Measurement of the ßß decay half-life of 130Te with the NEMO-3 detector.

We report results from the NEMO-3 experiment based on an exposure of 1275 days with 661 g of (130)Te in the form of enriched and natural tellurium foils. The ßß decay rate of (130)Te is found to be greater than zero with a significance of 7.7 standard deviations and the half-life is measured to be T(½)(2ν) = [7.0 ± 0.9(stat) ± 1.1(syst)] × 10(20) yr. This represents the most precise measurement of this half-life yet published and the first real-time observation of this decay.

Akt is transferred to the nucleus of cells treated with apoptin, and it participates in apoptin-induced cell death.

OBJECTIVES: The phosphatidylinositol 3-kinase (PI3-K)/Akt pathway is well known for the regulation of cell survival, proliferation, and some metabolic routes. MATERIALS AND METHODS: In this study, we document a novel role for the PI3-K/Akt pathway during cell death induced by apoptin, a tumour-selective inducer of apoptosis. RESULTS: We show for the first time that apoptin interacts with the p85 regulatory subunit, leading to constitutive activation of PI3-K. The inhibition of PI3-K activation either by chemical inhibitors or by genetic approaches severely impairs cell death induced by apoptin. Downstream of PI3-K, Akt is activated and translocated to the nucleus together with apoptin. Direct interaction between apoptin and Akt is documented. Co-expression of nuclear Akt significantly potentiates cell death induced by apoptin. Thus, apoptin-facilitated nuclear Akt, in contrast to when in its cytoplasmic pool, appears to be a positive regulator, rather than repressor of apoptosis. CONCLUSIONS: Our observations indicate that PI3-K/Akt pathways have a dual role in both survival and cell death processes depending on the stimulus. Nuclear Akt acts as apoptosis stimulator rather than as a repressor, as it likely gains access to a new set of substrates in the nucleus. The implicated link between survival and cell death pathways during apoptosis opens new pharmacological opportunities to modulate apoptosis in cancer, for example through the manipulation of Akt's cellular localization.

Inflammatory response, reactive oxygen species, programmed (necrotic-like and apoptotic) cell death and cancer.

In this short review we attempt to establish and/or strengthen connections between clinical, inflammatory manifestation of cancer, inflammatory processes driven by lipoxy-metabolites and their contribution to immortalized phenotype and apoptosis inhibition. Particularly the resemblance between symptoms of inflammation and signs associated with cancer chemotherapy and/or cytokine therapy is illustrated. In this context the role of apoptosis and necrosis in inflammation as well as the role of RedOx processes and lipid-oxidizing enzymes particularly cyclooxygenase-2 (COX-2) and also to lesser extend the 5-lipooxygenase (5-LOX) is highlighted. The multitude of biological effects of reactive oxygen species is shortly summarized and some aspects of it are being discussed in greater detail. Apoptotic cell death is discussed in the context of the "resolve-phase" of an inflammatory response. The disturbance of apoptosis is mainly deliberated in the framework of insufficient removal of immuno-effector cells that may cause autoimmunity. The role of COX-2 in apoptosis resistance is being highlighted mainly in the context of malignant transformation. The mechanism of cell death (apoptotic or necrotic) and its influence on the immune system and potential benefits of necrotic cell death induction during cancer chemotherapy is indicated.

Development and application of an enzyme immunoassay for karasurin A, an effective protein component of Trichosanthes kirilowii Max. var. japonicum Kitam.

