Maps Anabolic Pdf Free Download BETTER

I have a slight tear in the meniscus (not enough to do surgery) that makes squats/deadlifts very difficult. I would want to use MAPS anabolic only for upper body. Would that work within the program or any other thoughts.

The osteo-anabolic effects of intermittent parathyroid hormone (PTH) treatment require insulin-like growth factor (IGF) signaling through the IGF-I receptor. A major downstream target of the IGF-I receptor (via Akt) is the mammalian target of rapamycin (mTOR), a kinase involved in protein synthesis. We investigated whether the bone-building effects of intermittent PTH require functional mTOR signaling. Mice were treated with daily PTH 1-34 (0, 10, 30, or 90 microg/kg) for 6 weeks in the presence or absence of rapamycin, a selective inhibitor of mTOR. We found that all PTH doses were effective in enhancing bone mass, whether rapamycin was present or not. Rapamycin had little to no effect on the anabolic response at low (10 microg) PTH doses, small effects in a minority of anabolic measures at moderate doses (30 microg), but the anabolic effects of high-dose PTH (90 microg) were consistently and significantly suppressed by rapamycin ( approximately 4-36% reduction). Serum levels of Trap5b, a marker of resorption, were significantly enhanced by rapamycin, but these effects were observed whether PTH was absent or present. Our data suggest that intermittent PTH, particularly at lower doses, is effective in building bone mass in the presence of rapamycin. However, the full anabolic effects of higher doses of PTH are significantly suppressed by rapamycin, suggesting that PTH might normally activate additional pathways (including mTOR) for its enhanced high-dose anabolic effects. Clinical doses of intermittent PTH could be an effective treatment for maintaining or increasing bone mass among patients taking rapamycin analogs for unrelated health issues.

Maps Anabolic Pdf Free Download

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In pulmonary arterial hypertension (PAH), inflammation promotes a fibroproliferative pulmonary vasculopathy. Reductionist studies emphasizing single biochemical reactions suggest a shift toward glycolytic metabolism in PAH; however, key questions remain regarding the metabolic profile of specific cell types within PAH vascular lesions in vivo. We used RNA-Seq to profile the transcriptome of pulmonary artery endothelial cells (PAECs) freshly isolated from an inflammatory vascular injury model of PAH ex vivo, and these data were integrated with information from human gene ontology pathways. Network medicine was then used to map all aa and glucose pathways to the consolidated human interactome, which includes data on 233,957 physical protein-protein interactions. Glucose and proline pathways were significantly close to the human PAH disease module, suggesting that these pathways are functionally relevant to PAH pathobiology. To test this observation in vivo, we used multi-isotope imaging mass spectrometry to map and quantify utilization of glucose and proline in the PAH pulmonary vasculature at subcellular resolution. Our findings suggest that elevated glucose and proline avidity underlie increased biomass in PAECs and the media of fibrosed PAH pulmonary arterioles. Overall, these data show that anabolic utilization of glucose and proline are fundamental to the vascular pathology of PAH.

Osteoporosis, a disease characterized by increased bone fragility and fracture risk, affects over 20% of the ever-growing elderly population. It is important to further our knowledge of bone cell biology so we can develop new bone anabolic treatments. By combining genomic and bioinformatic tools against the backdrop of osteogenic differentiating human mesenchymal stromal cells, we have identified a previously unidentified bone anabolic compound that induces osteoblast differentiation in a subset of the hMSC population through cytoskeletal changes and increased bone morphogenetic protein 2 activity. Through this novel approach we identified an important mechanism of lineage allocation and demonstrated the significance of cytoskeletal organization in osteogenic differentiation, providing us with a novel mechanism for bone formation to target for new osteoporosis treatments.

Technical Abstract: Rates of protein accrual are largely affected by rates of protein degradation. Determining how proteolytic pathways are affected by catabolic and anabolic signals will contribute to the understanding of the impact and regulation these pathways have on protein turnover. Real time RT-PCR was used to investigate changes in expression of proteolytic genes in rainbow trout (Oncorhynchus mykiss) in response to feed deprivation, anabolic hormones, or both. After two weeks of feed deprivation white muscle expression of the cathepsins and the ubiquitin ligase protein F-box were increased 50% and 500%, respectively. Treatment with insulin-like growth factor (IGF-I) reduced weight loss during feed deprivation and prevented the upregulation of these genes, suggesting that IGF-I reduced protein loss by reducing the capacity for proteolysis via the proteasome and cathepsin pathways. Mechanisms for the actions of metabolic hormones were investigated further using myocyte cell culture. Myocyte treatment with IGF-I or insulin reduced expression of the ubiquitin ligase proteins F-box and MuRF in a dose-dependent manner via PI3K/AKT activation and FOXO phosphorylation. Therefore, the anabolic properties of these hormones partially results from their ability to reduce protein degradation by decreasing transcription of ubiquitin ligases, which target proteins to the proteasome. Additionally, F-box mRNA abundance in liver and muscle was positively correlated with feed conversion (feed/gain) and negatively correlated with body weight in liver, suggesting that a reduced capacity to degrade proteins results in better feed conversion and growth performance. ff782bc1db