Due to the growing number of applications of cadmium oxide nanoparticles (CdO NPs), there is a concern about their potential deleterious effects. The objective of our study was to investigate the effect of CdO NPs on the immune response, renal and intestine oxidative stress, blood antioxidant defence, renal fibrotic response, bone density and mineral content. Six-week-old female ICR mice were exposed to CdO NPs for 6 weeks by inhalation (particle size: 9.82 nm, mass concentration: 31.7 μg CdO/m3, total deposited dose: 0.195 μg CdO/g body weight). CdO NPs increased percentage of thymus CD3e+CD8a+ cells and moderately enhanced splenocyte proliferation and production of cytokines and chemokines. CdO NPs elevated pro-fibrotic factors (TGF-β2, α-SMA and collagen I) in the kidney, and concentrations of AGEs in the intestine. The ratio of GSH and GSSG in blood was slightly reduced. Exposure to CdO NPs resulted in 10-fold higher Cd concentration in tibia bones. No differences were found in bone mass density, mineral content, bone area values, bone concentrations of Ca, P, Mg and Ca/P ratio. Our findings indicate stimulation of immune/inflammatory response, oxidative stress in the intestine, starting fibrotic response in kidneys and accumulation of CdO NPs in bones of mice.

• Klíčová slova
• Cadmium oxide nanoparticles, Inhalation, Mice, Nanotoxicology,
• MeSH
• aplikace inhalační MeSH
• buněčná imunita účinky léků   MeSH
• cytokiny metabolismus   MeSH
• fibróza chemicky indukované   MeSH
• kovové nanočástice aplikace a dávkování   toxicita   MeSH
• ledviny účinky léků   patologie   MeSH
• lymfatické uzliny účinky léků   MeSH
• myši inbrední ICR MeSH
• oxidační stres účinky léků   MeSH
• oxidy aplikace a dávkování   toxicita   MeSH
• slezina účinky léků   MeSH
• sloučeniny kadmia aplikace a dávkování   toxicita   MeSH
• střeva účinky léků   MeSH
• thymus účinky léků   MeSH
• tibie účinky léků   MeSH
• zvířata MeSH
• Check Tag
• ženské pohlaví MeSH
• zvířata MeSH
• Publikační typ
• časopisecké články MeSH
• Názvy látek
• cadmium oxide MeSH Prohlížeč
• cytokiny MeSH
• oxidy MeSH
• sloučeniny kadmia MeSH

Tyrosine kinase inhibitors are being developed for therapy of malignancies caused by oncogenic FGFR signaling but little is known about their effect in congenital chondrodysplasias or craniosynostoses that associate with activating FGFR mutations. Here, we investigated the effects of novel FGFR inhibitor, ARQ 087, in experimental models of aberrant FGFR3 signaling in cartilage. In cultured chondrocytes, ARQ 087 efficiently rescued all major effects of pathological FGFR3 activation, i.e. inhibition of chondrocyte proliferation, loss of extracellular matrix and induction of premature senescence. In ex vivo tibia organ cultures, ARQ 087 restored normal growth plate architecture and eliminated the suppressing FGFR3 effect on chondrocyte hypertrophic differentiation, suggesting that it targets the FGFR3 pathway specifically, i.e. without interference with other pro-growth pathways. Moreover, ARQ 087 inhibited activity of FGFR1 and FGFR2 mutants associated with Pfeiffer, Apert and Beare-Stevenson craniosynostoses, and rescued FGFR-driven excessive osteogenic differentiation in mouse mesenchymal micromass cultures or in ex vivo calvarial organ cultures. Our data warrant further development of ARQ 087 for clinical use in skeletal disorders caused by activating FGFR mutations.

