Trends and characteristics associated with dietary triggers and psychological distress in patients with irritable bowel syndrome: a cross-sectional study.

OBJECTIVE: Diet, visceral sensitivity, and psychological distress play an important role in Irritable Bowel Syndrome (IBS). This study focused on the relation between IBS severity, foods, visceral sensitivity, and anxiety/depression. PATIENTS AND METHODS: Patients with IBS were investigated through (1) IBS-symptoms severity score (SSS), (2) self-reported food intolerance, (3) visceral sensitivity index (VSI), and (4) Hospital Anxiety and Depression Scale (HADS). Seventy-seven patients agreed to participate in the survey. Of them, 64 (83%) showed IBS according to Rome IV criteria and were included in the final analysis. Patients with IBS-D were 30 (47%), with IBS-C 27 (42%), and with IBS-M 7 (11%). RESULTS: Fifty-eight patients (90%) considered at least one foodstuff as IBS trigger. Amine-rich foods represented a symptom trigger for 77% of patients, those with lectin for 70%, IACs by 48%, and capsaicin by 37%. Overweight was significantly associated with amine-rich foods (p=0.015), age >45 years (p=0.001) and non-smoking condition (p=0.033) with lectin-rich foods, male gender (p=0.005) and overweight (p=0.027) with capsaicin-containing foods. A positive VSI score was found in 59% of patients, and non-smoking condition was significantly associated (OR 10.03; p=0.009). No factors were associated with a positive HADS score, shown by 80% of patients. Severe IBS was shown by 63% of patients, being amine-rich foods (p=0.024), overweight (p=0.020), and female gender (p=0.029) independent risk factors while marriage/cohabiting a protective one (p=0.038). Amine-rich foods are an independent risk factor for severe IBS, along with overweight and female gender. CONCLUSIONS: Clinicians should pay more attention to self-reported food intolerance in IBS patients. A personalized therapy including dietary advice as part of treatment could be of great benefit.

Allochthonous bioaugmentation in ex situ treatment of crude oil-polluted sediments in the presence of an effective degrading indigenous microbiome.

Oil-polluted sediment bioremediation depends on both physicochemical and biological parameters, but the effect of the latter cannot be evaluated without the optimization of the former. We aimed in optimizing the physicochemical parameters related to biodegradation by applying an ex-situ landfarming set-up combined with biostimulation to oil-polluted sediment, in order to determine the added effect of bioaugmentation by four allochthonous oil-degrading bacterial consortia in relation to the degradation efficiency of the indigenous community. We monitored hydrocarbon degradation, sediment ecotoxicity and hydrolytic activity, bacterial population sizes and bacterial community dynamics, characterizing the dominant taxa through time and at each treatment. We observed no significant differences in total degradation, but increased ecotoxicity between the different treatments receiving both biostimulation and bioaugmentation and the biostimulated-only control. Moreover, the added allochthonous bacteria quickly perished and were rarely detected, their addition inducing minimal shifts in community structure although it altered the distribution of the residual hydrocarbons in two treatments. Therefore, we concluded that biodegradation was mostly performed by the autochthonous populations while bioaugmentation, in contrast to biostimulation, did not enhance the remediation process. Our results indicate that when environmental conditions are optimized, the indigenous microbiome at a polluted site will likely outperform any allochthonous consortium.

Surgery for a gastric Dieulafoy's lesion reveals an occult bleeding jejunal diverticulum. A case report.

BACKGROUND: Jejunal diverticulosis is an uncommon disease and usually asymptomatic. It can be complicated not only by diverticulitis, but by hemorrhage, perforation, intussusception, volvulus, malabsorption and even small bowel obstruction due to enteroliths formed and expelled from these diverticula. METHODS: We describe a case of an occult bleeding jejunal diverticulum, casually discovered in a patient that was taken to surgery for a Dieulafoy's lesion after unsuccessful endoscopic treatment. We performed a gastric resection together with an ileocecal resection.Macroscopic and microscopic examinations confirmed the gastric Dieulafoy's lesion and demonstrated the presence of another source of occult bleeding in asymptomatic jejunal diverticulum. DISCUSSION: The current case emphasizes that some gastrointestinal bleeding lesions, although rare, can be multiple and result in potentially life-threatening bleeding. The clinician must be mindful to the possibility of multisite lesions and to the correlation between results of the investigations and clinical condition of the bleeding patient.