A method was developed for specific estimation of the content of a non-enzymatic protein, karasurin A, in fractions taken during the extraction and purification processes from a natural source. Anti-karokon serum was elicited in rabbits immunized with fragments of karokon, a dried root tuber of Trichosanthes kirilowii Max. var. japonicum Kitam. Rabbit antibody specific for karasurin A was identified in anti-karokon serum by the Western blotting method. After separation by SDS-PAGE, protein bands of purified karasurin A and extracted proteins from a medicinal herb which is a karasurin A source were reacted with anti-karokon serum followed by treatment with horseradish peroxidase (HRP)-labeled Fab' of goat anti-rabbit IgG, and then bound HRP-labeled second antibody on protein bands was developed to brown by reaction with a substrate solution of the used enzyme. A novel selected antibody enzyme immunoassay (SAEIA) for karasurin A was developed using selective binding of anti-karasurin A antibody in anti-karokon serum to solid phase karasurin A and HRP-labeled Fab' of the second antibody as the tracer. Specific estimation of the content of karasurin A in several fractions taken during the isolation and purification processes of the protein were possible using the SAEIA method.

Eccentric and concentric torque and power of the knee extensors of females.

The purpose of this study was to compare differences in eccentric and concentric peak torque and power measurements of knee extensors at different velocities. The subjects included 21 females between the ages of 19 and 28, who had no history of knee pain or abnormality. Eccentric and concentric contractions of the knee extensors of the dominant leg of each subject were tested on an isokinetic dynameter at 60 degrees/s, 120 degrees/s and 180 degrees/s. Eccentric peak torque was greater than concentric at each of the three velocities tested, whereas eccentric power was significantly greater only at the two higher velocities. The lack of change in concentric peak torque between 120 degrees/s and 180 degrees/s contrasted with results of other studies, probably owing to methodological differences. Eccentric torque increased from 60 degrees/s to 120 degrees/s, but decreased again at the highest velocity. Both concentric and eccentric power increased with velocity.

The effect of propranolol and verapamil on atrial and atrioventricular refractory periods in man.

The atrial effective (ERP) and relative (RRP) refractory periods were examined at high atrial pacing rates in 12 patients before and after intravenous injection of propranolol, and in 5 patients before and after injection of verapamil, using the technique of paired pacing. Seven of the patients had A-V block grade II-III and 10 patients had sinus rhythm. The range of atrial ERP in all patients was found to be 200 to 270 msec. and the range of atrial RRP was 230 to 330 msec. The atrial ERP and RRP were longer at a pacing rate of 160 per minute than at a pacing rate of 240 per minute. The conduction delay between the second impulse and the atrial depolarization was found to be due to increased interval between the stimulus and the start of the depolarization wave. The atrial ERP increased after injection of propranolol in 8 of 12 patients, decreased in 3 patients and was unchanged in one patient. The atrial RRP increased in 7 patients, decreased in one patient and was unchanged in 4 patients. In all patients the changes were of moderate degree. The conduction delay between the stimulating impulse and the atrial response was shorter after propranolol in 7 patients, longer in one patient and unchanged in 4 patients. The ERP of the atrioventricular conducting tissue was 220 to more than 380 millisec. After injection of propranolol it increased in all of 3 patients in whom it could be measured. After injection of verapamil no significant effects on the atrial ERP and RRP were found. ERP of the atrioventricular conducting tissue was lengthened in 4 of 5 patients, and the degree of A-V block during rapid atrial pacing increased after injection of verapamil. It is suggested that the effect of propranolol on atrial arrhythmias is due to its effect on ectopic pacemaker activity rather than any effect on the refractory period of the atrium. The effects of verapamil on the atrioventricular conducting tissue may explain some of the antiarrhythmic effects of this drug.

Long-term anticoagulant therapy after myocardial infarction in women.

A multicentre trial from five medical departments in Oslo has been carried out to determine the value in women patients of one year's long-term anticoagulant therapy. Follow-up long-term laboratory control and anticoagulant dosage were performed at one centre (the Rikshospitalet). One hundred and fifty-nine patients were assigned randomly into two similar well-matched groups (control and treatment). Dosage was controlled by Thrombotest, aiming at 10-20% levels, and 50% of the tests were less than 14%. Compared with the control group, the treatment group showed a significant reduction in mortality and in reinfarction rate. No serious bleeding complications occurred. It is concluded that women benefit as much as men from long-term anticoagulant therapy.