scholarly journals The influence of in-vivo mechanical behaviour of the Achilles tendon on the mechanics, energetics and apparent efficiency of bouncing gaits

2021 ◽  
Author(s):  
Andrea Monte ◽  
Francesca Nardello ◽  
Riccardo Magris ◽  
Paolo Tecchio ◽  
Paola Zamparo
Keyword(s):  
Achilles Tendon ◽  
Mechanical Power ◽  
Whole Body ◽  
Plantar Flexors ◽  
Inverse Dynamic ◽  
Body Level ◽  
Positive Correlations ◽  
Bouncing Gaits

In this study, we used kinematic, kinetic, metabolic and ultrasound analysis to investigate the role of elastic energy utilisation on the mechanical and physiological demands of a movement task that primarily involves the plantar-flexors muscles (hopping) to determine the contribution of tendon work to total mechanical work and its relationship with apparent efficiency (AE) in bouncing gaits. Metabolic power (PMET) and (positive) mechanical power at the whole-body level (PMEC) were measured during hopping at different frequencies (2, 2.5, 3 and 3.5 Hz). The (positive) mechanical power produced during the Achilles tendon recoil phase (PTEN) was obtained by integrating ultrasound data with an inverse dynamic approach. As a function of hopping frequency, PMEC decreased steadily and PMET exhibited a U-shape behaviour, with a minimum at about 3 Hz. AE (PMEC/PMET) showed an opposite trend and was maximal (about 0.50) at the same frequency when also PTEN was the highest. Positive correlations were observed: i) between PTEN and AE (AE=0.22+0.15.PTEN, R2=0.67, P<0.001) and the intercept of this relationship indicates the value of AE that should be expected when tendon work is nil; ii) between AE and tendon gearing (Gt=DMTU length/Dmuscle belly length) (R2=0.50, P<0.001), a high Gt indicates that the muscle is contracting more isometrically thus allowing the movement to be more economical (and efficient); iii) between Gt and PTEN (R2=0.73, P<0.001) and this indicates that Gt could play an important role in the tendon's capability to store and release mechanical power.

scholarly journals l-Cysteine-mediated modulation of copper trafficking in prostate cancer cells: an in vitro and in vivo investigation with 64Cu and 64Cu-PET

Metallomics ◽  
2020 ◽  
Vol 12 (10) ◽  
pp. 1508-1520
Author(s):  
Joanna J. Bartnicka ◽  
Fahad Al-salemee ◽  
George Firth ◽  
Philip J. Blower
Keyword(s):  
Prostate Cancer ◽  
Amino Acids ◽  
Cancer Cells ◽  
Whole Body ◽  
Prostate Cancer Cells ◽  
Copper Trafficking ◽  
Body Level

This article reports a novel role of thiol amino acids in modulating intracellular retention of copper in cancer cells and employs PET imaging with 64Cu to investigate this effect on the whole body level.

scholarly journals Role of antennary structure of N-linked sugar chains in renal handling of recombinant human erythropoietin

Blood ◽  
1995 ◽  
Vol 86 (11) ◽  
pp. 4097-4104 ◽  
Author(s):  
T Misaizu ◽  
S Matsuki ◽  
TW Strickland ◽  
M Takeuchi ◽  
A Kobata ◽  
...  
Keyword(s):  
Whole Body ◽  
Renal Handling ◽  
Sugar Chain ◽  
Erythroid Progenitor ◽  
Human Erythropoietin ◽  
Sugar Chains ◽  
Effective Transfer ◽  
Branched Structure

