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Biomedical subjects

T Sanner

Publications and source records attributed to T Sanner.

At least 19 recordsLinked to original sources
PubMed1999

[How to enforce the prohibition of sales of tobacco to minors?].

The introduction in 1996 of a ban on the sale of tobacco to persons under the age of 18 in Norway does not seem to have reduced the extent of smoking among minors. One reason may be that Norway's 20,000 tobacconists have not respected the age limit. A representative sample of households was randomly selected from a database containing all telephone numbers in Norway. Of the 6,135 households contacted, 2,054 households contained young people aged 13 to 20 years. Of these, 1,011 persons participated in the telephone survey. 75% of the tobacco smoked by 13-17-year-olds is bought by the minors themselves or by other minors. 70% of smokers under the age of 18 report not being asked how old they were when they bought or tried to buy tobacco. Only 48% had been denied purchase of tobacco during the last three months. The systematic anti-smoking efforts being instituted in the schools would be much more effective if they were backed up by the tobacconists through effective enforcement of the 18-year age limit for the purchase of tobacco.

Adolescent↗
PubMed1999

[How to reduce illegal sales of tobacco to minors?].

Of the tobacco consumed by young people between the ages of 13 and 17 in Norway, 75% is bought by minors. The Ministry of Health has requested the tobacconist's trade association to improve the enforcement of the 18-year age limit for the purchase of tobacco. After identifying 122 scientific articles through searches in Medline and Sociological Abstracts, we have reviewed the scientific literature on the effects of compliance-enhancing measures designed by the authorities in other countries. Four types of measures, including sanctions against tobacconist, have been used to improve age limit compliance. Voluntary agreements lead to higher tobacconist compliance; however, 20% of them still sell tobacco to minors. This is enough for young people not to report changes in availability or changes in smoking habits. Frequent spot tests, threats of fines or the revoking of licence have led to fewer young smokers. We conclude that the present Norwegian efforts at increasing tobacconist compliance are unlikely to lead to fewer smokers among minors.

Adolescent↗
PubMed1999

Passive smoking, sudden infant death syndrome (SIDS) and childhood infections.

1. A number of cohort and case-control studies have shown clear, dose-related associations between maternal smoking and infant death. The strongest relationships were found when the mother smoked during pregnancy as well as postnatally. Maternal smoking during pregnancy increases the risk for SIDS in most studies, whereas it appears that maternal smoking only postnatally also leads to an increase in risk. In addition, smoking only by the father appears to increase the risk for SIDS, but this is not seen in all studies. 2. Exposure of children to environmental tobacco smoke (ETS) increases the risk of having night cough and respiratory infections (bronchitis, bronchiolitis, pneumonia), especially during the first 2 years of life. An increased risk is also seen in studies not distinguishing between upper and lower respiratory diagnoses. Long-term breastfeeding may have a protective effect on ETS-increased risk of lower respiratory tract illness. One study of older children reports that ETS combined with allergy increased the risk of acute respiratory tract infections above that due to ETS alone. 3. The number of new episodes and duration of otitis media with effusion in young children is positively correlated with ETS exposure. Especially infants with lower birth weights had a high risk of recurrent otitis media during the first year of life when the mother was a heavy smoker. 4. Passive smoking has been reported as a risk factor in meningococcal disease and tuberculosis in young children.

Child↗
PubMed1998

Role of Cx43 phosphorylation and MAP kinase activation in EGF induced enhancement of cell communication in human kidney epithelial cells.

Epidermal growth factor (EGF) has been found to induce enhanced gap junctional intercellular communication (GJIC) in the human kidney epithelial cell line K7. This is in contrast to what is reported for other cell types, which all show decreased GJIC in response to EGF. In the present study it is shown that 12-O-tetradecanoylphorbol-13-acetate (TPA) and EGF induce similar phosphorylation pattern of the gap junction protein connexin43 (Cx43) in K7 cells, although their effects on GJIC are opposite. Tyrosine phosphorylation of a 42 kD protein was observed to be induced concomitantly with phosphorylation of Cx43. EGF was however found to induce only serine phosphorylation of Cx43, indicating that the tyrosine kinase activity of the EGF receptor was not directly affecting the gap junction protein. The 42 kD protein phosphorylated on tyrosine was identified to be a mitogen activated protein (MAP) kinase. Both EGF and TPA was found to activate MAP kinase in these cells. Phosphorylation of Cx43 and enhancement of GJIC in response to EGF occurred with difference in time course. Phosphorylation of Cx43 was completed within 15 min, while the enhanced GJIC appeared 2-3 h later. It is therefore possible that regulation of synthesis or transport of Cx43 is responsible for the increase in GJIC, rather than direct involvement of Cx43 phosphorylation. This is in support of our previous finding that protein synthesis is necessary for EGF induced upregulation of GJIC in K7 cells.