• Klíčová slova
• ARQ 087, Achondroplasia, Craniosynostosis, FGFR, Fibroblast growth factor receptor, Inhibitor, Skeletal dysplasia,
• MeSH
• aniliny farmakologie   terapeutické užití   MeSH
• bezbuněčný systém MeSH
• buněčná diferenciace * účinky léků   MeSH
• buněčné kultury MeSH
• chinazoliny farmakologie   terapeutické užití   MeSH
• chondrocyty účinky léků   metabolismus   patologie   MeSH
• extracelulární matrix účinky léků   metabolismus   MeSH
• fibroblastový růstový faktor 2 farmakologie   MeSH
• končetinové pupeny patologie   MeSH
• kraniosynostózy farmakoterapie   genetika   patologie   MeSH
• krysa rodu Rattus MeSH
• kur domácí MeSH
• lebka patologie   MeSH
• mutace genetika   MeSH
• myši MeSH
• orgánové kultury - kultivační techniky MeSH
• proliferace buněk účinky léků   MeSH
• receptory fibroblastových růstových faktorů genetika   MeSH
• signální transdukce * MeSH
• stárnutí buněk účinky léků   MeSH
• tibie účinky léků   patologie   MeSH
• zvířata MeSH
• Check Tag
• krysa rodu Rattus MeSH
• myši MeSH
• zvířata MeSH
• Publikační typ
• časopisecké články MeSH
• Názvy látek
• aniliny MeSH
• chinazoliny MeSH
• derazantinib MeSH Prohlížeč
• fibroblastový růstový faktor 2 MeSH
• receptory fibroblastových růstových faktorů MeSH

OBJECTIVE: Statins are widely used drugs for cholesterol lowering, which were recently found to counteract the effects of aberrant fibroblast growth factor receptor (FGFR3) signaling in cell and animal models of FGFR3-related chondrodysplasia. This opened an intriguing therapeutic possibility for human dwarfing conditions caused by gain-of-function mutations in FGFR3, although the mechanism of statin action on FGFR3 remains unclear. Here, we determine the effect of statins on FGFR signaling in chondrocytes. DESIGN: Cultured chondrocyte cell lines, mouse embryonic tibia cultures and limb bud micromasses were treated with FGF2 to activate FGFR signaling. The effects of atorvastatin, fluvastatin, lovastatin and pravastatin on FGFR3 protein stability and on FGFR-mediated chondrocyte growth-arrest, loss of extracellular matrix (ECM), induction of premature senescence and hypertrophic differentiation were evaluated. RESULTS: Statins did not alter the level of FGFR3 protein expression nor produce any effect on FGFR-mediated inhibition of chondrocyte proliferation and hypertrophic differentiation in cultured chondrocyte cell lines, mouse tibia cultures or limb bud micromasses. CONCLUSION: We conclude that statins do not inhibit the FGFR signaling in chondrocytes. Therefore the statin-mediated rescue of FGFR3-related chondrodysplasia, described before, is likely not intrinsic to the growth plate cartilage.

• Klíčová slova
• Achondroplasia, Chondrocytes, FGF signaling, Statins,
• MeSH
• buněčná diferenciace účinky léků   MeSH
• buněčné linie MeSH
• chondrocyty účinky léků   metabolismus   MeSH
• chondrogeneze účinky léků   MeSH
• končetinové pupeny účinky léků   metabolismus   MeSH
• krysa rodu Rattus MeSH
• kultivované buňky MeSH
• lidé MeSH
• myši MeSH
• receptor fibroblastových růstových faktorů, typ 3 antagonisté a inhibitory   metabolismus   MeSH
• signální transdukce účinky léků   MeSH
• statiny farmakologie   MeSH
• techniky tkáňových kultur MeSH
• tibie účinky léků   embryologie   růst a vývoj   MeSH
• zvířata MeSH
• Check Tag
• krysa rodu Rattus MeSH
• lidé MeSH
• myši MeSH
• zvířata MeSH
• Publikační typ
• časopisecké články MeSH
• práce podpořená grantem MeSH
• Názvy látek
• receptor fibroblastových růstových faktorů, typ 3 MeSH
• statiny MeSH

Our goal was to determine if venlafaxine has a negative effect on bone metabolism. Rats were divided into three groups. The sham-operated control group (SHAM), the control group after orchidectomy (ORX), and the experimental group after orchidectomy received venlafaxine (VEN ORX) in standard laboratory diet (SLD) for 12 weeks. Bone mineral content (BMC) was measured by dual energy X-ray absorptiometry (DXA). Bone marker concentrations of carboxy-terminal cross-linking telopeptide of type I collagen (CTX-I), osteoprotegerin (OPG), amino-terminal propeptide of procollagen type I (P1NP), bone alkaline phosphatase (BALP), sclerostin and bone morphogenetic protein 2 (BMP-2) were examined in bone homogenate. The femurs were used for biomechanical testing. Compared to the ORX group we found lower BMD in the diaphysis area of the femur in the VEN ORX group, suggesting a preferential effect on cortical bone. Of the bone metabolism markers, there was significant decrease (ORX control group versus VEN ORX experimental group) in BALP levels and increase in sclerostin and CTX-I levels, suggesting a decrease in osteoid synthesis and increased bone resorption. The results suggest that the prolonged use of venlafaxine may have a negative effect on bone metabolism. Further studies are warranted to establish whether venlafaxine may have a clinically significant adverse effect on bone.