Acute endovascular treatment (< 48 hours) of uncoilable ruptured aneurysms at non-branching sites using silk flow-diverting devices.

A blood blister-like (BBL) or dissecting aneurysm should be carefully considered if located at a non-branching site of the supra-clinoid internal carotid artery (ICA). Several surgical and endovascular treatment methods have been proposed but they all carry a relatively high risk of morbidity and mortality. This study evaluated the effectiveness of a novel Silk flow-diverting device (SFD) placed in the early acute stage. Three patients presenting with acute subarachnoid haemorrhage caused by small blister-like aneurysms of the carotid siphon were treated within 48 hours after admission by placement of SFDs. More than one device was placed to cover the lesion. None of the patients were premedicated and started anti-platelet therapy during the procedure. All aneurysms were successfully occluded. A good outcome was observed in two out of three treated patients. No thromboembolic or haemorrhagic event occurred during or after the procedures, or during follow-up (6-14 months). SFD prevented rebleeding and the use of these devices could be proposed as an option to treat fragile uncoilable BBL aneurysms, even in the early acute phase without anti-platelet premedication. Larger studies and long-terms results are necessary.

Association between Developmental Venous Anomalies and Cavernous Angiomas: a Retrospective MR Study.

Developmental venous anomalies (DVA) are large veins usually arranged in a cluster around a collector vein draining directly into the superficial and deep venous systems. Since the introduction of magnetic resonance imaging DVA have been disclosed more frequently. Many studies suggested and then confirmed the association between cavernous angioma and developmental venous anomaly, described for the first time by Roberson in 1974. The aim of our study was a retrospective assessment of the case series at our institution, namely to determine the frequency of the association between developmental venous anomaly and cavernous and analyse the relation between the two lesions.

Carotid Stenting without Angioplasty and without Protection: The Advantages of a Less Invasive Procedure.

SUMMARY: Endovascular stenting is a consolidated alternative to thrombendarterectomy in the treatment of extracranial carotid artery atheromasic stenosis. The most common complication of stenting is a distal embolism causing clinically silent orsymptomatic cerebral ischaemia. To prevent this complication distal embolism protection devices are often used but their effectiveness remains unsettled. In addition, there is some evidence that distal embolism may actually be triggered by the protection systems due to clot formationat their distal surface or in the intimal lesions these systems cause. Another rarer complicationis hyperperfusion syndrome arising during both stenting and thrombendarterectomy but more common in endovascular procedures. To avoid these complications the Neuroradiology Service at Bellaria Hospital (Bologna Local Health Trust) has devised a mini-invasive carotid stenting technique that does not require either distal embolism protection or angioplasty. The technique uses only the radial force exerted by the self-expanding stent to widen the atherosclerotic stenosis slowly and gradually. The goal of treatment has also changed from a prompt restoration of the atheromasic vessel's original calibre to slow transformation of the hemodynamic significance of the stenosis. The technique's success lies mainly in selecting the stenosis to treat using CT angiography to analyse plaque morphology and structure.We used the technique to treat 83 stenotic lesions in 75 patients. The study aims to describe and discussour experience.

Transmigrated intrauterine device discovered 17 years after its insertion.

We present the case of an intraperitoneal IUD incidentally noted on lumbar spine X-rays and confirmed by CT. This was secondary to asymptomatic uterine perforation occurred at the time of insertion 17 years before.

The functional ccpA gene is required for carbon catabolite repression in Lactobacillus plantarum.

We report the characterization of the ccpA gene of Lactobacillus plantarum, coding for catabolite control protein A. The gene is linked to the pepQ gene, encoding a proline peptidase, in the order ccpA-pepQ, with the two genes transcribed in tandem from the same strand as distinct transcriptional units. Two ccpA transcription start sites corresponding to two functional promoters were found, expression from the upstream promoter being autogenously regulated through a catabolite-responsive element (cre) sequence overlapping the upstream +1 site. During growth on ribose, the upstream promoter showed maximal expression, while growth on glucose led to transcription from the downstream promoter. In a ccpA mutant strain, the gene was transcribed mainly from the upstream promoter in both repressing and non repressing conditions. Expression of two enzyme activities, beta-glucosidase and beta-galactosidase, was relieved from carbon catabolite repression in the ccpA mutant strain. In vivo footprinting analysis of the catabolite-controlled bglH gene regulatory region in the ccpA mutant strain showed loss of protection of the cre under repressing conditions.