Antibodies↗
PubMed1997

Effects of peroxisome proliferators and 12-O-tetradecanoyl phorbol-13-acetate on intercellular communication and connexin43 in two hamster fibroblast systems.

Effects of 12-O-tetradecanoyl phorbol 13-acetate (TPA) and the hepatic peroxisome proliferators (HPPs) clofibrate, methyl clofenapate (MCP), di(2-ethylhexyl)phthalate (DEHP) and mono(2-ethylhexyl)phthalate (MEHP) were studied in 2 gap junctional intercellular communication (GJIC) systems, metabolic cooperation in V79 cells and microinjection/dye transfer in Syrian hamster embryo (SHE) cells and V79 cells. TPA inhibited GJIC in both systems but was considerably more potent in V79 cells. SHE cells showed a rapid and transient inhibition of GJIC after exposure to HPPs, with maximal inhibition occurring at 5-15 min. The transient inhibition could be caused by metabolization of the compounds. Clofibrate and MEHP produced strong inhibition of metabolic cooperation in V79 cells at high concentrations, while the effect of MCP and DEHP was lower. However, DEHP, MEHP and clofibrate strongly inhibited dye transfer in V79 cells after a 30 min exposure. Clofibrate also showed a dose- and time-dependent effect on dye transfer in V79 cells. The phosphorylation status of the gap junction protein connexin43 (Cx43) changed minimally in SHE cells after exposure to TPA or HPPs. Cx43 from V79 cells was strongly affected by TPA, but not by HPPs. Immunofluorescence of Cx43 disappeared in both cell types when they were exposed to TPA and MEHP, but not to the other HPPs. Thus, there is no direct correlation between the inhibition of GJIC and changes in the phosphorylation status of Cx43 or the appearance of Cx43 in immunofluorescence experiments. The discrepancies may partly be explained by binding of accessory proteins to Cx43. We point out sequences that may be involved in such binding.

Animals↗
PubMed1997

Induction of phosphotyrosine in the gap junction protein, connexin43.

The protein-tyrosine phosphatase inhibitors pervanadate, permolybdate, H2O2, and to a much lesser extent vanadate, increased the amount of cellular phosphotyrosine and induced tyrosine phosphorylation of connexin43 (Cx43) in early passage hamster embryo fibroblasts. The presence of phosphotyrosine in Cx43 immunoprecipitates from pervanadate-treated cells was shown by a phosphotyrosine-specific antibody and a phosphotyrosine-specific phosphatase. Pervanadate-induced Cx43 tyrosine phosphorylation was further verified by phosphoamino acid analysis, while no phosphotyrosine was present in control cells. This is the first observation of tyrosine phosphorylation of connexins in normal cells.

Animals↗
PubMed1997

Potency grading in carcinogen classification.

In 1992 the United Nations Conference on Environment and Development decided to harmonize carcinogen classification systems. A proposal for a harmonized classification system is currently being considered by the Organization for Economic Cooperation and Development (OECD). In many countries, classification of a chemical as carcinogenic triggers labeling requirements. Implicit in the labeling requirements are often restrictions on the sale of consumer products and workplace regulations. Many of the current classification systems for carcinogens use a single concentration limit for the minimum concentration of a carcinogen in a preparation (mixture) that requires labeling. For high-potency carcinogens, one concentration limit may not adequately express the hazard, whereas for low-potency carcinogens, one limit may overestimate the hazard caused by the carcinogen in the preparation (mixture). The potency grading system discussed consists of three potency groups: high-, medium-, and low-potency carcinogens. It is envisioned that the different classes will trigger different labeling requirements. In the process of potency grading, a preliminary conclusion as to whether a substance shows high, medium, or low potency is initially based on a tumorigenic dose descriptor. The preliminary potency evaluation may then be modified after due consideration of a number of additional elements. These may include evaluation of the dose-response curve; site-, species-, strain-, and sex-specific activity; mechanisms including genotoxicity; mechanistic relevance to humans; toxicokinetics; and other factors. The potency grading system discussed is applicable to most carcinogen classification systems, including that currently being considered by the OECD.

