Computer-aided detection in musculoskeletal projection radiography: A systematic review

ObjectivesTo investigated the accuracy of computer-aided detection (CAD) software in musculoskeletal projection radiography via a systematic review.Key findingsFollowing selection screening, eligible studies were assessed for bias, and had their study characteristics extracted resulting in 22 studies being included. Of these 22 three studies had tested their CAD software in a clinical setting; the first study investigated vertebral fractures, reporting a sensitivity score of 69.3% with CAD, compared to 59.8% sensitivity without CAD. The second study tested dental caries diagnosis producing a sensitivity score of 68.8% and specificity of 94.1% with CAD, compared to sensitivity of 39.3% and specificity of 96.7% without CAD. The third indicated osteoporotic cases based on CAD, resulting in 100% sensitivity and 81.3% specificity.ConclusionThe current evidence reported shows a lack of development into the clinical testing phase; however the research does show future promise in the variation of different CAD systems.     

Imaging update on soft tissue sarcoma

Soft tissue sarcomas (STS) are rare tumours presenting as soft tissue lumps. Ultrasound is often the primary modality for the initial assessment, with MRI the mainstay for lesion characterisation. PET/CT along with other emerging MRI sequences are used in certain situations as an adjunct and problem solving tool in STS staging and assessment of disease recurrence. Recent advances include the promise of whole body MRI, hybrid PET/MRI, diffusion weighted imaging, dynamic contrast enhanced MRI and advances in artificial intelligence. This article discusses current concepts in extremity STS imaging and highlights recent advances.     

Lysophosphatidic acid-induced IL-8 secretion involves MSK1 and MSK2 mediated activation of CREB1 in human fibroblast-like synoviocytes

Lysophosphatidic acid (LPA) is a pleiotropic lipid mediator that promotes motility, survival, and the synthesis of chemokines/cytokines such as interleukin-8 (IL-8) and interleukin-6 by human fibroblast-like synoviocytes from patients with rheumatoid arthritis (RAFLS). In those cells LPA was reported to induce IL-8 secretion through activation of various signaling pathways including p38 mitogen-activated protein kinase (p38 MAPK), p42/44 MAPK, and Rho kinase. In addition to those pathways we report that mitogen- and stress-activated protein kinases (MSKs) known to be activated downstream of the ERK1/2 and p38 MAPK cascades and CREB are phosphorylated in response to LPA. The silencing of MSKs with small-interfering RNAs and the pharmacological inhibitor of MSKs SB747651A shows a role for both MSK1 and MSK2 in LPA-mediated phosphorylation of CREB at Ser-133 and secretion of IL-8 and MCP-1. Whereas CREB inhibitors have off target effects and increased LPA-mediated IL-8 secretion, the silencing of CREB1 with short hairpin RNA significantly reduced LPA-induced chemokine production in RAFLS. Taken together the data clearly suggest that MSK1 and MSK2 are the major CREB kinases in RAFLS stimulated with LPA and that phosphorylation of CREB1 at Ser-133 downstream of MSKs plays a significant role in chemokine production.     

MSK1和RSK2介导的组蛋白磷酸化对人结直肠癌细胞恶性表型的影响

背景:ERK-MAPK信号通路与消化系肿瘤的发生、发展密切相关。前期研究发现抑制ERK-MAPK信号转导可能通过抑制其下游效应分子MSK1、RSK2活性而降低组蛋白H3磷酸化水平,进而下调原癌蛋白c-fos表达,抑制人结直肠癌细胞增殖。目的:探讨MSK1、RSK2与组蛋白磷酸化对人结直肠癌细胞肿瘤相关基因表达和恶性表型的影响。方法:以不同浓度ERK-MAPK阻断剂U0126干预人结肠癌细胞株HCT1 16和SW11 16,或以RNA干扰技术靶向沉默细胞中的MSK1、RSK2表达,分别采用CCK-8实验、流式细胞分析和蛋白质印迹法检测经不同处理的肿瘤细胞的增殖情况、细胞周期分布以及MSK1、RSK2磷酸化位点、组蛋白H3磷酸化水平和MSK1、RSK2、c-fos蛋白表达。结果:U0126能阻断人结直肠癌细胞MSK1(Thr581)、RSK2(Ser386)的磷酸化活化,转染MSK1 siRNA或RSK2 siRNA能特异性抑制MSK1、RSK2表达,导致组蛋白H3(Set10)磷酸化水平降低,c-fos蛋白表达下调,肿瘤细胞发生G0/G1期阻滞,细胞增殖显著受抑(P均<0.05)。结论:阻断ERK-MAPK信号转导可能通过抑制MSK1(Thr581)、RSK2(Ser386)磷酸化活化及其介导的组蛋白H3磷酸化而下调肿瘤相关基因如c-fos表达,从而抑制人结直肠癌细胞的恶性表型。     

