Food Cent$--implementing and evaluating a nutrition education project focusing on value for money

The photophysics and polarization of the phosphorescence and delayed fluorescence of erythrosin in conditions compatible with the current biological applications of the dye (aqueous buffers at pH 7.4 at ambient temperatures) and in ethanol have been studied as a function of dye concentration (10(-7)-10(-5) M) and temperature (245-333 K). The emission decay is strictly single exponential and the detailed kinetic analysis of all the rate processes connected with the emitting T1 state showed that (1) the lowering of the emission lifetime at the higher temperatures is due to a very efficient self-quenching process, (2) the back intersystem crossing rate T1-->S1 is temperature dependent (delta ETS approximately 7 kcal mol-1) but the T1-->S0 is not (Ea < 0.1 kcal mol-1) and (3) both intersystem crossing processes are very sensitive to solvent polarity, which accounts for the solvent dependence of the phosphorescence yield and lifetime. The high value of the phosphorescence anisotropy (r0 = 0.25 +/- 0.006) is independent of the excitation and emission wavelengths, and its evolution in time accurately reflects the rotational restrictions in solid solutions. The relevance of these findings to studies with protein-dye conjugates is also outlined to facilitate the design and interpretation of phosphorescence depolarization experiments that probe the microsecond-ms dynamics of biomolecules and supramolecular systems.     

Activators of the nuclear receptor PPARgamma enhance colon polyp formation

A high-fat diet increases the risk of colon, breast and prostate cancer. The molecular mechanism by which dietary lipids promote tumorigenesis is unknown. Their effects may be mediated at least in part by the peroxisome proliferator-activated receptors (PPARs). These ligand-activated nuclear receptors modulate gene expression in response to fatty acids, lipid-derived metabolites and antidiabetic drugs. To explore the role of the PPARs in diet-induced carcinogenesis, we treated mice predisposed to intestinal neoplasia with a synthetic PPARgamma ligand. Reflecting the pattern of expression of PPARgamma in the gastrointestinal tract, treated mice developed a considerably greater number of polyps in the colon but not in the small intestine, indicating that PPARgamma activation may provide a molecular link between a high-fat diet and increased risk of colorectal cancer.     

Comparison of tamoxifen effects on the actions of triiodothyronine or growth hormone in the ovariectomized-hypothyroid rat

Recent studies have suggested that a subset of estrogen responses arise via modulation of triiodothyronine (T3) actions, and depend on T3 for expression: other estrogen responses are not T3-dependent. Moreover, tamoxifen acts as a full estrogen agonist in T3-dependent responses but behaves as an antiestrogen in T3-independent responses. T3 directly induces a variety of metabolic enzymes and proteins, and also induces rat growth hormone (GH). Thus, some T3-dependent tamoxifen effects might reflect modulation of GH rather than T3 actions. To address this issue, tamoxifen effects on somatotropic and metabolic actions of T3 and GH were compared in ovariectomized rats with methimazole-induced hypothyroidism. Rats were given T3 (10 micrograms/kg/day) or ovine GH (2 mg/kg/day) with or without tamoxifen (0.5 mg/kg/day) for 30 days. GH was poorly effective in producing a sustained increase in somatic growth in hypothyroid rats compared to T3; nonetheless, GH effects to increase body weight, tibia length and serum insulin-like growth factor I while decreasing fat mass and evoking small increases in body temperature were not inhibited by tamoxifen. Tamoxifen also did not inhibit GH trends to increase tibia bone mineral density. T3 increased body temperature, insulin-like growth factor I levels and all measures of somatic growth and, unlike GH, increased food intake and tended to decrease tibia bone mineral density. Tamoxifen inhibited the somatotropic actions of T3 (including increases in insulin-like growth factor I levels), and produced significant increases in tibia bone mineral density only in T3-treated rats. Tamoxifen had no effect on T3 actions to increase food intake or body temperature. T3 alone increased fat mass and exhibited a tendency to decrease serum triglycerides: tamoxifen had no effect on these parameters in the absence of T3. However, coadministration of tamoxifen with T3 produced a marked decrease in fat mass and increased serum triglycerides. GH had no effect on serum triglycerides in either the presence or absence of tamoxifen. Serum glucose levels appeared normal in all groups. The data indicate that multiple tamoxifen effects on growth and metabolism may reflect modulation of T3 rather than GH actions.     

