Helicobacter pylori and Barrett’s esophagus: a protective factor or a real cause?

Notwithstanding the definite aetiopathogenetic path of certain diseases, the relationship between Helicobacter pylori (H. pylori) and Barrett’s esophagus (BE), a condition that increases the risk for dysplasia and consequently adenocarcinoma of the distal esophagus and esophagogastric junction, remains uncertain. This paper reviews the current scientific literature with emphasis on the protective correlation between H. pylori infection and BE and demonstrates that a causal relationship has not been disproved with certainty. Furthermore, H. pylori infection could pose a risk for the onset of gastroesophageal reflux disease (GERD), which could in turn trigger BE, a precancerous lesion, and subsequently cause cancer. By analyzing the current available data, this article tries to verify that H. pylori infection is the underlying cause of esophageal cancer.

Colorectal cancer: an update on the effects of lycopene on tumor progression and cell proliferation.

Colorectal cancer (CRC) is one of the most common cancers worldwide. Various factors, including oxidative stress, where excessive productions of reactive oxygen species (ROS) and reactive nitrogen species (RNS) occur, contribute to its pathogenesis. Numerous studies have investigated the effect of antioxidant substances derived from food such as fruits and vegetables; however, data on Lycopene are still rare. Studies on HT-29 colorectal cancer cells and on animal models have shown that lycopene has effects on cell proliferation and on the progression of the CRC by interacting with various cellular signaling pathways. This analysis of the literature focused on the antioxidant effect of lycopene, a substance that is found in the tomato.

Tea catechins induce crosstalk between signaling pathways and stabilize mast cells in ulcerative colitis.

It is well documented that nutraceuticals, in general, and Green tea catechins, in particular, possess a potential therapeutic value in inflammatory bowel diseases (IBD) due to their anti-oxidative and anti-inflammatory effects. This study aimed to investigate the possible mechanism of action of catechins in a rat model of colitis induced by 2.4.6 trinitrobenzene sulfonic acid (TNBS). Thirty-five young adult Sprague-Dawley rats were divided into four groups: normal control (n=5), catechins (n=9), TNBS (n=9) and TNBS plus catechins (n=12) treated. Catechin in the form of Epigallocatechin-3-gallate (EGCG) was administered daily by intraperitoneal injection, 1 week before the induction date of UC. Biopsies of the descending colon were collected on days 3, 10 and 17, and partly frozen for molecular studies or fixed for light microscopy. The status of intestinal tissue alterations and mast cells number were also assessed, as well as the mRNA expressions of IL-6, TNF-a and NF-kB, and determination of ROS expression. Histological data depicted a significant amelioration in the TNBS- and EGCG-treated rats compared to the non-treated animals. Catechin expressed strong anti-inflammatory and anti-oxidant effects, ameliorated ulcerative colitis and stabilized mast cells. The mechanism of action occurred basically through the NF-kB pathway and possibly through a crosstalk with other pathways.

Estrogens control inflammation in experimental colitis.

There is now a wealth of experimental evidence indicating that the deficit in endogenous estrogen facilitates the onset of inflammation that can be antagonized by estrogen replacement therapy. This work investigated the role of estrogen in the control of intestinal inflammation in a panel of colitis models, focusing on the morphological changes, the activity of mast cells, the expression of cytokines (IL-1beta, IL-6, and TNF-alpha), fibronectin and reactive oxygen species. Two hundred adult male rats were divided into 4 groups: colitis was induced in Group I and Group II but only the latter was treated with estrogen; Group III received estrogen only, and Group IV saline. Colitis was induced in 4 models using: iodoacetamide; iodoacetamide + enteropathogenic E. coli; 2, 4, 6-Trinitrobenzene sulfonic acid; and dextran sulfate sodium salt. Macroscopic and microscopic evaluations of abdominal structures as well as molecular analysis were made on days 7, 14, 28 and 56. There was a significant improvement in the health condition of the estrogen-treated rats: the inflammation scores were reduced by at least 10-15%, the number of mast cells in the colon decreased by 30%, fibronectin expression was only 50% and reactive oxygen species decreased by 30%. In addition, there was a significant decrease in TNF-alpha, IL-6 and IL-1beta expression by about 25%. In conclusion, there was an improvement in the inflammatory status in all estrogen-treated groups through the duration of the experiment at all-time points. In addition, there was less tissue necrosis as depicted by less fibronectin and a marked antioxidant effect.

