Caffeinated energy drinks in the Canadian context: health risk assessment with a focus on cardiovascular effects.

In Canada, caffeinated energy drinks (CEDs) currently sold under Temporary Marketing Authorizations must meet strict eligibility criteria. These criteria, which include compositional and labelling requirements, were developed based on the outcome of a health risk assessment conducted by Health Canada (HC) in 2013. HC updated its assessment by reviewing new information with the focus on potential cardiovascular effects associated with the consumption of CEDs available for sale in Canada.

Deltoid ligament reconstruction: a novel technique with biomechanical analysis.

Background: Deltoid ligament insufficiency has been shown to decrease tibiotalar contact area and increase peak pressures within the lateral ankle mortise. This detrimental effect may create an arthritic ankle joint if left unresolved. Reconstructive efforts thus far have been less than satisfactory.

Urinary bladder incarceration and infarction by an intra-abdominal fat pad in a Virginia opossum (Didelphis virginiana).

A 2.5-year-old, female opossum had acute stranguria. Based on radiography and ultrasonographic examination a cystic structure was identified in the caudal abdomen associated with bilateral hydroureter and hydronephrosis.

Effects of caffeine on human health.

Caffeine is probably the most frequently ingested pharmacologically active substance in the world. It is found in common beverages (coffee, tea, soft drinks), in products containing cocoa or chocolate, and in medications. Because of its wide consumption at different levels by most segments of the population, the public and the scientific community have expressed interest in the potential for caffeine to produce adverse effects on human health.

Analysis of sequence specificity of 5-bromodeoxyuridine-induced reversion in cells containing multiple copies of a mutant gpt gene.

For studies on molecular mechanisms of mutagenesis, it would be advantageous to transfer mutant genes with specific alterations into mammalian cells and use the transformed cells in reversion analyses. In the present paper, we describe an efficient method for analyzing reversion events occurring in cells that possess multiple copies of a mutational target gene. This method involves amplification of the chromosomally integrated target genes with the polymerase chain reaction (PCR) and restriction endonuclease digestion of the amplified product.

Induction of terminal differentiation-resistant epidermal cells in mouse skin and in papillomas by different initiators during two-stage carcinogenesis.

Carcinogen treatment of normal mouse epidermal cells causes some cells, if cultured under the appropriate conditions, to continue to proliferate instead of terminally differentiate, forming foci at 37 degrees C in medium with a calcium level above 0.1 mM. We have examined these Calcium (Ca)-resistant cells formed in the skin of SENCAR mice after treatment with the carcinogen initiator 7,12-dimethylbenz[a]anthracene (DMBA) followed by tumor promotion with 12-O-tetradecanoylphorbol-13-acetate (TPA).

Acetic acid, a potent agent of tumor progression in the multistage mouse skin model for chemical carcinogenesis.

Acetic acid, a very weak tumor promoter in the multistage mouse skin model for chemical carcinogenesis, was found to be very effective at enhancing cancer development, when applied during the progression phase of the model. Papilloma-bearing mice when repeatedly treated with acetic acid had a greater carcinoma incidence and a greater conversion of papillomas to carcinomas than vehicle treated mice. Selective cytotoxicity is discussed as a possible mechanism.

Effect of exogenous glutathione on tumor progression in the murine skin multistage carcinogenesis model.

Oxidative stress has been suggested to play an integral role in the cancer process. It may be particularly significant during tumor progression, where there is likely to be a large amount of free radicals generated by infiltrating inflammatory cells and dying tumor cells. In order to test this hypothesis, a variety of free radical scavengers and antioxidants were assessed for their ability to inhibit tumor progression.

Sequential alterations in growth control and cell dynamics of rat hepatocytes in early precancerous steps in hepatocarcinogenesis.

This set of experiments is the second of a series designed to explore alterations in cell dynamics and growth control of new populations of hepatocytes that appear to play a role in the carcinogenic process induced in the liver by chemical carcinogens. This is part of an ongoing study of the biochemical and molecular basis for cancer development. A rat model for hepatocarcinogenesis, the resistant hepatocyte model, was chosen with its synchrony of several steps in the process.

Critical genetic determinants and molecular events in multistage skin carcinogenesis.

Carcinogenesis can be operationally and mechanistically divided into at least three major stages--initiation, promotion, and progression. Variations among stocks and strains of mice to susceptibility to multistage skin and liver carcinogenesis appear to be more related to alterations in tumor promotion than tumor initiation; however, the critical events have not been determined. In the mouse skin model the first stage is thought to involve the interaction of a tumor initiator with the genetic material of stem cells leading to an alteration in some aspect of growth control, differentiation, or both.

Cell cycle kinetics of rat hepatocytes in early putative preneoplastic lesions in hepatocarcinogenesis.

This set of experiments is the first of a series designed to explore facets of cell proliferation of hepatocytes during the carcinogenic process induced in liver by chemical carcinogens. A rat model for hepatocarcinogenesis, the resistant hepatocyte model, was used. A major advantage of this model is the unusual degree of synchrony in the early steps.

Failure of glutathione to prevent liver cancer development in rats initiated with diethylnitrosamine in the resistant hepatocyte model.

This study was undertaken to observe whether the administration of reduced glutathione intragastrically to male Fischer 344 rats during the precancerous steps of liver carcinogenesis has any protective effect on the development of hepatocellular carcinoma. Hepatocyte nodules were induced in the liver with a single initiating dose of diethylnitrosamine followed by selection of resistant hepatocytes to generate nodules by a two week exposure to dietary 2-acetylaminofluorene coupled with partial hepatectomy. Animals had hepatocyte ('hyperplastic') nodules when examined by laparotomy at three months.