To elucidate the role of the branched structure of sugar chains of human erythropoietin (EPO) in the expression of in vivo activity, the pharmacokinetic profile of a less active recombinant human EPO sample (EPO-bi) enriched with biantennary sugar chains was compared with that of a highly active control EPO sample enriched with tetraantennary sugar chains. After an intravenous injection in rats, 125I-EPO-bi disappeared from the plasma with 3.2 times greater total body clearance (Cltot) than control 125I-EPO. Whole-body autoradiography after 20 minutes of administration indicated that the overall distribution of radioactivity is similar, but 125I-EPO-bi showed a higher level of radioactivity in the kidneys than control 125I-EPO. Quantitative determination of radioactivity in the tissues also indicated that radioactivity of 125I-EPO-bi in the kidneys was two times higher than that of control 125I-EPO. The difference in plasma disappearance between 125I-EPO-bi and control 125I-EPO was not observed in bilaterally nephrectomized rats. The distribution of 125I-EPO-bi to bone marrow and spleen was similarly inhibited by simultaneous injection of excess amounts of either the nonlabeled EPO-bi or control EPO. These results indicate that the low in vivo biologic activity of EPO-bi results from rapid clearance from the systemic circulation by renal handling. Thus, the well-branched structure of the N-linked sugar chain of EPO is suggested to play an important role in maintaining its higher plasma level, which guarantees an effective transfer to target organs and stimulation of erythroid progenitor cells.

Autoimmune disorder phenotypes in Hvcn1-deficient mice

2013 ◽  
Vol 450 (2) ◽  
pp. 295-301 ◽  
Author(s):  
Mari Sasaki ◽  
Akihiro Tojo ◽  
Yoshifumi Okochi ◽  
Nana Miyawaki ◽  
Daisuke Kamimura ◽  
...  
Keyword(s):  
T Cells ◽  
Autoimmune Disorder ◽  
Whole Body ◽  
Activated T Cells ◽  
Proton Channels ◽  
Voltage Gated ◽  
In The Wild ◽  
Body Level ◽  
Deficient Mice

Hv channels (voltage-gated proton channels) are expressed in blood cells, microglia and some types of epithelial cells. In neutrophils Hv channels regulate the production of reactive oxygen species through regulation of membrane potential and intracellular pH. Hv channels have also been suggested to play a role in sperm physiology in the human. However, the functions of the Hv channel at the whole-body level are not fully understood. In the present paper we show that Hvcn1 (voltage-gated hydrogen channel 1)-knockout mice show splenomegaly, autoantibodies and nephritis, that are reminiscent of human autoimmune diseases phenotypes. The number of activated T-cells was larger in Hvcn1-deficient mice than in the wild-type mice. Upon viral infection this was remarkably enhanced in Hvcn1-deficient mice. The production of superoxide anion in T-cells upon stimulation with PMA was significantly attenuated in the Hvcn1-deficient mice. These results suggest that Hv channels regulate T-cell homoeostasis in vivo.

Studies of the antibody-dependent killing of schistosomula of Schistosoma mansoni employing haptenic target antigens. Analysis of mechanisms responsible for the rejection of parasites in vivo

Parasitology ◽  
1981 ◽  
Vol 83 (3) ◽  
pp. 543-558
Author(s):  
Gina Moser ◽  
F. von Lichtenberg ◽  
A. Sher
Keyword(s):  
Schistosoma Mansoni ◽  
Passive Immunization ◽  
Early Response ◽  
Challenge Infection ◽  
Delayed Hypersensitivity ◽  
Whole Body ◽  
Hypersensitivity Response ◽  
Time Points

SUMMARYSchistosomula, surface labelled with trinitrophenyl (TNP) target antigens were tested for their susceptibility to killing by humoral- or cell-mediated anti-TNP effector mechanisms in vivo. It was found that mice passively immunized with anti-TNP serum effectively rejected an intravenous (i.v.) challenge infection with TNP-labelled schistosomula. In contrast, mice which demonstrated a strong TNP-specific, delayed hypersensitivity response to the haptenated larvae as evidenced by ear swelling, were unable to eliminate the same challenge infection. Significant passive immunization against TNP-labelled schistosomula was shown to require microlitre quantities of anti-TNP serum and could be conferred with an IgG fraction purified from the serum. The role of cells in the antibody-dependent rejection of TNP-labelled schistosomula was investigated using histopathological methods. In passively immunized mice, haptenated larvae elicited neutrophil-enriched focal reactions in the lungs and showed evidence of degeneration as early as 2 h after injection. These cellular reactions were not observed in recipients which had received prior whole-body irradiation. Nevertheless, by 24 h TNP-labelled larvae were found to have been killed in the lungs of the irradiated mice despite the absence of significant cellular attack. The above observations suggest that the antibody-dependent destruction of haptenated schistosomula results from two overlapping responses, an early response mediated by radio-sensitive cells and a second, radio-resistant response manifesting its effects at later time points. Since mice genetically deficient in the fifth component of complement fail to develop the later response, it probably reflects the effect of the lytic pathway of complement on the parasite.

