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Consumer interest in food products, including fresh vegetables, with health promoting properties is rising. In fresh vegetables, these properties include vitamins, minerals, dietary fiber, and secondary compounds, which collectively impart a large portion of the dietary, nutritional or health value associated with vegetable intake. Many, including farmers, aim to increase the health-promoting properties of fresh vegetables on the whole but they face at least three obstacles. First, describing crop composition in terms of its nutrition-based impact on human health is complex and there are few, if any, accepted processes and associated metrics for assessing and managing vegetable composition on-farm, at the origin of supply. Second, data suggest that primary and secondary metabolism can be 'in conflict' when establishing the abundance versus composition of a crop. Third, fresh vegetable farmers are rarely compensated for the phytochemical composition of their product. The development and implementation of a fresh vegetable 'nutritional yield' index could be instrumental in overcoming these obstacles. Nutritional yield is a function of crop biomass and tissue levels of health-related metabolites, including bioavailable antioxidant potential. Data from a multi-factor study of leaf lettuce primary and secondary metabolism and the literature suggest that antioxidant yield is sensitive to genetic and environmental production factors, and that changes in crop production and valuation will be required for fresh vegetable production systems to become more focused and purposeful instruments of public health.

Forty-nine schools (N = 5,680 fifth and sixth grade students) were assigned to pre test/treatment, pretest/no treatment, no pretest/treatment, and no pretest/no treat ment conditions in the context of an alcohol misuse prevention study. At the first posttest, five months after the pretest and two months after the intervention, the effects of the pretest and of the intervention were examined. The analyses showed that failure to correct for the design effect due to clustering within schools resulted in the overestimation of the significance of treatment and pretest effects. After correction for the design effect, a significant treatment effect in the hypothesized direction was found with respect to students' awareness of the content of the curriculum. As hypo thesized, significant treatment effects on the alcohol use and misuse measures had not yet developed but are expected to occur at subsequent posttest occasions. Significant pretest effects were found for indices measuring trouble with peers resulting from students' alcohol use, students' internal health locus of control, and their perceptions of adults as a locus of control for their health. Two of the three pretest effects were in the direction that would be hypothesized if the pretest were providing the same impe tus as the intervention. Implications of these findings for school-based substance abuse prevention programs are discussed.

Serum lipoproteins have received considerable notoriety as risk factors for atherosclerotic disease, yet the kinetic factors that determine serum concentrations are often unappreciated. Simple compartmental models for lipoprotein kinetics are herein presented which integrate key features of lipoprotein metabolism and allow prediction of very low-density lipoprotein and low-density lipoprotein levels in a wide variety of clinical circumstances. Possible changes in kinetic parameters responsible for hyperlipidemia in obesity, insulin resistance, diabetes, carbohydrate (sugar)-induced hypertriglyceridemia, alcoholic type V hyperlipemia, polyunsaturated fat diets, and several pharmacological interventions are discussed. Key features of lipoprotein metabolism are briefly reviewed.

Treatment of mice in vivo with 5% w/v ethanol given in a liquid diet causes marked changes in spleen, peripheral blood, and thymus lymphocytes. In both the thymus and spleen, there is an acute cellular depletion resulting in a significant decrease in gross tissue size and cell number. In spleen and peripheral blood, the percentage of T lymphocytes is increased relative to B lymphocytes, but the ratio of CD4+/CD8+ T cell sub‐populations remains unchanged. Splenic natural killer (NK) cell activity is increased in ethanol‐consuming mice, although the percentage of NK1.1+ cells is relatively unchanged.

