Panama, Panama

Columbus University
Panama, Panama

Columbus University may refer to: Columbus University a university in Panama Columbus State University in the U.S. state of Georgia Columbus University established by the Knights of Columbus and later merged into Catholic University of America Ohio State University in Columbus, Ohio The fictional school depicted in the film "Higher Learning". Columbus University , an unaccredited institution of higher learning in Louisiana Wikipedia.

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Tursi A.,Gastroenterology Service | Papa A.,Columbus University | Danese S.,IBD Unit | Danese S.,IBD Center
Alimentary Pharmacology and Therapeutics | Year: 2015

Background The incidence of diverticulosis and diverticular disease of the colon, including diverticulitis, is increasing worldwide, and becoming a significant burden on national health systems. Treatment of patients with diverticulosis and DD is generally based on high-fibre diet and antibiotics, respectively. However, new pathophysiological knowledge suggests that further treatment may be useful. Aim To review the current treatment of diverticulosis and diverticular disease. Methods A search of PubMed and Medline databases was performed to identify articles relevant to the management of diverticulosis and diverticular disease. Major international conferences were also reviewed. Results Two randomised controlled trials (RCT) found the role of antibiotics in managing acute diverticulitis to be questionable, particularly in patients with no complicating comorbidities. One RCT found mesalazine to be effective in preventing acute diverticulitis in patients with symptomatic uncomplicated diverticular disease. The role of rifaximin or mesalazine in preventing diverticulitis recurrence, based on the results of 1 and 4 RCTs, respectively, remains unclear. RCTs found rifaximin and mesalazine to be effective in treating symptomatic uncomplicated diverticular disease. The use of probiotics in diverticular disease and in preventing acute diverticulitis occurrence/recurrence appears promising but unconclusive. Finally, the role of fibre in treating diverticulosis remains unclear. Conclusions Available evidence suggests that antibiotics have a role only in the treatment of complicated diverticulitis. It appears to be some evidence for a role for rifaximin and mesalazine in treating symptomatic uncomplicated diverticular disease. Finally, there is not currently adequate evidence to recommend any medical treatment for the prevention of diverticulitis recurrence. © 2015 John Wiley & Sons Ltd.

Mocci G.,Brotzu Hospital | Marzo M.,Columbus University | Papa A.,Columbus University | Armuzzi A.,Columbus University | Guidi L.,Columbus University
Journal of Crohn's and Colitis | Year: 2013

The clinical introduction of tumour necrosis factor (TNF) inhibitors has deeply changed the treatment of inflammatory bowel diseases (IBD). It has demonstrated impressive efficacy as compared to alternative treatments, allowing for the chance to achieve near-remission and long-term improvement in function and quality of life and to alter the natural history of Crohn's disease (CD) and ulcerative colitis (UC). As a consequence of longer follow-up periods the number of side effects which may be attributed to treatment with biologics is growing significantly. Cutaneous reactions are among the most common adverse reactions. These complications include injection site reactions, cutaneous infections, immune-mediated complications such as psoriasis and lupus-like syndrome and rarely skin cancers. We review the recent literature and draw attention to dermatological side effects of anti-TNF therapy of inflammatory bowel disease. © 2013 European Crohn's and Colitis Organisation.

Masola V.,University of Padua | Gambaro G.,Columbus University | Tibaldi E.,University of Padua | Onisto M.,University of Padua | And 2 more authors.
Biochimica et Biophysica Acta - Molecular Cell Research | Year: 2011

Diabetic nephropathy is one of the main causes of end-stage renal disease, in which the development of tubular damage depends on factors such as high glucose levels, albuminuria and advanced glycation end-product. In this study, we analyzed the involvement of heparanase, a heparan sulfate glycosidase, in the homeostasis of proximal tubular epithelial cells in the diabetic milieu. In vitro studies were performed on a wild-type and stably heparanase-silenced adult tubular line (HK2) and HEK293. Gene and protein expression analyses were performed in the presence and absence of diabetic mediators. Albumin and advanced glycation end-product, but not high glucose levels, increased heparanase expression in adult tubular cells via the AKT/PI3K signaling pathway. This over-expression of heparanase is then responsible for heparan sulfate reduction via its endoglycosidase activity and its capacity to regulate the heparan sulfate-proteoglycans core protein. In fact, heparanase regulates the gene expression of syndecan-1, the most abundant heparan sulfate-proteoglycans in tubular cells. We showed that heparanase is a target gene of the diabetic nephropathy mediators albumin and advanced glycation end-product, so it may be relevant to the progression of diabetic nephropathy. It could take part in several processes, e.g. extracellular-matrix remodeling and cell-cell crosstalk, via its heparan sulfate endoglycosidase activity and capacity to regulate the expression of the heparan sulfate-proteoglycan syndecan-1. © 2011 Elsevier B.V.

