Self-identified strategies to manage intake of tempting foods: cross-sectional and prospective associations with BMI and snack intake.

OBJECTIVES: Individuals often use self-directed strategies to manage intake of tempting foods, but what these strategies are and whether they are effective is not well understood. This study assessed the frequency of use and subjective effectiveness of self-directed strategies in relation to BMI and snack intake. DESIGN: A cross-sectional and prospective study with three time points (T1: baseline, T2: 3 months and T3: 3 years). At T1, demographics, frequency of use and subjective effectiveness of forty-one identified strategies were assessed. At T2 and T3, current weight was reported, and at T2 frequency of snack intake was also recorded. SETTING: Online study in the UK. PARTICIPANTS: Data from 368 participants (Mage = 34·41 years; MBMI = 25·06 kg/m2) were used for analysis at T1, n = 170 (46·20 % of the total sample) at T2 and n = 51 (13·59 %) at T3. RESULTS: Two strategy factors were identified via principal axis factoring: (1) diet, exercise, reduction of temptations, and cognitive strategies, and (2) planning, preparation and eating style. For strategy 1, frequency of use, but not subjective effectiveness, was positively related to BMI at T1. Subjective effectiveness predicted an increase in BMI from T1 and T2 to T3. No relationship to snack intake was found. For strategy 2, frequency of use was negatively related to BMI at T1. Neither frequency of use nor subjective effectiveness were related to changes in BMI over time, but subjective effectiveness was negatively correlated with unhealthy snack intake. CONCLUSION: Self-directed strategies to reduce the intake of tempting foods are not consistently related to BMI or snack intake.

Associations between dietary variety, portion size and body weight: prospective evidence from UK Biobank participants.

'Dietary variety' has been identified as a factor associated with food intake. Whilst this relationship may have longer-term benefits for body weight management when eating low-energy, nutrient-dense foods, it may increase the risk of overconsumption (and body adiposity) when foods are high energy density. This study sought to further explore pathways underpinning the relationship between dietary variety and body weight, by considering energy density as a moderating factor and portion size as a mediating factor in this relationship. Using prospective data from the UK Biobank, dietary variety scores (DVS), cumulative portion size and energy density were derived from 24-h dietary recall questionnaires at baseline and follow-up. BMI, whole-body fat percentage and fat-free mass were included as outcomes. Contrary to predictions, linear multiple regression models found some evidence of a negative, direct association between DVS and body weight outcomes at baseline (b = -0·13). Though dietary variety was significantly associated with larger portions across time points (b = 41·86-82·64), a moderated mediation effect was not supported at baseline or follow-up (Index ≤ 0·035). Taken together, these findings provide population-level evidence to support a positive association between variety and food intake, which in turn has potential implications for body weight management, both in terms of moderating food intake and benefitting diet quality.

Friend virus production and heme synthesis in primary mouse spleen cell cultures.

A cell culture method has been developed in which spleen cells from Friend virus (FV) infected mice can be studied for virus production as well as erythroid differentiation. Primary spleen cell cultures from plethoric Balb/c mice were initiated at 24, 48 or 73 h after FV infection. These cells manifested a well-defined wave of heme synthesis at approximately 64, 48, or 23 h, respectively, of cell culture. Assays for spleen focus-forming virus (SFFV) and helper murine leukemia virus (MuLV-F) production in these cultures revealed that the peak rates of production of both viruses occurred at essentially the same time as the peaks of heme synthesis. The time at which the peaks of virus production and heme synthesis occurred in vitro was related to the time interval after infection (80-105 h) rather than the time at which the cells were placed in cell culture or the number of hours of cell culture. Medium change experiments suggested that the temporal relation between heme synthesis and virus production was an intrinsic feature of FVP infected cells in this in vitro system.

Influenza type A virus infection of suckling mice pre-exposed to insecticide carrier.

Suckling CD-1 outbred mice exposed topically to insecticide carrier (IC), a mixture of emulsifiers and solvent, were rendered less sensitive to infection with lethal doses of influenza type A/PR8/34 (H0N1) virus than untreated and mock-treated control mice. Decreased sensitivity to influenza type A/PR8/34 virus infection was evidenced by a significant increase in the mean percent survival of the mice. In addition, a 10- to 100-fold reduction in the 50% lethal titer of the stock virus was observed in IC-treated mice relative to untreated mice. Decreased sensitivity was virus dose related and occurred within a dose range of 2 to 8 X LD50. No decrease in mortality rate was observed as a function of exposure to IC.

Influenza type A virus infection of mice exposed in utero to chlordane; survival and antibody studies.

