An Experience of Ischemic Limb Salvage Associated with Myositis Ossificans of the Left Thigh

A case of ischemic limb salvage associated with myositis ossificans of the left thigh in a 66-year-old man was reported. The patient had a medical history of cerebral palsy and a cervical spinal cord injury, and had an operative past history of hip arthroplasty for fracture of the left femoral neck 10 years before. He showed ischemic symptoms such as paleness, coldness, and loss of the left dorsal arterial pulsation in the left toe, and had a rapidly growing mass in the left thigh. Roentgenography and computed tomography showed a mass 10 cm by 10 cm by 8 cm in size with severe calcification in the left quariceps muscle. Occlusion of the left common femoral artery was found in the arteriogram. Surgery was carried out in order to establish an accurate diagnosis and to rescue the left lower limb. The arterial pulsation was recovered as the result of completely resecting the left quariceps muscle tumor. The pathohistological diagnosis was of myositis ossificans in the quariceps muscle of the thigh. Etidronate disodium was administered in order to prevent a recurrence postoperatively. The patient has been well for the 13 months since surgery

A Case Report of Substernal Goiter

A case of substernal goiter is reported. A 78-year-old female was admitted to our hospital with no symptoms. Chest roentgenography on admission showed that a mass of 3 by 5 cm in size with calcification located in the substernal region. Computed tomography of the chest and aortography revealed that the mass was attached to the trachea, but the connection to the great vessels was not clear. Pathological findings of the incisional biopsy specimen showed thyroid tissue with no evidence of malignancy. Our clinical diagnosis was substernal goiter. Surgery was not carried out in this case, based on the literature. Surgery is indicated in case of malignancy or in cases with severe illness such as respiratory disorder and superior vena cava syndrome

HSF1 and HSF3 cooperatively regulate the heat shock response in lizards

<div><p>Cells cope with temperature elevations, which cause protein misfolding, by expressing heat shock proteins (HSPs). This adaptive response is called the heat shock response (HSR), and it is regulated mainly by heat shock transcription factor (HSF). Among the four HSF family members in vertebrates, HSF1 is a master regulator of <i>HSP</i> expression during proteotoxic stress including heat shock in mammals, whereas HSF3 is required for the HSR in birds. To examine whether only one of the HSF family members possesses the potential to induce the HSR in vertebrate animals, we isolated cDNA clones encoding lizard and frog <i>HSF</i> genes. The reconstructed phylogenetic tree of vertebrate HSFs demonstrated that HSF3 in one species is unrelated with that in other species. We found that the DNA-binding activity of both HSF1 and HSF3 in lizard and frog cells was induced in response to heat shock. Unexpectedly, overexpression of lizard and frog HSF3 as well as HSF1 induced HSP70 expression in mouse cells during heat shock, indicating that the two factors have the potential to induce the HSR. Furthermore, knockdown of either HSF3 or HSF1 markedly reduced HSP70 induction in lizard cells and resistance to heat shock. These results demonstrated that HSF1 and HSF3 cooperatively regulate the HSR at least in lizards, and suggest complex mechanisms of the HSR in lizards as well as frogs.</p></div