Masola V.,University of Padua | Secchi M.F.,University of Padua | Gambaro G.,Columbus University | Onisto M.,University of Padua
Current Cancer Drug Targets | Year: 2014

Heparanase is the unique and specific functional endoglycosidase capable of cleaving heparan sulfate (HS) chains. It exerts its enzymatic activity catalyzing the cleavage of the β (1, 4)-glycosidic bond between glucuronic acid and glucosamine residue. HS cleavage results in remodelling of the extracellular matrix as well as in regulating the release of many HS-linked molecules such as growth factors, cytokines and enzymes involved in inflammation, wound healing and tumour invasion. A pro-metastatic and pro-angiogenic role for this enzyme has been widely demonstrated in many primary human tumours since high levels of heparanase correlate with lymph node and distant metastasis, elevated micro vessel density and reduced survival of cancer patients. Recently, data have been reported that heparanase regulates heparan sulfate proteoglycan syndecan-1 and promotes its shedding from the cell surface. Shed syndecan-1 in turn controls tumour growth, metastasis and neo-angiogenesis mainly by promoting growth-factor signaling in the tumour milieu. Considering that, once inactivated, there are no other molecules capable of performing the same function, it is evident how this enzyme may be an effective and attractive drug target. Several heparanase inhibitors have been developed and some of them have undergone clinical trials showing efficacy against tumours. In this mini-review we will discuss current knowledge of heparanase involvement in cancer as well as its targeted inhibition as a promising therapeutic option in tumour treatment. © 2014 Bentham Science Publishers.

Masola V.,University of Verona | Masola V.,University of Padua | Zaza G.,University of Verona | Secchi M.F.,University of Padua | And 3 more authors.
Biochimica et Biophysica Acta - Molecular Cell Research | Year: 2014

Epithelial-mesenchymal transition (EMT) of tubular cells is one of the mechanisms which contribute to renal fibrosis and transforming growth factor-β (TGF-β) is one of the main triggers. Heparanase (HPSE) is an endo-β-D-glucuronidase that cleaves heparan-sulfate thus regulating the bioavailability of growth factors (FGF-2, TGF-β). HPSE controls FGF-2-induced EMT in tubular cells and is necessary for the development of diabetic nephropathy in mice. The aim of this study was to investigate whether HPSE can modulate the expression and the effects of TGF-β in tubular cells. First we proved that the lack of HPSE or its inhibition prevents the increased synthesis of TGF-β by tubular cells in response to pro-fibrotic stimuli such as FGF-2, advanced glycosylation end products (AGE) and albumin overload. Second, since TGF-β may derive from sources different from tubular cells, we investigated whether HPSE modulates tubular cell response to exogenous TGF-β. HPSE does not prevent EMT induced by TGF-β although it slows its onset; indeed in HPSE-silenced cells the acquisition of a mesenchymal phenotype does not develop as quickly as in wt cells. Additionally, TGF-β induces an autocrine loop to sustain its signal, whereas the lack of HPSE partially interferes with this autocrine loop. Overall these data confirm that HPSE is a key player in renal fibrosis since it interacts with the regulation and the effects of TGF-β. HPSE is needed for pathological TGF-β overexpression in response to pro-fibrotic factors. Furthermore, HPSE modulates TGF-β-induced EMT: the lack of HPSE delays tubular cell transdifferentiation, and impairs the TGF-β autocrine loop. © 2014 Elsevier B.V.

Fabris A.,University of Verona | Lupo A.,University of Verona | Ferraro P.M.,Columbus University | Anglani F.,University of Padua | And 3 more authors.
Kidney International | Year: 2013

Medullary sponge kidney (MSK) is a renal malformation typically associated with nephrocalcinosis and recurrent calcium nephrolithiasis. Approximately 12% of recurrent stone formers have MSK, which is generally considered a sporadic disorder. Since its discovery, three pedigrees have been described in which an apparently autosomal dominant inheritance was suggested. Here, family members of 50 patients with MSK were systematically investigated by means of interviews, renal imaging, and biochemical studies in an effort to establish whether MSK is an inheritable disorder. Twenty-seven MSK probands had 59 first-and second-degree relatives of both genders with MSK in all generations. There were progressively lower mean levels of serum calcium, urinary sodium, pH, and volume, combined with higher serum phosphate and potassium from probands to relatives with bilateral, to those with unilateral, and to those unaffected by MSK. This suggests that most affected relatives have a milder form of MSK than the probands, which would explain why they had not been so diagnosed. Thus, our study provides strong evidence that familial clustering of MSK is common, and has an autosomal dominant inheritance, a reduced penetrance, and variable expressivity. © 2012 International Society of Nephrology.

