Number of results to display per page
Search Results
5402. Bone fracture induces reflex muscle atrophy which is sex-dependent
- Creator:
- Urbancová, H., Hník, P., and Vejsada, R.
- Type:
- article, model:article, and TEXT
- Subject:
- bone fracture, muscle atrophy, and deafferentation
- Language:
- English
- Description:
- Longlasting nociceptive stimulation is known to cause atrophy of adjacent muscles. The aim of this study was to determine further the possible mechanisms of this pathological phenomenon. Unilateral fracture of the paw was performed under pentobarbital anaesthesia in several experimental groups (n = 8-11) of female and male rats. Dry muscle weights of the soleus (SOL), extensor digitorum longus (EDL), gastrocnemius (GA) and tibialis anterior (TA) were determined 7 days following the bone fracture and compared to the weight of contralateral control muscles. To demonstrate the reflex origin of this atrophy, deafferentation of the paw by dorsal root section (L4_5) was performed before or after unilateral fracture of hindlimb metatarsal bones. In female rats, the fracture resulted in a significant loss of muscle weight in all the four muscles examined. When the hindlimb was deafferented prior to the fracture, no muscle atrophy developed, and neither did deafferentation itself cause any appreciable change in muscle weight except in male rats. This supports the concept that this type of atrophy is reflex in origin. Deafferentation, when performed after the fracture, did not prevent the weight loss in extensor muscles (SOL, GA), while the flexors (EDL, TA) did not in general lose any weight. The results in male rats had a similar trend as in female rats, although the weight loss was significantly smaller. Our results showed that the mechanism of reflex muscle atrophy following metatarsal bone fracture involves a component which is dependent on afferent information from the injured paw. Differences in the degree of affection of different muscle types (extensors vs flexors, slow vs fast muscles) and of female and male rats suggest that the muscle atrophy is the result of a complex process that probably also involves hormonal mechanisms.
- Rights:
- http://creativecommons.org/licenses/by-nc-sa/4.0/ and policy:public
5403. Bone grafts in periodontal therapy
- Creator:
- Sukumar, Sujith
- Type:
- model:article and TEXT
- Language:
- English
- Rights:
- http://creativecommons.org/publicdomain/mark/1.0/ and policy:public
5404. Bone marrow necrosis: a rare complication of herbal treatment with Hypericum perforatum (St. John´s wort)
- Creator:
- Demiroglu, Yusuf Ziya
- Type:
- model:article and TEXT
- Language:
- English
- Rights:
- http://creativecommons.org/publicdomain/mark/1.0/ and policy:public
5405. Bone marrow-derived cells participate in composition of the satellite cell niche in intact and regenerating mouse skeletal muscle
- Creator:
- Čížková, D., Komárková, Z., Bezrouk, A., Macháčková, L., Vávrová, J., Filip, S., and Mokrý, J.
- Format:
- bez média and svazek
- Type:
- model:article and TEXT
- Subject:
- satellite cells, bone marrow cells, satellite cell niche, transplantation, and skeletal muscle regeneration
- Language:
- English
- Description:
- The cellular components of the satellite cell niche participate in the regulation of skeletal muscle regeneration. Beside myogenic cells at different developmental stages, this niche is formed by cells of the immune system, the interstitial connective tissue and the vascular ystem. Unambiguous determination of the origin of these cell types could contribute to optimization of the cell-based therapy of skeletal muscle disorders. In our work, we intravenously transplanted mouse GFP+ unseparated bone marrow cells into whole-body lethally irradiated immunocom-petent mice four weeks before cardiotoxin-induced injury of the recipients’ skeletal muscles. Seven and 28 days after the toxin injection, the injured regenerating and contralateral intact muscles were examined for identification of GFP+ bone marrow-derived cells by direct fluorescence, protein immunohistochemistry and immunogold transmission electron microscopy. In both the intact and injured muscles, GFP positivity was determined in immune cells, mainly in macrophages, and in interstitial spindle-shaped cells. Moreover, in the injured muscles, rare GFP+ endothelial cells of the blood vessels and newly formed myotubes and muscle fibres were present. Our results confirmed the ability of bone marrow-derived cells to contribute to the cellular component of the satellite cell niche in the intact and regenerating skeletal muscle. These cells originated not only from haematopoietic stem cells, but obviously also from other stem or progenitor cells residing in the bone marrow, such as multipotent mesenchymal stromal cells and endothelial progenitors. and Corresponding author: Dana Čížková