• Klíčová slova
• BALP, Bone mineral density, CTX-I, SNRI, Venlafaxine,
• MeSH
• absorpční fotometrie MeSH
• alkalická fosfatasa metabolismus   MeSH
• bederní obratle diagnostické zobrazování   účinky léků   MeSH
• biologické markery metabolismus   MeSH
• biomechanika MeSH
• femur diagnostické zobrazování   účinky léků   MeSH
• genetické markery MeSH
• inhibitory zpětného vychytávání serotoninu a noradrenalinu toxicita   MeSH
• kolagen typu I metabolismus   MeSH
• kosti a kostní tkáň účinky léků   metabolismus   účinky záření   MeSH
• kostní denzita účinky léků   MeSH
• kostní morfogenetické proteiny metabolismus   MeSH
• kostní morfogenetický protein 2 metabolismus   MeSH
• lidé MeSH
• orchiektomie * MeSH
• osteoprotegerin metabolismus   MeSH
• peptidové fragmenty metabolismus   MeSH
• peptidy metabolismus   MeSH
• potkani Wistar MeSH
• prokolagen metabolismus   MeSH
• remodelace kosti účinky léků   MeSH
• tibie účinky léků   metabolismus   MeSH
• venlafaxin hydrochlorid toxicita   MeSH
• zvířata MeSH
• Check Tag
• lidé MeSH
• zvířata MeSH
• Publikační typ
• časopisecké články MeSH
• práce podpořená grantem MeSH
• Názvy látek
• alkalická fosfatasa MeSH
• biologické markery MeSH
• Bmp2 protein, rat MeSH Prohlížeč
• collagen type I trimeric cross-linked peptide MeSH Prohlížeč
• genetické markery MeSH
• inhibitory zpětného vychytávání serotoninu a noradrenalinu MeSH
• kolagen typu I MeSH
• kostní morfogenetické proteiny MeSH
• kostní morfogenetický protein 2 MeSH
• osteoprotegerin MeSH
• peptidové fragmenty MeSH
• peptidy MeSH
• procollagen Type I N-terminal peptide MeSH Prohlížeč
• prokolagen MeSH
• Sost protein, rat MeSH Prohlížeč
• Tnfrsf11b protein, rat MeSH Prohlížeč
• venlafaxin hydrochlorid MeSH

Recent studies have shown that atorvastatin influences bone metabolism. We investigated its bone protective effect in orchidectomised rats after 12 weeks of treatment. Eight-week-old rats were divided into 3 groups: sham-operated group, control group after orchidectomy and experimental group after orchidectomy with atorvastatin administration (12 mg/kg/day). Bone mineral density and bone marker concentrations of aminoterminal propeptide of procollagen type I (PINP), osteoprotegerin (OPG), insulin-like growth factor 1 (IGF-1) in serum, and carboxy-terminal cross-linking telopeptide of type I collagen (CTX-I), bone alkaline phosphatase (BALP), bone morphogenetic protein 2 (BMP-2) in bone homogenate were measured. Total serum calcium and tibial calcium content was determined. Femurs were used for three-point bending test of the shaft and compression testing of the femoral neck. Bone markers (CTX-I, BALP, BMP-2) in control rats were higher vs. sham-operated rats. Atorvastatin reduced CTX-I, BMP-2 and OPG compared to controls. IGF-1 was decreased in control rats vs. sham-operated rats; atorvastatin increased IGF-1 vs. control rats. Atorvastatin exerts a positive effect on bone metabolism by increasing bone mineral density of the whole body, which had decreased under the effects of orchidectomy. Three-point bending test revealed an increase in maximal load values of the left femurs after atorvastatin administration compared to controls. The diameter of the left femur and length of both femurs were increased after atorvastatin administration compared to controls. Our findings suggest that atorvastatin has a beneficial effect on bone metabolism in orchidectomised rats by decreasing bone turnover, with resulting improvement in bone mineral density and bone biomechanical properties.

