This study aimed to investigate the effects of suboccipital muscle inhibition technique (SMIT) on active range of motion (AROM) of the ankle joint, lunge angle (LA), and balance in healthy adults, according to the duration of its application. A total of 80 participants were randomly allocated to the 4-min suboccipital muscle inhibition (SMI) group (SMI_4M, n = 20), 8-min SMI group (n = 20), 4-min sham-SMI (SSMI) group (n = 20), and 8-min SSMI group (n = 20). Accordingly, the SMIT and sham SMIT were applied for 4 min or 8 min in the respective groups. AROM of dorsiflexion and LA were assessed, and a single leg balance test (SLBT) was performed before and after the intervention. AROM (4 min, p < 0.001; 8 min, p < 0.001), LA (4 min, p < 0.001; 8 min, p < 0.001), and SLBT (4 min, p < 0.001; 8 min, p < 0.001) significantly improved after SMI application. Compared with the SSMI group, the SMI group showed a significant increase in AROM (p < 0.001), LA (p < 0.001), and SLBT (p < 0.001). Except for SLBT (p = 0.016), there were no significant interactions between intervention and application duration. The results suggest that the SMIT, at durations of both 4 and 8 min, could be effective tools for improving AROM, LA, and balance.

Although methyl-tertiary butyl ether (MTBE) is the only clinical topical agent for gallstone dissolution, its use is limited by its side effects mostly arising from a relatively low boiling point (55 °C). In this study, we developed the gallstone-dissolving compound containing an aromatic moiety, named 2-methoxy-6-methylpyridine (MMP) with higher boiling point (156 °C), and compared its effectiveness and toxicities with MTBE. The dissolubility of MTBE and MMP in vitro was determined by placing human gallstones in glass containers with either solvent and, then, measuring their dry weights. Their dissolubility in vivo was determined by comparing the weights of solvent-treated gallstones and control (dimethyl sulfoxide)-treated gallstones, after directly injecting each solvent into the gallbladder in hamster models with cholesterol and pigmented gallstones. In the in vitro dissolution test, MMP demonstrated statistically higher dissolubility than did MTBE for cholesterol and pigmented gallstones (88.2% vs. 65.7%, 50.8% vs. 29.0%, respectively; P < 0.05). In the in vivo experiments, MMP exhibited 59.0% and 54.3% dissolubility for cholesterol and pigmented gallstones, respectively, which were significantly higher than those of MTBE (50.0% and 32.0%, respectively; P < 0.05). The immunohistochemical stains of gallbladder specimens obtained from the MMP-treated hamsters demonstrated that MMP did not significantly increase the expression of cleaved caspase 9 or significantly decrease the expression of proliferation cell nuclear antigen. This study demonstrated that MMP has better potential than does MTBE in dissolving gallstones, especially pigmented gallstones, while resulting in lesser toxicities.

Sun WY, et al. J Breast Cancer. 2025 Mar;28:e11. https://doi.org/10.4048/jbc.2024.0262

Tumor necrosis factor-α (TNF-α)-driven inflammatory reaction plays a crucial role in the initiation of liver fibrosis. We herein attempted to design genetically engineered adipose-derived stem cells (ASCs) producing etanercept (a potent TNF-α inhibitor), and to determine the anti-fibrotic potential of the secretome released from the etanercept-synthesizing ASCs (etanercept-secretome). First, we generated the etanercept-synthesizing ASCs by transfecting the ASCs with mini-circle plasmids containing the gene insert encoding for etanercept. We subsequently collected the secretory material released from the etanercept-synthesizing ASCs and determined its anti-fibrotic effects both in vitro (in thioacetamide [TAA]-treated AML12 and LX2 cells) and in vivo (in TAA-treated mice) models of liver fibrosis. We observed that while etanercept-secretome increased the viability of the TAA-treated AML12 hepatocytes (p = 0.021), it significantly decreased the viability of the TAA-treated LX2 HSCs (p = 0.021). In the liver of mice with liver fibrosis, intravenous administration of the etanercept-secretome induced significant reduction in the expression of both fibrosis-related and inflammation-related markers compared to the control group (all Ps < 0.05). The etanercept-secretome group also showed significantly lower serum levels of liver enzymes as well as pro-inflammatory cytokines, such as TNF-α (p = 0.020) and IL-6 (p = 0.021). Histological examination of the liver showed the highest reduction in the degree of fibrosis in the entanercept-secretome group (p = 0.006). Our results suggest that the administration of etanercept-secretome improves liver fibrosis by inhibiting TNF-α-driven inflammation in the mice with liver fibrosis. Thus, blocking TNF-α-driven inflammation at the appropriate stage of liver fibrosis could be an efficient strategy to prevent fibrosis.

The variations in the tibialis posterior tendon (TPT) could not be defined by previous classification; thus, this study used a larger-scale cadaver with the aim to classify the types of TPT insertion based on the combination of the number and location of TPT insertions. A total of 118 feet from adult formalin-fixed cadavers were dissected (68 males, 50 females). The morphological characteristics and measurements of TPT insertion were evaluated. Four types of TPT insertions were classified, wherein the most common type was type 4 (quadruple insertions, 78 feet, 66.1%), which was divided into four new subtypes that were not defined in the previous classification. The second most common type was type 3 (triple insertions, 25 feet, 21.2%) with three subtypes, including the new subtype. Type 2 was found in 13 feet (11%), and the rarest type was type 1 (2 feet, 1.7%), wherein the main tendon was only attached to the navicular bone and the medial cuneiform bone. We suggest high morphological variability of the TPT in relation to the insertion location, along with the possibility of significant differences according to race and gender. Moreover, this classification will help clinicians understand adult flatfoot deformity-related posterior tibial tendon dysfunction (PTTD).