The Use of Rice in Brewing

Rice could be a useful raw material for the production of a gluten-free beer-like beverage. In today’s beer brewing industry, rice is primarily used as an adjunct in combination with barley malt. But, recently, there is some information about rice malt for brewing an all-rice malt beer. The use of rice as an adjunct in brewing is described highlighting the quality attributes of the final beer. The rice grain quality attributes of different samples are reported in order to evaluate their attitude to malting and brewing and also considering their enzymatic activity. Then, the different brewing processes to produce all-rice malt beers will be described and the final gluten-free rice beers is evaluated and compared to a barley malt beer. Finally, the levels of major aroma-active components of an all-rice malt beer and the results of the sensory analysis assessing the beer-like character of the rice beverage are reported. The obtained beer samples show a content of volatile compounds comparable with a barley malt beer. The sensory profile of the rice malt beer is similar to a barley malt beer in aroma, taste and mouthfeel

A novel mutation in SACS gene in a family from southern Italy

A form of autosomal recessive spastic ataxia (ARSACS) has been described in the Charlevoix and Saguenay regions of Quebec. So far a frameshift and a nonsense mutation have been identified in the SACS gene. The authors report a new mutation (1859insC), leading to a frameshift with a premature termination of the gene product sacsin, in two sisters from consanguineous parents. The phenotype is similar to previously described patients with ARSACS

Chelating properties of beer: Implications on calcium homeostasis in PE/CA-PJ15 cells

Abstract Beer contains a large variety of different molecules, of which some can chelate Ca 2+. Here, we show that in PE/CA-PJ15 cells, an experimental model previously employed to investigate Ca 2+ homeostasis, chemical entities with Ca 2+ -chelating properties can markedly impact intra- and extra-cellular levels of the metal ion. This was consistently shown by commercial beers, as well as aliquots of unfinished product taken during the last step (clarification) of the brewing process. Our data suggest that a large number of molecules with chelating properties, can cross the cell membrane and, thus, potentially lead to important biological effects associated with changes in Ca 2+ homeostasis. In this regard, when PE/CA-PJ15 cells were exposed to H 2 O 2 in order to experimentally prompt an oxidative stress, beer antagonized a non-capacitative Ca 2+ entry that was otherwise elicited by H 2 O 2 in its absence. Higher Ca 2+ -chelating activity of stout, as compared to lager beer, suggest that melanoidins, which are generally present in dark malts, are major chelating agents in dark beers. Further, based on dose-response determinations, we report, for the first time, that Ferulic Acid can bind both intra- and extra-cellular Ca 2+ and, as one of the most abundant hydroxycinnamic acids in malted barley, largely account for Ca 2+ chelation. These results support the notion that beer may be considered a natural source of chemical entities that, based on their binding activity to Ca 2+ and, possibly, other metal ions, might be considered as nutritional supplements, detoxification agents, or antibiotics

Sphingosine-1-phosphate modulates vascular permeability and cell recruitment inacute inflammation in vivo.

The sphingosine kinase (SPK)/sphingosine-1-phosphate (S1P) pathway recently has been associated with a variety of inflammatory-based diseases. The majority of these studies have been performed in vitro. Here, we have addressed the relevance of the SPK/S1P pathway in the acute inflammatory response in vivo by using different well known preclinical animal models. The study has been performed by operating a pharmacological modulation using 1) L-cycloserine and DL-threo-dihydrosphingosine (DTD), S1P synthesis inhibitors or 2) 2-undecyl-thiazolidine-4-carboxylic acid (BML-241) and N-(2,6-dichloro-4-pyridinyl)-2-[1,3-dimethyl-4-(1-methylethyl)-1H-pyrazolo[3,4-b]pyridin-6-yl]-hydrazinecarboxamide (JTE-013), specific S1P(2) and S1P(3) receptor antagonists. After local injection of carrageenan in mouse paw S1P release significantly increases locally and decreases during the resolution phase. Expression of SPKs and S1P(2) and S1P(3) receptors is increased in inflamed tissues. Administration of L-cycloserine or DTD caused a significant anti-inflammatory effect. By using different animal models we have also demonstrated that the SPK/S1P pathway contributes to changes in vascular permeability and promotes cell recruitment. The S1P effect on cell recruitment results is receptor-mediated because both JTE-013 and BML-241 inhibited zymosan-induced cell chemotaxis without effect on vascular leakage. Conversely, changes in vascular permeability involve mainly SPK activity, because compound 48/80-induced vascular leakage was significantly inhibited by DTD. In conclusion, the SPK/S1P pathway is involved in acute inflammation and could represent a valuable therapeutic target for developing a new class of anti-inflammatory drugs

Genetic Ablation Of The Fpr1 Gene Prevents Emphysema In Mice Chronically Exposed To Cigarette Smoke

INTRODUCTION: Cigarette smoke (CS) is the main causative factor of COPD in man. Morphological features of COPD including emphysema and chronic bronchitis associated with mucus hypersecretion can be induced in mice by chronic CS exposure. The peptide fMLP (N-formyl-L-methionyl-L-leucyl-L-phenylalanine) is an active component of cigarette smoke (CS). fMLP interacts on the neutrophil and macrophage membranes with a high-affinity receptor subtype (FPR) and with a low-affinity subtype FPRL1 promoting a chemotactic response, superoxide anion production and degranulation. fMLP-receptors are found to be increased in the lavage fluids from cigarette smokers and subjects with COPD. To date, the role of FPRs in COPD remains poorly understood. We examined whether FPR contributes to lung damage induced by CS, by comparing the response of FPR knockout (Fpr1-/-) mice with that of wild-type (WT) C57 Bl/6 mice. METHODS and RESULTS: After chronic exposure to CS (3 cigarettes/day, 5 days/week for 7 months) WT mice showed significant foci of emphysema disseminated throughout the lung parenchyma with a significant increase of the mean linear intercept (+ 21 %) and a decrease of the internal surface area (– 13 %). Air-control groups and smoke exposed Fpr1-/- mice showed no areas of emphysema. Acute smoke exposure (5 cigarettes/day, for 3 days) caused in WT mice a 3,7 fold and a 1,3 fold increase in BALF neutrophils and macrophages, respectively. Fpr1 ablation in mice prevented after CS exposure the increase of neutrophils and macrophages by 73 and 42%, respectively. CONCLUSIONS: This study supports a role for FPR signalling in the development of CS-induced emphysema