• MeSH
• atorvastatin MeSH
• biologické markery metabolismus   MeSH
• femur účinky léků   metabolismus   MeSH
• inhibitory kostní resorpce farmakologie   terapeutické užití   MeSH
• kosti a kostní tkáň metabolismus   MeSH
• kostní denzita účinky léků   MeSH
• krysa rodu Rattus MeSH
• kyseliny heptylové farmakologie   terapeutické užití   MeSH
• modely nemocí na zvířatech MeSH
• orchiektomie škodlivé účinky   MeSH
• osteoporóza farmakoterapie   metabolismus   MeSH
• pevnost v tlaku účinky léků   MeSH
• potkani Wistar MeSH
• pyrroly farmakologie   terapeutické užití   MeSH
• tibie účinky léků   metabolismus   MeSH
• vápník krev   metabolismus   MeSH
• zvířata MeSH
• Check Tag
• krysa rodu Rattus MeSH
• mužské pohlaví MeSH
• zvířata MeSH
• Publikační typ
• časopisecké články MeSH
• práce podpořená grantem MeSH
• Názvy látek
• atorvastatin MeSH
• biologické markery MeSH
• inhibitory kostní resorpce MeSH
• kyseliny heptylové MeSH
• pyrroly MeSH
• vápník MeSH

Tobacco, containing nicotine as the principal pharmacologically active chemical, has been identified as being a risk factor for the development of osteoporosis. Thirty-two male Wistar rats of two months of age were castrated or sham operated to evaluate the effects of long-term administration (four months) of nicotine in drinking water (9.0 mg/kg/day). The presence of cotinine in urine confirmed successful delivery of nicotine. The bones were tested mechanically by a three point bending test in a Mini Bionix (MTA) testing system. The bones from castrated rats were characterized by a reduction in bone density as well as ash, calcium and phosphate content. Castration significantly altered mechanical properties of bone (9%) and femoral cortical thickness. When intact rats were treated with a high dose of nicotine, nicotine had negative effect on tibial bone density as well as ash, calcium, phosphate content and significantly altered the mechanical properties of bone (12%) and femoral cortical thickness compared to intact animals. Nicotine itself does not exert any anti-androgenic effect and does not produce changes in the weight of seminal vesicles. Nicotine-induced bone loss is associated with high bone turnover in the male rats as expressed by increased TrACP and B-ALP. When castrated rats were treated with the high dose of nicotine the changes in bone density resulting from castration were not further potentiated. These results document the efficacy of nicotine at high doses to cause bone loss and loss of bone mechanical strength in intact rats. The results of the present study may be interpreted as supporting the hypothesis of nicotine as a risk factor for osteoporosis.

• MeSH
• alkalická fosfatasa krev   MeSH
• čas MeSH
• femur účinky léků   MeSH
• kostní denzita účinky léků   MeSH
• krysa rodu Rattus MeSH
• nikotin aplikace a dávkování   farmakologie   MeSH
• orchiektomie * MeSH
• pevnost v tlaku účinky léků   MeSH
• potkani Wistar MeSH
• tibie účinky léků   MeSH
• zvířata MeSH
• Check Tag
• krysa rodu Rattus MeSH
• mužské pohlaví MeSH
• zvířata MeSH
• Publikační typ
• časopisecké články MeSH
• hodnotící studie MeSH
• práce podpořená grantem MeSH
• srovnávací studie MeSH
• Názvy látek
• alkalická fosfatasa MeSH
• nikotin MeSH

Castration of male rats leads to increased bone turnover and osteopenia. This study was conducted to examine the effects of the aminobisphosphonate alendronate on castration-induced bone changes. Bisphosphonates are drugs that inhibit bone turnover by decreasing the resorption. Since they suppress bone remodeling, they may also prevent the repair of microdamage and decrease bone strength. Although the mechanical properties of bones are directly related to the determination of fracture risk, bisphosphonate effects on the related variables have scarcely been investigated. Twenty-four male Wistar rats at two months of age were castrated or sham-operated to evaluate the effects of long-term administration (six months) of sodium alendronate at a dose of 1 mg/kg/day. The bones were tested mechanically by a three-point bending test in a Mini Bionix (MTS) testing system. High bone remodeling seen in castrated rats expressed by increased TrACP and B-ALP was suppressed by alendronate administration. Bone from castrated rats was characterized by a reduction in bone density as well as ash, calcium and phosphate content. Castration significantly altered mechanical properties of bone and femoral cortical thickness. When castrated rats were treated with high dose of alendronate, the changes in bone density resulting from castration were entirely prevented, and mechanical analysis revealed preserved mechanical strength of femur and cortical thickness. We conclude that castration induces cortical bone loss associated with high bone turnover in the male rat, and this bone loss can be prevented by alendronate through the inhibition of osteoclastic activity, while preserving the mechanical properties of bone. These results document the efficacy of alendronate, even at high doses, in preventing bone loss, loss of bone mechanical strength, and the rise in biochemical bone turnover indicators due to castration in rats, and raises the possibility that a alendronate could be equally effective in humans.