Previous studies carried out by others have shown that in utero exposure of mice to chlordane effects a significant depression of cell-mediated immunity (CMI) at 100 days of life without adversely affecting the humoral immune system. In the studies reported herein we assessed the effect of in utero exposure to various doses of chlordane on the response of 38-day-old mice to influenza type A virus infection in terms of relative levels of mortality, mean day of death, and the levels of antiviral antibody in the primary and secondary immune response to the virus. In utero exposure to chlordane effected enhanced survival to influenza type A virus infection relative to mock-treated animals. No significant differences were noted in the mean day of death of chlordane-treated and mock-treated mice. A significant enhancement in the levels of antiviral antibody was noted in the chlordane-treated female mice but not male mice in both the primary and secondary immune response to the virus.

The effect of prenatal chlordane exposure on specific anti-influenza cell-mediated immunity.

Previous studies in our laboratory have documented that in utero chlordane exposure caused a significant enhancement in the survival of the offspring to influenza A virus infection, and a depressed delayed type hypersensitivity (DTH) response to oxazolone. To correlate these 2 effects, we assayed influenza A virus-specific DTH response, and found that it was significantly decreased in chlordane-treated offspring. Virus-specific T-cell blastogenesis was also assayed in chlordane-treated animals. No significant differences due to the chlordane treatment were found in virus-specific T-cell blastogenesis, suggesting that the DTH depression did not result from a paucity of antigen-reactive T-cells. To determine whether enhanced survival was due, in part, to the effects of chlordane on virus replication, rather than on immunological alteration alone, the kinetics of influenza virus replication in the lungs of chlordane- and vehicle-treated animals were determined. In utero chlordane treatment caused no significant differences in in vivo virus replication. These data suggest that increased survival was due to a decrease in virus-specific DTH and its associated pathology.

The effect of prenatal chlordane exposure on the delayed hypersensitivity response of BALB/c mice.

Previous studies in our laboratory have indicated that in utero chlordane exposure caused a significant enhancement in the survival of the offspring to influenza virus infection. Further studies, reported here, show that the non-specific delayed type hypersensitivity (DTH) response to oxazolone at 100 days of age, but not at 30 days of age, was significantly depressed. In contrast, the Con A-induced blastogenic response of spleen cells from chlordane-treated offspring was not depressed and was, in fact, significantly enhanced. However, neither the response to PHA nor to LPS mitogens was significantly altered. In utero exposure to chlordane significantly depressed the mixed lymphocyte reactivity (MLR) of spleen cells from male offspring, whereas females showed no significant alteration of MLR. The significant depression of the DTH and MLR responses supports our previous reports of enhanced survival of influenza virus infection following in utero exposure to chlordane, since active DTH contributes to the pathology of influenza virus infection in mice. The normal or enhanced T-cell mitogen response suggested that the chlordane-induced depression of DTH and MLR was not due to overt toxicity to T-cells.

Cytotoxic T-lymphocyte and NK responses in mice treated prenatally with chlordane.

It has been reported previously that BALB/c mice, treated in utero with chlordane, showed increased survival to influenza A/PR/8/34 [H1N1] (influenza) virus as young adults. To determine the possible role of cell-mediated immunity (CMI) on this effect, cytotoxic T-lymphocyte (CTL) and natural killer (NK) cell activities were assessed on chlordane-exposed offspring at 100 and 200 days post partum. The CTL response of these offspring showed no significant change from that obtained from their sex- and age-matched control counterparts exposed prenatally to the vehicle. NK responses of chlordane-exposed female offspring were significantly higher at 100 days of age but not at 200 days of age. Although male offspring that were exposed to chlordane prenatally showed no difference in NK cell activity at 100 days of age, NK cell activity was significantly less in chlordane-treated animals than controls at 200 days of age. Thus, prenatal treatment of mice with chlordane had varying effects on the NK cell activity of adult offspring, depending on the sex and age of the animal. It is concluded that the previously reported increase in survival to influenza is due to a resolution of the infection by normal CTL and NK cell activities coupled with a decrease in delayed-type hypersensitivity (DTH)-mediated pathology.

Methyl gallate, methyl-3,4,5-trihydroxybenzoate, is a potent and highly specific inhibitor of herpes simplex virus in vitro. I. Purification and characterization of methyl gallate from Sapium sebiferum.

A potent anti-herpetic compound was identified and purified to homogeneity from the leaves of Sapium sebiferum by plaque reduction assay using herpes simplex virus type 2. The chemical structure of the purified compound was determined by mass spectroscopy and proton and carbon-13 nuclear magnetic resonance as methyl gallate, methyl-3,4,5-trihydroxybenzoate. This is the first demonstration that methyl gallate is a potent anti-herpetic compound in vitro, present in high concentration in the leaves of S. sebiferum, a Chinese folk medicine for shingles.

Methyl gallate, methyl-3,4,5-trihydoxybenzoate, is a potent and highly specific inhibitor of herpes simplex virus in vitro. II. Antiviral activity of methyl gallate and its derivatives.

