Various types of tumors can affect the subungual space, including benign solid tumors (glomus tumor, subungual exostosis, soft-tissue chondroma, keratoacanthoma, hemangioma, lobular capillary hemangioma), benign cystic lesions (epidermal and mucoid cysts), and malignant tumors (squamous cell carcinoma, malignant melanoma). Imaging plays an important role in the detection and differentiation of subungual tumors because of their small size, nonspecific clinical manifestations, and functional significance. Ultrasonography (US)-in particular, high-resolution US with color Doppler studies-provides useful information regarding tumor size, location, shape, and internal characteristics (cystic, solid, or mixed), but it is limited in the further characterization of tissue. Magnetic resonance (MR) imaging has an important role in categorizing tumors according to their anatomic location, pathologic origin, and signal characteristics. There is some overlap between the US and MR imaging features of subungual tumors; however, certain features can allow accurate diagnosis and expedite management when correlated with clinical and pathologic findings.

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The features of heterogeneous echotexture, internal echogenic foci in scattered-dot pattern, and a hypoechoic rim or posterior shadowing itself could be discriminative ultrasonographic criteria for differentiating pilomatricomas from other subcutaneous tumors.

Many factors are associated with the development of low back pain. Among them, exercise, obesity, smoking, age, educational level and stress are the most common. This study examined the association of these factors with low back pain. An additional aim was to determine a procedure for preventing low back pain. This study analyzed the responses to a questionnaire sent to 772 individuals who had undergone a medical examination at this hospital in 2003 and excluded the individuals who had shown symptoms or their test results indicated a particular disease. Assuming that there were no variables, individuals who exercised regularly 3-4 times per week would have a lower chance of having low back pain than those who did not exercise regularly. The analysis revealed that individuals with a college degree or higher education have a lower chance of experiencing low back pain than those with only a high school education or even college drop-outs. When the other variables were constant, age, extent of obesity (body mass index), smoking and level of stress were not found to affect the development of low back pain. The level of education was associated with the development of low back pain. However, regular exercise 3-4 times per week or more would be most effective in reducing the incidence and duration of low back pain.

A number of therapeutic strategies for treating Alzheimer's disease have focused on reducing amyloid burden in the brain. Amongst these approaches, the expression of amyloid β peptide (Aβ)-degrading enzymes in the brain has been shown to be effective, but to date not practical for treating patients. We report here a novel strategy for lowering amyloid burden in the brain by peripherally expressing the Aβ-degrading enzyme neprilysin on leukocytes in the 3×Tg-AD mouse model of Alzheimer's disease. Through transplantation of lentivirus transduced bone marrow cells, the Aβ-degrading protease neprilysin was expressed on the surface of leukocytes. This peripheral neprilysin reduced soluble brain amyloid β peptide levels by ~30% and lowered the accumulation of amyloid β peptides by 50-60% when transplantation was performed at both young and early adult age. In addition, peripheral neprilysin expression reduced amyloid dependent performance deficits as measured by the Morris Water Maze. Unlike other methods designed to lower amyloid β peptide levels in blood, which cause a net increase in peptide, neprilysin expression results in the catabolism of the amyloid β peptide to small innocuous peptide fragments. These findings demonstrate that peripherally expressed neprilysin, and likely other amyloid β peptide degrading enzymes, has the potential for being utilized as a therapeutic approach to prevent and treat Alzheimer's disease and suggest this approach should be further explored.

Independently of the lipid-lowering effects, statin has been reported to attenuate the development of diabetic cardiomyopathy. However, the effect of statin in glucose-controlled diabetic condition has not been demonstrated. We evaluated the effect of fluvastatin on cardiac function, fibrosis, and angiotensin-converting enzyme-2 (ACE2) expression in glucose-controlled diabetic rats. Male Wistar rats were randomly divided into four groups: control (Group C), diabetes (Group D), diabetes with insulin (Group I), and diabetes with insulin and fluvastatin (Group I+F). Diabetes was induced by a single injection of streptozotocin (65 mg/kg). After 8 weeks, the hearts were extracted following echocardiographic evaluation. Cardiac fibrosis was analyzed using Masson's trichrome stain. Collagens I and III and ACE2 expressions were evaluated by immunohistochemistry and western blot. Group D showed reduced cardiac systolic function compared to the other groups (all P < 0.05). However, diastolic function estimated by E/A ratio was significantly decreased in groups D and I (median: 0.88 and 1.45, respectively) compared to groups C and I+F (2.97 and 2.15) (all P < 0.05). Cardiac fibrosis was more severe in groups D and I than in groups C and I+F (all P < 0.05) on Masson's trichrome stain. On immunohistochemistry, ACE2 expression was significantly decreased only in group D (all P < 0.05). However, collagen I and III showed higher expressions in group D compared to groups C and I+F while no significant difference was observed compared with group I (all P < 0.05). On western blot, collagen I and ACE2 expressions in group D (median: 1.78 and 0.35, respectively) were significantly different from groups C (references: 1) and I+F (0.76 and 1.21) (all P < 0.05), but not from group I (1.19 and 0.92). Our study suggested a combination of fluvastatin and insulin would be more effective than insulin alone in diabetic hearts. However, the exact mechanism remains to be elucidated.

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