- Rights:
- http://creativecommons.org/publicdomain/mark/1.0/ and policy:public
5406. Bone metabolism: a note on the significance of mouse models
- Creator:
- Raška, O., Klára Bernášková, and Ivan Raška
- Type:
- article, články, model:article, and TEXT
- Subject:
- Fyziologie člověka a srovnávací fyziologie, kostní metabolismus, osteoklasty, osteoporóza, obezita, diabetes mellitus, bone metabolism, osteoclasts, osteoporosis, obesity, bone remodeling, osteoblast, osteocalcin, 14, and 612
- Language:
- English
- Description:
- This minireview briefly surveys the complexity of regulations governing the bone metabolism. The impact of clinical studies devoted to osteoporosis is briefly summarized and the emphasis is put on the significance of experimental mouse models based on an extensive use of genetically modified animals. Despite possible arising drawbacks, the studies in mice are of prime importance for expanding our knowledge on bone metabolism. With respect to human physiology and medicine, one should be always aware of possib le limitations as the experimental results may not be, or may be only to some extent, transposed to humans. If applicable to humans, results obtained in mice provide new clues for assessing un foreseen treatment strategies for patients. A recent publication representing in our opinion the important breakthrough in the field of bone metabolism in mice is commented in detail. It provides an evidence that skeleton is endocrine organ that affects energy metabolism and osteocalcin, a protein specifically synthesized and secreted by osteoblasts, is a hormone involved. If confirmed by other groups and applicable to humans, this study provides the awaited connection of long duration between bone disorders on one hand and obesity and diabetes on the other., O. Raška, K. Bernášková, I. Raška Jr., and Obsahuje seznam literatury
- Rights:
- http://creativecommons.org/licenses/by-nc-sa/4.0/ and policy:public
5407. Bone microstructure of mice after prolonged taurine treatment
- Creator:
- Martiniakova, M. , Sarocka, A., Babosova, R. , Galbavy, D. , Kapusta, E., Goc, Z., Formicki, G. , and Omelka, R.
- Format:
- bez média and svazek
- Type:
- model:article and TEXT
- Subject:
- taurine, bone, mouse, and microstructure
- Language:
- English
- Description:
- Taurine, a sulphur - containing amino acid, has been termed a functional nutrient. Its synthetic form is a common ingredient in supplements and energy drinks. There is no information concerning taurine impact on bone microstructure after prolonged supplemental use. Also, differences in bone parameters of mice following taurine exposure are unknown. In this study, a detailed microstructure of compact and trabecular bone tissues of mice subchronically exposed to taurine was determined. Animals (n=12) were segregated into three groups: E1 group – mice received 20 mg/kg b.w. of taurine per day during 8 weeks; E2 group – mice were fed by taurine at a dose of 40 mg/kg b.w. for 8 weeks and a control (C) group. Decreased density of secondary osteons, increased sizes of primary osteon's vascular canals (P<0.05) were observed in taurine – treated animals. Cortical bone thickness, trabecular thickness were decreased (P<0.05) in E1 group, and relative volume of trabecular bone was lower (P<0.05) in E2 group as compared to C group. According to our results, prolonged taurine exposure at the doses used in this study can negatively affect both compact and trabecular bone tissues microstructure.
- Rights:
- http://creativecommons.org/publicdomain/mark/1.0/ and policy:public
5408. Bone mineral density and body composition in men with multiple sclerosis chronically treated with low-dose glucocorticoids
- Creator:
- Vít Zikán, Michaela Týblová, Ivan Raška, Eva Havrdová, Luchavová, M., Dana Michalská, and Aleš Kuběna
- Type:
- article, články, model:article, and TEXT
- Subject:
- Fyziologie člověka a srovnávací fyziologie, fyziologie člověka, human physiology, bone mineral density, body composition, multiple sclerosis, osteoporosis, glucocorticoid treatment, 14, and 612
- Language:
- English
- Description:
