The influence of the type of contraction on the masseter muscle EMG power spectrum

Different behaviours of the EMG power spectrum across increasing force levels have been reported for the masseter muscle. A factor that could explain these different behaviours may be the type of contraction used, as was recently shown for certain upper limb muscles⁵. The purpose of this study was to compare, between two types of isometric contractions, the behaviour of EMG power spectrum statistics (median frequency (MF) and mean power frequency (MPF)) obtained across increasing force levels. Ten women exerted, while biting in the intercuspal position, three 5 s ramp contractions that increased linearly from 0 to 100% of the maximal voluntary contraction (MVC). They also completed three step contractions (constant EMG amplitude) at each of the following levels: 20, 40, 60 and 80% MVC. EMG signals from the masseter muscle were recorded with miniature surface electrodes. The RMS, as well as the MPF and MF of the power spectrum were calculated at 20, 40, 60 and 80% MVC for each type of contraction. As expected, the RMS values showed similar increases with increasing levels of effort for both types of contractions. Different behaviours for both MPF (contraction^*force interaction, ANOVA, P<0.05) and MF (contraction^*force interaction, ANOVA, P>0.05) across increasing levels of effort were found between the two types of contraction. The use of step contractions gave rise to a decrease of both MPF and MF with increasing force, while the use of ramp contractions gave rise to an increase in both statistics up to at least 40% MVC followed by a decrease at higher force levels. These findings suggest that the type of contraction used does influence the behaviour of the spectral statistics across increasing force levels and that this could explain the differences obtained in previous studies for the masseter muscle.     

[Fréquence des maladies transmises sexuellement chez des étudiants universitaires.]

OBJECTIVE: To estimate the incidence rate of sexually transmitted diseases (STDs) among university students and evaluate the associated sociodemographic factors. DESIGN: Mail survey in April 1990. Included in the questionnaire were questions about the subjects'' STD experience since their admission to the university and the type and date of the infection. SUBJECTS: Of the 19,682 undergraduate students 2920 subjects, in 10 groups of 292, were randomly selected. A total of 1731 (59.4%) completed the questionnaire. MAIN OUTCOME MEASURES: Estimated annualized incidence rates of genital human papillomavirus infection and Chlamydia infection. RESULTS: The estimated annualized incidence rates of genital human papillomavirus and Chlamydia infections were 2.2% and 1.5% respectively. Among the students who indicated being infected with genital human papillomavirus 59% were 18 to 21 years old (p < 0.05), 76% were women (p < 0.01) and 69% had more than one sexual partner (p < 0.01). No statistically significant associations were observed between age, sex and Chlamydia infection. On the other hand, 95% of the cases of Chlamydia infection were found among those who had more than one sexual partner (p < 0.01). CONCLUSION: University students continue to have sexual activities at risk for STDs and should be specifically targetted by general practitioners and health services in an effort to slow the spread of STDs.     

Comparable Rates of Gene Loss and Functional Divergence after Genome Duplications Early in Vertebrate Evolution

Duplicated genes are an important source of new protein functions and novel developmental and physiological pathways. Whereas most models for fate of duplicated genes show that they tend to be rapidly lost, models for pathway evolution suggest that many duplicated genes rapidly acquire novel functions. Little empirical evidence is available, however, for the relative rates of gene loss vs. divergence to help resolve these contradictory expectations. Gene families resulting from genome duplications provide an opportunity to address this apparent contradiction. With genome duplication, the number of duplicated genes in a gene family is at most 2(n), where n is the number of duplications. The size of each gene family, e.g., 1, 2, 3, . . . , 2(n), reflects the patterns of gene loss vs. functional divergence after duplication. We focused on gene families in humans and mice that arose from genome duplications in early vertebrate evolution and we analyzed the frequency distribution of gene family size, i.e., the number of families with two, three or four members. All the models that we evaluated showed that duplicated genes are almost as likely to acquire a new and essential function as to be lost through acquisition of mutations that compromise protein function. An explanation for the unexpectedly high rate of functional divergence is that duplication allows genes to accumulate more neutral than disadvantageous mutations, thereby providing more opportunities to acquire diversified functions and pathways.     

