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Polyphenols are the main contributors for the wines color and also for others characteristics of wines such as astringency and bitterness. Samples of wines (red and white) were analyzed following to assess their polyphenols and anthocyanin's content in relation with their color characteristics. The properties of red (Fetească Neagră) and white wines (Fetească Albă from Cotnari vineyard) were compared to the wine made of grape hybrid cultivar Othello. Also the grape must obtained of hybrid cultivar Othello was analyzed. Polyphenols and anthocyanins were assessed by UV-VIS spectrophotometric methods. Polyphenols content was analyzed using Folin-Ciocalteu method and was expressed as gallic acid. Calibration with gallic acid as standard polyphenolic substance was previously performed. The method for determining anthocyanins is based on their property to be discolored by sulfites. Permanganate index was also determined to evaluate the reducing characteristics of wines by titration against potassium permanganate in the presence of Indigo carmine as redox indicator. Glories chromatic parameters such as color intensity, tonality, %Yellow, %Red and %Blue were established. Polyphenol of the analyzed wines ranged between 47-2653 mg/L polyphenols while the anthocyanins were 0-245 mg/L. Permanganate index was in the range of 14-87 ml KMnO4/L. The polyphenols content of the wine made of hybrid cultivar Othello was lower than that of red wine (Fetească Neagră). The color intensity was significant lower than that of Feteasca Neagră wines. [ABSTRACT FROM AUTHOR]

Lipoxygenase-derived lipid mediators can modulate inflammation and are stimulated in response to influenza infections. We report an effect of 8-lipoxygenase (ALOX8) on the recovery of mice after infection with Influenza virus X31. We compared the responses of 3- and 6-month-old mice with a deletion of ALOX8 (ALOX8−/−) to influenza infections with those of age-matched littermate wild-type mice (ALOX8+/+). The duration of illness was similar in 3-month-old ALOX8−/− and ALOX8+/+ mice. However, the 6-month-old ALOX8−/− mice showed a prolonged state of illness compared with ALOX8+/+ mice, as evidenced by reduced body temperatures, reduced locomotor activities, and delayed weight recovery. Although residual viral RNA in the lungs at day 10 post-inoculation was significantly influenced by the age of the ALOX8−/− mice, there were no significant differences between ALOX8−/− and ALOX8+/+ mice within the same age groups. The levels of cytokines interleukin 6 (IL-6) and keratinocyte chemoattractant (KC) differed significantly between 6-month-old ALOX8−/− and ALOX8+/+ mice 10 days after viral inoculation. Our data suggest that ALOX8 deficiency in mice leads to impaired recovery from influenza infection in an age-dependent manner. [ABSTRACT FROM AUTHOR]

Shift work (SW) is viewed as a risk factor for the development of many serious health conditions, yet prospective studies that document such risks are rare. The current study addressed this void by testing the hypothesis that long-term exposure to repeated diurnal phase shifts, mimicking SW, will accelerate disease onset or death in inbred mice with genetic risk of developing cancer, diabetes, or autoimmune disease. The data indicate that 1) life-long exposure to simulated SW accelerates death in female cancerprone AKR/J mice; 2) a significant proportion of male NON/ShiLtJ mice, which have impaired glucose tolerance but do not normally progress to type 2 diabetes, develop hyperglycemia, consistent with diabetes (that is, blood glucose 250 mg/dL or greater) after exposure to simulated SW for 8 wk; and 3) MRL/MpJ mice, which are prone to develop autoimmune disease, showed sex-related acceleration of disease development when exposed to SW as compared with mice maintained on a stable photocycle. Thus, longterm exposure to diurnal phase shifts that mimic SW reduces health or longevity in a wide variety of disease models. Our approach provides a simple way to assess the effect of chronic diurnal disruption in disease development in at-risk genotypes.

