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The purpose of this study was to investigate the site- and sex-differences in the morphological and mechanical properties of the plantar fascia (PF) in humans. The thickness and shear wave velocity (SWV) of PF at five different sites between the medial calcaneal tubercle and the second toe were measured for 40 healthy young participants (20 males and 20 females) using supersonic shear imaging (SSI). The thickness and SWV measurements were highly repeatable (ICC ≥ 0.93). The proximal sites of PF around the calcaneal attachment were significantly thicker and stiffer (higher SWV values) than the middle and distal sites (p < 0.05). In addition, females had significantly thinner PF in proximal and middle sites than males, while being significantly stiffer in regardless of the sites, compared with males (p < 0.05). The results of the present study partly support previous findings on the site- and sex-differences in PF morphology, and further reveal inhomogeneity and sex-specificity of PF stiffness. The present study widely opens the possibility of evaluating PF functions in vivo.

Non-small cell lung cancer (NSCLC) accounts for most lung cancer diagnoses. Statins preferentially inhibit the proliferation of mesenchymal- over epithelial-like cells in various types of cancer, including NSCLCs. However, the mechanisms underlying the differential statin sensitivity of mesenchymal and epithelial cancer cells remain unknown. Statins inhibit YAP/TAZ, effectors of the Hippo pathway, via depletion of geranylgeranyl pyrophosphate. Here, we aimed to elucidate the mechanisms underlying statin sensitivity in mesenchymal cancer. We explored the anticancer effects of atorvastatin and its association with YAP/TAZ activity in NSCLC cell lines with different epithelial-mesenchymal phenotypes. Atorvastatin significantly reduced the proliferation, migration, and invasion of mesenchymal-like cells, while showing negligible effect on epithelial-like cells. Atorvastatin also inhibited YAP/TAZ nuclear localization and downstream gene expression in mesenchymal cells but did not affect epithelial cells. Small interfering (si) RNA-mediated inhibition of both YAP and TAZ reduced the proliferation of all NSCLC cell lines tested, regardless of phenotype, indicating that sensitivity to YAP/TAZ inhibition and statins differ. In summary, our results suggest that inhibited YAP/TAZ nuclear localization by statins differs between epithelial and mesenchymal NSCLC cell lines, resulting in differential statin sensitivity.

Human steady-state locomotion modes are symmetrical, leading to symmetric mechanical function of human feet in general; however, track distance running in a counterclockwise direction exposes the runner’s feet to asymmetrical stress. This may induce asymmetrical adaptation in the runners’ foot arch functions, but this has not been experimentally tested. Here, we show that the plantar fascia (PF), a primary structure of the foot arch elasticity, is stiffer for the left than the right foot as a characteristic of runners, via a cross-sectional study on 10 track distance runners and 10 untrained individuals. Shear wave velocity (index of tissue stiffness: SWV) and thickness of PF and foot dimensions were compared between sides and groups. Runners showed higher PF SWV in their left (9.4 ± 1.0 m/s) than right (8.9 ± 0.9 m/s) feet, whereas untrained individuals showed no bilateral differences (8.5 ± 1.5 m/s and 8.6 ± 1.7 m/s, respectively). Additionally, runners showed higher left to right (L/R) ratio of PF SWV than untrained men (105.1% and 97.7%, respectively). PF thickness and foot dimensions were not significantly different between sides or groups. These results demonstrate stiffer PF in the left feet of runners, which may reflect adaptation to their running-specific training that involves asymmetrical mechanical loading.

The iliotibial band (ITB) is the lateral thickening of the fascia lata. The ITB has been extensively studied for its relevance to injury, but not much is known about its elastic properties. We aimed to investigate the site- and joint angle-dependence of ITB elasticity. We tested twelve healthy males (22–30 years; in vivo) and twelve male cadavers (69–93 years; cadaver). The Young’s modulus of the ITB was measured in the longitudinal direction at five sites (over the proximal, middle, and distal bellies of the vastus lateralis (VL), superior border of the patella, and between femur and tibia) of the right limb, by ultrasound shear wave elastography (in vivo) and the tensile test (cadaver). Joint angle-dependence was also studied for nine different positions (knee angles at 0, 25, 90˚ x hip angles at 0, 40, 90˚) (in vivo). Over VL, the ITB was more compliant at the distal (17.6–190.1 kPa; in vivo, 219.4 ± 68.8 MPa; cadaver, mean ± SD) than other sites (24.2–221.4 kPa, 337.9–362.7 MPa). The ITB at the superior border of the patella and between femur and tibia was stiffer in vivo (31.8–271.8 and 50.9–208.8 kPa), while it was more compliant in cadavers (113.4 ± 63.7 and 130.4 ± 73.7 MPa), compared to other sites. The ITB became stiffer associated with increasing hip extension angle and knee flexion angle, and the hip remarkably affecting the values regardless of site (in vivo). Our findings have clinical significance with respect to the site- and joint angle-dependence of ITB-related overuse injury.

