Study on the effects of arm abduction angle and cushion support during sonographic examination on the stiffness of supraspinatus muscle of sonographers using shear wave elastography.

OBJECTIVES: The incidence of work-related musculoskeletal disorder remains high in sonography. The aims of this study are to determine the changes in muscle stiffness with different arm abduction angles, and to investigate the effect of cushion support on reducing muscle load in the supraspinatus when sonographers scan with the arm abducted to different angles. METHODS: This is a prospective crossover study. Twenty-three healthy female subjects aged between 20 and 23 years were included. Subjects were instructed to simulate performing standardized abdominal ultrasound scans. The changes in muscle stiffness of supraspinatus, measured as shear modulus, at rest and at 30°, 45°, and 60° arm abduction angles with and without cushion support were evaluated using shear-wave elastography. Styrofoam support was used for the cushion support. RESULTS: Mean shear moduli of supraspinatus were 27.77 ± 5.84 kPa at rest and 41.63 ± 7.09 kPa, 63.88 ± 14.43 kPa, and 89.76 ± 16.55 kPa for 30°, 45°, and 60° arm abduction respectively, which corresponds to 53%, 116% increase in muscle stiffness when scanning arm abducted from 30° to 45° and 60° (p < .001). After applying cushion support, shear moduli dropped to 24.04 ± 5.60 kPa, 31.98 ± 6.06 kPa, 37.47 ± 5.61 kPa for arm abducted to 30°, 45°, and 60° respectively (p < .001). The muscle stiffnesses between 30° abduction without support and 60° abduction with support had no significant difference (p > .05). CONCLUSIONS: Muscle stiffness of supraspinatus increased with increasing arm abduction angle during ultrasound scanning. Utilizing cushion support underneath the arm was effective in reducing muscle stiffness in supraspinatus. Our results provide scientific justification on postural modifications for sonographers.

Piper sarmentosum Roxb. Attenuates Beta Amyloid (Aß)-Induced Neurotoxicity Via the Inhibition of Amyloidogenesis and Tau Hyperphosphorylation in SH-SY5Y Cells.

BACKGROUND: In Alzheimer's disease, accumulation of beta amyloid (Aß) triggers amyloidogenesis and hyperphosphorylation of tau protein leading to neuronal cell death. Piper sarmentosum Roxb. (PS) is a traditional medicinal herb used by Malay to treat rheumatism, headache and boost memory. It possesses various biological effects, such as anti-cholinergic, anti-inflammatory, anti-oxidant and anti-depressant-like effects. OBJECTIVE: The present study aimed to investigate neuroprotective properties of PS against Aß-induced neurotoxicity and to evaluate its potential mechanism of action. METHODS: Neuroprotective effects of hexane (HXN), dichloromethane (DCM), ethyl acetate (EA) and methanol (MEOH) extracts from leaves (L) and roots (R) of PS against Aß-induced neurotoxicity were investigated in SH-SY5Y human neuroblastoma cells. Cells were pre-treated with PS for 24 h followed by 24 h of induction with Aß. The neuroprotective effects of PS were studied using cell viability and cellular reactive oxygen species (ROS) assays. The levels of extracellular Aß and tau proteins phosphorylated at threonine 231 (pT231) were determined. Gene and protein expressions were assessed using qRT-PCR analyses and western blot analyses, respectively. RESULTS: Hexane extracts of PS (LHXN and RHXN) protected SH-SY5Y cells against Aß-induced neurotoxicity, and decreased levels of extracellular Aß and phosphorylated tau (pT231). Although extracts of PS inhibited Aß-induced ROS production, it was unlikely that neuroprotective effects were simply due to the anti-oxidant capacity of PS. Further, mechanistic study suggested that the neuroprotective effects of PS might be due to its capability to regulate amyloidogenesis through the downregulation of BACE and APP. CONCLUSION: These findings suggest that hexane extracts of PS confer neuroprotection against Aß- induced neurotoxicity in SH-SY5Y cells by attenuating amyloidogenesis and tau hyperphosphorylation. Due to its neuroprotective properties, PS might be a potential therapeutic agent for Alzheimer's disease.

Soluble CD146 Is a Novel Marker of Systemic Congestion in Heart Failure Patients: An Experimental Mechanistic and Transcardiac Clinical Study.

BACKGROUND: Soluble CD146 (sCD146), is an endothelial marker with similar diagnostic power as natriuretic peptides in decompensated heart failure (HF). While natriuretic peptides are released by the failing heart, sCD146 may be released by veins in response to stretch induced by systemic congestion in HF. This study investigated the source, effects of vascular stress on release and prognostic properties of sCD146 in HF. METHODS: In a peripheral venous stress study, plasma concentrations of sCD146 and N-terminal probrain natriuretic-peptide (NT-proBNP) were measured in 44 HF patients at baseline and after 90 min of unilateral forearm venous congestion. In addition, sCD146 and NT-proBNP were measured in peripheral vein (PV) and coronary sinus (CS) blood samples of 137 HF patients and the transcardiac gradient was calculated. Those patients were followed for major adverse cardiovascular events (MACE) during 2 years. RESULTS: The induction of venous stress was associated with a pronounced increase in circulating concentrations of sCD146 in the congested arm (+60 µg/L) compared to the control arm (+16 µg/L, P = 0.025), while no difference in NT-proBNP concentrations was seen. In contrast to positive transcardiac gradient for NT-proBNP, median sCD146 concentrations were lower in CS than in PV (396 vs 434, P < 0.001), indicating a predominantly extracardiac source of sCD146. Finally, increased PV concentrations of sCD146 were associated with higher risk of MACE at 2 years. CONCLUSIONS: Soluble CD146 is released from the peripheral vasculature in response to venous stretch and may reflect systemic congestion in chronic HF patients.