psoriasis (and perhaps chronic respiratory disease) under the comprehensive term "barrier organ disease" wherein an epithelial surface with sensor systems rules contacts between outer antigens and a reactive underneath tissue, with the balance between inflammation and quiescence kept at any time by mucosal permeability. IBD is thus viewed as a polyfactorial/polygenic/syndromic disorder, embedded into a galaxy of immune conditions offering multiple points of attack. This mindset of splitting the IBDs into pathogenic categories may allow overcoming the uniformly targeting of a single cytokine by biological drugs, in favor of demarcating the boundaries between different disease-subtype-specific indications, and paving the way to future personalized strategies.
    World journal of gastrointestinal pharmacology and therapeutics. 08/2014; 5(3):169-74.
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    ABSTRACT: Data on the efficacy of Peg-interferon/ribavirin therapy for chronic hepatitis C are mostly derived from treatment of selected patients enrolled in clinical trials. This study aimed to assess the effectiveness of Peg-interferon/ribavirin therapy in "real world" chronic hepatitis C patients in Italy.
    Digestive and Liver Disease 05/2014; · 2.89 Impact Factor
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    Journal of pharmacology & pharmacotherapeutics. 04/2014; 5(2):151-2.
  • Digestive and Liver Disease 03/2014; 46:S134. · 2.89 Impact Factor
  • Digestive and Liver Disease 03/2014; 46:S134. · 2.89 Impact Factor
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    ABSTRACT: Objective: To explore the type and frequency of the unwanted effects following use of non-steroidal anti-inflammatory drugs (NSAIDs) and antibiotics in a gastroenterological out-patient setting . Methods: We analyzed a gastroenterological database which includes 151 inflammatory bowel disease (IBD) patients followed between January 2008 and December 2009. The key-words included NSAIDs and antibiotics. Results: Of 19 cases treated with NSAIDs, 8 displayed convincing evidence linking them with the subsequent development of IBD. Of 44 antibiotic mentions, 7 documents alluded to macrolide prescriptions, which were followed by induction or relapse of IBD in 5; all of the newly diagnosed cases of IBD were endoscopically proven, and one ran a fulminant course requiring emergency colectomy; 4 of 5 prescriptions of amoxycillin/clavulanic acid were accompanied by toxicity (three hepatitides and one reactivated IBD). Overall, the frequency of unwanted effects was 36% for both NSAIDs and antibiotics. Conclusion: We suggest that NSAIDs and antibiotics (specifically of the macrolide structure) can induce gut and hepatic damage, significantly enhancing co-morbidities in gastroenterologic out-patients, with break of cost-containment guidelines. Therefore, caution is advisable in prescribing NSAIDs and antibiotics in this setting. Though retrospective and possibly biased, the current data coincide with both bench work and epidemiological evidence.
    Current drug safety. 01/2014; 9(2):133-7.
  • Giovanni C Actis, Floriano Rosina
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    ABSTRACT: The pathogenesis of the two inflammatory bowel diseases (IBDs) phenotypes ulcerative colitis (UC) and Crohn's disease (CD) has remained elusive, thus frustrating attempts at defining a cure. IBD often presents as a complex inflammatory process wherein colon lesions (UC) or widespread ulceration and fissure (CD) might be accompanied by ancillary extra-intestinal manifestations involving the eye, skin, joints or liver, but also by full-blown "autoimmune" disorders from psoriasis and multiple sclerosis to rheumatoid arthritis; attempts at unraveling a link or a hierarchical order in these entities have proven almost fruitless. More recently, the input of genetics has suggested that the IBDs might be multi-organ inflammatory processes, elicited by a large number of low-penetrance susceptibility genes, with environmental factors needed to induce full-blown disease. At a noteworthy exception to this rule, the description of the nucleotide-oligomerization domain (NOD) gene mutations in CD came at the beginning of the 2000s: the NOD-LRR are part of a highly conserved microbial sensor system which respond to bacterial peptidoglycans by mounting an inflammatory response. At least in Caucasian patients, the prevalently loss-of-function mutation of NOD permitted to unexpectedly define CD as an immune deficiency state, and upon its recent description in apparently unrelated disorders such as the Blau syndrome (a granulomatous pediatric syndrome), and perhaps in psoriasis and chronic obstructive pulmonary disorders, has contributed to revolutionize our view of IBD and CD in particular. The latter affection, together with psoriasis and chronic pulmonary disease can now be included into a newly identified category named "barrier organ disease", wherein a barrier organ is defined as a large mucosal or epithelial surface with an abundant metagenomic microbial population and an underneath reactive tissue, the whole structure being in contact with the outer environment and capable to react to it. Personalized treatments and empowerment of research across different disease phenotypes should be the advantages of this novel mindset.