We have investigated a relationship between two detoxication systems, metabolic detoxication through the cytochrome P-450 (P-450) pathway and resistance to infection through interferon (IFN), in mice infected with influenza virus following exposure to coal dust (CD) and diesel exhaust (DE) particulates. Mice were exposed by inhalation to filtered air (FA; control), CD, or DE for 1 month and then inoculated intranasally (IN) with influenza virus. During infection, 7-ethoxycoumarin deethylase (7ECdeEt'ase) and ethylmorphine demethylase (EMdeMe'ase) (monooxygenases), and NADPH cytochrome c reductase (NADPH c red'ase) were measured in liver microsomes. Temporal patterns of enzyme activities were observed with control animals. EMdeMe'ase and NADPH c red'ase exhibited peak values at Day 4 postinfection (27.6 and 482 nmole/min/mg protein, respectively), compared to initial activities (9.1 and 307 nmole/min/mg protein, respectively). 7ECdeEt'ase activity decreased between Days 1-3 postvirus infection and thereafter returned to the original value (1.7 nmole/min/mg protein). When the mice were first exposed to CD or DE particulates for 1 month prior to influenza infection, changes in enzyme temporal patterns were observed. The increased EMdeMe'ase activity at Day 4 was not observed in mice exposed to CD and was reduced in mice exposed to DE. Preexposure to either particulate resulted in the abolition of the increased Day 4 activity of NADPH c red'ase. The 7ECdeEt'ase postinfection temporal pattern was not affected by a preexposure to either particulate. Estimates of the enzyme activities after the 1-month exposure to FA, CD, or DE but before virus infection indicated no changes due to particulate exposure alone. Under these conditions of particulate exposure and virus infection, serum IFN levels in the mice used in this study peaked at Days 4-5 and were unaffected by the 1-month preexposure to CD or DE (Hahon et al., (1985). The data suggest the relationship that exists between metabolic detoxication and resistance to infection in normal mice was altered during a short-term preexposure to CD or DE.

The inhalation toxicity of an ethanol-gasoline mixture was investigated in rats. Groups of 15 male and 15 female rats were exposed by inhalation to 6130 ppm ethanol, 500 ppm gasoline or a mixture of 85% ethanol and 15% gasoline (by volume, 6130 ppm ethanol and 500 ppm gasoline), 6 h a day, 5 days per week for 4 weeks. Control rats of both genders received HEPA/charcoal-filtered room air. Ten males and ten females from each group were killed after 4 weeks of treatment and the remaining rats were exposed to filtered room air for an additional 4 weeks to determine the reversibility of toxic injuries. Female rats treated with the mixture showed growth suppression, which was reversed after 4 weeks of recovery. Increased kidney weight and elevated liver microsomal ethoxyresorufin-O-deethylase (EROD) activity, urinary ascorbic acid, hippuric acid and blood lymphocytes were observed and most of the effects were associated with gasoline exposure. Combined exposure to ethanol and gasoline appeared to exert an additive effect on growth suppression. Inflammation of the upper respiratory tract was observed only in the ethanol-gasoline mixture groups, and exposure to either ethanol and gasoline had no effect on the organ, suggesting that an irritating effect was produced when the two liquids were mixed. Morphology in the adrenal gland was characterized by vacuolation of the cortical area. Although histological changes were generally mild in male and female rats and were reversed after 4 weeks, the changes tended to be more severe in male rats. Brain biogenic amine levels were altered in ethanol- and gasoline-treated groups; their levels varied with respect to gender and brain region. Although no general interactions were observed in the brain neurotransmitters, gasoline appeared to suppress dopamine concentrations in the nucleus accumbens region co-exposed to ethanol. It was concluded that treatment with ethanol and gasoline, at the levels studied, produced mild, reversible biochemical hematological and histological effects, with some indications of interactions when they were co-administered.

A 45 year old man with metastatic colon cancer presented with uncontrollable abdominal wall pain. Transversus abdominis plane (TAP) block with ropivacaine and methylprednisolone was performed with excellent pain relief, which allowed a significant weaning of the patient's opioid requirements. A second TAP block was performed with a 33% ethanol solution (ethanol and ropivacaine) with excellent pain relief. The neurolytic block appeared to offer better pain control for more than 5 days after placement until the patient finally succumbed to his illness.

