Yasuo Kuroki

Constitutive c-fos expression in osteoblastic MC3T3-E1 cells stimulates osteoclast maturation and osteoclastic bone resorption.

The effect of culture supernatants of c‐fos‐transfectcd MC3T3‐El osteob[aslic cells on osteoclastic bone resorption was studied. Human c‐fos cDNA was integrated in the expression vector pH8. and the cells were transfected using the calcium phosphate precipitation technique. Osteoclastic bone resorplion was quantified by the pit formation assay, and the osteoclast maturation from precursor was assessed by the generation of tartrate‐resistant acid phosphatase (TRAP)‐positive multinucleated cells (MNC). The culture supernatants of MC3T3‐E1 transfectants constitulively expressing c‐fos gene enhanced osteoclast‐like MNC formation from haematopoietic blast cells compared with those of control transfectants (P<0‐0l). The culture supernatants also promoted osteoclastic bone resorption: the pit number. lI8‐7±38‐5, was significantly higher than 19‐0+10‐1 of the control (p<0‐05). The absorption area. 12394+3145 mm2, was significantly larger than 1646+314 mm2 of the control (p<0‐05). The culture supernatants also promoted bone resorption by purified chick osteoclasts (P<005). The results show that constitutive expression of c‐fos gene in osteoblastic MC3T3‐EI cells stimulates osteoclast rnaturation and osteoclastic bone resorption by releasing humoral mediator(s).

Age distribution of circulatingα-interferon

A sensitive radioimmunoassay showed that circulating α-interferon in the plasma of healthy individuals was low in children and reached the highest level in the young adult, then declined gradually with age. Circulating α-interferon was 0.201±0.059 ng/ml in males (n=19) and 0.184±0.076 ng/ml in females (n=14) at ages 30–39 years old. It was noted that circulating α-interferon was maintained up to a certain level even in elderly individuals.

Fasciitis: what is the significance of various forms?

I n this issue, Kim et al. (1) describe a patient with unusual fasciitis. The 33-year-old woman presented with thickening of both arms and lower legs. She had no arthritis, scleroderma, or myositis. Eosinophilic fasciitis, typically found in association with chronic graft versus host reaction, was not seen in this patient. A skin biopsy of the right calf area of the patient revealed fibrinoid degeneration of fascia and dense inflammatory cell infiltration along fascia. Although lymphocyte infiltration existed in the dermis, no evidence of adnexal destruction typical of systemic sclerosis was found in the dermis, and eosinophils were not found in the tissues or increased in the peripheral blood. Her fasciitis is therefore not only unusual but presented in a unique form (2). It should be noted that her fasciitis was improved after 3 months of treatment with cyclosporin and prednisolone. When the clinical features of fasciitis are reviewed, a well-known form is eosinophilic fasciitis. In 1974, Schulman (3) described a new syndrome characterized by the rapid onset of a woody induration of the skin and adjacent tissue with marked peripheral blood eosinophilia and histologic evidence of thickening of fascia. Rodnan et al. (4) called this “eosinophilic fasciitis,” and the disease was further characterized by many investigators (5). There is also another condition called “nodular fasciitis.” This is one of the most common benign soft tissue lesions and is characterized by proliferation of fibroblasts (6). In contrast, necrotizing fasciitis is potentially a lethal infection of the deep subcutaneous tissues that progresses to destroy fat and fascia (7). Group A beta hemolytic streptococcus is the most common etiology, whereas the majority of cases are polymicrobial in nature, and coinfection with synergistic, facultative, aerobic, and anaerobic gas-forming organisms takes place (8). This condition is sometimes seen in association with periarteritis nodosa (9). Macrophagic myofasciitis is a rare and unique inflammatory myopathy first reported from France. The symptoms included myalgia, arthralgia, systemic asthenia, muscle weakness, and fever. Abnormal laboratory findings included elevated creatine kinase levels, marked increase of erythrocyte sedimentation rate, and myopathic changes in electromyography (10). Histologic examination showed a perifascicular infiltration of the cells with a CD68 , CD1a , S100 monocyte/ macrophage lineage. Myofasciitis can also occur after irradiation (11). A somewhat similar but distinct syndrome called tumor necrosis factor (TNF) receptor–associated periodic syndrome was reported in 1999 from the United States (12). This syndrome is characterized genetically by mutations in the TNF receptor I gene (12). The syndrome is characterized clinically by recurrent episodes of fever in conjunction with localized inflammation at various sites. Myalgia is the most frequent and characteristic form of localized inflammation and is often associated with an erythematous macular rash in the overlying skin, which progresses centrifugally. When biopsy specimens were examined, the prominent feature was “monocytic fasciitis,” which was typically ac-

Schizophyllan Augments Development of Immunoglobulin-Secreting Cells upon Costimulation with Staphylococcus Aureus Cowan I

This case highlights the necessity ofevaluating the nutritional status of patients before initiating INH therapy, especially in the Hlv-positive population. The onset of peripheral neuropathy (ten days in this case) is different from previous reports (three months to six years) but is explained by the poor nutritional status of the patient and his probable vitamin B. deficiency prior to initiating INH therapy. Pyridoxine should be initiated concurrently with INH in the HIV population and these patients should be considered at risk for the development of peripheral neuropathy precipitated by INH.