A physical and functional analysis of the newly-identified bglGPT operon of Lactobacillus plantarum.

A newly-identified bglGPT operon of Lactobacillus plantarum was isolated and expressed in Escherichia coli. The sequence analysis of the cloned DNA fragment showed three open reading frames encoding (i) a 237-amino acid protein (BglG), (ii) a 577-amino acid protein (BglP) and (iii) a 486-amino acid protein (BglT). BglG, BglP and BglT were shown to be homologous to the BglG family of transcriptional antiterminators, to permeases of the phosphoenolpyruvate-dependent phosphotransferase system and to beta-glucosidases, respectively. Complementation of E. coli mutant strains showed that BglP and BglT are a permease and a beta-glucosidase active on the beta-glucosides, 5-bromo-4-chloro-3-indolyl-beta-D-glucopyranoside and p-nitrophenyl-beta-D-glucoside, respectively. BglG was also shown to promote expression of a bglG-lacZ gene fusion in an E. coli bglG(-) background. A ribonucleic antiterminator sequence, the antiterminator-responsive cis-element and a 'catabolite responsive element', were found downstream of the transcriptional start point. Transcription of the operon was repressed 10-fold in L. plantarum cells grown on glucose as compared to ribose.

Autoimmunity to tropomyosin isoforms in ulcerative colitis (UC) patients and unaffected relatives.

Autoimmunity to cytoskeletal protein tropomyosin (TM) has been demonstrated in UC. However, the TM isoforms involved in this IgG-mediated autoimmune response in UC and the possible presence of serum IgG antibodies against TM (hTMs IgG) in unaffected UC relatives are unknown. The aim of this study was to investigate the human TM (hTM) isoforms recognized by serum IgG from UC and to explore whether hTM IgG antibodies are present in healthy UC relatives. We studied 33 UC patients with 58 unaffected relatives, 31 Crohn's disease (CD) patients with 31 unaffected relatives and 20 controls (C). Serum IgG against four recombinant hTM isoforms (hTM1, 2, 3, 5) were tested by ELISA. p-ANCA were tested by ELISA and immunofluorescence. Serum hTM1 and hTM5 IgG were higher in UC patients than in CD and C (P<0.005). Among UC patients 52% were seropositive for hTM1 and 64% for hTM5 (P<0.001 versus CD and C). In UC, hTM5 IgG were higher in p-ANCA+ than in ANCA- patients (P=0.04). In UC relatives hTM1 IgG were higher than in CD relatives and C (P<0.01). UC relatives were more frequently seropositive for hTM1 than hTM5 IgG (P=0.001). while probands were more frequently seropositive for hTM5 IgG (P=0.008). We conclude that autoimmunity to hTMI and hTM5 is a feature of UC, while hTM1 IgG differentiate UC relatives from controls. A genetic susceptibility to immune recognition of hTM isoforms in UC is suggested.

Expression of the bglH gene of Lactobacillus plantarum is controlled by carbon catabolite repression.

A newly identified bglH gene coding for a phospho-beta-glucosidase of Lactobacillus plantarum was isolated and expressed in Escherichia coli. The sequence analysis of the cloned DNA fragment showed an open reading frame encoding a 480-amino-acid protein with a calculated molecular mass of 53 kDa. The bglH gene was shown to be expressed on a monocistronic transcriptional unit. Its transcription was repressed 10-fold in L. plantarum cells grown on glucose compared to the beta-glucoside salicin as a sole carbon source. A catabolite-responsive element (CRE) spanning from -3 to +11 with respect to the transcriptional start point was found, and its functionality was assessed by mutational analysis. In vitro and in vivo DNA binding experiments suggested the occurrence of a DNA-protein complex at the CRE site, which would mediate glucose repression of bglH expression.

Interleukin 12 is expressed and actively released by Crohn's disease intestinal lamina propria mononuclear cells.

