After bacterial cell division, the daughter cells are still covalently interlinked by the peptidoglycan network which is resolved by specific hydrolases (autolysins) to release the daughter cells. In staphylococci, the major autolysin (Atl) with its two domain enzymes, N-acetylmuramyl-L-alanine amidase (AmiA) and β-N-acetylglucosaminidase (GlcA), resolves the peptidoglycan to release the daughter cells. Internal deletions in each of the enzyme domains revealed defined morphological alterations such as cell cluster formation in ΔamiA, ΔglcA and Δatl, and asymmetric cell division in the ΔglcA. A most important finding was that GlcA activity requires the prior removal of the stem peptide by AmiA for its activity thus the naked glycan strand is its substrate. Furthermore, GlcA is not an endo-β-N-acetylglucosaminidase but an exo-enzyme that cuts the glycan backbone to disaccharides independent of its O-acetylation modification. Our results shed new light into the sequential peptidoglycan hydrolysis by AmiA and GlcA during cell division in staphylococci.As the prevalence of diabetes continues to climb, the number of individuals living with diabetic complications will reach an unprecedented magnitude. The emergence of new glucose-lowering agents - sodium-glucose cotransporter 2 inhibitors and incretin therapies - has markedly changed the treatment landscape of type 2 diabetes mellitus. In addition to effectively lowering glucose, incretin drugs, which include glucagon-like peptide 1 receptor (GLP1R) agonists and dipeptidyl peptidase 4 (DPP4) inhibitors, can also reduce blood pressure, body weight, the risk of developing or worsening chronic kidney disease and/or atherosclerotic cardiovascular events, and the risk of death. Although kidney disease events have thus far been secondary outcomes in clinical trials, an ongoing phase III trial in patients with diabetic kidney disease will test the effect of a GLP1R agonist on a primary kidney disease outcome. Experimental data have identified the modulation of innate immunity and inflammation as plausible biological mechanisms underpinning the kidney-protective effects of incretin-based agents. These drugs block the mechanisms involved in the pathogenesis of kidney damage, including the activation of resident mononuclear phagocytes, tissue infiltration by non-resident inflammatory cells, and the production of pro-inflammatory cytokines and adhesion molecules. GLP1R agonists and DPP4 inhibitors might also attenuate oxidative stress, fibrosis and cellular apoptosis in the kidney.Pleiotrophin (PTN) is a cytokine that is upregulated in different neuroinflammatory disorders. Using mice with transgenic PTN overexpression in the brain (Ptn-Tg), we have found a positive correlation between iNos and Tnfα mRNA and Ptn mRNA levels in the prefrontal cortex (PFC) of LPS-treated mice. PTN is an inhibitor of Receptor Protein Tyrosine Phosphatase (RPTP) β/ζ, which is mainly expressed in the central nervous system. see more We aimed to test if RPTPβ/ζ is involved in the modulation of neuroinflammatory responses using specific inhibitors of RPTPβ/ζ (MY10 and MY33-3). Treatment with MY10 potentiated LPS-induced microglial responses in the mouse PFC. Surprisingly, MY10 caused a decrease in LPS-induced NF-κB p65 expression, suggesting that RPTPβ/ζ may be involved in a novel mechanism of potentiation of microglial activation independent of the NF-κB p65 pathway. MY33-3 and MY10 limited LPS-induced nitrites production and iNos increases in BV2 microglial cells. SH-SY5Y neuronal cells were treated with the conditioned media from MY10/LPS-treated BV2 cells. Conditioned media from non-stimulated and from LPS-stimulated BV2 cells increased the viability of SH-SY5Y cultures. RPTPβ/ζ inhibition in microglial cells disrupted this neurotrophic effect of microglia, suggesting that RPTPβ/ζ plays a role in the neurotrophic phenotype of microglia and in microglia-neuron communication.Medical treatments such as high-intensity focused ultrasound, hyperthermic laser lipolysis or radiofrequency are employed as a minimally invasive alternatives for targeted tissue therapies. The increased temperature of the tissue triggers various thermal effects and leads to an unavoidable damage. As targeted tissues are generally located below the surface, various approaches are utilized to prevent skin layers from overheating and irreparable thermal damages. These procedures are often accompanied by cooling systems and protective layers accounting for a non-trivial detection of the subsurface temperature peak. Here, we show a temperature peak estimation method based on infrared thermography recording of the surface temperature evolution coupled with a thermal-diffusion-based model and a time-dependent data matching algorithm. The performance of the newly developed method was further showcased by employing hyperthermic laser lipolysis on an ex-vivo porcine fat tissue. Deviations of the estimated peak temperature remained below 1 °C, as validated by simultaneous measurement of depth temperature field within the tissue. Reconstruction of the depth profile shows a good reproducibility of the real temperature distribution with a small deviation of the peak temperature position. A thermal camera in combination with the time-dependent matching bears the scope for non-contact monitoring of the depth temperature profile as fast as 30 s. The latest demand for miniaturization of thermal cameras provides the possibility to embed the model in portable thermal scanners or medical laser technologies for improving safety and efficiency.Spectrally selective solar absorbers (SSAs), which harvest heat from sunlight, are the key to concentrated solar thermal systems. An ideal SSA must have an absorptivity of unity in the solar irradiance wavelength region (0.3-2.5 [Formula see text]m), and its infrared thermal emissivity must be zero to depress spontaneous blackbody irradiation (2.5-25 [Formula see text]m). Current SSA designs which utilize photonic crystals, metamaterials, or cermets are either cost-inefficient due to the complexity of the required nanofabrication methods, or have limited applicability due to poor thermal stability at high temperatures. We conceptually present blackbody-cavity solar absorber designs with nearly ideal spectrally selective properties, capable of being manufactured at scale. The theoretical analyses show that the unity solar absorptivity of the blackbody cavity and nearly zero infrared emissivity of the SSA's outer surface allow for a stagnation temperature of 880 [Formula see text]C under 10 suns. The performance surpasses state-of-the-art SSAs manufactured using nanofabrication methods.see more
For further actions, you may consider blocking this person and/or reporting abuse
Top comments (0)