In vivo physiological cross-sectional area and specific force are reduced in the gastrocnemius of elderly men

2005 ◽  
Vol 99 (3) ◽  
pp. 1050-1055 ◽  
Author(s):  
Christopher I. Morse ◽  
Jeanette M. Thom ◽  
Neil D. Reeves ◽  
Karen M. Birch ◽  
Marco V. Narici
Keyword(s):  
Achilles Tendon ◽  
Voluntary Contraction ◽  
Pennation Angle ◽  
Specific Force ◽  
Plantar Flexor ◽  
Moment Arm ◽  
Plantar Flexors ◽  
Elderly Men ◽  
Cross Sectional

Sarcopenia and muscle weakness are well-known consequences of aging. The aim of the present study was to ascertain whether a decrease in fascicle force (Ff) could be accounted for entirely by muscle atrophy. In vivo physiological cross-sectional area (PCSA) and specific force (Ff/PCSA) of the lateral head of the gastrocnemius (GL) muscle were assessed in a group of elderly men [EM, aged 73.8 yr (SD 3.5), height 173.4 cm (SD 4.4), weight 78.4 kg (SD 8.3); means (SD)] and for comparison in a group of young men [YM, aged 25.3 yr (SD 4.4), height 176.4 cm (SD 7.7), weight 79.1 kg (SD 11.9)]. GL muscle volume (Vol) and Achilles tendon moment arm length were evaluated using magnetic resonance imaging. Pennation angle and fiber fascicle length (Lf) were measured using B-mode ultrasonography during isometric maximum voluntary contraction of the plantar flexors. PCSA was estimated as Vol/Lf. GL Ff was calculated by dividing Achilles tendon force by the cosine of θ, during the interpolation of a supramaximal doublet, and accounting for antagonist activation level (assessed using EMG), Achilles tendon moment arm length, and the relative PCSA of the GL within the plantar flexor group. Voluntary activation of the plantar flexors was lower in the EM than in the YM (86 vs. 98%, respectively, P < 0.05). Compared with the YM, plantar flexor maximal voluntary contraction torque and Ff of the EM were lower by 47 and 40%, respectively ( P < 0.01). Both Vol and PCSA were smaller in the EM by 28% ( P < 0.01) and 16% ( P < 0.05), respectively. Also, pennation angle was 12% smaller in the EM, whereas there was no significant difference in Lf between the YM and EM. After accounting for differences in agonists and antagonists activation, the Ff/PCSA of the EM was 30% lower than that of the YM ( P < 0.01). These findings demonstrate that the loss of muscle strength with aging may be explained not only by a reduction in voluntary drive to the muscle, but mostly by a decrease in intrinsic muscle force. This phenomenon may possibly be due to a reduction in single-fiber specific tension.

scholarly journals Ablation of 3-Phosphoinositide-Dependent Protein Kinase 1 (PDK1) in Vascular Endothelial Cells Enhances Insulin Sensitivity by Reducing Visceral Fat and Suppressing Angiogenesis

2012 ◽  
Vol 26 (1) ◽  
pp. 95-109 ◽  
Author(s):  
Kazuhito Tawaramoto ◽  
Ko Kotani ◽  
Mitsuru Hashiramoto ◽  
Yukiko Kanda ◽  
Tomoki Nagare ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Insulin Sensitivity ◽  
Protein Kinase ◽  
Vascular Endothelial Cells ◽  
Whole Body ◽  
Vascular Endothelial ◽  
Dependent Protein Kinase ◽  
Dependent Protein

