Analgesic effect of the electromagnetic resonant frequencies derived from the NMR spectrum of morphine.

Exposure to various types of electromagnetic fields (EMFs) affects pain specificity (nociception) and pain inhibition (analgesia). Previous study of ours has shown that exposure to the resonant spectra derived from biologically active substances' NMR may induce to live targets the same effects as the substances themselves. The purpose of this study is to investigate the potential analgesic effect of the resonant EMFs derived from the NMR spectrum of morphine. Twenty five Wistar rats were divided into five groups: control group; intraperitoneal administration of morphine 10 mg/kg body wt; exposure of rats to resonant EMFs of morphine; exposure of rats to randomly selected non resonant EMFs; and intraperitoneal administration of naloxone and simultaneous exposure of rats to the resonant EMFs of morphine. Tail Flick and Hot Plate tests were performed for estimation of the latency time. Results showed that rats exposed to NMR spectrum of morphine induced a significant increase in latency time at time points (p < 0.05), while exposure to the non resonant random EMFs exerted no effects. Additionally, naloxone administration inhibited the analgesic effects of the NMR spectrum of morphine. Our results indicate that exposure of rats to the resonant EMFs derived from the NMR spectrum of morphine may exert on animals similar analgesic effects to morphine itself.

Solid state and solution studies of a vanadium(III)-L-cysteine compound and demonstration of its antimetastatic, antioxidant and inhibition of neutral endopeptidase activities.

Reaction of one equivalent of vanadium(III) chloride with three equivalents of l-cysteine(H2Cys) in methyl alcohol affords a VIII-Cys compound that is formulated as [VIII(Hcys)3].2HCl.2.5H2O 1. The solid state characterization of 1 was performed by microanalysis, circular dichroism (CD) and infrared studies as well as room temperature magnetic susceptibility. These studies have shown coordination of each HCys- ligand to the VIII atom through an amine nitrogen and a carboxylate oxygen atoms. Solution studies of 1 were carried out in water and methanol by UV-visible, CD and electron paramagnetic resonance (EPR) spectroscopies. According to these studies, it was evident that despite the progressive oxidation of 1 to oxovanadium(IV) species, some V(III) species were also present in solution after several hours. Compound 1, VIVOSO4.5H2O and l-cysteine were examined for their total antioxidant capacity (TAC) and lag time. Compound 1 exhibited significantly greater total antioxidant capacity and lag time values than l-cysteine. VIVOSO4.5H2O did not show any total antioxidant capacity or lag time. The inhibition of neutral endopeptidase (NEP) activity caused by 1, VIVOSO4.5H2O and thiorphan was also measured. Compound 1, at a concentration of 10(-3) M, showed inhibition of NEP activity as potent as thiorphan at 10(-6) M, while VIVOSO4.5H2O in the same concentration exhibited less than 50% inhibitory activity than that of thiorphan at 10(-6) M. Moreover, the antimetastatic effects of compound 1, l-cysteine and VIVOSO4.5H2O were examined on Wistar rats, treated with 3,4-benzopyrene. The results revealed that 1 prevents significantly lung metastases (only 9.5% of animals treated with 1 showed metastases), whereas 47-52% of the rats of the control group and those treated with l-cysteine and VIVOSO4.5H2O exhibited metastases.

Cardiovascular and pulmonary adaptations during short-term 15° and 30° head-down posture in healthy male volunteers.

INTRODUCTION: Healthy male volunteers were investigated for cardiopulmonary adaptations to a head-down posture (HDT). METHODS: Thirty-three volunteers were enrolled in this study. Their changes in cardiopulmonary parameters at 15° and 30° HDT, for 7.5 minutes in each posture, were studied using echocardiography. Spirometric measurements of pulmonary function were performed during sitting and supine positions, and 15° and 30° HDT, while measurements of blood pressure, carotid blood flow, and electrocardiographic (ECG) and echocardiographic examinations were performed in the supine position and under 15° and 30° HDT. RESULTS: A significant increase (p<0.05) in mean, systolic, and diastolic pressure, and a decrease in heart rate (p<0.05) were observed during the HDT postures. Right ventricular diameter increased (p<0.05) from supine to 15° and 30° HDT. Forced vital capacity, forced expiratory volume in 1 s, and peak flow rate decreased significantly from supine to 15° and 30° HDT. Maximum ventilatory volume decreased significantly only from the sitting to the supine posture and then remained steady in the HDT postures. CONCLUSIONS: During short-term HDT, the cardiovascular system maintains a stable ejection fraction, with a significant in heart rate, and a decrease in pulmonary ventilation.

Serum and tissue selenium levels in gastric cancer patients and correlation with CEA.

BACKGROUND: An inverse relationship between selenium (Se) intake and cancer mortality is evident in humans. MATERIALS AND METHODS: In eighty patients who had been operated on for primary gastric cancer, serum Se and carcinoembryonic antigen (CEA) levels were measured preoperatively using a fluorometric and immunoradiometric assay (IRMA), respectively. RESULTS: The serum Se levels were 43+/-6.3 microg l(-1) in the patient group and 68.7+/-4.5 microg l(-1) in healthy individuals (p<0.001). The serum CEA was 12+/-1.9 U ml(-1) in the gastric cancer patients and 2.1 U ml(-1) in the control group (p<0.001). The Se tissue concentrations were 2,640+/-220 mg g(-1) in excised neoplastic tissue and 685+/-115 mg g(-1) in non-neoplastic tissue (p<0.001). An inverse correlation between Se and CEA serum levels was found (r=-0.782). There was no correlation between serum/tissue Se concentration and disease stage/histological type or gender in the patient group.

Vitamin C transiently arrests cancer cell cycle progression in S phase and G2/M boundary by modulating the kinetics of activation and the subcellular localization of Cdc25C phosphatase.

Regulation of cell cycle progression involves redox (oxidation-reduction)-dependent modification of proteins including the mitosis-inducing phosphatase Cdc25C. The role of vitamin C (ascorbic acid, ASC), a known modulator of the cellular redox status, in regulating mitotic entry was investigated in this study. We demonstrated that vitamin C inhibits DNA synthesis in HeLa cells and, mainly the form of dehydroascorbic acid (DHA), delays the entry of p53-deficient synchronized HeLa and T98G cancer cells into mitosis. High concentrations of Vitamin C caused transient S and G2 arrest in both cell lines by delaying the activation of the M-phase promoting factor (MPF), Cdc2/cyclin-B complex. Although vitamin C did not inhibit the accumulation of cyclin-B1, it may have increased the level of Cdc2 inhibitory phosphorylation. This was achieved by transiently maintaining Cdc25C, the activator of Cdc2, both in low levels and in a phosphorylated on Ser216 inactive form that binds to 14-3-3 proteins contributing thus to the nuclear exclusion of Cdc25C. As expected, vitamin C prevented the nuclear accumulation of Cdc25C in both cell lines. In conclusion, it seems that vitamin C induces transient cell cycle arrest, at least in part, by delaying the accumulation and the activation of Cdc25C.