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The preoperative localisation of small parathyroid adenomas improves when introducing Tc-99m-Sestamibi SPECT to multiphase contrast-enhanced CT.
Regulation of glucose homeostasis is a fundamental process to maintain blood glucose at a physiological level, and its dysregulation is associated with the development of several metabolic diseases. Here, we report on a zebrafish mutant for Aldo-keto-reductase 1a1b (akr1a1b) as a regulator of gluconeogenesis. Adult akr1a1b -/- mutant zebrafish developed fasting hypoglycemia, which was caused by inhibiting phosphoenolpyruvate carboxykinase (PEPCK) expression as rate-limiting enzyme of gluconeogenesis. Subsequently, glucogenic amino acid glutamate as substrate for gluconeogenesis accumulated in the kidneys, but not in livers, and induced structural and functional pronephros alterations in 48-hpf akr1a1b -/- embryos. Akr1a1b -/- mutants displayed increased nitrosative stress as indicated by increased nitrotyrosine, and increased protein-S-nitrosylation. Inhibition of nitrosative stress using the NO synthase inhibitor L-NAME prevented kidney damage and normalized PEPCK expression in akr1a1b -/- mutants. Thus, the data have identified Akr1a1b as a regulator of gluconeogenesis in zebrafish and thereby controlling glucose homeostasis.Vision is essential for vertebrates including humans. Sustained vision is accomplished by retinoid metabolism, the "visual cycle," where all-trans retinol (atROL) is incorporated into the retinal pigment epithelium (RPE) from photoreceptors presumably through decade-long missing receptor(s). Here, we show that the LDL-related receptor-5 (Lrp5) protein is linked to the retinol binding protein 1a (Rbp1a), the transporter of atROL in the visual cycle, by generating and analyzing the digenic eyes shut homolog +/- ; lrp5 +/- zebrafish, the same form of gene defect detected in a human case of inherited retinal degeneration. Global gene expression analysis followed by genetic study clarified that rbp1a played a role downstream of lrp5. Rbp1a protein was colocalized with Lrp5 protein at microvilli of RPE cells. Furthermore, Rbp1a directly bound to the C-terminal intracellular region of Lrp5 in vitro. Collectively, these results strongly suggest that Lrp5 is a potent candidate of the receptor of atROL in the visual cycle.In this work, a spinel single-crystalline Li1.1Mn1.9O4 has been successfully synthesized using β-MnO2 nanotubes as the self-sacrifice template. The tubular morphology was retained through solid-state reactions, attributed to a minimal structural reorganization from tetragonal β-MnO2 to spinel Li1.1Mn1.9O4. find more The materials were investigated as sorbents for lithium recovery from LiCl solutions, recycled using H2SO4 and (NH4)2S2O8. Li1.1Mn1.9O4 nanotubes exhibited favorable lithium extraction behavior due to tubular nanostructure, single-crystalline nature, and high crystallinity. (NH4)2S2O8 eluent ensures the structural stability of Li1.1Mn1.9O4 nanotube, registering a Li+ adsorption capacity of 39.21 mg g-1 (∼89.73% of the theoretical capacity) with only 0.08% manganese dissolution after eight adsorption/desorption cycles, compared to that of 1.21% for H2SO4. It reveals the degradation of sorbent involves with the volume change, Mn reduction, and Li/Mn ratio depletion. New strategies, based on nanotube adsorbent and (NH4)2S2O8 eluent, can extract lithium ions at satisfactorily high degrees while effectively minimizing manganese dissolution.Several treatments have been attempted in amyotrophic lateral sclerosis (ALS) animal models and patients. Recently, transplantation of bone marrow-derived mononuclear cells (MNCs) was investigated as a regenerative therapy for ALS, but satisfactory treatments remain to be established. To develop an effective treatment, we focused on mesenchymal stem cells (MSCs) expressing hepatocyte growth factor, glial cell line-derived neurotrophic factor, and insulin-like growth factor using human artificial chromosome vector (HAC-MSCs). Here, we demonstrated the transplantation of MNCs with HAC-MSCs in ALS mice. As per our results, the progression of motor dysfunction was significantly delayed, and their survival was prolonged dramatically. Additional analysis revealed preservation of motor neurons, suppression of gliosis, engraftment of numerous MNCs, and elevated chemotaxis-related cytokines in the spinal cord of treated mice. Therefore, growth factor-expressing MSCs enhance the therapeutic effects of bone marrow-derived MNCs for ALS and have a high potential as a novel cell therapy for patients with ALS.ATP is required for mammalian cells to remain viable and to perform genetically programmed functions. Maintenance of the ΔG'ATP hydrolysis of -56 kJ/mole is the endpoint of both genetic and metabolic processes required for life. Various anomalies in mitochondrial structure and function prevent maximal ATP synthesis through OxPhos in cancer cells. Little ATP synthesis would occur through glycolysis in cancer cells that express the dimeric form of pyruvate kinase M2. Mitochondrial substrate level phosphorylation (mSLP) in the glutamine-driven glutaminolysis pathway, substantiated by the succinate-CoA ligase reaction in the TCA cycle, can partially compensate for reduced ATP synthesis through both OxPhos and glycolysis. A protracted insufficiency of OxPhos coupled with elevated glycolysis and an auxiliary, fully operational mSLP, would cause a cell to enter its default state of unbridled proliferation with consequent dedifferentiation and apoptotic resistance, i.e., cancer. The simultaneous restriction of glucose and glutamine offers a therapeutic strategy for managing cancer.The relative contribution of the two phagosomal catabolic processes, oxidative and metabolic, was assessed in the killing of Pseudomonas aeruginosa in phagosomes of alveolar macrophages (AMs) from wild-type (p47-phox +/+ ) or NOX-defective (p47-phox -/- ) mice. Free radical release and degradative acidification within AM phagosomes is sequential and separable. The initial NOX activity, identifiable as a transient alkalinization, leads to fast bacterial wall permeabilization by ROS. This is followed by V-ATPase-induced acidification and enzymatic bacterial degradation contributed through phagosomal-lysosomal fusion. The alkalinization/acidification ratio was variable among phagosomes within single cells of a given genotype and not as a function of macrophage M1 or M2 classification, possibly owing to uneven distribution of phagosomal transporter proteins. Irregular, excessive NOX activity prevents phago-lysosomal fusion, and the lack of V-ATPase-induced acidification leads to bacterial stasis in the phagosome.
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