An Arabic language version of the health promotion lifestyle profile

BACKGROUND: Characteristic features of cholesteatoma of the middle ear are destruction of the bone and a high tendency for recurrent disease. The choice of surgical procedure is determined by audiological results and the rate of recurrent cholesteatoma. PATIENTS: One hundred fifty patients who underwent primary cholesteatoma surgery were investigated 3-5 years postoperatively. Preoperative and postoperative audiological results and rate of revision surgery were compared for the respective surgical procedures. All cholesteatomas were treated with an open surgical technique. The lateral attic walls and cholesteatomas were removed. RESULTS: Cholesteotoma recurred in 15 patients (10%). Primary reconstruction of the ossicular chain with a tympanoplasty (type III) was performed in 98 patients in the first operation. Approximately 80% of patients treated with a type III tympanoplasty had a maximum postoperative air-bone gap of 20 dB in the main speech range, depending on the frequency. In about 50% of patients, this value was 10 dB or less. Comparison of preoperative and postoperative conductive hearing loss between 250 Hz and 8000 Hz revealed an improvement (p < 0.05) of 10 dB (500 Hz, 3000 Hz, 4000 Hz) and 15 dB (250 Hz, 1500 Hz, 2000 Hz, 8000 Hz). CONCLUSIONS: In our opinion, a second look operation should be performed in cases where a large cholesteatoma cannot be removed with sufficient reliability. This applies especially to a cholesteatoma in the oval window. Here, we suggest second-look surgery after one year.     

Recognition of synthetic oligopeptides from nonstructural proteins NS1 and NS3 of dengue-4 virus by sera from dengue virus-infected children

OBJECTIVE: To investigate the correlation between soluble forms of the intercellular adhesion molecule (sICAM-1) and vascular cell adhesion molecule (sVCAM-1) and the severity of pre-eclampsia or its possible consequences for fetal growth. DESIGN: Prospective observational study. SETTING: Institute of Medical Genetics, University of Oslo, Department of Medical Genetics and Haematological Research Laboratory, Ullev?l University Hospital; and the Department of Obstetrics and Gynaecology, The National Hospital, Oslo, Norway. PARTICIPANTS: Seventy-six women with normotensive pregnancies and 157 women with pre-eclampsia divided into three subgroups: mild, severe and pre-eclampsia with fetal growth retardation. METHODS: ELISA-measurements of plasma sICAM-1 and sVCAM-1 were performed in a group of healthy pregnant normotensive women and three groups of women with varying degrees of pre-eclampsia. RESULTS: sICAM-1 concentrations were higher in the pre-eclampsia group compared with the control group, but this difference was not statistically significant. Plasma concentrations of sVCAM-1 were significantly greater (P < 0.0001) in all pre-eclampsia subgroups (835.34, 855.25 and 964.05 ng/mL) compared with the control group (667.62 ng/mL). Within the pre-eclampsia group, plasma concentration of sVCAM-1 was significantly higher in the subgroup exhibiting fetal growth retardation (P = 0.03) compared with mild pre-eclampsia. CONCLUSION: The observed increases in plasma concentrations of sVCAM-1 suggest that measurements of this adhesion molecule may be useful in monitoring pregnancies with respect to the development of pre-eclampsia or fetal growth retardation.     

Elevated nocturnal profiles of serum leptin in patients with depression

Leptin, the protein product of the obese (ob) gene, has been suggested to play a role in the regulation of food intake. As depressive episodes are frequently characterized by loss of appetite, reduced food intake and weight loss, altered leptin secretion might also be expected in patients with depression. Therefore, we examined nocturnal (10.00 p.m. to 7.00 a.m.) secretion of leptin, cortisol, ACTH and growth hormone (GH) in a group of 15 patients with depression and age- and sex-matched controls (age range 23-71 years). In addition, the effects of pulsatile administration of growth hormone-releasing hormone (GHRH), thought to be an endogenous antagonist of corticotropin-releasing hormone (CRH), which in turn is believed to play a critical role for the pathophysiology of depression, on nocturnal hormone secretion were assessed. Patients with depression showed a trend towards elevated nocturnal cortisol secretion (F = 3.8, p < 0.05). Nocturnal serum leptin was significantly higher in patients, despite a reported weight loss (F = 8, p < 0.05), but showed the same sexual dimorphism as in controls (F = 20.9, p < 0.01). No significant differences were seen between patients and controls with regard to plasma GH and ACTH. GHRH treatment increased GH secretion in both patients and controls, while the other hormones were not affected. Furthermore, serum leptin was correlated with body mass index (BMI) in controls, but not in patients with depression, supporting an altered regulation of leptin secretion in depressive illness. Finally, we provide some evidence that in young female patients the normal nocturnal leptin surge is blunted. As glucocorticoids can prevent the fasting-induced decline in serum leptin, we propose that hypercortisolism in depression might counteract the reduction in leptin secretion caused by decreased food intake and weight loss. Elevated serum leptin in depression might in turn further promote CRH release, as shown in animals and, hence, contribute to HPA system hyperactivity seen in depression.