Muscle thickness and echo-intensity changes of the quadriceps femoris muscle during a strength training program

IntroductionUltrasound (US) has an important role in musculoskeletal (MSK) evaluation, allowing the study of muscle morphology and function. Muscle thickness (MT) and muscle echo-intensity (EI) are two important parameters that may quantify muscle structural adaptations to a variety of stimuli. The aim was to explore the potential of quantitative US imaging for assessing the adaptations and responses of the muscle tissue to increased contractile activity using B-mode US. This study was centred on the quadriceps femoris muscle contractile activity on MT and EI.Methods and materialsTwenty-eight young male adults participated in the study, divided in a control group and two training groups performing concentric or eccentric strength training, respectively. The effect of a 15-week strength program was studied on MT and EI in several regions of the heads of the quadriceps femoris using B-mode US. All images acquisitions and measurements were done by the same experience sonographer.ResultsStrength training resulted in an increase of MT at all muscles and sites (p < 0.05), except the VM. Strength training failed in changing EI in most of the quadriceps femoris, except in the VI and some regions of the VL. No statistically significant differences were observed in our quantitative US parameters between concentric and eccentric training (p > 0.05).ConclusionThese results emphasise the value of MT as a quantifiable muscle US method for evaluating muscle adaptation to exercise training. However, the inconsistency of the EI values indicates that more studies are needed to develop it as an accurate diagnostic tool.     

Inhibition of the Rho/ROCK pathway prevents neuronal degeneration in vitro and in vivo following methylmercury exposure

Methylmercury (MeHg) is an environmental neurotoxicant which induces neuropathological changes in both the central nervous and peripheral sensory nervous systems. Our recent study demonstrated that down-regulation of Ras-related C3 botulinum toxin substrate 1 (Rac1), which is known to promote neuritic extension, preceded MeHg-induced damage in cultured cortical neurons, suggesting that MeHg-mediated axonal degeneration is due to the disturbance of neuritic extension. Therefore we hypothesized that MeHg-induced axonal degeneration might be caused by neuritic extension/retraction incoordination. This idea brought our attention to the Ras homolog gene (Rho)/Rho-associated coiled coil-forming protein kinase (ROCK) pathway because it has been known to be associated with the development of axon and apoptotic neuronal cell death. Here we show that inhibition of the Rho/ROCK pathway prevents MeHg-intoxication both in vitro and in vivo. A Rho inhibitor, C3 toxin, and 2 ROCK inhibitors, Fasudil and Y-27632, significantly protected against MeHg-induced axonal degeneration and apoptotic neuronal cell death in cultured cortical neuronal cells exposed to 100 nM MeHg for 3 days. Furthermore, Fasudil partially prevented the loss of large pale neurons in dorsal root ganglia, axonal degeneration in dorsal spinal root nerves, and vacuolar degeneration in the dorsal columns of the spinal cord in MeHg-intoxicated model rats (20 ppm MeHg in drinking water for 28 days). Hind limb crossing sign, a characteristic MeHg-intoxicated sign, was significantly suppressed in this model. The results suggest that inhibition of the Rho/ROCK pathway rescues MeHg-mediated neuritic extension/retraction incoordination and is effective for the prevention of MeHg-induced axonal degeneration and apoptotic neuronal cell death.