Force trace characteristics in anterior cruciate ligament deficient and uninjured knees during a maximal isometric task

Anterior cruciate ligament (ACL) deficiency has been shown to alter the muscle function of the leg. This study aimed to investigate differences in force trace characteristics of a maximal isometric task between ACL deficient and uninjured knees. Six ACL injured and uninjured participants completed maximal adduction, extension, and flexion isometric contractions. Peak, mean, standard deviation (SD), coefficient of variance (CV), frequency and signal regularity were calculated for all trials. Mean flexion force was larger in the ACL intact (0.91 N/kg) compared to their deficient (0.67 N/kg; p<0.05) knee. SD, CV and frequency composition of the extension trial differed between limbs in the uninjured (p<0.05). Analysis of variability, frequency and regularity of a signal may provide information on the function of the knee

Force trace characteristics in anterior cruciate ligament deficient and uninjured knees during a maximal isometric task

Anterior cruciate ligament (ACL) deficiency has been shown to alter the muscle function of the leg. This study aimed to investigate differences in force trace characteristics of a maximal isometric task between ACL deficient and uninjured knees. Six ACL injured and uninjured participants completed maximal adduction, extension, and flexion isometric contractions. Peak, mean, standard deviation (SD), coefficient of variance (CV), frequency and signal regularity were calculated for all trials. Mean flexion force was larger in the ACL intact (0.91 N/kg) compared to their deficient (0.67 N/kg; p<0.05) knee. SD, CV and frequency composition of the extension trial differed between limbs in the uninjured (p<0.05). Analysis of variability, frequency and regularity of a signal may provide information on the function of the knee

Therapeutic modulators of hepatic stellate cells for hepatocellular carcinoma

Hepatocellular carcinoma (HCC) is the most common type of primary tumor in the liver and is a leading cause of cancer-related death worldwide. Activated hepatic stellate cells (HSCs) are key components of the HCC microenvironment and play an important role in the onset and progression of HCC through the secretion of growth factors and cytokines. Current treatment modalities that include chemotherapy, radiotherapy and ablation are able to activate HSCs and remodel the tumor microenvironment. Growing evidence has demonstrated that the complex interaction between activated HSCs and tumor cells can facilitate cancer chemoresistance and metastasis. Therefore, therapeutic targeting of activated HSCs has emerged as a promising strategy to improve treatment outcomes for HCC. This review summarizes the molecular mechanisms of HSC activation triggered by treatment modalities, the function of activated HSCs in HCC, as well as the crosstalk between tumor cells and activated HSCs. Pathways of activated HSC reduction are discussed, including inhibition, apoptosis, and reversion to the inactivated state. Finally, we outline the progress and challenges of therapeutic approaches targeting activated HSCs in the development of HCC treatment.Qi Ruan, Haolu Wang, Leslie J. Burke, Kim R. Bridle, Xinxing Li, Chun-Xia Zhao, Darrell H.G. Crawford, Michael S. Roberts, and Xiaowen Lian