Příspěvek přináší komparaci životních osudů a osobnostního vývoje dvou archeologů německého původu, Bolko von Richthofena a Helmuta Preidela. Cílem tohoto srovnání má být zodpovězení otázky před- a poválečné kontinuity nacionálních mýtů, stereotypů a schémat v uvažování německých vědců, kteří působili v tzv. německých východních územích a kteří se po roce 1945 angažovali v tzv. vyhnaneckých organizacích. and The article presents a comparison of the fates and personality developments of two archaeologists of German origin: Bolko von Richthofen and Helmut Preidel. The aim of this comparison is to address the issues of the pre-war and post-war continuity of national myths, stereotypes and schemes in the reflections of German scientists who were active in the so-called eastern German territories and who became involved in expellee organisations after their forced resettlement in the Federal Republic of Germany.
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.
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
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
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.