Minimally invasive plate osteosynthesis (MIPO) has been used for humeral shaft fractures, but concerns exist about soft tissue injuries. The purpose of this study was to report the surgical technique and clinical outcomes of MIPO using a helical plate for metadiaphyseal complex humeral shaft fractures. Twelve patients with acute displacement involving proximal and middle third humeral shaft fractures (AO type C) were treated using the MIPO technique with a helical plate. Fracture union, complications, and functional outcomes were evaluated using the Constant-Murley score and Mayo Elbow Performance Score (MEPS) at final follow-up. All fractures united at an average of 17.9 weeks. No major complications, such as neurovascular injury, infection, and nonunion, were observed. Mean Constant-Murley and MEPS scores at final follow-up were 88.6 and 97.9, respectively. A MIPO technique using a helical plate can be a useful surgical option for metadiaphyseal complex fractures of the humeral shaft.
Photoresponses and microwave characteristics of an area-variable varactor diode are investigated in the frequency range up to 7 GHz. It is demonstrated that the on/off ratio of its capacitance corresponds to 18.5 at 1 GHz. The capacitance is also significantly altered by photoillumination, and a maximum on/off ratio of 450% is achieved at 1 GHz with 1045 nW light power.
Additional file 8: Table S7. Analysis of MAPK/ERK target genes in extra-renal tissues. The gene expression changes identified in embryonic kidney were also quantified by qPCR in E12.5 mouse lungs and adult liver slices cultured for 24h in the presence of MEK inhibitor U0126. The analyzed genes are listed in “Gene” column followed by Yes/No to indicate whether the expression pattern observed in MAPK/ERK-deficient embryonic kidney was recapitulated in the extra-renal tissue. “Regulation” column shows whether the given gene expression was up- or down-regulated by MEK inhibition and indicates the potential statistical significance (*=p<0.05; **=p<0.01; ***=p<0.001).
The in vivo niche and basic cellular properties of nephron progenitors are poorly described. Here we studied the cellular organization and function of the MAPK/ERK pathway in nephron progenitors. Live-imaging of ERK activity by a Förster resonance energy transfer biosensor revealed a dynamic activation pattern in progenitors, whereas differentiating precursors exhibited sustained activity. Genetic experiments demonstrate that MAPK/ERK activity controls the thickness, coherence, and integrity of the nephron progenitor niche. Molecularly, MAPK/ERK activity regulates niche organization and communication with extracellular matrix through PAX2 and ITGA8, and is needed for CITED1 expression denoting undifferentiated status. MAPK/ERK activation in nephron precursors propels differentiation by priming cells for distal and proximal fates induced by the Wnt and Notch pathways. Thus, our results demonstrate a mechanism through which MAPK/ERK activity controls both progenitor maintenance and differentiation by regulating a distinct set of targets, which maintain the biomechanical milieu of tissue-residing progenitors and prime precursors for nephrogenesis.
Alterations in metabolic pathways are gaining attention as important environmental factors affecting life span, but the determination of specific metabolic pathways and enzymes involved in life span remains largely unexplored. By applying an NMR-based metabolomics approach to a calorie-restricted yeast (Saccharomyces cerevisiae) model, we found that alanine level is inversely correlated with yeast chronological life span. The involvement of the alanine-metabolizing pathway in the life span was tested using a deletion mutant of ALT1, the gene for a key alanine-metabolizing enzyme. The mutant exhibited increased endogenous alanine level and much shorter life span, demonstrating the importance of ALT1 and alanine metabolic pathways in the life span. ALT1's effect on life span was independent of the TOR pathway, as revealed by a tor1 deletion mutant. Further mechanistic studies showed that alt1 deletion suppresses cytochrome c oxidase subunit 2 expression, ultimately generating reactive oxygen species. Overall, ALT1 seems critical in determining yeast life span, and our approach should be useful for the mechanistic studies of life span determinations.
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