Impact of juçara (Euterpe edulis) fruit waste extracts on the quality of conventional and antibiotic-free broiler meat.

Juçara (Euterpe edulis) is a native Brazilian palm tree from the Atlantic Forest, whose fruit-processing waste can present high concentration of antioxidant compounds. This research was assessed to determine the antioxidant potential of juçara waste extracts aiming to reduce the lipid and protein oxidation processes on conventional and antibiotic-free broiler meat throughout 9 d during refrigerated storage. The juçara waste extracts were obtained by microwave-assisted extraction. Two different extracts were tested based on the optimum point obtained when checking total phenolic (TPC) contents (Extract P) and antioxidant activity (Extract A) based on a previous study. The treatments using conventional and antibiotic-free broiler meat included: chicken patties without antioxidant addition (AFBNC and CBNC), with synthetic antioxidant (BHT) (AFBPC and CBPC), with Extract P (AFBEP and CBEP) and with Extract A (AFBEA and CBEA), totaling 8 treatments. Antioxidant activity of extracts along with TPC, flavonoid, anthocyanin, and tannin contents of extracts and patties were assessed. Proximate composition, fatty acid profile, lipid and protein oxidation process, and instrumental color were analyzed in patty treatments. Although both extracts had similar content of TPC and tannin, extract A presented the highest anthocyanin, while extract P exhibited the highest flavonoid. While extract A exhibited the highest antioxidant activity, extract P was highly influential in the stability of lipid oxidative degradation in both types of broiler meat (AFBEP and CBEP), and as successful as BHT (AFBPC and CBPC). In addition, extract P was also able to stabilize protein oxidation in conventional broiler meat (CBEP) from the third day, until the end of the storage period. Therefore, the fruit waste extract P of juçara can be a promising source of natural antioxidants to prevent the oxidative process in conventional and antibiotic-free broiler meat.

Everybody loves cheese: crosslink between persistence and virulence of Shiga-toxin Escherichia coli.

General cheese manufacturing involves high temperatures, fermentation and ripening steps that function as hurdles to microbial growth. On the other hand, the application of several different formulations and manufacturing techniques may create a bacterial protective environment. In cheese, the persistent behavior of Shiga toxin-producing Escherichia coli (STEC) relies on complex mechanisms that enable bacteria to respond to stressful conditions found in cheese matrix. In this review, we discuss how STEC manages to survive to high and low temperatures, hyperosmotic conditions, exposure to weak organic acids, and pH decreasing related to cheese manufacturing, the cheese matrix itself and storage. Moreover, we discuss how these stress responses interact with each other by enhancing adaptation and consequently, the persistence of STEC in cheese. Further, we show how virulence genes eae and tir are affected by stress response mechanisms, increasing either cell adherence or virulence factors production, which leads to a selection of more resistant and virulent pathogens in the cheese industry, leading to a public health issue.

Adipokine Gene Single-Nucleotide Polymorphisms in Portuguese Obese Adolescents: Associations with Plasma Concentrations of Adiponectin, Resistin, IL-6, IL-1ß, and TNF-α.

BACKGROUND: The genetic contribution to obesity and to circulating adipokine levels has not been completely clarified. We aimed to evaluate adipokine genes' single-nucleotide polymorphism (SNP) prevalence and its association with circulating adipokine levels and risk factors for cardiovascular disease in an obese Portuguese pediatric population. METHODS: Two hundred forty-eight obese adolescents (mean age 13.4 years old; 47.2% females) participated in a cohort study. We screened 12 SNPs by direct sequencing in five adipokine genes: adiponectin (ADIPOQ: rs16861194, rs17300539, rs266729, rs2241766, rs1501299), interleukin-1ß (IL-1ß; rs1143627), IL-6 (IL-6; rs1800795), tumor necrosis factor-α (TNF-α; rs1800629), and resistin (RETN; rs1862513, rs3219177, rs3745367, rs3745368). Biochemical analysis included determination of circulating adipokines, C-reactive protein (CRP) levels, lipid profile, and markers of insulin resistance. RESULTS: Compared to males, females presented higher circulating levels of insulin, adiponectin, IL-6, resistin, and leptin concentrations, but lower TNF-α levels. No statistically significant differences were found for genotype or allelic distributions between genders. In the whole sample population, adiponectin levels were influenced by ADIPOQ rs17300539 (c.-1138G>A; lower in subjects with GG genotype). When only males were considered, IL-1ß, IL-6, and TNF-α levels were associated with ADIPOQ rs1501299 (c.214 + 62G>T; higher in GG subjects). TNF-α concentrations were modulated by TNF-α rs1800629 (c.-488G>A; lower in GG males), RETN rs1862513 (c.-216C>G; higher in CC subjects), and RETN rs3219177 (c.118 + 39C>T; higher in CC subjects). Leptin levels were influenced by IL-1ß rs1143627 (c.-118C>T) presenting TT individuals' lower levels. CONCLUSIONS: Our data demonstrate that in pediatric obese patients, some adipokine gene SNPs have an association with circulating adipokine levels and lipid profile.