Abstract The phosphatidylinositol 3-kinase signaling pathway in vascular endothelial cells is important for systemic angiogenesis and glucose metabolism. In this study, we addressed the precise role of the 3-phosphoinositide-dependent protein kinase 1 (PDK1)-regulated signaling network in endothelial cells in vivo, using vascular endothelial PDK1 knockout (VEPDK1KO) mice. Surprisingly, VEPDK1KO mice manifested enhanced glucose tolerance and whole-body insulin sensitivity due to suppression of their hepatic glucose production with no change in either peripheral glucose disposal or even impaired vascular endothelial function at 6 months of age. When mice were fed a standard diet at 6 months of age and a high-fat diet at 3 months of age, hypertrophy of epididymal adipose tissues was inhibited, adiponectin mRNA was significantly increased, and mRNA of MCP1, leptin, and TNFα was decreased in the white adipose tissue of VEPDK1KO mice in comparison with controls. Consequently, both the circulating adiponectin levels and the activity of hepatic AMP-activated protein kinase were significantly increased, subsequently enhancing whole-body insulin sensitivity and energy expenditure with increased hepatic fatty acid oxidation in VEPDK1KO mice. These results provide the first in vivo evidence that lowered angiogenesis through the deletion of PDK1 signaling not only interferes with the growth of adipose tissue but also induces increased energy expenditure due to amelioration of the adipocytokine profile. This demonstrates an unexpected role of PDK1 signaling in endothelial cells on the maintenance of proper glucose homeostasis through the regulation of adipocyte development.

scholarly journals Mesenchymal Igf2 is a major paracrine regulator of pancreatic growth and function

2019 ◽  
Author(s):  
Constanze M. Hammerle ◽  
Ionel Sandovici ◽  
Gemma V. Brierley ◽  
Nicola M. Smith ◽  
Warren E. Zimmer ◽  
...  
Keyword(s):  
Ex Vivo ◽  
Whole Body ◽  
Imprinted Genes ◽  
Paracrine Signalling ◽  
Genetic Mechanisms ◽  
Pancreatic Epithelium ◽  
And Function ◽  
Maternal Glucose

AbstractThe genetic mechanisms that determine the size of the adult pancreas are poorly understood. Here we demonstrate that many imprinted genes are highly expressed in the pancreatic mesenchyme, and explore the role of Igf2 in-vivo. Mesenchyme-specific Igf2 deletion results in acinar and beta-cell hypoplasia, postnatal whole-body growth restriction and maternal glucose intolerance during pregnancy. Surprisingly, mesenchymal mass is unaffected, suggesting that the mesenchyme is a developmental reservoir of IGF2 used for paracrine signalling. The unique actions of mesenchymal IGF2 are demonstrated by the absence of phenotypes upon Igf2 deletion in the developing pancreatic epithelium. Furthermore, increased IGF2 activity specifically in the mesenchyme, through Igf2 loss-of-imprinting or Igf2r deletion, leads to pancreatic acinar overgrowth. Ex-vivo exposure of primary acinar cells to exogenous IGF2 increases cell proliferation and amylase production through AKT signalling. We propose that mesenchymal Igf2, and perhaps other imprinted genes, are key developmental regulators of adult pancreas size and function.

BODY ORGAN CYTOCHROME OXIDASE ACTIVITY IN COLD- AND WARM-ACCLIMATED RATS

1963 ◽  
Vol 41 (9) ◽  
pp. 1847-1854 ◽  
Author(s):  
Ladislav Janský
Keyword(s):  
Steady State ◽  
Cytochrome Oxidase ◽  
Oxidase Activity ◽  
Whole Body ◽  
Cytochrome Oxidase Activity ◽  
Full Capacity ◽  
Body Organ ◽  
Total Body

The cytochrome oxidase activity was estimated in homogenates of the whole body and in nine body organs of cold- and warm-acclimated rats. The total body cytochrome oxidase activity expressed in terms of oxygen consumption was similar in cold- and warm-acclimated rats. In cold-acclimated animals the total cytochrome oxidase activity did not differ from maximal steady state metabolism measured in vivo, while in warm-acclimated rats the total cytochrome oxidase activity was almost twice as great as the maximal steady state metabolism. The results indicate that warm-acclimated rats do not utilize the full capacity of the cytochrome system and that cold-acclimation makes full exploitation of the oxidase capacity possible. In cold-acclimated rats the cytochrome oxidase activity of the muscles comprised 57% of the total, the liver 22.5%, and the skin 6%, with smaller roles for other organs. The role of the liver was greater in cold-acclimated than in warm-acclimated rats.