The role of peripherally and centrally acting acetaldehyde in ethanol‐induced conditioned taste aversion (CTA) was investigated using various enzyme manipulations. Cyanamide, an aldehyde dehydrogenase inhibitor (ALDH) elevates blood acetaldehyde levels in the presence of ethanol. Concurrent administration with 4‐methylpyrazole (4MP), an alcohol dehydrogenase inhibitor, prevents peripheral accumulation of acetaldehyde by cyanamide. Under both treatment conditions brain and liver ALDH activity is inhibited. Water‐deprived rats were pretreated 4 hr prior to fluid presentation with intraperitoneal injections of saline (S+S), 4‐methylpyrazole (4MP+S), cyanamide (S+C), or 4‐methylpyrazole + cyanamide (4MP+C). Subsequently, animals were presented with a novel saccharin solution followed immediately by intraperitoneal injection of one of three doses of ethanol (0.4, 0.8, or 1.2 g/kg) or saline vehicle on four occasions. Results suggested that animals pretreated with cyanamide (groups S+C and 4MP+C) drank significantly less saccharin after conditioning with a subthreshold dose of ethanol (0.4 g/kg) in comparison to groups S+S and 4MP+S. Moreover, at the conditioning dose of 1.2 g/kg, cyanamide‐treated animals demonstrated an attenuation of CTA compared to the other two groups. These effects cannot be attributed to elevated blood acetaldehyde levels since pretreatment with 4MP+C prevented peripheral acetaldehyde accumulation. A characteristic common to both cyanamide‐treated groups was the inhibition of brain ALDH. It is therefore suggested that brain ALDH may play a role in the mediation of ethanol‐induced CTAs. It is conceivable that ALDH plays this role by regulating the levels of acetaldehyde in brain.

Background: Chronic alcohol consumption has been demonstrated to be deleterious to bone health. However, binge drinking is the prevalent form of drinking in young people, which was the impetus for the present study to determine the effect of week‐end and week‐long binge drinking on bone health in a young actively growing animal model. Methods: Four‐week‐old, female, Sprague‐Dawley rats were given the amount of 5% alcohol by gavage to be equivalent to a 63 kg woman drinking six beers a day for either 2 or 5 consecutive days per week. Results: There were no changes in the 5‐day binge animals, but the 2‐day binge animals were hypocalcemia Similarly, 2‐day binge animals had slightly increased bone chemistry and histomorphometric values for both tibia and femur, but only femur length, dry weight, and ash weight as well as femur density, presented either as g/ml or ash weight per unit volume, were increased by a statistically significant level. Cross‐section periosteal Mineral Apposition Rate (MAR) was significantly decreased in the 2‐day alcohol fed animals. Conclusions: Actively growing rats given 5% alcohol by gavage for 2 days per week have an increased bone length, bone weight, and bone density. The interpretation of these results must be viewed with great caution because studies of chronic alcohol consumption, and many studies of acute drinking, clearly indicate deleterious effects of alcohol on bone health. Those fed alcohol for 5 days per week showed no change.

Abstract In this study, a multi-phase, two-dimensional model that integrates the bipolar plate (BP) and gas diffusion layer (GDL) interfacial morphology was developed to understand the effects of this interface on mass, charge and heat transport and performance of polymer electrolyte fuel cells (PEFCs). Two different case studies were performed. The first case assumes a perfect contact interface between the BP and GDL, whereas in the second case, the BP|GDL interfacial layer was incorporated as a separate domain based on the measured BP|GDL morphology. In the BP|GDL interface case, the interfacial voids were assumed to be filled with liquid water to investigate the role of the interfacial voids. For both cases, the effects of different current densities on the in-plane temperature, saturation, and oxygen concentration distribution in the GDL were investigated. Simulations indicate that the Ohmic and concentration losses are increased due to the inclusion of the realistic BP|GDL interface. The electrical contact resistance contribution of the BP|GDL interface was predicted to be 3.8 mΩcm 2 . The saturation in the GDL was found to be higher for the BP|GDL interface case, which results in higher concentration losses. The temperature was predicted to be slightly higher for the BP|GDL interface case, which could be attributed to the higher thermal contact resistance due to the fewer contact regions at the interface.