A new method for the noninvasive determination of abdominal muscle feedforward activity based on tissue velocity information from tissue Doppler imaging.

Rapid arm movements elicit anticipatory activation of the deep-lying abdominal muscles; this appears modified in back pain, but the invasive technique used for its assessment [fine-wire electromyography (EMG)] has precluded its widespread investigation. We examined whether tissue-velocity changes recorded with ultrasound (M-mode) tissue Doppler imaging (TDI) provided a viable noninvasive alternative. Fourteen healthy subjects rapidly flexed, extended, and abducted the shoulder; recordings were made of medial deltoid (MD) surface EMG and of fine-wire EMG and TDI tissue-velocity changes of the contralateral transversus abdominis, obliquus internus, and obliquus externus. Muscle onsets were determined by blinded visual analysis of EMG and TDI data. TDI could not distinguish between the relative activation of the three muscles, so in subsequent analyses only the onset of the earliest abdominal muscle activity was used. The latter occurred <50 ms after the onset of medial deltoid EMG (i.e., was feedforward) and correlated with the corresponding EMG onsets (r = 0.47, P < 0.0001). The mean difference between methods was 20 ms and was likely explained by electromechanical delay; limits of agreement were wide (-40 to +80 ms) but no greater than those typical of repeated measurements using either technique. The between-day standard error of measurement of the TDI onsets (examined in 16 further subjects) was 16 ms. TDI yielded reliable and valid measures of the earliest onset of feedforward activity within the anterolateral abdominal muscle group. The method can be used to assess muscle dysfunction in large groups of back-pain patients and may also be suitable for the noninvasive analysis of other deep-lying or small/thin muscles.     

The dynamic microbiome

While our genomes are essentially static, our microbiomes are inherently dynamic. The microbial communities we harbor in our bodies change throughout our lives due to many factors, including maturation during childhood, alterations in our diets, travel, illnesses, and medical treatments. Moreover, there is mounting evidence that our microbiomes change us, by promoting health through their beneficial actions or by increasing our susceptibility to diseases through a process termed dysbiosis. Recent technological advances are enabling unprecedentedly detailed studies of the dynamics of the microbiota in animal models and human populations. This review will highlight key areas of investigation in the field, including establishment of the microbiota during early childhood, temporal variability of the microbiome in healthy adults, responses of the microbiota to intentional perturbations such as antibiotics and dietary changes, and prospective analyses linking changes in the microbiota to host disease status. Given the importance of computational methods in the field, this review will also discuss issues and pitfalls in the analysis of microbiome time-series data, and explore several promising new directions for mathematical model and algorithm development.     

Laboratory workshop on the characterization of anti-platelet antibodies in immune thrombocytopenic purpura

The aim of this laboratory workshop was to evaluate the state of knowledge concerning the demonstration of membrane glycoprotein specific anti-platelet antibodies. The main interest lay in investigating whether specific antibody detection offers possibilities to distinguish the chronic from the acute form of ITP. In five laboratories four different methods were applied to demonstrate such antibodies. These methods are briefly described and compared. In all, except two, of the 45 ITP samples anti-platelet antibodies could be detected by at least one participating laboratory, in 85% of the samples antibodies were found by two or more laboratories. For seven out of eight control samples no positive results were reported. The comparison of glycoprotein specific anti-platelet antibodies shows partly considerable differences which may be due to the different methods as well as the different antibodies used (monoclonal antibody against membrane glycoprotein and antihuman globulin sera). This laboratory workshop leads to the conclusion that by exchange of reagents and patient samples the different methods may be compared and evaluated. The results obtained allowed no further characterization of ITP. All participants agreed on the usefulness of further similar laboratory workshops.     

Functional significance of the A-current

This work considers the response to simulated synaptic inputs of an excitable membrane model. The model is essentially of the Hodgkin-Huxley type, but contains an A-current in addition to sodium and delayed-rectifier potassium channels. The results were compared with previous simulations in which the stimulus was an injected current. These two types of stimuli give somewhat different results because synaptic stimuli directly change the membrane resistance, whereas injected current does not. The results of synaptic stimulation were similar to injected current in that very low frequencies of action potentials were elicited only where the stimulus was slightly above threshold. For most of the range of synaptic inputs that produced oscillatory behavior, the A-current had little effect on oscillation frequency. With synaptic stimuli as with injected current, the model membrane's spiking behavior does not begin immediately when an excitatory stimulus is imposed on a quiescent state. The delay before spiking is closely related to the inactivation time of the A-current. The synaptic results were different from the injected current results in that when substantial inhibition was present, the ability to produce very-low-frequency spiking was absent, even just above the excitatory threshold. The higher the degree of inhibition, the narrower the range of spike frequencies that could be elicited by excitation. At very high inhibition, no degree of excitation could elicit spiking.     

Metabolism of deoxycytidine in isolated perfused organs

Summary The metabolism of deoxycytidine-U-¹⁴C was studied in isolated perfused normal and regenerating rat liver, in perfused rat intestine and in isolated perfused mouse liver. A technique to perfuse mouse liver is described. Catabolism of dCyd is very slow in organs of the rat whereas it is rapid in those of the mouse. Nevertheless, incorporation into liver DNA does not differ markedly between the species. The quantitative aspects of dCyd metabolism in the isolated organs are discussed.

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Zusammenfassung Der Stoffwechsel von Deoxycytidin-U-¹⁴C wurde in isoliert perfundierter normaler und regenerierter Rattenleber, in Rattendarm und in normaler Mäuseleber untersucht. Eine Methode zur Perfusion der Mäuseleber wird beschrieben. Der Abbau von Deoxycytidin ist langsam in Rattenorganen, jedoch rasch in Mäuseleber. Dabei sind zwischen den beiden Tierarten keine großen Unterschiede beim Einbau in Leber-DNA zu verzeichnen. Die quantitativen Aspekte des Deoxycytidinstoffwechsels in isolierten Organen werden diskutiert.

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Abbreviations used in text and figures dCyd deoxyoytidine - dThd deoxythymidine - dUrd deoxyuridine - dCMP deoxyoytidine monophosphate - BAIBA ß-aminoisobutyrio acid This is publication No. 754 of the Euratom Biology Division, Contract 078-69 BIAC.