Chronic alcohol consumption is a major risk factor for cancer of upper aero-digestive tract (oro-pharynx, hypopharynx, larynx and oesophagus), the liver, the colo-rectum and the breast. Evidence has accumulated that acetaldehyde is predominantly responsible for alcoholassociated carcinogenesis. Acetaldehyde is carcinogenic and mutagenic, binds to DNA and protein, destroys the folate molecule and results in secondary cellular hyper-regeneration. Acetaldehyde is produced by mucosal and cellular alcohol dehydrogenase, cytochrome P450 2E1 and through bacterial oxidation. Its generation and/or its metabolism is modulated as a result of polymorphisms or mutations of the genes responsible for these enzymes. Acetaldehyde can also be produced by oral bacteria. Smoking, which changes the oral bacterial flora, also increases salivary acetaldehyde. Cigarette smoke and some alcoholic beverages, such as Calvados, contain acetaldehyde. In addition, chronic alcohol consumption induces cytochrome P450 2E1 enxyme activity in mucosal cells, resulting in an increased generation of reactive oxygen species and in an increased activation of various dietary and environmental carcinogens. Deficiencies of riboflavin, Zn, folate and possibly retinoic acid may further enhance alcohol-associated carcinogenesis. Finally, methyl deficiency as a result of multiple alcoholinduced changes leads to DNA hypomethylation. A depletion of lipotropes, including methionine, choline, betaine and S-adenosylmethionine, as well as folate, results in the hypomethylation of oncogenes and may lead to DNA strand breaks, all of which are associated with increased carcinogenesis.Chronic alcohol consumption: Cancer: Acetaldehyde: Cytochrome P450 2E1:Alcohol-nutrient interactionsChronic excessive alcohol consumption is a strong risk factor for cancer of the upper aero-digestive tract (oral cavity, pharynx, hypopharynx, larynx, oesophagus), the liver, the colo-rectum and the breast. A great number of epidemiological studies have demonstrated the correlation between alcohol ingestion and the occurrence of cancer in these organs . These studies clearly show that the ingestion of all types of alcoholic beverage is associated with an increased cancer risk, which suggests that ethanol is the common ingredient that causes this effect. The exact mechanism of ethanol-associated carcinogenesis has remained obscure, since ethanol is not a carcinogen. Multiple mechanisms are involved in alcoholassociated cancer development, including the effect of acetaldehyde (AL; the first metabolite of ethanol oxidation), the induction of cytochrome P450 2E1 (CYP2E1) leading to the generation of reactive oxygen species and enhanced procarcinogen activation, modulation of cellular regeneration and nutritional deficiencies. These mechanisms have been the subject of recent reviews ). In the present paper major emphasis is given to the most recent observations contributing to the elucidation of the mechanisms involved in alcohol-associated carcinogenesis, such as genetic factors and alcohol-nut...

In this paper, we report a transistor model that has successfully led to the identification of a non visual defect. This model was based on detailed electrical characterization of a MOS NFET exhibiting a threshold voltage (Vt) of just about 40mv lower than normal. This small Vt delta was based on standard graphical extrapolation method in the usual linear Id-Vg plots. We observed, using a semilog plot, two slopes in the Id-Vg curves with Vt delta magnified significantly in the subthreshold region. The two slopes were attributed to two transistors in parallel with different Vts. We further found that one of the parallel transistors had short channel effect due to a punch-through mechanism. It was proposed and ultimately confirmed the cause was due to a dopant defect using scanning capacitance microscopy (SCM) technique.

In this paper, we report a device model that has successfully described the characteristics of an anomalous CMOS NFET and led to the identification of a non-visual defect. The model was based on detailed electrical characterization of a transistor exhibiting a threshold voltage (Vt) of about 120mv lower than normal and also exhibiting source to drain leakage. Using a simple graphical simulation, we predicted that the anomalous device was a transistor in parallel with a resistor. It was proposed that the resistor was due to a counter doping defect. This was confirmed using Scanning Capacitance Microscopy (SCM). The dopant defect was shown by TEM imaging to be caused by a crystalline silicon dislocation.

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