Changes in upper airways microbiota in ventilator-associated pneumonia.

BACKGROUND: The role of upper airways microbiota and its association with ventilator-associated pneumonia (VAP) development in mechanically ventilated (MV) patients is unclear. Taking advantage of data collected in a prospective study aimed to assess the composition and over-time variation of upper airway microbiota in patients MV for non-pulmonary reasons, we describe upper airway microbiota characteristics among VAP and NO-VAP patients. METHODS: Exploratory analysis of data collected in a prospective observational study on patients intubated for non-pulmonary conditions. Microbiota analysis (trough 16S-rRNA gene profiling) was performed on endotracheal aspirates (at intubation, T0, and after 72 h, T3) of patients with VAP (cases cohort) and a subgroup of NO-VAP patients (control cohort, matched according to total intubation time). RESULTS: Samples from 13 VAP patients and 22 NO-VAP matched controls were analyzed. At intubation (T0), patients with VAP revealed a significantly lower microbial complexity of the microbiota of the upper airways compared to NO-VAP controls (alpha diversity index of 84 ± 37 and 160 ± 102, in VAP and NO_VAP group, respectively, p-value < 0.012). Furthermore, an overall decrease in microbial diversity was observed in both groups at T3 as compared to T0. At T3, a loss of some genera (Prevotella 7, Fusobacterium, Neisseria, Escherichia-Shigella and Haemophilus) was found in VAP patients. In contrast, eight genera belonging to the Bacteroidetes, Firmicutes and Fusobacteria phyla was predominant in this group. However, it is unclear whether VAP caused dysbiosis or dysbiosis caused VAP. CONCLUSIONS: In a small sample size of intubated patients, microbial diversity at intubation was less in patients with VAP compared to patients without VAP.

Influence of dietary inclusion of tannin extracts from mimosa, chestnut and tara on volatile compounds and flavour in lamb meat.

Tannins are compounds able to form complexes with proteins limiting their ruminal degradation and thus the synthesis of some odour-active compounds may be inhibited. Tannins are broadly divided in condensed tannins (CT) and hydrolysable tannins (HT). The study aimed to assess the influence of dietary inclusion of three commercial tannin extracts, namely mimosa (Acacia mearnsii; CT), chestnut (Castanea sativa; HT) or tara (Caesalpinia spinosa; HT) on volatile profile and flavour of meat and kidney fat from lambs. Comisana male lambs were divided into four groups (n = 9 each) and fed for 75 days with a concentrate-based diet (CON) or CON supplemented with 4% of one of the tannin extracts. Tannins reduced "pastoral" odour in perirenal fat of lambs the meat of which was characterized by a very low perception of this attribute. It may be assumed that p-cresol and 8-methylnonanoic acid mostly contributed to "pastoral" odour expression in the diet without condensed or hydrolysable tannins.

Influence of dietary cardoon meal on volatile compounds and flavour in lamb meat.

Cardoon meal is a by-product retained after oil extraction from the seeds of cultivated Cynara cardunculus var. altilis that has been proposed as a valuable resource for animal feeding. The study aimed to assess the influence of its dietary inclusion on volatile profile and flavour of meat and kidney fat from lambs. Fifteen Sarda × Comisana male lambs were randomly divided in two groups and fed for 75 days with a concentrate-based diet containing 15% cardoon meal (CMD, n = 7) or dehydrated alfalfa (CON, n = 8). Cardoon meal inclusion reduced the "barnyard/animal" odour perceived by a trained panel in kidney fat, which could be associated with the aromatic compound p-cresol (4-methylphenol), detected only in CON diet. Considering the other aroma volatiles regarded as the main contributors for the characteristic lamb flavour, both diets were characterized by moderate to low levels of 4-methyloctanoic acid, skatole and indole while 4-methylnonanoic acid and 4-ethyloctanoic acid were not detected.

