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Objective: To investigate whether probiotic bacteria given perioperatively may adhere to the colonic mucosa, reduce concentration of pathogens in stools, and modulate local immune function. Design: Prospective, randomized, double-blind, clinical trial. Methods: Thirty-one patients undergoing elective colorectal resection for cancer were allocated to receive either placebo (group A, n = 10), or a dose of 107 of a mixture of Bifidobacterium longum (BB536) and Lactobacillus jonhsonii (La1) (group B, n = 11), or the same mixture at a concentration of 109 (group C, n = 10). Probiotics or placebo were given orally in 2 doses/day for 3 days before operation. The same treatment continued postoperatively from day 2 to 4. Stools were collected before treatment (day -4), during surgery (day 0), and 5 days after operation. During the operation, colonic mucosa samples were harvested to evaluate bacterial adherence and to phenotype dendritic cell subsets by surface antigen expression (flow cytometry). Presence of BB536 and La1 was evaluated by the random amplified polymorphism DNA method. Results: The 3 groups were balanced for baseline and surgical parameters. BB536 was never found at any time point studied. At day 0, La1 was present in 60% of patients in group C in either stools or biopsy, in 27.2% in B, and none in the placebo group (p = 0.02, group C vs. A). There was a linear correlation between dose given and number of adherent La1 (p = 0.01). The rate of mucosal colonization by Enterobacteriaceae was 30% in group C, 82% in group B, and 70% in group A (p = 0.03, C vs. B). Enterobacteriaceae count in stools was 2.4 (log10 scale) in C, 4.2 in B, and 4.5 in A (p = 0.07). The same trend was observed for colonizing enterococci. La1 was not found at day +5. After ex vivo stimulation with lipopolysaccharides, groups C and B had a lower proliferation rate compared with group A. Moreover, dendritic phenotypes CD83-123, CD83-HLADR, and CD83-11c (markers of activation) were significantly less expressed in patients colonized with LA1 (p < 0.05). Conclusions: La1, but not BB536, adhere to the colonic mucosa, affect intestinal microbiota by reducing the concentration of pathogens, and modulate local immunity. [ABSTRACT FROM AUTHOR]

The article provides information on a study on the effect of hospital volume on outcome of pancreaticoduodenectomy (PD) in Italy. 1576 patients were involved in the study who underwent PD in 2003 and the hospitals were allocated to 4 volume groups. It was found that increasing hospital volume was associated with decreased mortality rate and the length of postoperative stay was lessened in very-high volume hospitals.

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Background Literature data report an association between some vitamin D receptor (VDR) polymorphisms and different kinds of tumours, including malignant melanoma (MM). Only three VDR polymorphisms ( FokI, TaqI and A-1012G) have been investigated in association with the presence of cutaneous MM or the development of metastases. Objectives The present paper analyses for the first time the association between BsmI polymorphism and MM prevalence together with Breslow thickness. In addition, the FokI single nucleotide polymorphism was also determined. Methods One hundred and one patients with MM and 101 healthy donors matched for age and sex were enrolled. Molecular VDR typing was performed by means of restriction fragment length polymorphism analysis. Results All cases and controls were in Hardy–Weinberg equilibrium for BsmI, FokI and A-1012G. Significant associations were found between the BsmI bb genotype frequency and MM ( P = 0·02) along with Breslow thickness ( P = 0·001). This same behaviour was not observed for the FokI or A-1012G polymorphisms. Multivariate logistic regression analysis confirmed these significant results after correction for age, gender, skin type and MM localization. Conclusions Although the biological meaning of the effects exerted by BsmI polymorphism is still under debate, the statistical association found in the present study suggests that further work should be done to verify this variant as a possible risk marker for MM and its aggressiveness, also considering that the real association may be due to other unknown genes linked to the BsmI b allele. [ABSTRACT FROM AUTHOR]