Maintenance of internal pH and an electrochemical gradient in Trypanosoma brucei

The internal pH value (pHi) of the long-slender bloodstream form of Trypanosoma brucei was estimated from the distribution of 14C-labeled 5,5-dimethyl-2,4-oxazolidinedione or 14C-labeled methyl amine between the intracellular space of the cells and the medium. The pHi of T. brucei remained relatively constant at 7.0-7.2 throughout an extracellular pH (pHo) range of 6.0-8.0. The maintenance of an internal pH more acidic than the environment appears to be a unique feature. Preincubation of T. brucei with carbonyl cyanide m-chlorophenyl hydrazone (CCCP) or CCCP + valinomycin had no appreciable effect on the delta pH across the T. brucei membrane when the external pH was 8.0. However, when the external pH was 6.0, CCCP abolished the observed delta pH. Nigericin significantly dissipated the delta pH across the T. brucei membrane at all pHo values. These data suggest that under physiological conditions, the maintenance of a delta pH across the bloodstream-form T. brucei membrane may be by a mechanism other than an energy-dependent gradient, whereas an energy-dependent pump may be needed for maintaining the pHi in an acidic environment. The electrical potential (delta psi) across the trypanosomal plasma membrane was also estimated using the lipophilic cation, [3H]tetraphenyl-phosphonium bromide. It appears dependent on both the external pH and the external salt conditions. Under ionic conditions similar to the host bloodstream, it ranges from -76 to -160 mV over an external pH range of 6.0 to 8.0, with an estimated value of -155.5 +/- 0.7 at the physiological pH.(ABSTRACT TRUNCATED AT 250 WORDS)     

A model invalidation-based approach for elucidating biological signalling pathways,applied to the chemotaxis pathway in R. sphaeroides

Background  

Developing methods for understanding the connectivity of signalling pathways is a major challenge in biological research. For this purpose, mathematical models are routinely developed based on experimental observations, which also allow the prediction of the system behaviour under different experimental conditions. Often, however, the same experimental data can be represented by several competing network models.     

The electro-mechanical delay of the erector spinae muscle: influence of rate of force development, fatigue and electrode location.

Electro-mechanical delay (EMD) values of the erector spinae muscle were obtained using a technique based on the cross-correlation between the force and the electromyogram (EMG). Seven subjects performed a series of 20 submaximal dynamic isometric contractions in a seated position at two frequencies (0.5 Hz and 1 Hz) to study the influence of the rate of force development on EMD. Mean EMD values of 125.7 (SD 28.1) ms (1 Hz) and 136.8 (SD 28.6) ms (0.5 Hz) were shown to differ significantly (P = 0.02). This finding supports the hypothesis that EMD is inversely related to the rate of force development and implies that the time to stretch the series elastic component is an important factor determining EMD. After performing a series of fatiguing contractions EMD did not differ significantly from the control value. Multiple regression analysis showed that maximal voluntary contraction force (MVC) and endurance time of the fatiguing exercise correlated significantly with EMD. The site from which the EMG signal was recorded had no significant influence on EMD. However, the coefficient of correlation between force and the EMG-signal differed significantly between electrode positions. The magnitude of the EMD values found emphasized the need to account for this delay when interpreting temporal patterns of activation of the muscles in, for example, lifting tasks.     

Urotensin II and urocortin trigger the expression of myostatin, a negative regulator of cardiac growth, in cardiomyocytes

Urotensin II (UII) and urocortin (UCN) are potent contributors to the physiopathology of heart failure. Our study investigated the effects of UII and UCN on the expression of myostatin (Mstn) in primary culture of adult cardiomyocytes. Adult rat cardiomyocytes were stimulated for 48 h with UII and UCN. Cell size and protein content were determined. Mstn gene expression was determined by real time quantitative polymerase chain reaction. Treatment with UII and UCN stimulates hypertrophy of adult cardiomyocytes. This effect was associated with a twofold increase of Mstn gene expression. We have established for the first time that the two hypertrophic peptides UII and UCN stimulate the expression of Mstn.