The human triceps surae (two gastrocnemii and soleus) has aponeuroses in the proximal and distal aspects, the latter of which insert into the calcaneus by sharing the common Achilles tendon. These tendinous tissues are known to have elasticity and upon muscle contraction the aponeurosis is stretched both longitudinally (along the muscle's line of action) and transversely. Higher aponeurosis transverse deformability has been documented, but there is a paucity of information on the morphology and mechanical properties of human aponeurosis. This study aimed to identify morphological and mechanical characteristics of the human triceps surae aponeuroses. Twenty-five triceps surae muscle-tendon units were procured from 13 human donors (formalin fixed, 6 males, 7 females) aged 67-91 years. Specimens of aponeuroses were excised from the eight regions (posterior and anterior regions of the gastrocnemius medialis and lateralis, medial and lateral parts of soleus; proximal, middle, and distal sites each, 2-4 cm × 2-4 cm). Aponeurosis thickness was measured using a digital caliper. Uniaxial tensile tests were implemented to determine the mechanical properties of specimens loaded longitudinally (along the muscle's line of action) and transversely. The aponeurosis thickness showed significant differences between muscles and sites, while Young's modulus showed direction-dependent (longitudinal vs. transverse) differences within sites. Results show different morphology and mechanical properties of aponeuroses between synergist muscles. The reason for site-dependent differences in stiffness is due to a reduced aponeurosis thickness rather than a reduction in the material property. The anisotropic elastic feature (differences between longitudinal and transverse directions) of the aponeuroses was more pronounced than previous in vivo findings, suggesting inherent material design of the aponeurosis that matches three-dimensional contractile behavior of muscle fibers.

Cerebrospinal fluid (CSF) leakage is a rare but severe complication during dacryocystorhinostomy (DCR). Understanding the details of the anatomy of the lacrimal drainage system and skull base is essential to avoid this complication. We examined the positional relationship between the lacrimal sac and skull base using 16 cadavers (22 sides) and using computed tomographic images taken in 81 patients (81 sides). Consequently, the frontal sinus intervened between the lacrimal sac and skull base in 81.8–90.1% of cases. The lacrimal sac fundus and posterior lacrimal crest were far from the skull base/cribriform plate, and the skull base above the lacrimal sac was considerably thick. These results indicate that the risk of skull base injury and consequent CSF leakage during DCR is extremely low. However, surgeons should be cautious of this complication by indirect injury due to a twisting movement of a bone rongeur applied to the maxillary bone during creation of a bony window in patients with no interposition of the frontal and ethmoid sinuses between the lacrimal sac and skull base.

BackgroundEndothelial cells are known to grow on the luminal surface of arteriovenous grafts (AVGs) used in hemodialysis. Although endothelial cells are important for preventing infection, a detailed growth of endothelial cells in AVGs is unknown. This study sought to create a simpler animal model of AVGs and to investigate how endothelial cells form on the luminal surface.MethodsPolyethylene grafts were placed between the cervical artery and vein of Wistar rats. The grafts were removed at 6 h, 24 h, 3 days, or 7 days after placement. The luminal surface was observed under optical and polarizing microscopy and stained with endothelial cell markers (LEL, CD31), the progenitor cell marker CD34, and the macrophage marker ED-1.ResultsMicroscopy demonstrated many diffuse vascular endothelial cells on the luminal surface of AVGs after placement. While there was no difference in the number of LEL-positive cells between the arterial side (AS) and venous side (VS) at 6 h or 7 days, there were significantly more of these cells on the VS at both 24 h and 3 days (p < 0.05). Analysis at 24 h showed some CD31-positive cells and few CD34-positive cells.ConclusionsThis was the first study to use a simple rat model of AVG placement. Endothelial cell formation was initially more active on the VS than on the AS, but these cells subsequently increased in number across the luminal surface. Future clinical studies might contribute clinically by confirming whether AS versus VS puncture results in different infection rates.

