Probiotics Prevent Intestinal Barrier Dysfunction in Acute Pancreatitis in Rats via Induction of Ileal Mucosal Glutathione Biosynthesis

BACKGROUND: During acute pancreatitis (AP), oxidative stress contributes to intestinal barrier failure. We studied actions of multispecies probiotics on barrier dysfunction and oxidative stress in experimental AP. METHODOLOGY/PRINCIPAL FINDINGS: Fifty-three male Spraque-Dawley rats were randomly allocated into five groups: 1) controls, non-operated, 2) sham-operated, 3) AP, 4) AP and probiotics and 5) AP and placebo. AP was induced by intraductal glycodeoxycholate infusion and intravenous cerulein (6 h). Daily probiotics or placebo were administered intragastrically, starting five days prior to AP. After cerulein infusion, ileal mucosa was collected for measurements of E. coli K12 and (51)Cr-EDTA passage in Ussing chambers. Tight junction proteins were investigated by confocal immunofluorescence imaging. Ileal mucosal apoptosis, lipid peroxidation, and glutathione levels were determined and glutamate-cysteine-ligase activity and expression were quantified. AP-induced barrier dysfunction was characterized by epithelial cell apoptosis and alterations of tight junction proteins (i.e. disruption of occludin and claudin-1 and up-regulation of claudin-2) and correlated with lipid peroxidation (r>0.8). Probiotic pre-treatment diminished the AP-induced increase in E. coli passage (probiotics 57.4+/-33.5 vs. placebo 223.7+/-93.7 a.u.; P<0.001), (51)Cr-EDTA flux (16.7+/-10.1 vs. 32.1+/-10.0 cm/s10(-6); P<0.005), apoptosis, lipid peroxidation (0.42+/-0.13 vs. 1.62+/-0.53 pmol MDA/mg protein; P<0.001), and prevented tight junction protein disruption. AP-induced decline in glutathione was not only prevented (14.33+/-1.47 vs. 8.82+/-1.30 nmol/mg protein, P<0.001), but probiotics even increased mucosal glutathione compared with sham rats (14.33+/-1.47 vs. 10.70+/-1.74 nmol/mg protein, P<0.001). Glutamate-cysteine-ligase activity, which is rate-limiting in glutathione biosynthesis, was enhanced in probiotic pre-treated animals (probiotics 2.88+/-1.21 vs. placebo 1.94+/-0.55 nmol/min/mg protein; P<0.05) coinciding with an increase in mRNA expression of glutamate-cysteine-ligase catalytic (GCLc) and modifier (GCLm) subunits. CONCLUSIONS: Probiotic pre-treatment diminished AP-induced intestinal barrier dysfunction and prevented oxidative stress via mechanisms mainly involving mucosal glutathione biosynthesis.Original Publication:Femke Lutgendorff, Rian M Nijmeijer, Per A Sandström, Lena M Trulsson, Karl-Eric Magnusson, Harro M Timmerman, L Paul van Minnen, Ger T Rijkers, Hein G Gooszen, Louis M A Akkermans and Johan D Söderholm, Probiotics prevent intestinal barrier dysfunction in acute pancreatitis in rats via induction of ileal mucosal glutathione biosynthesis., 2009, PLoS ONE, (4), 2, e4512.http://dx.doi.org/10.1371/journal.pone.0004512Licensee: Public Library of Science (PLoS)http://www.plos.org

Use of zinc phosphate cement as a luting agent for Denzir™ copings: an in vitro study

BACKGROUND: The clinical success rate with zinc phosphate cemented Procera crowns is high. The objective with this study was to determine whether CADCAM processed and zinc phosphate cemented Denzir copings would perform as well as zinc phosphate cemented Procera copings when tested in vitro in tension. METHODS: Twelve Procera copings and twenty-four Denzir copings were made. After the copings had been made, twelve of the Denzir copings were sandblasted on their internal surfaces. All copings were then cemented with zinc phosphate cement to carbon steel dies and transferred to water or artificial saliva. Two weeks after cementation, half of the samples were tested. The remaining samples were tested after one year in the storage medium. All tests were done in tension and evaluated with an ANOVA. RESULTS: Sandblasted and un-sandblasted Denzir copings performed as well as Procera copings. Storage in water or artificial saliva up to one year did not decrease the force needed to dislodge any of the coping groups. Three copings fractured during testing and one coping developed a crack during testing. The three complete fractures occurred in Procera copings, while the partly cracked coping was a Denzir coping. CONCLUSION: No significant differences existed between the different material groups, and the retentive force increased rather than decreased with time. Fewer fractures occurred in Denzir copings, explained by the higher fracture toughness of the Denzir material. Based on good clinical results with zinc phosphate cemented Procera crowns, we foresee that zinc phosphate cement luted Denzir copings are likely to perform well clinically

Hydrolytic degradation of dental composites and effects of silane-treatment and filler fraction on compressive strength and thermal expansion of composites