Animals↗
PubMed1997

T25: a simplified carcinogenic potency index: description of the system and study of correlations between carcinogenic potency and species/site specificity and mutagenicity.

A simplified carcinogenic potency index, the T25, is proposed as a practical method for the inclusion of potency considerations in carcinogen classification systems. The T25 is the chronic daily dose in mg per kg bodyweight which will give 25% of the animals tumours at a specific tissue site, after correction for spontaneous incidence, within the standard life span of that species. Calculated T25 values of a set of 113 US National Cancer Institute/National Toxicology Program (NC/NTP) carcinogens showed excellent correlation (correlation coefficient 0.96, P < 0.0001) with the carcinogenic potency index TD50 of Peto et al. (1984). The mean of T25 values for 51 transspecies, multiple common site NCI/NTP carcinogens were 10-fold lower than those for 62 NCI/NTP single species, single site carcinogens. For these 113 carcinogens, the mean T25 values were approximately 3-fold lower for agents that were also mutagenic in Salmonella compared to the non-mutagenic agents.

Abdominal Neoplasms↗
PubMed1996

[Chemoprevention of cancer. Prevention of cancer in groups with increased risk].

The term chemoprevention is defined as the use of specific natural or synthetic chemical agents to reverse, suppress or prevent carcinogenic development to a tumour. Many potential chemopreventive substances are pharmacologic agents which may already be in use or are naturally occurring compounds. Short-term tests and animal models are available for identifying potential chemopreventive agents. There are several similarities between clinical chemopreventive trials and cancer prevention by dietary intervention. The cost and length of chemopreventive trials can be reduced by using validated biomarkers as endpoint instead of cancer. Experience from chemoprevention of cancer is limited, seen in relation to use of chemical agents to reduce cardiovascular disease. However, a number of international clinical trials are now going on to evaluate the use of pharmacological substances as potential chemopreventive agents.

Anticarcinogenic Agents↗
PubMed1996

[Health damages from passive smoking].

Environmental tobacco smoke is a complex mixture of many chemical substances. The term passive smoking is used when a person breathes in air contaminated by tobacco smoke. Active and passive smoking expose an individual to the same substances, but the relative concentrations of the various substances differ. Thus, under conditions where individuals are exposed to an amount of nicotine corresponding to their smoking 1/2 a cigarette, they will be exposed to an amount of nitrosodimethylamine corresponding to their smoking about five cigarettes. Exposure of children to environmental tobacco smoke is associated with increased risk of lower respiratory tract infections, middle ear infections and asthma. Accumulating evidence points to passive smoking as a risk factor for the sudden infant death syndrome. Long term exposure to environmental tobacco smoke increases risk of lung cancer and heart disease. It is estimated that in Norway, 50 non-smokers die of lung cancer and 300-500 of heart disease annually, as a result of long term exposure to environmental tobacco smoke.

Europe↗
PubMed1996

Carcinogen classification systems: similarities and differences.

An overview of regulatory classification systems on carcinogens in the Organization for Economic Cooperation and Development (OECD) countries is presented based on a questionnaire study. Most OECD countries have implemented legislation including classification systems and lists of carcinogens. Basically, there are two types of classifications systems. The major difference between the two is that in one system carcinogens are classified according to the weight of evidence for carcinogenic effects in humans, whereas in the other carcinogens are allocated to various groups according to potency. Even if the classification systems may differ, the substances classified as carcinogens are to a large extent the same. Classification of carcinogens will in many countries require hazard labeling. This labeling, i.e., the limit for labeling of substances and preparations, and risk phrases show considerable similarities, but differ in certain aspects. Several countries have restrictions on sale and/or use of carcinogens. There is a trend toward introducing more mechanistic considerations in the classification of carcinogens.

Carcinogens↗
PubMed1995

[Peroxisome proliferation and possible cancer hazard].

Approximately 80 chemicals, including hypolipidemic fibrates, have been shown to induce peroxisome proliferation in rodent liver. There is a strong concordance between this effect and development of liver cancer in rats and mice. There is evidence that the peroxisome proliferators induce cancer via a non-genotoxic, receptor-mediated mechanism. Both oxidative stress as a consequence of peroxisome proliferation and preferential growth of preneoplastic lesions following hepatocyte proliferation have been proposed as underlying processes in the neoplastic development. Peroxisome proliferation does not seem to occur in human liver to any significant extent. Therefore exposure to chemicals with such an effect apparently represents little, if any, human carcinogenic hazard.