Abscisic acid and the accumulation, biological activity and metabolism of four derivatives of [3H]gibberellin A1 in barley aleurone layers

Tritiated GA₁ and four of its synthetic derivatives were studiedin relation to their biological activity, uptake and metabolismby barley aleurone layers. Incubation was done in the presenceand absence of ABA. Tentative identification of some of themetabolites was made by TLC and GLC radiocounting of the metaboliteand its acid hydrolyzed derivative. Only GA₁ promoted -amylase synthesis. Uptake ranged from 20to 42%, varying with the derivative. ABA enhanced uptake of[³H]GA₁ and [³H]pseudoGA₁ and inhibited uptake of [³H]ketoGA₁the Wagner-Meerwein rearrangement product of [³H]GA₁ Uptakeof [³H]GA₁ methyl ester ([³H]GA₁-Me) and [³H]dihydroGA₁ wasunaffected by ABA. [³H]GA₁ was converted to an amphoteric GA₁ derivative ([³H]amphoGA₁)and [³H]GA₁-glycosyl ester. GA₁-Me was metabolized to four products,all of them GA₁ derivatives, including an apparent amphotericGA₁ derivative. DihydroGA₁ was quite stable; only one metabolitewas produced in sufficient yield to analyze. This product didnot cochromatograph with either of the expected acid hydrolyzedepimers of [³H]dihydroGA₁. [³H]ketoGA₁ was readily metabolizedto one product, probably the glycoside. [³H]pseudoGA₁ remainedessentially unmetabolized. Metabolism of all compounds testedwas not dramatically affected by ABA. Surprisingly, no metabolitesfrom hydroxylation at the 2-position were found. ¹ Present address: Monsanto Agricultural Co., 800 N. LindberghBlvd., St. Louis, MO 63166, U.S.A. (Received January 31, 1977; )     

Molecular studies on trypanothione reductase, a target for antiparasitic drugs

Trypanosoma and Leishmania are parasitic protozoa that cause a variety of diseases, which include African sleeping sickness and oriental sore. Attempts to determine pharmaceutically exploitable differences between host and parasite biochemistry have identified the unique trypanothione pathway as a possible target. This pathway includes the enzyme trypanothione reductase, the parasite analogue of glutathione reductase.     

Organization and Evolution of the Mammalian Genome: I. Polymorphism of H-2 Linked Loci

To test the hypothesis that the H-2 polymorphism is adaptive, the degree of polymorphism of loci linked to the H-2 complex on chromosome 17 of the house mouse was compared to the degree of polymorphism of loci located on other chromosomes. Published theoretical analyses show that polymorphisms subject to natural selection usually reduce the polymorphism of linked neutral loci. The first test of the hypothesis was based on data obtained from a survey of the polymorphism of 12 isozyme-encoding loci in wild house mice from Europe, North Africa and South America. Results of this test showed that, on the average, H-2-linked loci were as polymorphic as loci located on other chromosomes. In fact, the data suggested that H-2 linked loci might be more polymorphic than other loci. To test this hypothesis more rigorously, data for the 12 isozyme-encoding loci were augmented with data from published surveys of the polymorphisms of 59 loci in house mice from Europe and North America. Results of these tests showed that polymorphic loci linked to the H-2 complex tended to be more, rather than less, polymorphic than loci located on other chromosomes. The cluster of highly polymorphic loci seems to be related to linkage of these loci to the highly polymorphic H-2 complex, but the way in which the influence is exerted could not be readily explained.     