- The aim of the study was to compare the bone mineral density (BMD) and body composition between ambulatory male MS patients and control subjects and to evaluate the relationships among body composition, motor disability, glucocorticoids (GC) use, and bone health. Body composition and BMD were measured by dual-energy X-ray absorptiometry in 104 ambulatory men with MS (mean age: 45.2 years) chronically treated with low-dose GC and in 54 healthy age-matched men. Compared to age-matched controls, MS patients had a significantly lower total body bone mineral content (TBBMC) and BMD at all measured sites except for the radius. Sixty five male MS patients (62.5 %) met the criteria for osteopenia and twenty six of them (25 %) for osteoporosis. The multivariate analysis showed a consistent dependence of bone measures (except whole body BMD) on BMI. The total leg lean mass % was as an independent predictor of TBBMC. The Expanded Disability Status Scale (EDSS), cumulative GC dose and age were independent determinants for BMD of the proximal femur. We conclude that decreasing mobility in male MS patients is associated with an increasing degree of osteoporosis and muscle wasting in the lower extremities. The chronic low-dose GC treatment further contributes to bone loss., V. Zikán ... [et al.]., and Obsahuje seznam literatury
- Rights:
- http://creativecommons.org/licenses/by-nc-sa/4.0/ and policy:public
5409. Bone mineral density in patients with apolipoprotein E type 2/2 and 4/4 genotype
- Creator:
- Tomáš Štulc, Richard Češka, Aleš Hořínek, and Jan Štěpán
- Format:
- print, bez média, and svazek
- Type:
- article, články, journal articles, model:article, and TEXT
- Subject:
- Fyziologie člověka a srovnávací fyziologie, osteoporóza, vitamin K, osteoporosis, bone mineral density, bone turnover, apolipoprotein E, 14, and 612
- Language:
- English
- Description:
- The peak bone mass and the rate of bone loss are in part genetically determined. It has been suggested that bone mineral density (BMD) may be related to allelic variation in the apolipoprotein E (ApoE) gene locus. ApoE is important in the receptor-mediated clearance of chylomicron particles from the plasma, Apo E4 having the highest and Apo E2 the lowest receptor affinity. Chylomicrons are the main carrier of vitamin K in the plasma; vitamin K plays an important role in the carboxylation of osteocalcin. We have tested the hypothesis that persons with E4 variant would have lower BMD and increased bone turnover than those with E2 variant. A total of 18 ApoE 2/2 and ApoE 4/4 homozygotes were selected from 873 patients who were examined for the ApoE genotype. BMD in lumbar vertebral, femoral neck and distal forearm was measured and plasma concentrations of osteocalcin and C-terminal fragments of collagen (CTx) were determined. BMD values (expressed as T-score) at the three specified sites were -0.12± 1.72, -0.52± 1.32 and -0.52± 0.81 in ApoE 2/2 group and -0.24± 1.22, 0.00± 0.84 and -0.17± 1.07 in the ApoE 4/4 group. Plasma osteocalcin and CTx were within normal limits in both groups. In conclusion, we did not observe any association of ApoE genotype with BMD and biochemical markers of bone metabolism in ApoE 2/2 and ApoE 4/4 homozygotes., T. Štulc, R. Češka, A. Hořínek, J. Štěpán., and Obsahuje bibliografii
- Rights:
- http://creativecommons.org/licenses/by-nc-sa/4.0/ and policy:public
5410. Bone remodeling, particle disease and individual susceptibility to periprosthetic osteolysis
- Creator:
- Jiří Gallo, Milan Raška, František Mrázek, and Martin Petřek
- Format:
- print, bez média, and svazek
- Type:
- article, články, model:article, and TEXT
- Subject:
- Experimentální medicína, patologická fyziologie, osteoklasty, ortopedie, pathological physiology, osteoclasts, orthopedics, periprotetická osteolýza, osteoblast, periprosthetic osteolysis, particle disease, basic multicellular unit, 14, and 616-092
- Language:
- English
- Description:
- Bone remodeling is a tightly coupled process consisting of repetitive cycles of bone resorption and formation. Both processes are governed by mechanical signals, which operate in conjunction with local and systemic factors in a discrete anatomic structure designated a basic multicellular unit (BMU). The microenvironment around total joint arthroplasty is a dynamic and complex milieu influenced by the chemical and physical stimuli associated with servicing the prosthesis. A key factor limiting the longevity of the prosthesis is polyethylene wear, which induces particle disease, and this may lead to increased and prolonged activity of BMUs resulting in periprosthetic osteolysis. Several pathways regulating BMU function have been reported in the past, including RANKL/RANK/OPG/TRAF6, TNF-α/TNFR/TRAF1, and IL-6/CD126/JAK/STAT. Moreover, the expression and functional activity of all these molecules can be affected by variations in their genes. These may explain the differences in severity of bone defects or prosthetic failure between patients with similar wear rates and the same prosthesis. Simultaneously, this data strongly support the theory of individual susceptibility to prosthetic failure., J. Gallo, M. Raška, F. Mrázek, M. Petřek., and Obsahuje bibliografii a bibliografické odkazy
- Rights:
- http://creativecommons.org/licenses/by-nc-sa/4.0/ and policy:public