Coordination in vertical jumping

The present study was designed to investigate for vertical jumping the relationships between muscle actions, movement pattern and jumping achievement. Ten skilled jumpers performed jumps with preparatory countermovement. Ground reaction forces and cinematographic data were recorded. In addition, myoelectric activity (EMG) was recorded from seven leg muscles. EMG-signals were rectified and low-pass filtered to obtain EMG-levels. The latter, which were assumed to reflect activation levels, rose to a plateau in the sequence m. semitendinosus, long head of m. biceps femoris, m. gluteus maximus, m. vastus medialis, m. rectus femoris, m. soleus, m. gastrocnemius. It was attempted to link the EMG-pattern to the purpose of the push-off, namely to maximize the effective energy (Ey) of the mass center of the body (MCB). The term Ey designates the sum of the potential energy of MCB and the kinetic energy due to the vertical velocity of MCB. One of the requirements for maximization of Ey is that the mono-articular extensor muscles release as much energy as possible before toe-off occurs. It is argued that this requirement can only be satisfied if the vertical velocity differences between the proximal and distal ends of body segments reach their peaks in a sequence. The sequence that is realized by the pattern of muscular activation is upper body, upper legs, lower legs, feet. Another important requirement is that the mechanical energy released by the muscles is optimally used. This requirement can be satisfied by transportation of energy via the biarticular m. rectus femoris and m. gastrocnemius.     

The lepidopteran mitochondrial control region: structure and evolution

For several species of lepidoptera, most of the approximately 350-bp mitochondrial control-region sequences were determined. Six of these species are in one genus, Jalmenus; are closely related; and are believed to have undergone recent rapid speciation. Recent speciation was supported by the observation of low interspecific sequence divergence. Thus, no useful phylogeny could be constructed for the genus. Despite a surprising conservation of control-region length, there was little conservation of primary sequences either among the three lepidopteran genera or between lepidoptera and Drosophila. Analysis of secondary structure indicated only one possible feature in common--inferred stem loops with higher-than-random folding energies-- although the positions of the structures in different species were unrelated to regions of primary sequence similarity. We suggest that the conserved, short length of control regions is related to the observed lack of heteroplasmy in lepidopteran mitochondrial genomes. In addition, determination of flanking sequences for one Jalmenus species indicated (i) only weak support for the available model of insect 12S rRNA structure and (ii) that tRNA translocation is a frequent event in the evolution of insect mitochondrial genomes.      

Glutamine repeats and inherited neurodegenerative diseases: molecular aspects

Several dominantly inherited, late onset, neurodegenerative diseases are due to expansion of CAG repeats, leading to expansion of glutamine repeats in the affected proteins. These proteins are of very different sizes and, with one exception, show no sequence homology to known proteins or to each other; their functions are unknown. In some, the glutamine repeat starts near the N-terminus, in another near the middle and in another near the C-terminus, but regardless of these differences, no disease has been observed in individuals with fewer than 37 repeats, and absence of disease has never been found in those with more than 41 repeats. Protein constructs with more than 41 repeats are toxic to E. coli and to CHO cells in culture, and they elicit ataxia in transgenic mice. These observations argue in favour of a distinct change of structure associated with elongation beyond 37–41 glutamine repeats. The review describes experiments designed to find out what these structures might be and how they could influence the properties of the proteins of which they form part. Poly- -glutamines form pleated sheets of β-strands held together by hydrogen bonds between their amides. Incorporation of glutamine repeats into a small protein of known structure made it associate irreversibly into oligomers. That association took place during the folding of the protein molecules and led to their becoming firmly interlocked by either strand- or domain-swapping. Thermodynamic considerations suggest that elongation of glutamine repeats beyond a certain length may lead to a phase change from random coils to hydrogen-bonded hairpins. Possible mechanisms of expansion of CAG repeats are discussed in the light of looped DNA model structures.     

Development of cell surface saccharides on embryonic pancreatic cells

Using a battery of seven lectin-ferritin conjugates as probes for cell surface glycoconjugates, we have studied the pattern of plasmalemmal differentiation of cells in the embryonic rat pancreas from day 15 in utero to the early postpartum stage. Our results indicate that differentiation of plasmalemmal glycoconjugates on acinar, endocrine, and centroacinar cells is temporally correlated with development and is unique for each cell type, as indicated by lectin-ferritin binding. Specifically, (a) expression of adult cell surface saccharide phenotype can be detected on presumptive acinar cells as early as 15 d in utero, as indicated by soybean agglutinin binding, and precedes development of intracellular organelles characteristic of mature acinar cells; (b) maturation of the plasmalemma of acinar cells is reached after intracellular cytodifferentiation is completed, as indicated by appearance of Con A and fucoselectin binding sites only at day 19 of development; conversely, maturation of the endocrine cell plasmalemma is accompanied by "loss" (masking) of ricinus communis II agglutinin receptors; and (c) binding sites for fucose lectins and for soybean agglutinin are absent on endocrine and centroacinar cells at all stages examined. We conclude that acinar, centroacinar, and endocrine cells develop from a common progenitor cell(s) whose plasmalemmal carbohydrate composition resembles most closely that of the adult centroacinar cell. Finally, appearance of acinar lumina beginning at approximately 17 d in utero is accompanied by differenetiation of apical and basolateral plasmalemmal domains of epithelial cells, as indicated by enhanced binding of several lectin-ferritin conjugates to the apical plasmalemmal, a pattern that persists from this stage through adult life.     

