Status of nutrition labeling, health claims, and nutrient content claims for processed foods: 1997 Food Label and Package Survey

The Food and Drug Administration (FDA) conducts studies of food labels as part of its ongoing monitoring of the nutritional status of the US population. In 1994 FDA nutrition labeling rules were implemented and in 1997 the Food Label and Package Survey characterized various aspects of the labeling of processed, packaged foods, including nutrition labeling, health claims, and nutrient content claims. For the survey, FDA selected a multistage, representative sample of food products from the SCAN-TRACK food sales database (AC Nielsen Co, Schaumburg, Ill). FDA identified 58 product groups and selected those product classes from the database that accounted for 80% of sales in each group. From each product class, FDA selected the 3 top-selling product brands and randomly selected follower brands. Based on label information from a final sample of 1,267 food products, FDA determined the percentage of products sold that bear Nutrition Facts labels, health claims, and nutrient content claims. The purpose of this article was to present FDA findings regarding the status of food labels 3 years after implementation of the nutrition labeling rules. Nutrition-labeled products accounted for an estimated 96.5% of the annual sales of processed, packaged foods. An additional 3.4% of products sold were exempt from labeling regulations. Nutrient content claims and health claims appeared on an estimated 39% and 4%, respectively, of the products sold. Dietitians and other health care professionals can use this survey information to identify food types with specific label information and to assist the US consumer in making more varied and healthful food choices in the marketplace.     

Bacterial and mammalian DNA alkyltransferases sensitize Escherichia coli to the lethal and mutagenic effects of dibromoalkanes

Here we confirm and extend our previous studies demonstrating that the mutagenic potency of 1,2-dibromoethane (DBE) and dibromomethane (DBM) is markedly enhanced (not prevented) in bacteria expressing the O6- alkylguanine-DNA alkyltransferase (ATase) encoded by the Escherichia coli ogt gene. We demonstrate that, in close parallel with mutagenesis, the Ogt ATase sensitizes the bacteria to the lethal effects of these carcinogens, suggesting that one or more of the potentially mutagenic lesions induced by DBE and DBM in the presence of Ogt has additional lethal capacity. We further demonstrate that the sensitization to both lethality and mutagenesis by DBE and DBM is a property shared by other DNA alkyltransferases. This objective was accomplished by quantifying the induction of mutations and lethal events in ogt- ada- E. coli expressing an exogenous bacterial or mammalian ATase from a multicopy plasmid. Mammalian recombinant ATases enhanced the lethal and mutagenic actions of DBE and suppressed the lack of sensitivity of the vector- transformed bacteria to DBM. In most cases the order of effectiveness of the ATases ranked: murine > human > Ogt > rat. Further comparisons included the full-length Ada ATase from E. coli and a truncated Ada version (T-ada) that retains the O6-methylguanine binding domain of the protein. The full-length Ada ATase was effective in enhancing the lethality but not the mutagenicity induced by DBE and DBM. The T-ada ATase provided less sensitization than Ada to lethality by DBE, but of the three bacterial ATases T-ada yielded the highest sensitization to mutagenesis by this compound. T-ada and Ada ATases were in general less effective than the mammalian versions, with the exception of the rat recombinant ATase. The effectiveness of the different mammalian and bacterial ATases in promoting the deleterious actions of dibromoalkanes was compared with the effectiveness of these proteins in suppressing the lethal and mutagenic effects induced by N-nitroso-N-methylurea. The ability to sensitize E. coli to the lethal and mutagenic effects of DBE and DBM seems restricted to DNA alkyltransferase, since overexpression of thioredoxin (Trx) or glutaredoxin (Grx1) in ogt- ada- cells showed no effect, in spite of the reported potential of bioactive dihaloethane- derived species to alkylate Trx.      

Neural cell adhesion molecules, CaM kinase II and long-term memory in the chick

The intermediate and medial hyperstriatum ventrale (IMHV) of the chick brain is a site of recognition memory for filial imprinting. Previous results have demonstrated learning-related changes in the amounts of the three major isoforms of neural cell adhesion molecule (NCAM) in the left IMHV. The increases were present 24 h after training. The present study enquired whether the increases persisted and were present 48 h after training. The brain regions analysed were the left and right IMHV and the left and right hyperstriatum accessorium (HA), a visual projection area. The alpha-subunit of calcium/calmodulin protein kinase II (CaMKIIalpha) was also assayed. There were significant correlations between a measure of the strength of learning and the amount of NCAM 180 in the right IMHV (r = +0.65; p = 0.012) but not in the left, and in the left HA (r = -0.61; p = 0.02), but not in the right. There were no learning-related changes for CaMKIIalpha. We conclude that in IMHV the effects of imprinting on NCAM 180 are expressed mainly in the left IMHV 24 h after training, but 48 h after training are expressed mainly in the right IMHV.     

Amphetamine-induced anorexia: analysis with hypothalamic lesions and knife cuts

The present study examined the hypotheses that the midlateral perifornical region of the hypothalamus (PFH), at the level of the ventromedial nucleus, plays a crucial role in amphetamine (AMPH)-induced anorexia and that mediating fibers ascending to this brain region follow a midlateral course through the caudal hypothalamus. Electrolytic lesions that destroyed the PFH region attenuated the feeding suppression induced by intraperitoneal administration of AMPH. Lesions placed anterior, dorsal, or medial to this region, in contrast, did not decrease AMPH's effect. The medially-placed paraventricular nucleus lesion, in fact, enhanced drug response. Midlateral coronal wire-knife cuts in the caudal hypothalamus also attenuated AMPH anorexia. The crucial midlateral caudal hypothalamic cut also disrupted anorexia induced by direct injection of AMPH into the PFH area. The results obtained from the lesion data support the hypothesis that the PFH region is essential to AMPH's suppressive effect upon feeding, and the KC data suggest that crucial catecholamine fibers mediating this drug response ascend specifically through the midlateral portion of the hypothalamus.