Gambaro G.,Columbus University | Kong N.C.T.,National University of Malaysia
Journal of Nephrology | Year: 2010

Patients with primary and secondary chronic glomerular diseases are at significant risk for progression to end-stage renal disease. Unfortunately the treatment armamentarium is relatively limited in terms both of available agents and of specificity. Experimental evidence supports the idea that heparin-derived agents and glycosaminoglycans (GAGs) favorably affect primary and secondary renal diseases. While a number of clinical exploratory studies have addressed the effect of these agents in microalbuminuric and macroalbuminuric diabetic patients, very few have investigated their activity in nondiabetic renal conditions. This paper will review the experimental and clinical evidence on the use of GAGs in renal disease other than diabetic nephropathy, following the reports of experimental findings supporting their use and the possible mechanisms involved: anticoagulant and antiproliferative activity, effect on growth factors (PDGF, FGF2 and TGF-β1), inhibition of heparanase, macrophage renal infiltration and of the renin-angiotensin system, and decrease in proteinuria. Targeting these pathogenic loops with GAG treatment might be revealed to be very rewarding from a clinical point of view. Prospective randomized controlled trials with large case populations and definite entry criteria are clearly indicated. © 2010 Società Italiana di Nefrologia.

Gambaro G.,Columbus University | Danza F.M.,Gemelli University Hospital | Fabris A.,University of Verona
Current Opinion in Nephrology and Hypertension | Year: 2013

Purpose of review: After it was first described in 1939, medullary sponge kidney (MSK) received relatively little attention. This was because it was believed to have a low prevalence and because it was considered a benign condition. Studies in recent years have been changing these convictions however, hence the present review. Recent findings: Insight has been obtained on the genetic basis of this disease, supporting the hypothesis that MSK is due to a disruption at the 'ureteric bud-metanephric mesenchyme' interface. This explains why so many tubular defects coexist in this disease, and particularly a distal tubular acidification defect of which the highly prevalent metabolic bone disease is one very important consequence. In addition to the typical clinical phenotype of recurrent stone disease, other clinical profiles have now been recognized, that is, an indolent, almost asymptomatic MSK, and a rare form characterized by intractable, excruciating pain. Summary: Findings suggest the need for a more comprehensive clinical characterization of MSK patients. The genetic grounds for the condition warrant further investigation, and reliable methods are needed to diagnose MSK. © 2013 Wolters Kluwer Health | Lippincott Williams & Wilkins.

Marianetti T.M.,Columbus University
Minerva stomatologica | Year: 2011

Oligodontia may compromise the harmonious development of the masticatory system. The quantity and quality of agenesis determines the type of approach and the complexity of rehabilitative therapy. We present a case of a patient affected by oligodontia and maxillo-mandibular skeletal alterations, corrected by orthodontic and orthognatic surgical treatment, assisted by prosthetic-presurgical rehabilitation of the lower arch. After surgery the occlusion was finally restored by a definitive prosthesis modeled on the presurgical one and supported by the same residual dental elements. Photographic and cephalometric analysis have shown the stability of the results at 20 years follow-up. The case presented shows that the final prosthesis on the residual teeth in patients affected by oligodontia may represent a possible alternative to implanto-prosthetic rehabilitation, presenting lower cost and requiring less time for definitive occlusal rehabilitation.

Pelo S.,Columbus University
International journal of oral and maxillofacial surgery | Year: 2011

There are few studies on maxillomandibular skeletal alterations. Twenty-one patients with unilateral coronal craniosynostosis were analysed and compared with controls. Landmarks analysed were: sella-nasion-point A and B angles, point A-nasion-point B angle, interincisal angle, angle of superior incisor axis on the sella-nasion plane, lower incisor to mandibular plane angle, Frankfort mandibular plane angle, zygomatic-frontal suture (Z), point on the most concave part of pyramidal apophysis of the upper maxilla (Mx), antegonial incisure (AG), upper (UMT) and lower (LMT) molar teeth. Differences were significant for class II dentoskeletal occlusion (p<0.0001), mandibular hyperdivergence (p<0.0001), lingualization of superior incisor (p<0.005), deviation of inferior interincisal contralateral line to the synostosis (p<0.0001) in the plagiocephalic population. Compared with contralateral counterpoints, Z (p<0.05), Mx (p<0.005) and UMT (p<0.0005) on the affected side were closer to the midline; AG (p<0.0005) and LMT (p<0.05) were further from it. On the frontal plane, Z, Mx, UMT, LMT and AG on the affected side were higher. Vertical and transversal contraction of the jaw of the synostotic side and laterodeviation of the mandibular interincisal line of the contralateral synostotic were clear. The altered position of the glenoid cavity, anteriorized in unilateral coronal craniosynostosis, could be the cause of mandibular dentoskeletal asymmetry. Copyright © 2011 International Association of Oral and Maxillofacial Surgeons. Published by Elsevier Ltd. All rights reserved.

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