Rapid resolution of femoral head osteonecrosis after rotational acetabular osteotomy

The natural history of osteonecrosis of the femoral head is generally thought to be one of progressive deterioration if no intervention is undertaken. However, it is unknown whether surgical intervention is beneficial for patients with a small region of osteonecrosis. We observed rapid improvement of MRI findings after rotational acetabular osteotomy (RAO) was performed in a young patient with osteonecrosis of the femoral head. The band-like low signal area on T2-weighted images almost resolved by six months after surgery. He returned to work as an electrician by six months after surgery. Early surgical intervention such as RAO that alters the mechanical force acting on the necrotic region of the femoral head may accelerate the recovery of osteonecrosis and the improvement of symptoms

Metastatic breast carcinoma of the coracoid process: two case reports

<p>Abstract</p> <p>Background</p> <p>The coracoid process of the scapula is a rare site of involvement for metastatic disease or for primary tumors. We are unaware of any reports in the literature of pathologic coracoid process fractures and only one report of metastatic disease to the coracoid.</p> <p>Methods and Results</p> <p>In this case report, we present two cases with metastatic breast carcinoma of the coracoid process, one of which presented with a pathologic fracture of the coracoid.</p> <p>Conclusions</p> <p>An orthopaedic surgeon must be aware of the potential for metastatic disease to the coracoid as they may be the first medical provider to encounter evidence of malignant disease.</p

Regulation of Brown Fat Adipogenesis by Protein Tyrosine Phosphatase 1B

Protein-tyrosine phosphatase 1B (PTP1B) is a physiological regulator of insulin signaling and energy balance, but its role in brown fat adipogenesis requires additional investigation.To precisely determine the role of PTP1B in adipogenesis, we established preadipocyte cell lines from wild type and PTP1B knockout (KO) mice. In addition, we reconstituted KO cells with wild type, substrate-trapping (D/A) and sumoylation-resistant (K/R) PTP1B mutants, then characterized differentiation and signaling in these cells. KO, D/A- and WT-reconstituted cells fully differentiated into mature adipocytes with KO and D/A cells exhibiting a trend for enhanced differentiation. In contrast, K/R cells exhibited marked attenuation in differentiation and lipid accumulation compared with WT cells. Expression of adipogenic markers PPARγ, C/EBPα, C/EBPδ, and PGC1α mirrored the differentiation pattern. In addition, the differentiation deficit in K/R cells could be reversed completely by the PPARγ activator troglitazone. PTP1B deficiency enhanced insulin receptor (IR) and insulin receptor substrate 1 (IRS1) tyrosyl phosphorylation, while K/R cells exhibited attenuated insulin-induced IR and IRS1 phosphorylation and glucose uptake compared with WT cells. In addition, substrate-trapping studies revealed that IRS1 is a substrate for PTP1B in brown adipocytes. Moreover, KO, D/A and K/R cells exhibited elevated AMPK and ACC phosphorylation compared with WT cells.These data indicate that PTP1B is a modulator of brown fat adipogenesis and suggest that adipocyte differentiation requires regulated expression of PTP1B