Analysis of the UDP-glucuronosyltransferase gene in Portuguese patients with a clinical diagnosis of Gilbert and Crigler-Najjar syndromes.

We describe the molecular study in a cohort of 120 Portuguese patients with the clinical diagnosis of Gilbert syndrome and in one with the diagnosis of Crigler-Najjar syndrome type II, as well as a prenatal diagnosis of Crigler-Najjar syndrome type I. Among the 120 unrelated patients with Gilbert syndrome, 110 were homozygous for the [TA]7 allele ([TA]7/[TA]7), and one patient was a compound heterozygote for two different insertions ([TA]7/[TA]8). The remaining 9 patients were heterozygous for the TA insertion ([TA]6/[TA]7). Additional studies in these 9 patients revealed heterozygosity for the c.674T>G, c.488_491dupACCT and c.923G>A mutations, in 1, 1 and 4 patients, respectively. The patient with Crigler-Najjar syndrome type II was a compound heterozygote for [TA]7 and the c.923G>A mutation. The undocumented polymorphisms c.-1126C>T and c.997-82T>C were also detected in the course of this study. Prenatal diagnosis in a family with a boy previously diagnosed as Crigler-Najjar syndrome type I and homozygosity for the c.923G>A mutation revealed that the fetus was unaffected. Homozygosity for the [TA] insertion was found to be the most frequent cause of GS in our population. Identification of further mutations in the UGT1A1 gene was also seen to contribute significantly towards diagnosis.

A new case of (TA)8 allele in the UGT1A1 gene promoter in a Caucasian girl with Gilbert syndrome.

The authors describe a 5-year-old Caucasian girl, referred to their hospital for evaluation of an unconjugated hyperbilirubinemia (57.9 micromol/L) detected from blood analysis during an episode of fever. The molecular analysis of the TATA-box region of the UGT1A1 gene revealed that the patient was a compound heterozygote for two insertions, one TA and the other TATA [(TA)(7)/(TA)(8)]. This is the first case of (TA)8 allele found in a Portuguese Caucasian patient and the third found in the literature.

[Glucose-6-phosphate dehydrogenase deficiency, neonatal hyperbilirubinemia and Gilbert syndrome]. / Défice de glicose-6-fosfato desidrogenase, ictericia neonatal e sindroma de Gilbert.

The aim of this work was to evaluate the influence of abnormal UDP-glucoronosyltransferase-1 (UGT1A1) gene variant, on the incidence and severity of neonatal hyperbilirubinemia, in glucose-6-phosphate dehydrogenase (G6PD) deficient newborns. The A(TA)nTAA region in the promoter of the UGT1A1 gene was analysed in 20 children with G6PD deficiency. Fourteen of these children had the African type variant (G6PDA-) and 6 had different variants (G6PDNara, G6PDGuadalajara, G6PDDurham, G6PDTomah, G6PDAveiro e G6PDNashville) related to chronic nonspherocytic haemolytic anaemia (CNSHA). The existence of a positive history of neonatal hyperbilirubinemia, as well as its severity was registered. The incidence of neonatal hyperbilirubinemia was increased in this group of children (90%) and was not associated with abnormal alleles of the UGT1A1 gene. It was not possible to assess the influence of abnormal alleles in the severity of the neonatal hyperbilirubinemia. However, these abnormal alleles did not account for the severity of jaundice in children who presented variants related to CNSHA, since 5 were treated with an exchange transfusion and none presented abnormal alleles.