BACKGROUND & AIMS: Cell-mediated immunity is a feature of Crohn's disease (CD). The heterodimer interleukin (IL)-12, produced by phagocytes, induces T-cell cytokines, primarily interferon (IFN)-gamma. This study examined whether CD lamina propria mononuclear cells (LPMCs) express and release bioactive IL-12. METHODS: LPMCs were isolated from 13 patients with CD, 9 with ulcerative colitis (UC), and 13 controls. Messenger RNA for p40 and p35 IL-12 subunits was evaluated by reverse-transcription polymerase chain reaction. IL-12 was measured by enzyme-linked immunosorbent assay in LPMC culture supernatants. The INF-gamma-inducing effect of unstimulated LPMC supernatants was evaluated. RESULTS: Messenger RNA for both IL-12 subunits was detected in LPMCs of 11 of 13 patients with CD, 1 of 9 patients with UC, and 1 of 13 controls (P < 0.001). IL-12 was measured (10.5 +/- 2 pg/mL at 24 hours) in unstimulated CD LPMCs and was enhanced by pokeweed mitogen, lipopolysaccharide, and staphylococcal enterotoxin B. No IL-12 was detectable in 8 of 9 patients with UC and 12 of 13 control-unstimulated LPMCs. IL-12 induced by pokeweed mitogen and staphylococcal enterotoxin B in UC was lower than in CD and did not differ from controls. An IFN-gamma-inducing effect was restricted to unstimulated CD LPMC supernatants and was inhibited by an anti-IL-12 antibody in a dose-dependent fashion. CONCLUSIONS: IL-12 transcripts are expressed in CD intestinal tissues. CD LPMCs are up-regulated in their capability of releasing bioactive IL-12. Expression and release of bioactive IL-12 seem to differentiate CD from UC.

A new Bacillus subtilis gene with homology to Escherichia coli prc.

We report the cloning of a 2-kb PstI-BamHI fragment of Bacillus subtilis DNA carrying an open reading frame of 1398 bp, herein designated orfRM1. This orf was shown to be transcribed only during vegetative growth from a putative sigma A-specific promoter. The deduced amino acid sequence predicted a polypeptide of 51 kDa (466 aa), which shows significant percentage of identity with the Escherichia coli Prc protein. However no Prc-like phenotypes were observed in a B. subtilis orfRM1 deletion-insertion mutant.

Evidence against colonic mucosa colonisation by Helicobacter pylori. Lack of a specific antibody response in homogenates of rectal endoscopic biopsies.

Aim of this study is to provide indirect evidence that human colonic mucosa harbour Helicobacter pylori. The antibody response of IgG and IgA class against Helicobacter pylori was examined in autologous homogenate of gastric and rectal endoscopic biopsies from 26 patients and in rectal samples of a further 36. All had a documented (histology and/or serology) Helicobacter pylori status. Helicobacter pylori specific IgG and IgA were measured by an in-house ELISA. In Helicobacter pylori positive patients having both gastric and rectal homogenate, mean level of Helicobacter pylori IgG and IgA was higher in gastric than in rectal samples (0.810 +/- 0.668 optical density vs 0.329 +/- 0.509 optical density for IgG, p = 0.007 and 0.660 +/- 0.477 vs 0.116 +/- 0.229 for IgA, p < 0.001, respectively). In each patient, level of the two isotypes was clearly higher in gastric than in autologous rectal sample. In the overall study population, mean level of Helicobacter pylori IgG in rectal homogenate was not significantly (p = 0.16) different between Helicobacter pylori positive (48/62, 77%, 0.243 +/- 0.388 optical density) and negative (14/62, 23%; 0.095 +/- 0.088) patients. In same material, levels of Helicobacter pylori IgA were very low and undetectable either in Helicobacter pylori positive or negative patients. Although Helicobacter pylori IgG are detectable in rectal homogenates of Helicobacter pylori positive patients, present data suggest that these antibodies may not be local in origin but rather reflect circulating response. These observations do not support the view that large bowel mucosa is colonised by Helicobacter pylori.

Low Prevalence of p-ANCA in Unaffected Relatives of Patients with Ulcerative Colitis from a Mediterranean Area.