Effects of Isometric Scaling on Vertical Jumping Performance

Jump height, defined as vertical displacement in the airborne phase, depends on vertical takeoff velocity. For centuries, researchers have speculated on how jump height is affected by body size and many have adhered to what has come to be known as Borelli’s law, which states that jump height does not depend on body size per se. The underlying assumption is that the amount of work produced per kg body mass during the push-off is independent of size. However, if a big body is isometrically downscaled to a small body, the latter requires higher joint angular velocities to achieve a given takeoff velocity and work production will be more impaired by the force-velocity relationship of muscle. In the present study, the effects of pure isometric scaling on vertical jumping performance were investigated using a biologically realistic model of the human musculoskeletal system. The input of the model, muscle stimulation over time, was optimized using jump height as criterion. It was found that when the human model was miniaturized to the size of a mouse lemur, with a mass of about one-thousandth that of a human, jump height dropped from 40 cm to only 6 cm, mainly because of the force-velocity relationship. In reality, mouse lemurs achieve jump heights of about 33 cm. By implication, the unfavourable effects of the small body size of mouse lemurs on jumping performance must be counteracted by favourable effects of morphological and physiological adaptations. The same holds true for other small jumping animals. The simulations for the first time expose and explain the sheer magnitude of the isolated effects of isometric downscaling on jumping performance, to be counteracted by morphological and physiological adaptations.     

B30.2-like domain proteins: update and new insights into a rapidly expanding family of proteins

The B30.2 domain is a conserved region of around 170 amino acids associated with several different protein domains, including the immunoglobulin folds of butyrophilin and the RING finger domain of ret finger protein. We recently reported several novel members of this family as well as previously undescribed protein families possessing the B30.2 domain. Many proteins have subsequently been found to possess this domain, including pyrin/marenostrin and the midline 1 (MID1) protein. Mutations in the B30.2 domain of pyrin/marenostrin are implicated in familial Mediterranean fever, and partial loss of the B30.2 domain of MID1 is responsible for Opitz G/BBB syndrome, characterized by developmental midline defects. In this study, we scrutinized the available sequence data bases for the identification of novel B30.2 domain proteins using highly sensitive database-searching tools. In addition, we discuss the chromosomal localization of genes in the B30.2 family, since the encoded proteins are likely to be involved in other forms of periodic fever, autoimmune, and genetic diseases.      

Out of Africa and back again: nested cladistic analysis of human Y chromosome variation

We surveyed nine diallelic polymorphic sites on the Y chromosomes of 1,544 individuals from Africa, Asia, Europe, Oceania, and the New World. Phylogenetic analyses of these nine sites resulted in a tree for 10 distinct Y haplotypes with a coalescence time of approximately 150,000 years. The 10 haplotypes were unevenly distributed among human populations: 5 were restricted to a particular continent, 2 were shared between Africa and Europe, 1 was present only in the Old World, and 2 were found in all geographic regions surveyed. The ancestral haplotype was limited to African populations. Random permutation procedures revealed statistically significant patterns of geographical structuring of this paternal genetic variation. The results of a nested cladistic analysis indicated that these geographical associations arose through a combination of processes, including restricted, recurrent gene flow (isolation by distance) and range expansions. We inferred that one of the oldest events in the nested cladistic analysis was a range expansion out of Africa which resulted in the complete replacement of Y chromosomes throughout the Old World, a finding consistent with many versions of the Out of Africa Replacement Model. A second and more recent range expansion brought Asian Y chromosomes back to Africa without replacing the indigenous African male gene pool. Thus, the previously observed high levels of Y chromosomal genetic diversity in Africa may be due in part to bidirectional population movements. Finally, a comparison of our results with those from nested cladistic analyses of human mtDNA and beta-globin data revealed different patterns of inferences for males and females concerning the relative roles of population history (range expansions) and population structure (recurrent gene flow), thereby adding a new sex-specific component to models of human evolution.      

A model of open-loop control of equilibrium position and stiffness of the human elbow joint

According to the equilibrium point theory, the control of posture and movement involves the setting of equilibrium joint positions (EP) and the independent modulation of stiffness. One model of EP control, the α-model, posits that stable EPs and stiffness are set open-loop, i.e. without the aid of feedback. The purpose of the present study was to explore for the elbow joint the range over which stable EPs can be set open-loop and to investigate the effect of co-contraction on intrinsic low-frequency elbow joint stiffness (K _ilf). For this purpose, a model of the upper and lower arm was constructed, equipped with Hill-type muscles. At a constant neural input, the isometric force of the contractile element of the muscles depended on both the myofilamentary overlap and the effect of sarcomere length on the sensitivity of myofilaments to [Ca²⁺] (LDCS). The musculoskeletal model, for which the parameters were chosen carefully on the basis of physiological literature, captured the salient isometric properties of the muscles spanning the elbow joint. It was found that stable open-loop EPs could be achieved over the whole range of motion of the elbow joint and that K _ilf, which ranged from 18 to 42 N m·rad⁻¹, could be independently controlled. In the model, LDCS contributed substantially to K _ilf (up to 25 N m·rad⁻¹) and caused K _ilf to peak at a sub-maximal level of co-contraction.