Methyl gallate (MG), methyl-3,4,5-trihydroxybenzoate, was highly active against herpes viruses as determined by plaque reduction assay. Herpes simplex virus type 2, MS strain, was sensitive to MG at a mean 50% inhibitory concentration (IC50) of 0.224 micrograms/ml in monkey kidney cells. MG was specific for herpes viruses with the relative sensitivity HSV-2 greater than HSV-1 greater than CMV. Two RNA viruses tested were significantly less sensitive to MG. The structural components of MG which modulate the anti-herpetic activity were identified by analysis of chemical analogues. Our structural analyses indicated that three hydroxyl groups were required but were not sufficient for the anti-herpetic action of MG. The presence and chain length of the alkyl ester were also important to the anti-herpetic activity of MG. Methyl gallate may interact with virus proteins and alter the adsorption and penetration of the virion.

Effect of emulsifiers on influenza type A virus infection, in vivo and in vitro studies.

Results of in vitro studies carried out by other investigators suggest that insecticide emulsifiers enhance the replication of animal viruses possessing a single-stranded RNA genome. Based on this observation and on epidemiological findings, it has been postulated that insecticide emulsifiers and related compounds may be etiologically involved in Reye's syndrome. Reye's syndrome is an enigmatic pernicious disease of childhood causally associated with an antecedent viral infection, usually influenza, and putatively associated with exposure to environmental chemicals. The present study was carried out to assess the effects of emulsifiers on infection in vivo with influenza type A virus, a virus possessing a single-stranded RNA genome, using the suckling mouse as host, and in vitro using a susceptible line of mammalian cells. Three coded emulsifiers retrospectively identified as Atlox 3409F, Toximul MP8, and Triton X-100 were assayed at concentrations of 1.0, 2.5, 5.0, and 10.0 ppm. None of the emulsifiers enhanced the plaquing efficiency of influenza A/PR/8/34 (HON1) virus in Madin-Darby canine kidney cells (less than a twofold increase), nor did percutaneous application of these emulsifiers at a concentration of 21 parts per thousand in peanut oil enhance the lethality of influenza A/PR/8/34 (HON1) virus infection. Indeed, peanut oil alone, and in combination with the emulsifiers, lowered lethality relative to mice that were treated percutaneously in parallel with physiologic saline.

Cryosurvival of herpes simplex virus-2 during cryopreservation of human spermatozoa.

Herpes simplex virus (HSV) is a sexually transmitted agent which has potential association with cervical cancer, as well as with high morbidity and mortality in perinatal infection. Its incidence is estimated just after gonorrhea and Chlamydia trachomatis infections. Cryobanking of human semen is accepted worldwide in therapeutic use for both husband and donor. Serious consequences could follow the clinical applications of cryobanked human semen in insemination, if some ejaculates contain HSV and the virus survives the processing of semen in cryopreservation. There is then the likelihood of infection of the female, and through her, the child, generally during parturition.

Changes in the virus-host cell relationship in a stable non-virogenic cell line persistently infected with measles virus (BGM/MV).

A non-virogenic African green monkey kidney cell line BGM/MV persistently infected with a neurotropic mouse brain-adapted strain of measles virus, was found to have undergone significant changes in the virus-host cell relationship between passages 35 and 119. Rather than the stable non-cytopathic relationship previously reported in which approximately 100% of the cells contained measles antigens and less than 1% of the cells expressed cell surface measles antigen, we observed cyclic manifestations of c.p.e. together with changes in the percentage of cells expressing intracellular and cell surface measles antigens. Treatment of BGM/MV cells with actinomycin D effected an increase in the percentage of cells expressing cell surface virus haemagglutinin (HA) at times when the percentage of cells with surface HA was less than the percentage of cells with intracellular measles antigens. Superinfection studies employing measles virus and vesicular stomatitis virus revealed a consonant cyclic refractivity and essentially no refractivity, respectively. Endogenous, infectious measles virus was not detected nor was interferon. It was concluded that a host cell factor other than interferon was modulating the cyclic expression of the measles virus infection.

Induction of measles virus hemagglutinin in a persistently infected, nonvirogenic line of cells (BGM/MV).

BGM/MV cells carry measles virus antigens and nucleocapsid-like structures in their cytoplasm. There is no infectious virus demonstrable, and measles virus-induced cell surface changes detectable by hemadsorption (HAD) are absent. Treatment of cells with actinomycin D or cycloheximide or enucleation of cells with cytochalasin B induced surface changes in that the cells became HAD positive. 6-Azauridine treatment of cells did not inhibit the induction of HAD, suggesting that RNA synthesis was not required. Cycloheximide treatment of cells induced by enucleation inhibited the development of HAD, suggesting a requirement for protein synthesis.