: Antineutrophil-cytoplasmic-autoantibodies (p-ANCA) are strongly associated with ulcerative colitis (UC) and may represent an indicator of genetic susceptibility to UC. To further examine whether p-ANCA may serve as a genetic marker of UC we evaluated the frequency of p-ANCA in unaffected family members of UC from a defined geographic area. A total of 110 patients with UC and 90 unaffected family members (first- or second-degree relatives) were tested. Controls included: 58 Crohn's disease (CD) patients with 25 unaffected relatives and 52 irritable bowel syndrome (IBS) patients with 20 healthy family members. p-ANCA were detected by enzyme-linked immunoassay followed by immunofluorescence. p-ANCA were detected in 57 UC patients (51.8%). Six of 90 (6.6%) unaffected relatives were positive for p-ANCA and 4 of these were from two families. In 3 of 35 families the proband and at least one unaffected relative were p-ANCA-positive. In five families with more than one member affected by UC, p-ANCA were detected in 2 of 19 (10.5%) unaffected relatives. Six CD patients (10.3%) and one (1.9%) in the IBS group were positive for p-ANCA. One family member was positive in the CD family group and 1 was positive in the control family group. In the group of families recruited for this study, p-ANCA were not more frequent in unaffected relatives of UC patients than in controls, suggesting that at least in the geographic area considered for this study p-ANCA may not represent a definite subclinical marker of susceptibility for UC.

Control of ilvIH transcription during amino acid downshift in stringent and relaxed strains of Escherichia coli.

Transcription of the ilvIH operon was reduced during amino acid starvation of wild-type Escherichia coli. The effect was abolished by a relA mutation and was enhanced by a spoT mutation, thus suggesting a possible negative role of ppGpp accumulation on ilvIH transcription. No effect of amino acid downshift was observed on the synthesis of lrp mRNA, encoding the positive regulator (Lrp) of ilvIH transcription.

Utilization of cellobiose and other beta-D-glucosides in Agrobacterium tumefaciens.

Agrobacterium tumefaciens strain C58 was able to utilize carbon from cellobiose and some other beta-D-glucosides as efficiently as from glucose. beta-D-glucoside utilization was partially inducible and the induction was subject to catabolite repression by glucose, independently of the presence of cyclic AMP in the medium. It was also independent of Ti plasmid-encoded functions. beta-D-glucosides were hydrolysed by a single, cytoplasmic and constitutively expressed beta-glucosidase, which was active on non-phosphorylated substrates and insensitive to glucose inhibition.

Salivary specific IgG is a sensitive indicator of the humoral immune response to Helicobacter pylori.

In humans, salivary antibodies are secreted during humoral immune response. Helicobacter pylori infection is associated with systemic humoral immune response reflected by raised serum levels of specific IgG. The present study was aimed at exploring whether salivary concentrations of specific H. pylori IgG are a reliable indicator of H. pylori infection. Serum and salivary samples were obtained from 291 subjects attending the GI clinic and tested for H. pylori-specific IgG by a direct ELISA (94% sensitivity, 95% specificity for serum determinations) using a crude H. pylori sonicate as antigen. Data are given as optical density (mean +/- S.D.). Levels of salivary H. pylori IgG paralleled those of circulating specific IgG in the 291 subjects studied (0.981 +/- 0.431 vs. 0.777 +/- 0.682, respectively). A significant positive correlation was found between specific H. pylori IgG in sera and saliva samples (r = 0.981, P < 0.0001). An overall concordance between circulating and salivary H. pylori IgG was observed in 238 out of the 291 (81.7%) subjects. Salivary H. pylori IgG represent a sensitive marker of specific humoral immune response and they may substitute circulating H. pylori IgG measurement when sera samples are not available.

In vivo footprinting analysis of Lrp binding to the ilvIH promoter region of Escherichia coli.

An in vivo footprinting analysis of the ilvIH regulatory region of Escherichia coli showed that the transcription activator Lrp binds to six sites, scattered over 250 bp upstream of the transcriptional start point. When Lrp-mediated activation was impaired by the presence of exogenous leucine, only one promoter-distal site (site 2) was partially protected by Lrp binding. Equilibrium dialysis experiments showed the formation of an Lrp-leucine complex in vitro. These results suggest that leucine negatively affects ilvIH transcription because its interaction with Lrp reduces the efficiency of binding of the regulatory protein to the promoter region.