People who engage in shift work (SW) have increased risk of developing illnesses, including infectious diseases and various inflammatory conditions. We hypothesized that exposure to repeated cycles of diurnal disruption, mimicking SW, influences viral clearance, latent viral load, or viral reactivation from latency in mice infected with murine gammaherpesvirus (MuGHV). To test this idea, we inoculated BALB/cByJ and C.129S7(B6)-Ifng tm1Ts/J (IFNgKO) mice with MuGHV and housed them under either a stable light:dark (LD) cycle or one mimicking SW. Compared with BALB/cByJ mice, IFNgKO mice generally had higher levels of lytic virus during the 6-wk period after inoculation. In addition, more IFNgKO mice were positive for replicating virus than were BALB/cByJ mice. Exposure to SW did not alter these measures consistently. After the virus had entered the latent phase of infection, mice received either LPS or pyrogen-free saline intraperitoneally. Mice exposed to SW and then injected with LPS during latent infection had greater viral loads and more replicating virus in the lung at 7 d after injection than did either mice that received pyrogen-free saline or those exposed to LD and then treated with LPS. Some cytokine and chemokine concentrations were changed in lung collected 1 d after but not at 7 d after LPS administration. These findings suggest that exposure to repeated chronic diurnal disruption and an acute inflammatory challenge during latent MuGHV infection, in the context of impaired host immune competence, contribute to enhanced viral reactivity and an increased viral load that might trigger 'sickness behavior' symptoms of infectious disease and perhaps contribute to chronic fatigue syndrome.

To determine how housing density and ambient temperature interact to influence the physiology and behavior of mice, we systematically varied housing density (1 to 5 mice per cage) and ambient temperature (22, 26, or 30 °C) and measured effects on body weight, food intake, diurnal patterns of locomotor activity and core temperature, fecal corticosterone, and serum cytokine and adipokine panels. Temperatures inside cages housing 5 mice were 1 to 2 °C higher than the ambient temperature. As the housing density decreased, in-cage temperatures began to fall at a density of 2 or 3 mice per cage and did not differ from ambient temperature at 1 mouse per cage. Ambient temperature, but not housing density, significantly affected food intake. Although neither ambient temperature nor housing density affected core temperature or activity, hyperthermia and behavioral activation occurred during the 12-h period after cage change. Fecal concentrations of corticosterone metabolites and serum cytokines, chemokines, insulin, and leptin were not influenced by cage density and were only sporadically influenced by ambient temperature. Our data document that the number of mice housed per cage influences the intracage environmental conditions and that ambient temperature influences food intake even when temperatures are within or near recommended or thermoneutral ranges. We conclude that investigators should be cautious when changing the number of mice housed in a cage over the course of a study, because doing so significantly alters the cage environment to which remaining mice are exposed.

Many chronic diseases are associated with both fatigue and disrupted or nonrestorative sleep. In addition, so-called 'sickness behaviors' (for example, anorexia, anhedonia, reduced social interaction, fatigue) are common during infectious and inflammatory disease and have been linked to facets of the immune response. To study these relationships, we used murine gammaherpesvirus (MuGHV), a natural pathogen of wild rodents that provides an experimental model for studying the pathophysiology of an Epstein-Barr (EBV)-like γ-herpesvirus infection in mice. We exposed male and female C57BL/6J mice that were either uninfected or latently infected with MuGHV to either sleep fragmentation (SF) or control conditions and measured the effects on behavior and markers of inflammation. Exposure of infected male mice to SF during the normal somnolent (light) phase significantly reduced locomotor activity during the subsequent active phase, despite an intervening 6-h rest period. Infection was associated with significant increases in lung IFNγ and CXC motif ligand (CXCL) 10 in both male and female mice. In both infected and uninfected male mice, exposure to SF was associated with lower levels of IL1β and C-C motif ligand (CCL) 3 in lung. Exposure of infected female mice to SF led to reductions in lung IL2, CXCL1, and CCL 3. Thus, compared with control conditions, SF was generally associated with lower concentrations of various cytokines in lung. These findings, together with our previous work, indicate that complex interactions among several host factors likely contribute to the behavioral and inflammatory changes associated with viral infection and sleep disruption even in a well-controlled mouse model.