Cytoarchitecture of the Xenopus thymus following gamma-irradiation

Development ◽  
1987 ◽  
Vol 100 (1) ◽  
pp. 95-105
Author(s):  
JH Russ ◽  
JD Horton
Keyword(s):  
Gamma Irradiation ◽  
Tolerance Induction ◽  
Cell Types ◽  
Whole Body ◽  
Thymic Stromal Cells ◽  
Normal Architecture

This paper describes in vitro and in vivo attempts to deplete the 4- to 8-month-old Xenopus laevis (J strain) thymus of its lymphocyte compartment. Gamma irradiation (2-3000 rad) of the excised thymus, followed by two weeks in organ culture, is effective in removing lymphocytes, but causes drastic reduction in size and loss of normal architecture. In contrast, in vivo whole-body irradiation (3000 rad) and subsequent in situ residence for 8-14 days proves successful in providing a lymphocyte-depleted froglet thymus without loss of cortical and medullary zones. In vivo-irradiated thymuses are about half normal size, lack cortical lymphocytes, but still retain some medullary thymocytes; they show no signs of lymphocyte regeneration when subsequently organ cultured for 2 weeks. Light microscopy of 1 micron, plastic-embedded sections and electron microscopy reveal that a range of thymic stromal cell types are retained and that increased numbers of cysts, mucous and myoid cells are found in the thymus following whole-body irradiation. In vivo-irradiated thymuses are therefore suitable for implantation studies exploring the role of thymic stromal cells in tolerance induction of differentiating T lymphocytes.

Measuring whole-body actin/myosin protein breakdown in mice using a primed constant stable isotope-infusion protocol

2003 ◽  
Vol 104 (6) ◽  
pp. 585-590 ◽  
Author(s):  
Yvonne L. J. VISSERS ◽  
Maarten F. VON MEYENFELDT ◽  
Valeria B. BRAULIO ◽  
Yvette C. LUIKING ◽  
Nicolaas E. P. DEUTZ
Keyword(s):  
Stable Isotope ◽  
Total Protein ◽  
Myofibrillar Protein ◽  
Whole Body ◽  
Constant Infusion ◽  
Protein Breakdown ◽  
Net Protein ◽  
Infusion Protocol

To measure actin/myosin protein breakdown, the 24 h excretion of Nτ-methylhistidine (3MH) is used. However, in mice, this method is invalid. Therefore we have developed a liquid chromatography-MS technique to measure the tracer/tracee ratio and concentration of 3MH in plasma, enabling an in vivo primed constant infusion protocol with a deuterated stable isotope of 3MH. We tested this model by giving a primed constant infusion of L-[3-methyl-2H3]histidine, L-[phenyl-2H5]phenylalanine and L-[phenyl-2H2]tyrosine to three anaesthetized experimental groups: mice receiving saline intraperitoneally (i.p.) (CON), mice receiving saline i.p. and starved for 9 h (STA), and mice receiving lipopolysaccharide i.p. and starved for 9 h (STA + LPS). The contribution of myofibrillar to total protein breakdown was significantly lower in the STA group than the CON group (30±4% and 54±14% respectively; P<0.05), and was significantly higher in the STA + LPS group than the STA group (52±7% and 30±4% respectively; P<0.05). Whole-body myofibrillar protein breakdown, total protein breakdown, protein synthesis and net protein breakdown were not different between the groups. We conclude that this in vivo primed constant stable isotope-infusion protocol can give valuable information about the role of actin/myosin protein breakdown in mice.

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