Effects of isometric contraction of the quadriceps on the hardness and blood flow in the infrapatellar fat pad

[Purpose] This study aimed to clarify the influence of the isometric contraction of the quadriceps (ICQ) with low intensity on the circulation in the infrapatellar fat pad (IFP). [Participants and Methods] The participants were 7 males and 5 females, with an average age of 21.5 ± 1.4 years. IFP hardness was measured using shear wave ultrasound elastography and Biodex. Tissue oxygenation was measured via near-infrared spectroscopy using oxygenated hemoglobin (O2Hb), deoxygenated hemoglobin (HHb), and total hemoglobin (cHb) as indices. The mean values were calculated for three periods: 1 min of rest immediately before the exercise task (before ICQ), the lower limit of the 10 sets during the exercise task (during ICQ), and 3–4 min after the exercise task (after ICQ). IFP hardness was compared between resting conditions and ICQ, and tissue oxygenation was compared before, during, and after ICQ. [Results] ICQ significantly increased IFP hardness. Tissue hemoglobin, O2Hb, and cHb decreased significantly during ICQ and increased after ICQ compared to that before ICQ. HHb decreased during ICQ and recovered significantly after ICQ. [Conclusion] In healthy participants, low-intensity ICQ increases the hardness and oxygenation of the IFP. This study may partly explain the unknown pain relief mechanism of exercise therapy.     

Deposition of calcium pyrophosphate dihydrate crystals in the hand

A rare case with deposition of calcium pyrophosphate dihydrate crystals around the proximal portion of the first and second metacarpal bones is reported. The second metacarpal had a cystic lesion, and the cortex of the first metacarpal had irregular osteolytic change. There were degenerative changes in the first carpometacarpal joint, trapeziotrapezoid articulation, and second carpometacarpal joint. The patient had recurrent acute inflammatory attacks at the affected site. Initially the patient was thought to have tumoral calcinosis, or a calcifying soft-tissue tumor, with the possibility of a malignant tumor because of angiographic evidence of tumor stain and hypervascularity. Surgical biopsy with partial curettage of the calcified mass resulted in early recurrence of deposition of the crystals. Total excision would seem to be necessary to avoid recurrence.     

Potential therapeutic target secretogranin II might cooperate with hypoxia-inducible factor 1α in sunitinib-resistant renal cell carcinoma

Multitargeted receptor tyrosine kinase inhibitors, including vascular endothelial growth factor (VEGF) inhibitors, such as sunitinib, have been used as the primary targeted agents for patients with recurrent or distant metastasis of advanced renal cell carcinoma (RCC). However, endogenous or acquired sunitinib resistance has become a significant therapeutic problem. Therefore, we focused on mechanisms of sunitinib resistance in RCC. First, we undertook RNA sequencing analysis using previously established sunitinib-resistant RCC (SUR-Caki1, SUR-ACHN, and SUR-A498) cells. The results showed increased expression of secretogranin II (SCG2, chromogranin C) in SUR-RCC cells compared to parental cells. The Cancer Genome Atlas database showed that SCG2 expression was increased in RCC compared to normal renal cells. In addition, the survival rate of the SCG2 high-expression group was significantly lower than that of the RCC low-expression group. Thus, we investigated the involvement of SCG2 in sunitinib-resistant RCC. In vitro analysis showed that migratory and invasive abilities were suppressed by SCG2 knockdown SUR cells. As SCG2 was previously reported to be associated with angiogenesis, we undertook a tube formation assay. The results showed that suppression of SCG2 inhibited angiogenesis. Furthermore, coimmunoprecipitation assays revealed a direct interaction between SCG2 and hypoxia-inducible factor 1α (HIF1α). Expression levels of VEGF-A and VEGF-C downstream of HIF1α were found to be decreased in SCG2 knockdown SUR cells. In conclusion, SCG2 could be associated with sunitinib resistance through VEGF regulation in RCC cells. These findings could lead to a better understanding of the VHL/HIF/VEGF pathway and the development of new therapeutic strategies for sunitinib-resistant RCC.