    World journal of gastrointestinal pharmacology and therapeutics. 08/2013; 4(3):41-6.
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    ABSTRACT: Genome-wide association studies (GWAS) have successfully identified several loci associated with primary biliary cirrhosis (PBC) risk. Pathway analysis complements conventional GWAS analysis. We applied the recently developed linear combination test for pathways to datasets drawn from independent PBC GWAS in Italian and Canadian subjects. Of the Kyoto Encyclopedia of Genes and Genomes and BioCarta pathways tested, 25 pathways in the Italian dataset (449 cases, 940 controls) and 26 pathways in the Canadian dataset (530 cases, 398 controls) were associated with PBC susceptibility (P<0.05). After correcting for multiple comparisons, only the eight most significant pathways in the Italian dataset had FDR <0.25 with tumor necrosis factor/stress-related signaling emerging as the top pathway (P=7.38 × 10(-4), FDR=0.18). Two pathways, phosphatidylinositol signaling and hedgehog signaling, were replicated in both datasets (P<0.05), and subjected to two additional complementary pathway tests. Both pathway signals remained significant in the Italian dataset on modified gene set enrichment analysis (P<0.05). In both GWAS, variants nominally associated with PBC were significantly overrepresented in the phosphatidylinositol pathway (Fisher exact P<0.05). These results point to established and novel pathway-level associations with inherited predisposition to PBC that, on further independent replication and functional validation, may provide fresh insights into PBC etiology.Genes and Immunity advance online publication, 7 February 2013; doi:10.1038/gene.2013.1.
    Genes and immunity 02/2013; · 4.22 Impact Factor
  • Giovanni C Actis, Sonia Tarallo, Floriano Rosina
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    ABSTRACT: Colitis-associated cancer represents a long-standing problem, with two new factors adding to its importance: the diffusion of inflammatory bowel disease in developing countries, and the increased availability of effective drugs that control ulcerative colitis delaying or abrogating the need for a curative colectomy. The consolidated evidence that inflammation is the unique variable that factors in colitic cancer development has conferred impetus to the search and release of anti-inflammatory/immune suppressive molecules to pursue the goal of cancer chemoprevention. Cutting-edge research has provided breakthrough insights into the mechanism of the chemopreventive actions of mesalamines, thiopurines, and probiotics, and we expand on these topics. Despite these advancements, bedside evidence is still mixed and calls for further scrutiny. Nowadays, the clinician must continue to rely on classic preventive measures such as surveillance colonoscopy, and the early and aggressive use of drugs that permit to keep the degree of mucosal inflammation to a minimum.
    Inflammation & allergy drug targets. 11/2012;
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    ABSTRACT: We studied the toxicity of cyclosporin (CsA), azathioprine, and mesalamine in 94 patients with inflammatory bowel disease (IBD). 63 treatments with CsA (2mg/kg intravenously or 5 mg/kg orally); 57 with azathioprine (2 mg/kg); and 44 with mesalamine (3.2-4.8 gr) were included. After induction, oral CsA was continued for 6 months, azathioprine for a median of 14 months (range 1-201 mos), mesalamine until tolerated. CsA toxicity frequency 25%: withdrawal and colectomy in 3 cases. AZA toxicity rate: 43% with an overall time-to-onset of a median of 6 months (range 1-60 mos); withdrawal and colectomy in 7 cases; 62% of the events were other than leukopenia. Mesalamine toxicity rates: (13.6%) with one colectomy. Toxicity-related withdrawal of conventional IBD treatments is significant and leads to colectomy in ulcerative colitis. 50% of the thiopurine toxicities outrange the predicting power of the available pharmacogenomic assays; mesalamine often causes allergic lung dysfunction. Efforts are warranted to optimize this conventional treatment of IBD.
    Current clinical pharmacology. 05/2012; 7(3):209-13.
  • Journal of Hepatology 04/2012; 44:S12. · 10.40 Impact Factor
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    ABSTRACT: Representing the second cause of cancer-related death after lung cancer in men and breast cancer in women, colorectal cancer (CRC) is a major health problem in Italy. Obesity is reckoned to favor CRC; however, the underlying mechanisms are unclear. Recently, a single nucleotide polymorphism (SNP) in the fat mass and obesity associated (FTO) gene was found to be significantly associated with obesity. To establish whether the FTO SNP rs9939609 may represent a risk factor for CRC and adenoma in the Italian population. 1,037 subjects were enrolled in the study and divided in 3 groups: CRC (341 pts., M/F=197/144, mean age=65.17±11.16 years), colorectal adenoma (385 pts., M/F=247/138, mean age=62.49±13.01 years), healthy controls (311 pts., M/F=150/161, mean age=57.31±13.84 years). DNA was extracted from whole blood, and stored frozen for rs9939609 genotyping by real-time PCR. The frequency of the obesity-associated mutated A allele (AA+AT) on the FTO gene was 69.77% among controls, and 71.85% and 65.71% respectively among CRC and polyp patients. Compared to control subjects the AA+AT genotype had no significant effect on the risk for either CRC (OR=1.106; CI 95%=0.788-1.550; p=0.561) or colorectal adenomas (OR=0.830; CI 95%=0.602-1.144; p=0.255). We did not observe any association between the AA genotype and CRC/polyp localization and age at diagnosis. As measured in a patient subset, carriership of the risk alleles did not reflect in a significantly altered BMI. The obesity-linked FTO variants do not play a significant role in modulating the colorectal cancer risk in the Italian population.