• MeSH
• alendronát aplikace a dávkování   farmakologie   terapeutické užití   MeSH
• alkalická fosfatasa metabolismus   MeSH
• biomechanika MeSH
• izoenzymy metabolismus   MeSH
• kosti a kostní tkáň účinky léků   patologie   fyziologie   MeSH
• kostní denzita účinky léků   MeSH
• krysa rodu Rattus MeSH
• kyselá fosfatasa rezistentní k tartarátu MeSH
• kyselá fosfatasa metabolismus   MeSH
• orchiektomie * MeSH
• osteoklasty účinky léků   enzymologie   metabolismus   MeSH
• resorpce kosti patologie   prevence a kontrola   MeSH
• semenné váčky anatomie a histologie   účinky léků   MeSH
• tělesná hmotnost účinky léků   MeSH
• tibie účinky léků   metabolismus   MeSH
• vápník metabolismus   MeSH
• velikost orgánu účinky léků   MeSH
• zvířata MeSH
• Check Tag
• krysa rodu Rattus MeSH
• mužské pohlaví MeSH
• zvířata MeSH
• Publikační typ
• časopisecké články MeSH
• práce podpořená grantem MeSH
• Názvy látek
• alendronát MeSH
• alkalická fosfatasa MeSH
• izoenzymy MeSH
• kyselá fosfatasa rezistentní k tartarátu MeSH
• kyselá fosfatasa MeSH
• vápník MeSH

The pathophysiological processes underlying the development of diabetic osteopenia has not hitherto been elucidated. Induction of streptozotocin diabetes leads in our experiments to decrease of bone density, ash, mineral content and to thinner cortical width compared to control male rats. In order to investigate the pathogenetic role of bone resorption by osteoclasts in streptozotocin-induced diabetes, we determined the circulating levels of tartrate-resistant acid phosphatase (TRAP), a biochemical marker for bone resorption. Plasma TRAP values in diabetic rats did not differ from their corresponding controls. Streptozotocin diabetes by itself did not have any effect on the weight of seminal vesicles which are highly testosterone-dependent. Low doses of nitric oxide cause bone resorption, but higher doses of NO inhibit bone resorbing activity. We examined the effect of L-NAME (inhibitor of nitric oxide production) after six weeks of administration to diabetic rats. There was no further significant loss of bone mineral density, ash and mineral content or tibia weight in diabetic rats treated with L-NAME. L-NAME itself did not decrease bone metabolism. In our study no evidence of an increased bone resorption was found. Our results have indicated that a predominance of bone resorption over bone formation is not involved in the pathogenesis of diabetes-associated osteopenia. Inhibition of NO neither increased osteoclastic activity (TRAP) nor induced osteopenia in L-NAME-treated rats. This suggests a possibility that NO is not involved in the pathogenesis of diabetic osteopenia.

• MeSH
• experimentální diabetes mellitus krev   komplikace   patofyziologie   MeSH
• femur chemie   účinky léků   MeSH
• glykovaný hemoglobin analýza   MeSH
• inhibitory enzymů farmakologie   MeSH
• inzulin krev   MeSH
• izoenzymy krev   MeSH
• kosti a kostní tkáň účinky léků   metabolismus   patofyziologie   MeSH
• kostní denzita účinky léků   MeSH
• krevní glukóza analýza   účinky léků   MeSH
• krysa rodu Rattus MeSH
• kyselá fosfatasa rezistentní k tartarátu MeSH
• kyselá fosfatasa krev   MeSH
• metabolické nemoci kostí etiologie   prevence a kontrola   MeSH
• NG-nitroargininmethylester farmakologie   MeSH
• potkani Wistar MeSH
• semenné váčky účinky léků   MeSH
• synthasa oxidu dusnatého antagonisté a inhibitory   MeSH
• tělesná hmotnost účinky léků   MeSH
• tibie chemie   účinky léků   MeSH
• výsledek terapie MeSH
• zvířata MeSH
• Check Tag
• krysa rodu Rattus MeSH
• mužské pohlaví MeSH
• zvířata MeSH
• Publikační typ
• časopisecké články MeSH
• práce podpořená grantem MeSH
• Názvy látek
• glykovaný hemoglobin MeSH
• inhibitory enzymů MeSH
• inzulin MeSH
• izoenzymy MeSH
• krevní glukóza MeSH
• kyselá fosfatasa rezistentní k tartarátu MeSH
• kyselá fosfatasa MeSH
• NG-nitroargininmethylester MeSH
• synthasa oxidu dusnatého MeSH