Modulation of Beta2 and Beta3 integrins in experimental colitis induced by iodoacetamide and enteropathogenic E. coli.

Integrins can modulate the infiltration of inflammatory cells and the secretion of various inflammatory mediators, essential players in the pathogenesis of colitis. This study explores the role of beta2 and beta3 integrin signaling and their possible role in experimental colitis. A total of 160 adult male Sprague-Dawly rats were divided into 4 equal groups: methylcellulose, bacteria, iodoacetamide and iodoacetamide plus bacteria. Clinical symptoms and signs of colitis were checked daily and colonic tissues were biopsied on days 3, 14, 28, and 56 post induction. Histological studies along with histochemical analysis and polymerase chain reaction of beta2, beta3 and alphavbeta3 were performed according to standard procedures. The symptoms and signs were consistent with previously reported data on active colitis. The highest expression of beta3 integrin was in the combined treatment mostly on platelets, endothelial and inflammatory cells. In the same group, the expression of alphavbeta3 integrin complex reached the highest score after 56 days in all colonic layers. Beta2 integrin expression showed a 3-4-fold increase in the combined treatment group at all time points and kept increasing till day 56. It was mostly expressed in the mucosa and submucosa. In addition, the expression of both αvβ3 and αiiβ3 integrins was also elevated 2- to 10-fold, respectively, in the same colitis groups throughout the duration of the experiment. In conclusion, the combined treatment of IA and Enteropathogenic E. coli led to a significant upregulation of all the tested integrins throughout the experimental duration. Such upregulation of integrins could have contributed to the increase and chronicity of inflammation.

Rat model of burn wound healing: effect of Botox.

Animal models of burn play a crucial role in studying the mechanisms of burn wound progression and the factors that regulate various stages of healing. In this study, using a rat model, we assessed the effect of Botox in the healing process through parameters like transepidermal water loss (TEWL), histological alterations, transforming growth factor beta (TGF-beta1) and tumor necrosis factor alpha (TNF-alpha). Fifty Sprague-Dawley rats were inflicted with 5 cm2 second degree burn and divided into 2 groups; one group was injected intralesionally with Botox and the other with saline. Daily observation and transepidermal water loss measurement were performed. Biopsies were taken on days 0, 3, 8, 14, and 28 for histology and polymerase chain reaction, testing TGF-beta and TNF-alpha. The results showed no significant difference in TEWL except for slightly better preservation of moisture with Botox. Histology revealed relatively better and faster regeneration with Botox, delayed lower grade inflammation, and increase in fibroblasts. TNF-alpha had an acute increase of 21-fold then tapered down while TGF-beta levels increased on day 3 after TNF-alpha, peaked on day 8 and then started to decrease until complete healing. Botox improved the healing process and the cosmetic appearance of burn scar.

Review and update on the use of the microanastomotic coupler device for arterial anastomosis in free tissue transfer.

While a simple interrupted sutured anastomosis remains the gold standard in microsurgery, the introduction of the microanastomotic coupler device (MACD) has decreased procedure time and thrombosis risk, and improved the patency of venous anastomoses. The aim of this review is to update the evidence-based advantages of the MACD on arteries, based on clinical and experimental data, and to compare them to the hand-sewn approach in free flap transfer. All relevant articles that appeared in the PubMed and Medline/Ovid databases during the past three decades were reviewed. After exclusions, 11 studies were retained and discussed. The MACD had a generally shorter arterial anastomosis time, with improved flap survival and reduced ischaemia compared with the hand-sewn approach. The use of the MACD in arterial anastomosis is an efficient and less time-consuming alternative to the hand-sewn technique, provided that the selection of vessels is appropriate and the vessel diameter is large enough to do the anastomosis.

Frequency of the CCR5-delta 32 chemokine receptor gene mutation in the Lebanese population.

A direct correlation between HIV infection and mutation in the chemokine receptor (CCR5) gene has been established. However, such correlation has never been investigated in Lebanon. We report the frequency of the CCR5-delta 32 mutation in a random sample of 209 healthy, HIV-1 seronegative Lebanese aged 19-68. Overall, 4.8% were heterozygous for the mutation. Homozygosity was absent from our sample. The frequency for the CCR5-delta 32 allele was 2.5%. Distribution of the mutation was unaffected by sex, age, religion or educational level. The frequency in the Lebanese population is consistent with that in the origin of the mutation in northern Europe. This could be attributed to a gene flow into the Middle East from northern Europe.