Three-Dimensional Ankle Moments and Nonlinear Summation of Rat Triceps Surae Muscles

The Achilles tendon and epimuscular connective tissues mechanically link the triceps surae muscles. These pathways may cause joint moments exerted by each muscle individually not to sum linearly, both in magnitude and direction. The aims were (i) to assess effects of sagittal plane ankle angle (varied between 150° and 70°) on isometric ankle moments, in both magnitude and direction, exerted by active rat triceps surae muscles, (ii) to assess ankle moment summation between those muscles for a range of ankle angles and (iii) to assess effects of sagittal plane ankle angle and muscle activation on Achilles tendon length. At each ankle angle, soleus (SO) and gastrocnemius (GA) muscles were first excited separately to assess ankle-angle moment characteristics and subsequently both muscles were excited simultaneously to investigate moment summation. The magnitude of ankle moment exerted by SO and GA, the SO direction in the transverse and sagittal planes, and the GA direction in the transverse plane were significantly affected by ankle angle. SO moment direction in the frontal and sagittal planes were significantly different from that of GA. Nonlinear magnitude summation varied between 0.6±2.9% and −3.6±2.9%, while the nonlinear direction summation varied between 0.3±0.4° and −0.4±0.7° in the transverse plane, between 0.5±0.4° and 0.1±0.4° in the frontal plane, and between 3.0±7.9° and 0.3±2.3° in the sagittal plane. Changes in tendon length caused by SO contraction were significantly lower than those during contraction of GA and GA+SO simultaneously. Thus, moments exerted by GA and SO sum nonlinearly both in the magnitude and direction. The limited degree of nonlinear summation may be explained by different mechanisms acting in opposite directions.     

Preventing fatal diseases increases healthcare costs: cause elimination life table approach.

OBJECTIVES: To examine whether elimination of fatal diseases will increase healthcare costs. DESIGN: Mortality data from vital statistics combined with healthcare spending in a cause elimination life table. Costs were allocated to specific diseases through the various healthcare registers. SETTING AND SUBJECTS: The population of the Netherlands, 1988. MAIN OUTCOME MEASURES: Healthcare costs of a synthetic life table cohort, expressed as life time expected costs. RESULTS: The life time expected healthcare costs for 1988 in the Netherlands were 56,600 Pounds for men and 80,900 Pounds for women. Elimination of fatal diseases--such as coronary heart disease, cancer, or chronic obstructive lung disease--increases healthcare costs. Major savings will be achieved only by elimination of non-fatal disease--such as musculoskeletal diseases and mental disorders. CONCLUSION: The aim of prevention is to spare people from avoidable misery and death not to save money on the healthcare system. In countries with low mortality, elimination of fatal diseases by successful prevention increases healthcare spending because of the medical expenses during added life years.     

Über die Einwirkung karbonatfreier und kalkfreier Salzlösungen auf erwachsene Kalkschwämme und auf Entwicklungsstadien derselben

Ohne Zusammenfassung     

Brain (Na+, K+)-ATPase and Noradrenergic Activity: Effects of Hyperinnervation and Denervation on High-Affinity Ouabain Binding

Abstract: To examine the role of nerve-specific (Na⁺, K⁺)-ATPase in chronic changes in noradrenergic activity, we examined the effects of noradrenergic denervation and hyperinnervation on p -nitrophenylphosphatase activity and on total and nerve-specific ouabain binding. High-affinity and erythrosin B-sensitive binding were compared as measurements of nerve-specific binding. Hyperinnervation and denervation was produced in cerebellum and cerebral cortex, respectively, by 6-hydroxydopamine lesions of the dorsal noradrenergic bundle. Hyperinnervation increased, and denervation decreased, enzyme activity, high-affinity ouabain inhibition, and erythrosin B-sensitive ouabain binding. As (Nat⁺, K⁺)-ATPase has a major role in the regulation of neural excitability and energy metabolism, and the ouabain binding site has been shown to have endogenous ligands, these changes in (Na⁺, K⁺)-ATPase may be important in the long-term regulation of neuron function by norepinephrine.     

The geographic distribution of flavone-glycosylating genes in Silene pratensis (Rafn.) Godron and Gren. (Caryophyllaceae)

In Silene pratensis three loci (g, gl and fg) control the glycosylation of isovitexin. Three alleles are known for both the g-locus (g, g ^G and g ^X ) and the gl-locus (gl, gl ^A and gl ^R ); for the fg-locus there are only two alleles (fg and Fg). The distribution of these alleles over 285 European populations of S. pratensis has been investigated. It was concluded that there are three different chemical races within S. pratensis in Europe. The first race contains the populations in western and southern Europe and displays high frequencies of g ^G , gl and fg. The frequencies of g ^G and gl ^R are very high in the second chemical race, which can be found in the USSR, Scandinavia and eastern Poland. The third chemical race occurs in central Europe and in this race the frequencies of both g and gl ^R are high, Fg has low to moderate frequencies in the second and third groups. The alleles gl ^A and g ^X are seldom found in S. pratensis, but are present in the closely related S. dioica. They do occur with low frequencies in some populations of S. pratensis, possibly as a result of hybridization with S. dioica.     

