Complete Analytical Solution of the Statistical Rate Theory: Desorption from Solid/Solution Interfaces.

One of the essential steps in the design and regeneration of catalysts is desorption. Kinetics modeling of the desorption process is essential for a better understanding of this process. The statistical rate theory (SRT) method is one of the essential theoretical methods that can be used to study the rate of desorption. For the first time, a complete solution of the SRT equation for desorption from the solid surface to the solution phase (SRT-D) is reported. The new integrated equations are provided as the linear forms, which have been denoted as the SRT-LFD equations. The first complete analytical solution of the SRT-D equation is confirmed using the created data by numerical solution of the SRT-D equation and the experimental data. The perfect agreement between the obtained results of the SRT-LFD equations and the results of the created and experimental data confirms the accuracy of the obtained equations.

Investigation of Fractal-like Characteristics According to New Kinetic Equation of Desorption.

Most of the adsorbents have porous structures and a suitable kinetic model is essential for studying these systems. The kinetic Langmuir model is one of the first theoretical models, which can be used for desorption studies. In the present research, the fractal-like concept was added to the kinetic Langmuir model of desorption. A new integrated kinetic Langmuir equation was provided to investigate the rate of desorption from a solid surface. The preferred characteristic of the provided rate equation is the application of the fractal concept for the kinetic study of the desorption process from porous surfaces. The derivation of a new equation was confirmed using the generated data. The fractal-like concept for some experimental desorption studies was obtained. This parameter can show how the porous structure of an adsorbent can affect the desorption kinetics.

Elevation of phosphate levels impairs skeletal myoblast differentiation.

Hyperphosphatemic conditions such as chronic kidney disease are associated with severe muscle wasting and impaired life quality. While regeneration of muscle tissue is known to be reliant on recruitment of myogenic progenitor cells, the effects of elevated phosphate loads on this process have not been investigated in detail so far. This study aims to clarify the direct effects of hyperphosphatemic conditions on skeletal myoblast differentiation in a murine in vitro model. C2C12 murine muscle progenitor cells were supplemented with phosphate concentrations resembling moderate to severe hyperphosphatemia (1.4-2.9 mmol/l). Phosphate-induced effects were quantified by RT-PCR and immunoblotting. Immunohistochemistry was performed to count nuclear positive cells under treatment. Cell viability and metabolic activity were assessed by XTT and BrdU incorporation assays. Inorganic phosphate directly induced ERK-phosphorylation in pre-differentiated C2C12 myoblast cells. While phosphate concentrations resembling the upper normal range significantly reduced Myogenin expression (- 22.5%, p = 0.015), severe hyperphosphatemic conditions further impaired differentiation (Myogenin - 61.0%, p < 0.0001; MyoD - 51.0%; p < 0.0001). Analogue effects were found on the protein level (Myogenin - 42.0%, p = 0.004; MyoD - 25.7%, p = 0.002). ERK inhibition strongly attenuated phosphate-induced effects on Myogenin expression (p = 0.002). Metabolic activity was unaffected by the treatments. Our data point to a phosphate-induced inhibition of myoblast differentiation without effects on cell viability. Serum phosphate levels as low as the upper normal serum range significantly impaired marker gene expression in vitro. Investigation of cellular effects of hyperphosphatemia may help to better define serum cutoffs and modify existing treatment approaches of phosphate binders, especially in patients at risk of sarcopenia.

A journey through growth plates: tracking differences in morphology and regulation between the spine and the long bones in a pig model.

BACKGROUND CONTEXT: The process of linear growth is driven by axial elongation of both long bones and vertebral bodies and is accomplished by enchondral ossification. Differences in regulation between the two skeletal sites are mirrored clinically by the age course in body proportions. Whereas long bone growth plates (GPs) can easily be discriminated, vertebral GPs are part of the cartilaginous end plate, which typically shows important species differences. PURPOSE: The objective of this study was to describe and compare histologic, histomorphometric, and regulatory characteristics in the GPs of the spine and the long bones in a porcine model. MATERIALS AND METHODS: Two- and six-week-old piglet GPs of three vertebral segments (cervical, thoracic, and lumbar) and eight long bones (proximal and distal radius, humerus, tibia, and femur) were analyzed morphometrically. Further, estrogen receptors, proliferation markers, and growth factor expressions were examined by immunohistochemistry. RESULTS: Individual vertebral GPs were smaller in width and contained fewer chondrocytes than long bone GPs, although their proliferation activity was similar. Whereas the expression pattern of growth hormone-associated factors such as insulin-like growth factor (IGF)-1 and IGF-1 receptor (IGF-1R) was similar, estrogen receptor (ER)-ß and IGF-2 were distinctly expressed in the vertebral samples. CONCLUSIONS: Vertebral GPs display differential growth, with measurements similar to the slowest-growing GPs of long bones. Further investigation is needed to decipher the molecular basis of the differential growth of the spine and the long bones. Knowledge on the distinct mechanism will ultimately improve the assessment of clinically essential characteristics of spinal growth, such as vertebral elongation potential and GP fusion.