Aging and cancer: are telomeres and telomerase the connection?

There is substantial evidence for the progressive loss of the telomeric ends of chromosomes during aging, both in cell culture and in vivo. The loss of telomeres may eventually induce antiproliferative signals that result in cellular senescence. A hypothesis gaining prominence is that the activation of telomerase, a ribonucleoprotein enzyme that is important in maintaining telomere length stability, is necessary for the sustained growth of most tumors. The interrelationships between telomere shortening and aging, and how activation of telomerase may be necessary for cells to become immortal and malignant, are reviewed here.     

Transformation of the methylotrophic actinomycete Amycolatopis methanolica with plasmid DNA: stimulatory effect of a pMEA300-encoded gene

The concentration of endothelin-1 (ET-1) in the brain regions, heart, and throacic aorta of 1-, 4-, 6- and 8-week-old spontaneously hypertensive (SHR) and normotensive Wistar-Kyoto (WKY) rats was determined using radioimmunoassay. ET-1-like immunoreactivity in the brain regions of 1-week-old WKY and SHR rats was lower compared to older (6 and 8 weeks) rats. ET-1 levels in the central nervous system gradually increased with age in both SHR and WKY rats. However, the concentration of ET-1 in 8-week-old rats was lower in the brain regions of SHR compared to WKY rats. The concentration of ET-1 in the thoracic aorta of SHR (224 +/- 43 pg/g tissue) rats was lower than that of WKY (452 +/- 11 pg/g tissue) rats at 1 week of age. However, ET-1 levels gradually increased with age in SHR rats. By 8 weeks of age, levels of ET-1 in SHR (623 +/- 33 pg/g tissue) rats were higher compared to WKY (439 +/- 62 pg/g tissue) rats. In the heart, ET-1 levels were similar in WKY and SHR rats at 4 weeks of age, but at 8 weeks of age ET-1 levels were higher in SHR rats (364 +/- 33 pg/g tissue) compared to WKY rats (260 +/- 31 pg/g tissue). It appears that at 8 weeks of age when hypertension is fully expressed in rats, ET-1 levels are lower in the central nervous system and are higher in the thoracic aorta and heart of SHR compared to WKY rats.     

An adaptive linear combiner for on-line tracking of power systemharmonics

The paper presents a new approach for the estimation of harmonic components of a power system using a linear adaptive neuron called Adaline. The learning parameters in the proposed neural estimation algorithm are adjusted to force the error between the actual and desired outputs to satisfy a stable difference error equation. The estimator tracks the Fourier coefficients of the signal data corrupted with noise and decaying DC components very accurately. Adaptive tracking of harmonic components of a power system can easily be done using this algorithm. Several numerical tests have been conducted for the adaptive estimation of harmonic components of power system signals mixed with noise and decaying DC components     

Apnoea and bradycardia during epileptic seizures: relation to sudden death in epilepsy

OBJECTIVE: To record non-invasively ictal cardiorespiratory variables. METHODS: Techniques employed in polysomnography were used in patients with epilepsy undergoing EEG-video recording at a telemetry unit. RESULTS: Apnoea (> 10, range > 10-63, mean 24 s) was seen in 20 of 47 clinical seizures (three secondary generalised, 16 complex partial, and one tonic) and 10 of 17 patients. Apnoea was central in 10 patients, but obstructive apnoea was also recorded in three of 10. Oxyhaemoglobin saturation (SpO2) dropped to less than 85% in 10 seizures (six patients). An increase in heart rate was common (91% of seizures). Bradycardia/sinus arrest was documented in four patients (mean maximum RR interval 5.36, range 2.8-8.6 s) but always in the context of a change in respiratory pattern. CONCLUSION: Ictal apnoea was often seen. The occurrence of bradycardia in association with apnoea suggests the involvement of cardiorespiratory reflexes. Similar mechanisms may operate in cases of sudden death in epilepsy.     

Repair kinetics in pig epidermis: an analysis based on two separate rates of repair

Pig skin was irradiated using 90Sr/90Y plaques and the dose-related incidence of induced moist desquamation was determined. The repair of radiation-induced sublethal damage (SLD) was studied by fitting these response data to the generalized LQ equation for incomplete repair using quasilikelihood methods with binomial statistics, and either a Poisson or logistic link to relate the probability of response to the covariates. A Poisson response analysis based on the assumption that SLD was governed by two repair processes gave estimated repair half-times of 0.20 [(95% confidence limits) 0.12, 0.34] and 6.6 [4.3, 10.0] h. The estimates of the short and long repair half-times were significantly different, although there was no significant difference between the results using the Poisson and logistic modes of analyses. The partition coefficient for the longer repair process was 0.5 [0.34, 0.71] indicating that about 33% of SLD-derived lethal damage is associated with the longer repair process in the case of 'complete repair' protocols. However, this proportionation is, in general, protocol dependent for incomplete repair protocols. A chi2 test on the residual deviance showed that the assumption of two repair processes for SLD gave a superior fit to the data than a single repair process at a significance level >99%. The radiation dose to the assumed target cell population depends upon their depth from the skin surface, due to the relatively short range of the electron emission from the 90Sr/90Y plaques. However, further modelling analyses have shown that the estimated repair half-times were independent of the assumed target cell distribution in the skin. This is in contrast with the alpha/beta ratio, where different (clinically significant) estimates can be obtained depending upon the assumed target cell distribution. If the target cells were at 16 micrometer depth from the surface of the skin, the estimated value for the alpha/beta ratio using the biphasic repair model would be 4.6[3.6, 5.6] Gy(Poisson analysis). However, the estimates decrease with the assumed depth (distribution) of the target cells.