Regulatory gene mutations affecting arginine biosynthesis in Escherichia coli

Summary Mutants of Escherichia coli with altered regulation of arginine biosynthesis were isolated. The alterations in all of the mutants with increased levels of the biosynthetic enzymes were found to map in the argR locus. The mutants were grouped into three classes based on their effect on the regulatory behavior. Complementation studies with stable merodiploid strains demonstrated that the derepressed synthesis in the mutants was recessive to wild-type regulation.     

Physical mapping of genes on the F plasmid of Escherichia coli responsible for inhibition of growth of female-specific bacteriophages.

By correlating the resistance or sensitivity to female-specific phages of strains carrying F plasmids with deletions for part of the region 32.6 to 42.9 F, cloned F fragments, and other plasmids, it was shown that the pif loci are located near and clockwise to a point on F with coordinate 38.3 F.     

Regression analysis of recent changes in cardiovascular morbidity and mortality in The Netherlands.

OBJECTIVES: To test whether recent declines in mortality from coronary heart disease were associated with increased mortality from other cardiovascular diseases. DESIGN: Poisson regression analysis of national data on causes of death and hospital discharges. SETTING AND SUBJECTS: Population of the Netherlands, 1969-93. MAIN OUTCOME MEASURES: Annual changes in mortality from coronary heart disease, stroke, and other cardiovascular diseases and annual changes in hospital discharge rates for acute coronary events, stroke, and congestive heart failures. RESULTS: Patterns of cardiovascular mortality changed abruptly in 1987-93. Annual decline in mortality from coronary heart disease increased sharply for women and men: from -1.9% (95% confidence interval -2.2% to -1.6%) and -1.7% (-1.9% to -1.4%) respectively in 1979-86 to -3.1% (-3.5% to -2.6%) and -4.2% (-4.6% to -3.9%) in 1987-93. The longstanding decline in mortality from stroke levelled off: from annual change of -3.3% (-3.7% to -2.8%) and -3.2% (-3.7% to -2.8%) in 1979-86 to -0.1% (-0.7% to 0.4%) and -1.1% (-1.7% to -0.5%) in 1987-93. Mortality from other cardiovascular diseases, however, started to increase: from -2.0% (-2.4% to -1.6%) and -0.2% (-0.5% to 0.2%) in 1979-86 to 1.5% (1.0% to 2.0%) and 1.9% (1.5% to 2.3%) in 1987-93. Hospital discharge rates for acute coronary heart disease, congestive heart failure, and stroke increased during 1980-6. During 1987-93 discharge rates for stroke and coronary heart disease stabilised but rates for congestive heart failure increased. CONCLUSION: Improved management of coronary heart disease seems to have reduced mortality, but some of the gains are lost to deaths from stroke and other cardiovascular diseases. The increasing numbers of patients with coronary heart disease who survive will increase demands on health services for long term care.     

Establishment of reference values for the lysine acetylation marker Nɛ-acetyllysine in small volume human plasma samples by a multi-target LC–MS/MS method

Amino Acids - Cardiovascular disease (CVD) and chronic kidney disease (CKD) constitute substantial burdens for public health. The identification and validation of risk markers for CVD and CKD in...     

An integrated gene regulatory network controls stem cell proliferation in teeth

Epithelial stem cells reside in specific niches that regulate their self-renewal and differentiation, and are responsible for the continuous regeneration of tissues such as hair, skin, and gut. Although the regenerative potential of mammalian teeth is limited, mouse incisors grow continuously throughout life and contain stem cells at their proximal ends in the cervical loops. In the labial cervical loop, the epithelial stem cells proliferate and migrate along the labial surface, differentiating into enamel-forming ameloblasts. In contrast, the lingual cervical loop contains fewer proliferating stem cells, and the lingual incisor surface lacks ameloblasts and enamel. Here we have used a combination of mouse mutant analyses, organ culture experiments, and expression studies to identify the key signaling molecules that regulate stem cell proliferation in the rodent incisor stem cell niche, and to elucidate their role in the generation of the intrinsic asymmetry of the incisors. We show that epithelial stem cell proliferation in the cervical loops is controlled by an integrated gene regulatory network consisting of Activin, bone morphogenetic protein (BMP), fibroblast growth factor (FGF), and Follistatin within the incisor stem cell niche. Mesenchymal FGF3 stimulates epithelial stem cell proliferation, and BMP4 represses Fgf3 expression. In turn, Activin, which is strongly expressed in labial mesenchyme, inhibits the repressive effect of BMP4 and restricts Fgf3 expression to labial dental mesenchyme, resulting in increased stem cell proliferation and a large, labial stem cell niche. Follistatin limits the number of lingual stem cells, further contributing to the characteristic asymmetry of mouse incisors, and on the basis of our findings, we suggest a model in which Follistatin antagonizes the activity of Activin. These results show how the spatially restricted and balanced effects of specific components of a signaling network can regulate stem cell proliferation in the niche and account for asymmetric organogenesis. Subtle variations in this or related regulatory networks may explain the different regenerative capacities of various organs and animal species.