Some researchers have suggested that the weakest link of dental composites is the filler-matrix bond. However, due to incompleteness of information dealing with this bond and its stability in a humid environment, it was considered desirable to investigate the effect of water on this region, as well as the influence of filler bonding and filler fraction on compressive strength and thermal expansion Experimental composites containing different filler fractions of either silane-treated or untreated fillers were made. Compressive strength and coefficient of thermal expansion were determined using routine methods, while the hydrolytic degradation was investigated by measuring changes in concentrations of elements in the storage water using atomic absorption spectrophotometry. Scanning electron microscopic investigations were made on fractured samples. The diffusion coefficient of a representative resin system was determined gravimetrically. Seven commercial composites were investigated regarding hydrolytic degradation. The filler compositions of these composite materials were determined by emission spectroscopy or energy-dispersive x-ray analysis before storage in distilled water. This water was replaced and analyzed monthly using plasma spectrophotometry or atomic absorption spectrophotometry. After completed water storage the samples were fractured and investigated by use of scanning electron microscopy. From the results of these studies the following conclusions were drawn: 1. The compressive strength of composites changes linearly with increased filler fraction. Contrary to bonded fillers, composites containing unbonded fillers lost strength with increased filler fraction. 2. Water diffuses through the polymer matrix and attacks the filler particles. This degradation is most pronounced for untreated fillers containing glass modifying elements such as sodium, barium and strontium. 3. The resin, used as a matrix, influences the speed with which the hydrolytic degradation of the filler proceeds. 4. The hydrolytic degradation of the filler seemed to be associated with micro-crack formation occurring in the matrix. Of the investigated composites, the micro-filled resin showed the lowest frequency of such crack formations. 5. The coefficient of thermal expansion decreases linearly with increased filler fraction. Silane treatment did not influence this coefficient. 6. Using a simplified model to predict stresses in a particle filled composite indicates that rather high stress levels are induced in the polymer matrix due to polymerization shrinkage. This shrinkage induces radial compressive and tangential tensile stresses with respect to the filler surface. Increased filler fraction increases the tangential tensile stresses but reduces the compressive radial stresses.S. 1-66: sammanfattning, s. 67-168: 6 uppsatserdigitalisering@um

Clinical wear performance of eight experimental dental composites over three years determined by two measuring methods

The effect of matrix selection, filler composition, filler silanization, operator variations, and test site (dental clinic) on the wear rate of eight composites were evaluated, The wear was measured on replicas using both a microscopic and a laser scanning measuring method. The average wear rate on contact-free surfaces was 9.2 +/- 4.2 mum/month with the microscopic measurement and 8.5 +/- 3.7 mum/month with the laser scanner over the 36-month period. The urethane-based composites performed significantly better than those which were bisGMA-based. Restorations placed at one dental clinic showed significantly lower initial wear. There was also a significant difference between the operators that was most pronounced during the first 6 months. The other variable (filler composition and silane treatment) did not affect the wear rate significantly

http://urn.kb.se/resolve?urn=urn:nbn:se:liu:diva-17082 Probiotics Prevent Intestinal Barrier Dysfunction in Acute Pancreatitis in Rats via Induction of Ileal Mucosal

Probiotics prevent intestinal barrier dysfunction in acute pancreatitis in rats via induction of ileal mucosal glutathione biosynthesis

Probiotics induce systemic increase in GSH levels and GCL activity.

<p>After 5 days of pre-treatment with placebo (pla, n = 12) or probiotics (pro, n = 12), rats were subjected to acute pancreatitis (AP, n = 12), a sham-procedure (n = 12) or not operated (control, n = 5). Whole blood was sampled 1) before treatment, 2) after 5 days of pre-treatment, immediately before induction of AP and 3) six hours after induction of AP or sham-procedure. Time course of plasma GSH levels (A) and GCL activity in red blood cells (B) was monitored. The graphs show average (±SD). All analyses were run in duplicates. Comparisons were performed using ANOVA followed by Tukey's HSD. *<i>P</i><0.001, probiotics <i>vs.</i> placebo. Associations between (C) ileal lipid peroxidation, (D) bacterial passage, (E) ⁵¹Cr-EDTA flux, (F) ileal GSH content six hours after induction of AP and GCL activity in red blood cells immediately before subjection to AP.</p

Probiotics prevented disruption of tight junction proteins.

<p>After 5 days of pre-treatment with placebo (pla) or probiotics (pro), rats were subjected to acute pancreatitis (AP), or a sham-procedure. Ileal sections were stained with occludin, claudin-1 or -2 antibodies (green), counterstained with DAPI (blue) and visualized by confocal laser scanning microscopy. Bar = 500 µm. The higher magnification (100×/1.30) images shown in the insets are typical details of crypts (left) and villi (right). Probiotics prevented the deleterious effects of AP on occludin and caused redistribution of occludin to the apical surface (arrowhead). Acute pancreatitis-induced detachment of epithelial cells seems to be preceded by loss of claudin-1 (arrowhead) and was reduced by probiotic pre-treatment; though probiotics could not prevent the AP-induced formation of aggregates of claudin-1 in the cytosol (arrowhead). Probiotics prevented AP-associated up-regulation of claudin-2 in both crypts and villi (arrowhead). The patterns of staining are typical of that seen in 4 sections of 4 rats per group.</p