We studied changes in the local circulation and mineralization of the rat tibia under different experimental conditions. Four experiments were performed on a total of 155 female and male rats: after oophorectomy (OOX) or orchidectomy (ORX), after the administration of estradiol benzoate (EB, Agofollin Depot, 1 mg/rat once a week or 5 mg/kg body weight once every 5 days for 4 weeks), or after the administration of testosterone (T, Agovirin Depot, 25 mg/kg body weight once every 5 days for 4 weeks). We estimated 85Sr-microsphere uptake and blood flow in the tibia, density of the tibia, and ash weight per bone volume unit. The scheme of the experiments was uniform: experiment A--females--controls, OOX, EB, OOX + EB; experiment B--males--controls, ORX, EB, ORX + EB; experiment C--females--controls, OOX, T, OOX + T; experiment D--males--controls, ORX, T, ORX + T. A sham operation was performed on the animals in the uncastrated groups. The results showed that OOX and ORX stimulated the uptake of 85Sr-microspheres and bone blood flow and reduced both bone density and ash weight, whereas T inconstantly and EB constantly reduced 85Sr-microsphere uptake and bone blood flow and increased bone density and ash weight in both sham-operated and castrated animals. The described changes in the bone blood flow and mineral content under the given experimental conditions suggest a relation in the regulations of both processes, a possible association with resorption of bone, and the importance of the circulation of blood in the metabolism of bone tissue.

• MeSH
• estradiol farmakologie   MeSH
• kostní denzita účinky léků   fyziologie   MeSH
• krysa rodu Rattus MeSH
• orchiektomie MeSH
• ovarium fyziologie   MeSH
• regionální krevní průtok MeSH
• testis fyziologie   MeSH
• testosteron farmakologie   MeSH
• tibie krevní zásobení   účinky léků   fyziologie   MeSH
• zvířata MeSH
• Check Tag
• krysa rodu Rattus MeSH
• mužské pohlaví MeSH
• ženské pohlaví MeSH
• zvířata MeSH
• Publikační typ
• časopisecké články MeSH
• práce podpořená grantem MeSH
• Názvy látek
• estradiol MeSH
• testosteron MeSH

The aim of this study was to verify the possible role of prostaglandin (PG) in the increase in the bone blood flow of female rats after oophorectomy (OOX). In two experiments we determined blood flow in the tibia and distal femur (85Sr-microspheres) and 24-h incorporation of 45Ca and 3H-proline. Acetylosalicyclic acid (ASA, 0.13% in the food for 4 weeks) was used to suppress the production of PG. There was an increase in the bone blood flow after OOX (performed 4 weeks prior to the experiment), no change after ASA alone and significant reduction by ASA of the OOX-induced increase in the bone blood flow. In both groups of OOX females there was a decrease in tibial bone density and ash weight. The changes in 45Ca incorporation were similar to those in the blood flow while the changes in 3H-proline incorporation were not significant. Thus, the effect of ASA, i.e. suppression of the OOX-induced increase in the bone blood flow, is consistent with the possible role of PG (probably PGE2) in the increase in bone blood flow of OOX female rats.

• MeSH
• Aspirin farmakologie   MeSH
• femur krevní zásobení   účinky léků   fyziologie   MeSH
• kosti a kostní tkáň krevní zásobení   účinky léků   fyziologie   MeSH
• kostní denzita fyziologie   MeSH
• krysa rodu Rattus MeSH
• mikrosféry MeSH
• ovarektomie * MeSH
• prolin metabolismus   MeSH
• prostaglandiny metabolismus   fyziologie   MeSH
• regionální krevní průtok MeSH
• tibie krevní zásobení   účinky léků   fyziologie   MeSH
• tritium MeSH
• vápník metabolismus   MeSH
• zvířata MeSH
• Check Tag
• krysa rodu Rattus MeSH
• ženské pohlaví MeSH
• zvířata MeSH
• Publikační typ
• časopisecké články MeSH
• práce podpořená grantem MeSH
• Názvy látek
• Aspirin MeSH
• prolin MeSH
• prostaglandiny MeSH
• tritium MeSH
• vápník MeSH