Single injection of platelet-rich plasma in a rat Achilles tendon tear model.

The purpose of this study was to determine the efficacy of platelet-rich plasma (PRP) 1-injection during an Achilles tendon rat tear model. 80 male adult imbreded rats (Wistar Kyoto), underwent under surgical tendon rupture. 40 Animal (PRP group rats) were given a local injection with 0,25 mL of PRP, and 40 animal (control group) were given the same quantity of control solution. The rats were sacrified at 1, 2, 4 and 6 weeks (each time point, 20 rats of the each group) after surgical tear and tendon tissue was analysed by macroscopic aspect, histology, immunostaining and Real Time (RT)-PCR to evaluate tissue repair. PRP improved tendon remodelling by better coordination of the reconstructive process with earlier formation of tendon-like continuity only in the first week after surgery. However, after 2,4 and 6 weeks, Achilles tendons in the PRP group had no difference compared to the control group. Immunostaining and RT-PCR did not show any difference between PRP treated and untreated group. Based on these findings a single injection of PRP appear not useful for Achilles rat tendon tear.

Increased p21 expression in chondrocytes of achondroplasic children independently from the presence of the G380R FGFR3 mutation.

BACKGROUND: Achondroplasia (ACH) represents the major cause of dwarfism and is due to mutations in the fibroblast growth factor receptor 3 (FGFR3) gene. The cellular mechanisms involved in the reduced growth have been mainly described for in vitro or in vivo models, but few data have been obtained for humans. METHODS: Thirteen children with ACH were enrolled in the study; the presence of FGFR3 mutations was determined by restriction fragment length polymorphism analysis and sequencing, whereas protein expression in cartilage biopsy was assessed by immunohistochemistry. RESULTS: Chondrocytes in cartilage biopsies of ACH children were characterized by the presence of growth arrest mediated by STAT activation (both STAT1 and STAT5) and increased expression of p21 and cyclin D1, whereas no expression of either p53 or cyclin D3 could be detected. This mechanism was present in ACH children carrying the G380R mutation but also in a patient in whom no mutation could be detected in the entire coding region of the FGFR3 gene. CONCLUSIONS: These data thus demonstrate the presence of a common final mechanism involving p21 and possibly leading to a block in chondrocyte proliferation.

Hemochromatosis gene mutations and iron metabolism in celiac disease.

BACKGROUND AND OBJECTIVES: Iron deficiency anemia is a common manifestation of celiac disease, which may be due to genetic and environmental factors. HFE mutations, frequent in Caucasian populations, can cause increased intestinal iron absorption and thus could protect against the development of iron deficiency. The aim of this study was to evaluate the prevalence of HFE mutations and their effect on iron metabolism in Italian celiac patients at diagnosis and after a gluten-free diet. DESIGN AND METHODS: C282Y and H63D mutations were assessed by polymerase chain reaction (PCR) and restriction enzyme digestion in 203 patients with celiac disease and in 206 controls. HLA alleles were determined by sequence-specific primers and PCR. Duodenal histology was graded using Marsh's classification, and iron parameters measured by standard techniques. RESULTS: The frequency of the C282Y mutation was similar in celiac patients and controls (0.034 vs. 0.031); comparable frequencies were detected also for the H63D allele (0.170 vs. 0.136 in celiac patients and controls, respectively). Neither of the two HFE mutations affected iron indices in celiac patients at diagnosis, whereas a significant inverse correlation was detected between hemoglobin or ferritin and severity of histological damage (Marsh 3C or 3B vs. 3A, p<0.05 for both parameters). After a gluten-free diet, a slight increase in hemoglobin levels was observed in C282Y carriers as compared to controls, but only in female patients (p=0.044). INTERPRETATION AND CONCLUSIONS: In Italian patients with untreated celiac disease, HFE mutations do not constitute a protective factor against the development of iron deficiency, which seems to be mainly determined by the severity of the intestinal lesions.