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Bone marrow edema was not present on initial MR imaging of osteonecrosis. Bone marrow edema should be considered a marker for potential progression to advanced osteonecrosis, and careful examinations for osteonecrosis are necessary when bone marrow edema is seen.

The lubrication mechanism between the human flexor digitorum profundus tendon and the A2 pulley was investigated in vitro. The gliding resistance at the interface between the tendon and the pulley increased significantly after the tendon had been treated with a hyaluronidase solution. Alcian-blue staining of the surface of the tendon before and after it was treated with hyaluronidase suggested the presence of hyaluronate complex. Alcian blue-positive and hyaluronidase-sensitive materials, such as hyaluronate or proteoglycan, in the synovial membrane and the matrix of the tendon, may act as a boundary lubricant, facilitating the gliding and reducing the resistance between the tendon and the pulley.

PR domain-containing 16 (PRDM16) induces expression of brown fat-specific genes in brown and beige adipocytes, although the underlying transcription-related mechanisms remain largely unknown. Here, in vitro studies show that PRDM16, through its zinc finger domains, directly interacts with the MED1 subunit of the Mediator complex, is recruited to the enhancer of the brown fat-specific uncoupling protein 1 (Ucp1) gene through this interaction, and enhances thyroid hormone receptor (TR)-driven transcription in a biochemically defined system in a Mediator-dependent manner, thus providing a direct link to the general transcription machinery.Complementary cell-based studies show that upon forskolin treatment, PRDM16 induces Ucp1 expression in undifferentiated murine embryonic fibroblasts, that this induction depends on MED1 and TR, and, consistent with a direct effect, that PRDM16 is recruited to the Ucp1 enhancer. Related studies have defined MED1 and PRDM16 interaction domains important for Ucp1 versus Ppargc1a induction by PRDM16. These results reveal novel mechanisms for PRDM16 function through the Mediator complex.

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Changes of portal hemodynamics with the progression of chronic liver disease and changes caused by body posture and physical exercise were investigated using an ultrasonic pulsed Doppler flowmeter in healthy adults and in patients with chronic persistent hepatitis, chronic active hepatitis, and cirrhosis. Portal venous velocity was significantly reduced in patients with chronic active hepatitis, cirrhosis without a large splenorenal shunt, and cirrhosis with a large splenorenal shunt, compared with normal subjects and patients with chronic persistent hepatitis. Portal venous flow, by contrast, was significantly reduced only in patients with cirrhosis and a large splenorenal shunt compared with normal subjects and with the other three groups; there was no significant difference in portal venous flow among the latter four groups. Both portal venous velocity and flow showed a tendency toward further reduction in patients with cirrhosis who had hepatofugal flow of part of the superior mesenteric venous blood into the splenic vein and a large splenorenal shunt. Both exercise and posture change from supine to sitting significantly reduced portal venous velocity and portal venous flow in normal subjects, as well as in the patients with chronic liver disease.

To study the effects of habitual alcohol intake on the latency period for the development of liver cirrhosis and hepatocellular carcinoma (HCC), 158 patients with cirrhosis and 79 with HCC were analyzed with respect to age at the time of diagnosis. They were classified into four groups based on hepatitis B surface antigen (HBsAg) in serum, and the history of intake of more than one small bottle of Japanese "sake" or an equivalent per day for more than 10 years. The average age of HBsAg positive male cirrhotics with a drinking habit (n = 10) was 38.8 years, 10.5 years younger than that of those without a drinking habit (n = 8) (P less than 0.05). The average age of HBsAg negative cirrhotics with a drinking habit (n = 97) was 47.9 years, eight years younger than that of those not drinking (n = 36) (P less than 0.001). There was no significant difference in the laboratory data between these groups. The average age of the HBsAg positive HCC patients with a drinking habit (n = 20) was 48.9 years, nine years younger than that of those without a drinking habit (n = 12) (P less than 0.05). The average age of HBsAg negative male HCC cases with habitual intake of more than 126 ml of ethanol per day was 51.0 years (n = 8), ten years younger than that of nondrinking male HCC cases (n = 11) (P less than 0.05). These data suggest that habitual alcohol intake may promote the development of liver cirrhosis and HCC, especially in HBsAg carriers.