Adult↗
PubMed1994

[Smokeless health institutions--what progress was achieved so far?].

In August 1991, the Norwegian Ministry of Health and Social Affairs distributed their publication Plan of Action to Achieve Smoke-free Health Institutions. The goal was that all health institutions in Norway should have established a smoke-free environment for all employees before 1.1.1994. In March 1993 a questionnaire was sent to all health institutions. The purpose was to remind the institutions of the plan of action, and to evaluate the progress of the efforts to achieve smoke-free health institutions so far. Three types of institutions were included in this study: hospitals, institutions for the elderly, and psychiatric institutions, in all 1,437 institutions. The overall response rate was 33%. The response rate for the hospitals was 68%. A majority, 55%, have decided to establish a smoke-free environment for their employees. About two thirds of the institutions who had not made such a decision do not have any plans to do so. It is concluded that this study indicates a demand for further action in order to establish smoke-free health institutions in Norway. Stronger involvement seems to be needed, particularly on the part of the municipalities and countries, as owners of the institutions.

Evaluation Studies as Topic↗
PubMed1994

Effect of 1,1'-(2,2,2-trichloroethylidene)-bis(4-chlorobenzene) (DDT) on gap junctional intercellular communication and morphological transformation of Syrian hamster embryo cells.

The organochlorine insecticide 1,1'-(2,2,2-trichloroethylidene)bis(4-chlorobenzene) (DDT) did not induce or promote induction of morphological transformation in Syrian hamster embryo (SHE) cells, but it was a potent inhibitor of gap junctional intercellular communication (GJIC). The kinase inhibitor staurosporine did not affect DDT induced inhibition of GJIC, although it has been shown to decrease the inhibitory effect of 12-O-tetradecanoyl-phorbol-13-acetate (TPA) on GJIC. In addition, pretreatment with TPA made the cells refractory to further TPA induced inhibition of GJIC, while they remained sensitive to DDT. Thus, DDT and TPA inhibit GJIC through different mechanisms. Elevation of cellular cyclic adenosine monophosphate (cAMP) level by exposure to forskolin counteracted the inhibitory effect of DDT similar to that observed for TPA. Continuous exposure to DDT at concentrations near the effective concentration (50%) value (EC50 value) resulted in a slight recovery of GJIC following the initial inhibition. This recovery was not accompanied by the cells becoming refractory to further DDT induced inhibition of GJIC. The recovery of GJIC after removal of the DDT containing medium seemed to be related to a reduction in the amount of cell-associated DDT.

Animals↗
PubMed1994

Increased gap junctional intercellular communication in Syrian hamster embryo cells treated with oxidative agents.

The effects of K2CrO4, H2O2, benzoyl peroxide, menadione, KBrO3 and UV365nm on gap junctional intercellular communication (GJIC) have been studied in the 12-O-tetradecanoylphorbol-13-acetate (TPA)-sensitive Syrian hamster embryo (SHE) cell line BPNi. All agents were found to increase the level of GJIC by 50-100%. Also, in early passage SHE cells, a tendency for increased GJIC was found for the oxidative agents studied. Hydrogen peroxide was used as a model compound in the subsequent studies. The increase in GJIC was reversible, and it was not due to an increased non-junctional permeability. Hydrogen peroxide counteracted the TPA-induced decrease in GJIC, regardless of whether the cells were exposed to the compounds simultaneously or the cells were pre-exposed to TPA before addition of H2O2. The GJIC enhancement by H2O2 was slightly reduced by the addition of the hydroxyl radical scavenger dimethylsulphoxide or by the inhibition of catalase by amitrole. The cAMP/protein kinase A system is the only characterized signal transduction system that is known to increase GJIC in most cell types. Hydrogen peroxide did not increase the amount of cAMP (or cGMP) in BPNi cells, while forskolin and a phosphodiesterase inhibitor had to increase the cAMP level several-fold to affect GJIC to the same degree as the oxidative agents. Some inhibitors of protein kinase A were assayed for their ability to inhibit the increases in GJIC caused by H2O2 and forskolin. Staurosporine inhibited the forskolin-induced increase in GJIC, with much less effect on the H2O2-induced increase. H8, H88 and H89 had less effect than staurosporine on the forskolin-induced increase in GJIC. The results suggest that the cAMP/protein kinase A system may not be involved in the increase in GJIC caused by H2O2, although this cannot be completely ruled out.

Animals↗