The Volume of Subscapularis Muscle Remains Unaffected by Supraspinatus Tendon Tears: Three-dimensionally Reconstructed Magnetic Resonance Imaging Analysis.

BACKGROUND: This study aimed to compare the subscapularis muscle volume between the intact groups (group I) and supraspinatus tendon tear groups (group T) based on the sex and three different age groups. METHODS: Subjects with a group I and subjects with group T without any other lesions were retrospectively evaluated from among patients who received a magnetic resonance imaging (MRI) scan between January 2011 and December 2013. The MRI scans were studied by a consultant radiologist. The subscapularis muscle volume was compared according to the age and sex; the age groups were categorized as patients in their 40s, 50s, and 60s. The volume of subscapularis muscle was measured by three-dimensional reconstructed images acquired through the axial section of 1.5T MRI. RESULTS: No statistically significant differences were observed between subscapularis muscle volume of the group I and group T, except for male patients in their 50s (group I: 100,650 mm3 vs. group T: 106,488 mm3) and 60s (group I: 76,347 mm3 vs. group T: 99,549 mm3) (p<0.05). Males had a larger mean volume of subscapularis muscle than females, and the subscapularis muscle volume decreased in a linear manner with increasing age. CONCLUSIONS: Decrease in subscapularis muscle volume was observed with increasing age, and the impact of supraspinatus tear on subscapularis muscle volume is age and sex dependent.

Three-dimensional Capsular Volume Measurements in Multidirectional Shoulder Instability.

BACKGROUND: In a previous study undertaken to quantify capsular volume in rotator cuff interval or axillary pouch, significant differences were found between controls and patients with instability. However, the results obtained were derived from two-dimensional cross sectional areas. In our study, we sought correlation between three-dimensional (3D) capsular volumes, as measured by magnetic resonance arthrography (MRA), and multidirectional instability (MDI) of the shoulder. METHODS: The MRAs of 21 patients with MDI of the shoulder and 16 control cases with no instability were retrospectively reviewed. Capsular areas determined by MRA were translated into 3D volumes using 3D software Mimics ver. 16 (Materilise, Leuven, Belgium), and glenoid surface area was measured in axial and coronal MRA views. Then, the ratio between capsular volume and glenoid surface area was calculated, and evaluated with control group. RESULTS: The ratio between 3D capsular volume and glenoid surface area was significantly increased in the MDI group (3.59 ± 0.83 cm3/cm2) compared to the control group (2.53 ± 0.62 cm3/cm2) (p<0.01). CONCLUSIONS: From these results, we could support that capsular volume enlargement play an important role in MDI of the shoulder using volume measurement.

Regulation of RANKL-Induced Osteoclastogenesis by 635-nm Light-Emitting Diode Irradiation Via HSP27 in Bone Marrow-Derived Macrophages.

OBJECTIVE: This study was designed to investigate the effect of 635-nm irradiation from a light-emitting diode (LED) on osteoclastogenesis in receptor activator of nuclear factor kappa-B (NF-κB) ligand (RANKL)-stimulated mouse bone marrow-derived macrophages (BMMs). We determined whether 635-nm irradiation modulated the RANKL-induced osteoclastic signaling pathway in heat shock protein-27 (HSP27)-silenced cells and analyzed the functional cross talk between these factors in osteoclastic differentiation and activation. BACKGROUND: HSP27, a member of the small HSP family, regulates oxidative stress. Clinical reports suggest that low-level laser therapy or LED therapy (LEDT) could be an effective alternative treatment for osteolytic bone disease. METHODS: In control or HSP27-siRNA-treated BMMs, the effects of LED irradiation with 635 nm and 5 mW/cm2 on RANKL-induced osteoclastic differentiation and activity were assessed by measuring tartrate-resistant acid phosphatase (TRAP) and resorption pit formation. Quantitative real-time polymerase chain reaction and western blot assays were carried out to assess the mRNA expression of osteoclastogenesis-related genes and phosphorylation of c-Jun-N-terminal kinase (JNK), extracellular signal-regulated kinase 1/2 (ERK1/2), AKT, and p38, respectively. Intracellular reactive oxygen species (ROS) generation was measured using the 2',7'-dichlorodihydrofluorescein diacetate (H2DCF-DA) detection method. RESULTS: The 635-nm irradiation treatment significantly increased HSP27 expression and decreased intracellular ROS generation, as well as p38 and AKT phosphorylation, leading to reductions in the expression of c-fos, NFATc1, and DC-STAMP and TRAP activation and osteoclastic bone resorption in RANKL-induced BMMs. However, in HSP27-silenced BMMs, no change was observed. CONCLUSIONS: Thus, 635-nm irradiation modulates RANKL-induced osteoclastogenesis via HSP27 in BMMs. Thus, HSP27 may play a role in regulating the osteoclastic response to LEDT.

Activation of mitogen-activated protein kinases in hamster brains infected with 263K scrapie agent.

We investigated the expression, activation and distribution of c-Jun N-terminal kinases (JNKs), p38 mitogen-activated protein kinases (p38 MAPKs) and extracellular signal-regulated kinases (ERKs), using western blotting and immunohistochemistry, in the brains of hamsters infected with 263K scrapie agent, to clarify the role of these kinases in the pathogenesis of prion disease. The immunoblot analysis demonstrated that activation of JNK, p38 MAPK and ERK in whole brain homogenates was increased in infected animals. Phosphorylation of cAMP/calcium responsive element binding protein (CREB), a downstream transcription factor of active ERK, was significantly increased in scrapie-infected hamsters. The immunohistochemical study showed that active ERK was enhanced in infected hamsters compared with controls. Active ERK immunoreactivity was observed within neurons in the dentate gyrus and in glial fibrillary acidic protein (GFAP)-positive reactive astrocytes of infected animals. The expression level of c-Jun mRNA as well as protein, a substrate of active JNK, was increased in infected animals. A significant increase in JNK activity upon glutathione S-transferase (GST)-c-Jun was observed in infected compared with control animals. Phospho-c-Jun immunoreactivity was observed only in neurons of the thalamus in infected groups. These findings indicated that the JNK pathway was activated in the scrapie-infected group. The chronological activation of MAPKs using immunoblot analysis indicates that the kinases are sequentially activated during the pathophysiology of prion disease. Taken together, these results lend credence to the notion that MAPK pathways are dysregulated in prion disease, and also indicate an active role for this pathway in disease pathogenesis.

The expression of RANTES and chemokine receptors in the brains of scrapie-infected mice.

While chemokines play an important role in host defense, it has become abundantly clear that their expression is not solely restricted to immune cells. In this study, to investigate the role of chemokines in pathogenic mechanism of neurodegeneration in prion diseases, we determined the cerebral expression of RANTES, a major chemoattractant of monocytes and activated lymphocytes, and its receptors CCR1, CCR3 and CCR5 in ME7 scrapie-infected mice. The mRNA of RANTES gene was upregulated in the brains of scrapie-infected mice. Intense immunoreactivity of RANTES was observed only in glial fibrillary acidic protein (GFAP)-positive astrocytes of the hippocampus of the infected mice. In addition, the levels of mRNA expression of CCR1, CCR3, and CCR5 were increased in hippocampus of scrapie-infected brains compared to the values in controls. Immunostaining of CCR1, CCR3, and CCR5 was observed in reactive astrocytes of the hippocampal region of scrapie-infected brains. In addition, immunoreactivity of CCR5 was also observed in microglia of scrapie-infected brains. These results suggest that RANTES and its receptors may participate in amplifying proinflammatory responses and, thereby, exacerbate the neurodegeneration of prion diseases.