    European Journal of Internal Medicine 01/2012; 23(1):65-9. · 2.30 Impact Factor
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    ABSTRACT: Traditional knowledge of clinical, laboratorial, and endoscopic orders regarding ulcerative colitis and Crohn's disease has begun to be implemented by the revolutionary data from genetic studies. Ever since many decades ago it has been clear that inflammatory bowel diseases are complex multifactorial disorders wherein gut-confined and/or environmental factors must synergize with genetic components to effect the full-blown disorder. The sequencing of the human genome and the generation of public resources of single nucleotide polymorphisms permitted the conduction of powerful population based genome-wide association studies. The latter have increased the number of the identified susceptibility loci to 99. In this review we touched on two pathways that make true susceptibility genes for inflammatory bowel diseases; gene loci that confer specific risk for ulcerative colitis and Crohn's disease were discussed in detail.
    Inflammation & allergy drug targets. 12/2011; 10(6):447-54.
  • International Journal of Colorectal Disease 06/2011; 27(4):547-8. · 2.24 Impact Factor
  • Giovanni C Actis, Floriano Rosina, Ian R Mackay
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    ABSTRACT: Dysregulated inflammation in the gut, designated clinically as inflammatory bowel disease (IBD), is manifested by the prototypic phenotypes of an Arthus-like reaction restricted to the mucosa of the colon, as in ulcerative colitis, or a transmural granulomatous reaction, as in Crohn's disease, or an indeterminate form of the two polar types. That the inflammation of IBD can trespass the boundaries of the bowel has long been known, with articular, ophthalmologic, cutaneous, hepatobiliary or other complications/associations - some autoimmune and others not - affecting significant numbers of patients with IBD. Also notable is the frequency of diagnosis of IBD-type diseases on a background of systemic, (mostly myelo-hematological) disorders, associated with alterations of either (or both) innate or adaptive arms of the immune response. Finally, cases of IBD are reported to occur as an adverse effect of TNF inhibitors. Bone marrow transplant has been proven to be the only curative measure for some of the above cases. Thus, in effect, the IBDs should now be regarded as a systemic, rather than bowel-localized, disease. Genome-wide association studies have been informative in consolidating the view of three phenotypes of IBD (ulcerative colitis, Crohn's disease and mixed) and, notably, are revealing that the onset of IBD can be linked to polymorphisms in regulatory miRNAs, or to nucleotide sequences coding for regulatory lymphokines and/or their receptors. At the effector level, we emphasize the major role of the Th17/IL-23 axis in dictating the perpetuation of intestinal inflammation, augmented by a failure of physiological control by regulatory T-cells. In conclusion, there is a central genesis of the defects underlying IBD, which therefore, in our opinion, is best accommodated by the concept of IBD as more of a syndrome than an autonomous disease. This altered mindset should upgrade our knowledge of IBD, influence its medical care and provide a platform for further advances.
    Expert review of gastroenterology & hepatology 06/2011; 5(3):401-10.
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    Digestive and Liver Disease 03/2011; 43. · 2.89 Impact Factor
  • Digestive and Liver Disease 03/2011; 43. · 2.89 Impact Factor

Publication Stats

2k Citations
956.04 Total Impact Points


  • 2010
    • Presidio Sanitario San Camillo, Torino
      Torino, Piedmont, Italy
  • 2007
    • University of Texas Medical Branch at Galveston
      Galveston, Texas, United States
  • 1989–2005
    • Università degli Studi di Torino
      • Department of Medical Science
      Torino, Piedmont, Italy
  • 1999
    • University of California, Davis
      • Division of Rheumatology/Allergy/Clinical Immunology
      Davis, CA, United States
  • 1997
    • Università degli Studi di Bari Aldo Moro
      Bari, Apulia, Italy
    • Oxford University Hospitals NHS Trust
      • Department of Gastroenterology
      Oxford, ENG, United Kingdom
  • 1991
    • Ospedale San Giovanni Battista, ACISMOM
      Torino, Piedmont, Italy