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This study investigated the effects of AdipoRon, which is an agonist for adiponectin receptor 1 (AdipoR1) and AdipoR2, on the protein content, myotube diameter, and number of nuclei per myotube of C2C12 cells and skeletal muscle mass in C57BL/6J mice. AdipoRon suppressed the protein content, myotube diameter, and number of nuclei per myotube of C2C12 cells of C2C12 myotubes in a dose-dependent manner. Adiponectin-associated decline of protein content, diameter, and number of nuclei per myotube in C2C12 myotubes was partially rescued by knockdown of AdipoR1 and/or AdipoR2. Phosphorylation level of AMPK showed a trend to be increased by AdipoRon. A significant increase in phosphorylation level of AMPK was observed at 20 μM AdipoRon. Knockdown of AdipoR1 and/or AdipoR2 rescued AdipoRon-associated decrease in protein content of C2C12 myotubes. AdipoRon-associated increase in phosphorylation level of AMPK in C2C12 myotubes was suppressed by knockdown of AdipoR1 and/or AdipoR2. Successive intravenous injections of AdipoRon into mice caused a decrease in the wet weight of plantaris muscle (PLA), but not in soleus muscle (SOL). Mean fiber cross-sectional area of PLA, but not of SOL, was significantly decreased by AdipoRon administration. On the one hand, the expression level of phosphorylated AMPK and ubiquitinated protein in SOL and PLA muscles was upregulated by AdipoRon administration. On the other hand, AdipoRon administration induced no changes in the expression level of puromycin-labeled proteins in both SOL and PLA muscles. Expression level of adiponectin in extensor digitorum longus (EDL) muscle was increased by aging, but not in SOL muscle. Aging had no effect on the expression level of AdipoR1 and AdipoR2 in both muscles. Phosphorylation level of AMPK in EDL was increased by aging, but not SOL muscle. Results from this study suggest that high level of circulating adiponectin may induce skeletal muscle atrophy, especially fast-type muscle.

When skinned fibers from frog semitendinous muscle were mildly treated with trypsin, passive tension generation was remarkably reduced, and the hydrolysis of a-connectin to ,8-connectin simultaneously occurred. On immunoelectron microscopy, splitting of the connectin filaments at the A-I junction area in a sarcomere was seen. These observations strongly suggest that connectin filaments are responsible for passive tension generation as a parallel elastic component in a sarcomere.

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The internal mammary lymph node (IMLN) chain is a pathway through which breast lymphatic drainage flows. The internal mammary lymphatic vessel runs around the internal mammary artery and veins with IMLN in the parasternal intercostal spaces. IMLN metastasis, which forms a part of clinical TNM staging, may negatively affect the prognosis of primary breast cancer patients. IMLN metastasis is clinically detected using ultrasound, computed tomography, magnetic resonance imaging, and F-deoxyglucose positron emission tomography computed tomography. The uptake of radioactive tracers in IMLN with clinically negative axillary lymph nodes is often identified using sentinel lymph node mapping (SLNM) in primary breast cancer patients. The indication for IMLN biopsy or resection that is clinically detected or visualized using SLNM is controversial. The clinically suspicious IMLN may be considered for ultrasound-guided fine-needle aspiration. First IMLN recurrence needs to be biopsied. Irradiation of the breast, chest wall, and/or regional nodal irradiation, including IMLN, following lumpectomy or postmastectomy is recommended. Although radiation therapy for IMLN recurrence may improve clinical outcomes, it is also associated with pulmonary and cardiac toxicities. This review covers the local anatomy of IMLN, lymph drainage and image findings of IMLN with a discussion.

Duchenne muscular dystrophy is a lethal X-linked disease with no effective treatment. Progressive muscle degeneration, increased macrophage infiltration, and ectopic calcification are characteristic features of the mdx mouse, a murine model of Duchenne muscular dystrophy. Because dietary phosphorus/phosphate consumption is increasing and adverse effects of phosphate overloading have been reported in several disease conditions, we examined the effects of dietary phosphorus intake in mdx mice phenotypes. On weaning, control and mdx mice were fed diets containing 0.7, 1.0, or 2.0 g phosphorus per 100 g until they were 90 days old. Dystrophic phenotypes were evaluated in cryosections of quadriceps and tibialis anterior muscles, and maximal forces and voluntary activity were measured. Ectopic calcification was analyzed by electron microscopy to determine the cells initially responsible for calcium deposition in skeletal muscle. Dietary phosphorus overload dramatically exacerbated the dystrophic phenotypes of mdx mice by increasing inflammation associated with infiltration of M1 macrophages. In contrast, minimal muscle necrosis and inflammation were observed in exercised mdx mice fed a low-phosphorus diet, suggesting potential beneficial therapeutic effects of lowering dietary phosphorus intake on disease progression. To our knowledge, this is the first report showing that dietary phosphorus intake directly affects muscle pathological characteristics of mdx mice. Dietary phosphorus overloading promoted dystrophic disease progression in mdx mice, whereas restricting dietary phosphorus intake improved muscle pathological characteristics and function.

BackgroundLower tube voltage has advantages for CT angiography, such as improved contrastObjectiveTo evaluate the image quality of low-voltage (70 kV) CT for congenital heart disease and the ability of sinogram-affirmed iterative reconstruction to improve image quality.Materials and methodsForty-six children with congenital heart disease (median age: 109 days) were examined using dual-source CT. Scans were performed at 80 kV and 70 kV in 21 and 25 children, respectively. A nonionic iodinated contrast medium (300 mg I/ml) was used for the 80-kV protocol. The contrast medium was diluted to 75% (225 mgI/mL) with saline for the 70-kV protocol. Image noise was measured in the two protocols for each group by extracting the standard deviations of a region of interest placed on the descending aorta. We then determined whether sinogram-affirmed iterative reconstruction reduced the image noise at 70 kV.ResultsThere was more noise at 70 kV than at 80 kV (29 ± 12 vs 20 ± 4.8; P < 0.01). Sinogram-affirmed iterative reconstruction with grade 4 strength settings improved the noise (20 ± 5.9; P < 0.01) for the 70-kV group.ConclusionSinogram-affirmed iterative reconstruction improved the image quality of CT in congenital heart disease.