We collected audio-magnetotelluric (AMT) data across Usu volcano, Hokkaido, Japan, which erupted in 1977 and is still active. We had a profile of 17 sites perpendicular to the regional tectonic strike, which crossed the 1977 cryptodome, Usu-Shinzan. Tensor-decomposed data were interpreted by a two-dimensional inversion. Outside the crater rim, the resistivity structure is simple. The resistive somma lava is underlain by a conductive substratum, implying altered Tertiary or Quaternary rocks. In the crater, there are two resistive bodies bisected by a vertical conductor, which corresponds to Usu-Shinzan fault, located at the foot of the uplift. The vertical conductor was not detected in the AMT sounding in 1985. One of the possible causes of the development of the vertical conductor is a cold water supply from the surface into the vapor dominant fracture zone. One of the resistive bodies is located beneath Usu-Shinzan and implies an intrusive magma body which caused the 1977 uplift.

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Anticarbamazepine antibody was detected in a patient who had clinical signs of serum sickness induced by carbamazepine. Skin rash, fever, oedema, and lymphadenopathy are classic signs of severe adverse reaction, but although immunological hypersensitivity is thought to be a contributory factor, the presence of anticarbamazepine antibody has not previously been reported to our knowledge.Carbamazepine is widely used in the treatment of various forms of epileptic disorders.' 2 Although different side effects have been reported, skin rash is the most common adverse reaction. Exfoliative dermatitis, urticaria, toxic epidermal necrolysis, Stevens-Johnson syndrome, and a reaction similar to systemic lupus erythematosus have been reported.2 3 In some cases the skin rash is part of a severe illness affecting several organs, and immunological hypersensitivity is thought to contribute to the skin reaction.3 4 So far, however, we know of no report of the presence of anticarbamazepine antibody in any patient with severe skin reactions.We present a patient with the typical clinical manifestations of serum sickness, fever, eruption with oedema (particularly around the face and neck), and lymphadenopathy. The laboratory findings showed a decrease in complement C4 and an increase in C3a and C4a activity. Anticarbamazepine antibody was detected in the serum using an enzyme linked immunosorbent assay (ELISA). Methods BALB/C mice were given carbamazepine (1 g/kg) orally, and bled six hours later. The serum was used as the antigen.The anticarbamazepine antibody of serum from the patient was analysed by ELISA, a procedure that has been described elsewhere.5 Briefly, the mouse serum diluted (1:100) with 10 mM carbonate buffer was added to 96 well polyvinylchloride microtitre plates, and left for two hours at room temperature. The nonbinding sites were blocked with phosphate buffered saline containing 0 05% Tween 20 and 2% ovalbumin. Diluted human serum was added to the wells and incubated for one hour at 4°C. After three washings, 100 >t of appropriately diluted horseradish peroxidase conjugated goat antimouse Ig antiserum was added to each well. The plates were then incubated for one hour at 4°C and washed three times, and 200 tl of freshly prepared substrate solution containing 0-05% o-phenylendiamine and 0 0075% hydrogen peroxide in McIlvain buffer, pH 6-0, was added to each well. After 30 minutes of incubation at room temperature, absorbance was read at 405 nm with a Titertek Multiskan plate reader.Case report An 8 year old girl was admitted with fever and skin rash. Thirty seven days before admission carbamazepine 200 mg (10 mg/kg) had been prescribed because of a complex partial seizure. Twenty seven days before admission the first skin rash had appeared on her cheeks, but this disappeared within a few days. Twenty three days before admission, the dose of carbamazepine had been increased to 300 mg. The day before admission she had again developed maculopapular erythema on her face and neck, this time accompanied by fever...

The effect of recombinant immune interferon (IFN-gamma) on the expression and shedding of HLA antigens and of melanoma-associated antigens (MAA) by epidermal melanocytes was investigated by using serologic and immunochemical techniques. IFN-gamma enhances the expression and/or shedding of HLA class I antigens and of the cytoplasmic MAA defined by monoclonal antibody (MoAb) 465.12S and induces a slight reduction in the expression of the high m.w. melanoma-associated antigen (HMW-MAA). In agreement with the data in the literature, melanocytes incubated with IFN-gamma acquire HLA-DR, -DQ, and -DP antigens. Contrary to previous information in the literature, the effect is not restricted to HLA class II antigens, since IFN-gamma also induces the expression of the 96-kDa MAA recognized by MoAb CL203. The effect of IFN-gamma on HLA class II antigens and 96-kDa MAA is dose and time dependent and is specific, because recombinant leukocyte interferon affects the expression of neither type of antigen. In spite of the expression of HLA class II antigens, IFN-gamma-treated melanocytes do not acquire the ability to stimulate the proliferation of allogeneic lymphocytes. HLA-DR antigens are more susceptible to induction by IFN-gamma than HLA-DQ and -DP antigens, since the percentage of melanocytes acquiring HLA-DQ and -DP antigens is lower than that acquiring HLA-DR antigens. Furthermore, the dose of IFN-gamma is higher and the time of incubation is longer to induce HLA-DQ and -DP antigens than to induce HLA-DR antigens. The differential susceptibility of HLA-DR, -DQ, and -DP antigens as well as of melanocytes from various donors to the modulating effect of IFN-gamma may provide an explanation for the more frequent detection of HLA-DR than of HLA-DQ and -DP antigens in melanoma lesions and for the expression of HLA class II antigens by some, but not all, melanoma lesions.

We report on a patient with severe serum sickness induced by carbamazepine in whom anticarbamazepine IgG antibodies were detected in the serum. The T cells of the patient showed impairment of phytohemagglutinin-induced proliferation, and hypergammaglobulinemia was evident. The clinical features and immunological abnormalities were compatible with immunoblastic lymphadenopathy. Immunosuppressive factors were also detected in the patient. Their molecular weights ranged from 20,000 to 30,000 as evaluated by Sephadex G-200 gel filtration. Such immunosuppressive cytokines were not detected in other patients with carbamazepine allergy who did not develop the clinical manifestations of immunoblastic lymphadenopathy. These results suggest that the T cell functional deficiency of immunoblastic lymphadenopathy is induced by these immunosuppressive cytokines.