Linkage of Pgm-3 in the house mouse and homologies of three phosphoglucomutase loci in mouse and man

The discovery of a third phosphoglucomutase locus (Pgm-3) in the house mouse is reported. Three alleles are recognized on the basis of differences in electrophoretic mobility and enzymatic activity. Pgm-3 ^a (fast mobility and high activity) is present in inbred strain C57BL/10J and 24 other strains; Pgm-3 ^b (slow mobility and high activity) is present in LP/Pas and six other strains; and Pgm-3 ^c (no detectable activity in any tissue tested) is present in strain DBA/2J and 14 other strains. Seventy-four recombinant inbred strains derived from progenitors that differed at Pgm-3 were used to study genic linkage. Pgm-3 is on chromosome 9 and is linked to Sep-1, d, Mod-1, and Ltw-3. Gene order and recombination frequencies are estimated as d 3.8±1.8% Pgm-3 2.3±1.2% Mod-1. Substrate specificities and cofactor requirements show that mouse Pgm-1 is homologous with human Pgm-2, mouse Pgm-2 with human Pgm-1, and mouse Pgm-3 with human Pgm-3.This research was supported in part by NIH Research Grant GM18684 from the National Institute of General Medical Sciences to B.A.T. and by grants from NIH A105531-02 and the Volkswagon Foundation to Jan Klein. J.H.N. was a recipient of a Fellowship from the Max-Planck-Gesellschaft, Munich. G.S. and J.K. were supported by funds from the Deutsche Forschungsgemeinschaft.     

Effect of adrenaline on insulin secretion in rats treated chronically with adrenaline.

To determine whether rats could adapt to a chronic exogenous supply of adrenaline by a decrease in the well-known inhibitory effect of adrenaline on insulin secretion, plasma glucose and insulin levels were measured in unanesthetized control and adrenaline-treated rats (300 mug/kg twice a day for 28 days) during an adrenaline infusion (0.75 mug kg-1 min-1), after an acute glucose load (0.5 g/kg), and during the simultaneous administration of both agents. Chronic treatment with adrenaline did not modify the initial glucose levels but it greatly diminished the basal insulin values (21.57+/-2.48 vs. 44.69+/-3.3muU/ml, p less than 0.01). In the control rats, despite the elevated glucose concentrations, a significant drop in plasma insulin levels was observed within the first 15 min of adrenaline infusion, followed by a period of recovery. In the adrenaline-treated group, in which plasma glucose levels were lower than in control animals, plasma insulin levels did not drop as in control rats, but a significant increase was found after 30 min of infusion. During the intravenous glucose tolerance test, the plasma glucose and insulin responses showed similar patterns; however, during the concomitant adrenaline infusion, the treated rats showed a better glucose tolerance than their controls. These results indicate that rats chronically treated with adrenaline adapt to the diabetogenic effect of an infusion of adrenaline by have a lower inhibition of insulin release, although the lower basal insulin levels may indicate a greater sensitivity to endogenous insulin.     

Computation of aortic pulse wave velocity and aortic pulse wave velocity and aortic extensibility from pressure gradient measurements.

This study is concerned with the computation of aortic pulse wave velocity based on simultaneous recordings of the aortic pressure gradient and first-time derivative of aortic pressure. These variables were recorded by means of a double-lumen catheter introduced in the aorta of four anesthetized closed chest dogs, and connected to critically damped manometer systems. Results of aortic pulse wave velocity were then compared: (i) to the true phase velocity obtained from spectra of apparent phase velocity, and (ii) to the pulse wave velocity computed from the time shift between maximum slopes of the pressure wave. From the aortic valves to 37 cm down the aortic trunk, pulse wave velocity increased from 410-460 cm/s to approximately 600-800 cm/s. Based on the wave propagation equation presented of Bramwell and Hill (Bramwell, J.C., and Hill, A. V. 1922. Proc. R. Soc. 93, 298-306), volumetric extensibility coefficients were computed from pulse wave velocity data. Results indicated that, from the aortic valves to 37 cm down to the aorta, the mean volumetric extensibility decreased from 0.43-0.56% deltaV/cm H2O to 0.16-0.25% deltaV/cm H2O (1 cm H2O = 94.1 N/m2).