Effect of arm-shoulder fatigue on carpenters at work

The purpose of the study was to analyse the effect of arm-shoulder fatigue on manual performance. Ten experienced carpenters performed three standardized tasks (nailing, sawing and screwing). Electromyographic activity was recorded from six arm-shoulder muscles and the performances were video-filmed. After 45 min of standardized arm-cranking (arm-shoulder-fatiguing exercise of approximately 70%-80% maximal oxygen consumption), the tasks were repeated. The number of work movements and the time taken for each task were recorded and the quality of the work performed was compared. After the fatiguing exercise, only nailing was perceived as being harder and more mistakes were made during nailing and sawing. Movement performance was not influenced during nailing but was slightly slower during sawing and faster during screwing. However, there were increased mean EMG amplitudes in the upper trapezius and biceps muscles during nailing, in the upper trapezius, anterior deltoid and infraspinatus muscles during sawing and in the anterior deltoid muscle during screwing. Of the muscles studied the upper trapezius and anterior deltoid muscles increased their activity most after the arm-shoulder-fatiguing exercise.     

The effect of lipopolysaccharide desensitization on the regulation of in vivo induction of immunologic tolerance and antibody production and in vitro release of IL-1

As previously reported, LPS and 8-derivatized guanosine (both generators of IL-1 release), as well as IL-1 itself interfere with the in vivo induction of tolerance to DHGG in A/J mice. In the present studies it was demonstrated that desensitization of either A/J or CBA/CaJ mice with LPS aborts the ability of LPS to interfere with the induction of tolerance to DHGG. The abrogation of the ability of LPS to interfere with tolerance by LPS desensitization is not the result of neutralization of LPS by antibody produced to LPS during desensitization. Desensitization with LPS also aborts the interference with tolerance induction by 7-methyl-8-oxoguanosine. LPS desensitization inhibits the ability of LPS and/or 7-methyl-8-oxoguanosine to both convert a tolerogenic signal to an immunogenic signal and interfere with the induction of a tolerant state to a subsequent injection of Ag. The effects resulting from desensitization may be in part attributed to the depletion of IL-1. LPS desensitization also modulates the antibody response to injection of the AG, AHGG. Desensitization with LPS markedly suppresses the antibody response to a subsequent injection of AHGG in CBA/CaJ mice. Desensitization with LPS also inhibits the anti-HGG antibody response in A/J mice, but in this strain its effect is dependent on the route of injection of AHGG. In an experiment directly comparing the responses of normal and desensitized A/J mice to either intravenous or intraperitoneal injection of AHGG, desensitization only suppressed the response in mice injected with AHGG i.p.. Desensitization with LPS also inhibits the ability of LPS to act as an adjuvant in a subsequent antibody response to AHGG. Not only does desensitization interfere with the primary antibody response to AHGG, but it also interferes with the secondary response, suggesting that the primary injection after desensitization induces a state of immunologic tolerance.     

Purification and characterization of chick intestine brush border membrane Effects of 1α(OH) vitamin D3 treatment

A new technique has been developed for the isolation of membrane vesicles from the vitamin D-deficient and vitamin D-treated chick intestinal brush border membrane. The technique involves removal of nuclei from a low speed pellet by discontinuous sucrose gradient centrifugation. The resulting intact brush borders are then homogenized in 0.5 M Tris and the membrane fragments purified on a glycerol gradient. This preparation represents a 20-fold purification of the brush border marker sucrase. After 1α-hydroxyvitamin D₃ treatment there is a significant increase in membrane phospholipid phosphorous, an alteration in the fatty acid composition of the phosphatidylcholine fraction of membrane phospholipid, and a decrease in sucrase specific activity.