A whole-grain cereal-rich diet increases plasma betaine, and tends to decrease total and LDL-cholesterol compared with a refined-grain diet in healthy subjects

Epidemiological studies have repeatedly found that whole-grain (WG) cereal foods reduce the risk of several lifestyle-related diseases, though consistent clinical outcomes and mechanisms are elusive. To compare the effects of a WG-rich diet with a matched refined-grain (RG) diet on plasma biomarkers and bowel health parameters, seventeen healthy subjects (eleven females and six males) completed an exploratory cross-over study with a 2-week intervention diet based on either WG- or RG-based foods, separated by a washout of at least 5 weeks. Both diets were the same except for the use of WG (150g/d) or RG foods. Subjects undertook a 4h postprandial challenge on day 8 of each intervention diet. After 2 weeks, the WG diet tended to decrease plasma total and LDL-cholesterol (both P=0·09), but did not change plasma HDL-cholesterol, fasting glucose, C-reactive protein or homocysteine compared with the RG diet. Plasma betaine and alkylresorcinol concentrations were elevated after 1 week of the WG diet (P=0·01 and P<0·0001, respectively). Clostridium leptum populations in faeces were increased after the WG diet, along with a trend for decreased faecal water pH (P=0·096) and increased stool frequency (P<0·0001) compared with the RG diet. A short controlled intervention trial with a variety of commercially available WG-based products tended to improve biomarkers of CVD compared with a RG diet. Changes in faecal microbiota related to increased fibre fermentation and increased plasma betaine concentrations point to both fibre and phytochemical components of WG being important in mediating any potential health effect

Mouse Alpha-amylase Loci, Amy-1^a and Amy-2^a, are Closely Linked

We have cloned a contiguous 106×10³ base-pair long stretch of mouse DNA. The isolated chromosomal DNA segment contains the single copy gene Amy-1a that is strongly expressed in the parotid gland and, 23×10³ base-pairs downstream from it, one member of the pancreas-specific Amy-2a oligogene family. At least two of the four Amy-2a genes, including the copy linked to Amy-1a, are efficiently transcribed. The cloned DNA sequences do not appear to specify messenger RNAs other than those encoding alpha-amylase in pancreas, parotid gland or liver. Transcription termination on Amy-1a occurs within 3×10³ base-pairs downstream from the polyadenylation site in both parotid gland and liver, in which this gene is transcribed at different rates from different promoters

Different Tissue-Specific Expression of the Amylase Gene <i>Amy-1</i> in Mice and Rats

We cloned the rat alpha-amylase gene Amy-1 and compared its structure and expression with its mouse counterpart. The results showed that the general organization of the transcriptionally active rat Amy-1 gene was similar to that of its mouse counterpart; i.e., the rat gene also contained two independent transcriptional promoters. The distance between the two promoters in the rat gene was, however, more than double (6 kilobases) that measured in the mouse gene (2.8 kilobases). In addition, the rat genome also contained an independent, orphonlike version of the weaker Amy-1 promoter, which was transcriptionally silent. In spite of the similar overall organization of the Amy-1 genes in mouse and rat cells, an interesting difference was observed in the expression of the weak promoter in these two closely related rodents. In rats this promoter was significantly active only in liver cells, while in mice it was utilized with similar efficiencies in parotid, liver, and pancrease cells. Moreover, the transcripts produced in rat liver had a very heterogeneous population of 5' ends, located between 180 and 220 nucleotides upstream of the two homologous start sites observed for this promoter in mouse liver, even though the sequences around this region were strongly conserved between the two species

The Role of Prophage for Genome Diversification within a Clonal Lineage of Lactobacillus johnsonii: Characterization of the Defective Prophage LJ771▿ †

Two independent isolates of the gut commensal Lactobacillus johnsonii were sequenced. These isolates belonged to the same clonal lineage and differed mainly by a 40.8-kb prophage, LJ771, belonging to the Sfi11 phage lineage. LJ771 shares close DNA sequence identity with Lactobacillus gasseri prophages. LJ771 coexists as an integrated prophage and excised circular phage DNA, but phage DNA packaged into extracellular phage particles was not detected. Between the phage lysin gene and attR a likely mazE (“antitoxin”)/pemK (“toxin”) gene cassette was detected in LJ771 but not in the L. gasseri prophages. Expressed pemK could be cloned in Escherichia coli only together with the mazE gene. LJ771 was shown to be highly stable and could be cured only by coexpression of mazE from a plasmid. The prophage was integrated into the methionine sulfoxide reductase gene (msrA) and complemented the 5′ end of this gene, creating a protein with a slightly altered N-terminal sequence. The two L. johnsonii strains had identical in vitro growth and in vivo gut persistence phenotypes. Also, in an isogenic background, the presence of the prophage resulted in no growth disadvantage

Are there regional variations in the diagnosis surveillance, and control of methicillin-resistant Staphylococcus aureus?

SCOPUS: ar.jinfo:eu-repo/semantics/publishe