Chronic subdural hematoma (CSDH) is an angiogenic disease that is involved with many inflammatory mediators. Tie2 is predominantly expressed in the embryonic endothelium and plays an important role in the maturation and stabilization of the vasculature. Angiopoietin (Ang)1 and Ang2 are well-known ligands of the Tie2 receptor. We examined the expression of Ang1 and Ang2 in CSDH fluid and the expression of Tie-2 receptor and components of the angiogenic signaling pathways in the outer membrane of CSDH. Twenty-five samples of CSDH fluid and eight samples of outer membrane of CSDH were included. The concentrations of Ang1 and Ang2 in the CSDH fluid were measured using enzyme-linked immunosorbent assay (ELISA) kits. The expression of Tie2, phosphoinositide 3-kinase (PI3K), protein kinase B (Akt) mechanistic target of rapamycin (mTOR), GβL, 70 kDa ribosomal protein S6 kinase (p70S6K), eukaryotic initiation factor 4E (eIF-4E), and β-actin was examined by a Western blot analysis. The expression of Tie2, Akt, and mTOR was also examined by immunohistochemistry. The concentration of Ang2 in CSDH fluid was significantly higher than that in the serum or cerebrospinal fluid (CSF), and also higher than that of Ang1 in CSDH fluid. Tie2, PI3K, Akt, mTOR, GβL, p70S6K, and eIF-4E were detected in all cases. In addition, Tie2, Akt, and mTOR were localized in the endothelial cells of vessels in the CSDH outer membrane. Our data suggest that Ang2, although not Ang1, in CSDH fluid promotes angiogenesis in endothelial cells through the Tie2 receptor. The Ang2/Tie2 signaling pathway might therefore be a useful therapeutic target for treating the growth of intractable CSDH.

Background Sprengel’s deformity is a congenital abnormality of the shoulder girdle. Because scapular retraction, such as the Green procedure, is usually performed during childhood to improve esthetics and shoulder function, Sprengel’s deformity is rarely found in older patients. Case presentation We presented a unique case of a Japanese female cadaver with Sprengel’s deformity at the age of 80 years. Anatomical dissection and radiological imaging revealed musculoskeletal anomalies associated with Sprengel’s deformity, including Klippel–Feil syndrome, presence of an omovertebral bone, and absence of the trapezius muscle. In addition, bilateral cervical ribs were in contact with the brachial plexus. These anomalies may lead to numbness, pain, and limited range of motion of the neck and upper girdle with aging. Conclusions Because most adult patients with Sprengel’s deformity experience neck pain and limited movement of the shoulder, the presented case is a rare case of neglected Sprengel’s deformity in an 80-year-old cadaver.

Peritoneal membrane dysfunction in peritoneal dialysis (PD) is primarily attributed to angiogenesis; however, the integrity of vascular endothelial cells can affect peritoneal permeability. Hyaluronan, a component of the endothelial glycocalyx, is reportedly involved in preventing proteinuria in the normal glomerulus. One hypothesis suggests that development of encapsulating peritoneal sclerosis (EPS) is triggered by protein leakage due to vascular endothelial injury. We therefore investigated the effect of hyaluronan in the glycocalyx on peritoneal permeability and disease conditions. After hyaluronidase-mediated degradation of hyaluronan on the endothelial cells of mice, macromolecules, including albumin and β2 microglobulin, leaked into the dialysate. However, peritoneal transport of small solute molecules was not affected. Pathologically, hyaluronan expression was diminished; however, expression of vascular endothelial cadherin and heparan sulfate, a core protein of the glycocalyx, was preserved. Hyaluronan expression on endothelial cells was studied using 254 human peritoneal membrane samples. Hyaluronan expression decreased in patients undergoing long-term PD treatment and EPS patients treated with conventional solutions. Furthermore, the extent of hyaluronan loss correlated with the severity of vasculopathy. Hyaluronan on endothelial cells is involved in the peritoneal transport of macromolecules. Treatment strategies that preserve hyaluronan in the glycocalyx could prevent the leakage of macromolecules and subsequent related complications.