SUMMARYThe pathogenesis of avascular necrosis of bone (ANB) was investigated in 111 patients with systemic lupus erythematosus (SLE) (24 with ANB, 87 without ANB); patients' ages, corticosteroid treatment, clinical and laboratory features associated with SLE, and haemostatic profiles were all taken into account. The mean ages of patients with and without ANB at the time of diagnosis of SLE was 24-1 and 31*2 years respectively. The mean maximal daily dose of prednisolone in the group with ANB was 50*8 mg, which was significantly higher than the dose (41*8 mg) in the group without ANB. Disease features of SLE, such as Raynaud's phenomenon, hyperlipidaemia, nephrotic syndrome, hypertension, and disease activity, were not found to be related to ANB. The percentage of patients who had lupus anticoagulant as well as a shorter activated partial thromboplastin time was greater in those with ANB than in those without. Multiple factors may be involved in the pathogenesis of ANB in SLE, and it is suggested that haemostatic abnormalities, which could be influenced by corticosteroids and young ages, play some part in the development of ANB.Since 1960 when Dubois and Cozen suggested an association of avascular necrosis of bone (ANB) with systemic lupus erythematosus (SLE),1 ANB has continued to be one of the major problems during the course of SLE. Corticosteroids, which are used for most patients with SLE, have been implicated as one cause of ANB, 6 but multiple factors, such as vasculitis,7 8 fat emboli,9 10 Raynaud's phenomenon,6 11 and young ages,12 13 must contribute to its development. As ANB may result from interference with the blood supply,7 haemostatic abnormalities and factors which induce them could also contribute to its occurrence.In this study we attempted to determine the predisposing factors for ANB in SLE, considering particularly patients' ages, corticosteroid treatment, and haemostatic state.

The incidence of herpes zoster was determined in patients with systemic lupus erythematosus (SLE) and the cellular and humoral immunity to varicella zoster virus (VZV) investigated in 45 of these 92 patients.The incidence of herpes zoster was high, occurring in 40 patients (43%) Patients and methods PATIENTS WITH CONTROLSNinety two patients (89 women, three men) who fulfilled the criteria of the American Rheumatism Association for SLE20 were enrolled in this study. They had a mean age of 36-8 (range 19-68) years. The history of herpes zoster was obtained at interview with the patients and was confirmed by doctors' records.Cellular and humoral immunity to VZV was evaluated in 45 of these 92 patients (44 women and one man with a mean age of 37-2 (range 22-68) years) and in 15 healthy subjects with no history of zoster (11 women and four men with a mean age of 35-0 (23-52) years). Patients with a history of herpes zoster within the last six months were excluded from the immunological study. At the time of the immunological study 36 patients were receiving corticosteroids alone(1-25-30 mg/day of prednisolone) and nine were receiving corticosteroids and immunosuppressants (50 mg/day of cyclophosphamide or azathioprine).

In 1968-1981, a total of 3222 serum samples were collected from healthy subjects in Okinawa--in Ishigaki City, on Hateruma Island, and on Iriomote Island--and in Kyushu, in Fukuoka City and Nichinan City. These serum samples were tested for the presence of hepatitis B surface antigen (HBsAg) by reverse passive hemagglutination (RPHA), for antibody to hepatitis B surface antigen (anti-HBs) by passive hemagglutination (PHA) and radioimmunoassay (RIA), and for antibody to hepatitis B core antigen (anti-HBc) by RIA. Overall prevalence of HBsAg (7.5%), anti-HBs by PHA (41.0%) and RIA (56.4%), and anti-HBc (65.5%) in Okinawa was significantly higher than prevalence of HBsAg (2.4%), anti-HBs by PHA (24.7%) and by RIA (28.1%), and anti-HBc (30.9%) in Kyushu. In both areas, anti-HBc was more frequently detected than anti-HBs by both methods. In Okinawa, HBsAg was significantly more prevalent in males than in females. No significant differences by sex in other hepatitis B virus markers were found. On Iriomote Island and Ishigaki City, second samples were collected after intervals of 10 and 12 years, respectively. Over these periods, the prevalence of all hepatitis B virus markers decreased significantly for the 0-9 and 10-19 year age groups. These data suggest that hepatitis B infection among children has declined in recent years and that high prevalence of hepatitis B infection in adults may reflect high rates of infection in their childhood.

Monoclonal antibodies against etiological agents of Weil's disease were produced by cell fusion technology. Twenty hybridomas were produced through the fusion of P3×63Ag8.653 cells with spleen cells from BALB/c mice immunized against Leptospira interrogans serovar icterohaemorrhagiae RGA strain and serovar copenhageni Shiromizu and M20 strains. Reactivities of the antibodies produced by the hybridomas were determined by the microscopic agglutination test. Among the five hybridoma antibodies to the RGA strain, two reacted specifically to serovar icterohaemorrhagiae, two reacted to serovar icterohaemorrhagiae at a high titer and serovar copenhageni at a low titer, and one reacted to serovars icterohaemorrhagiae, copenhageni, pyrogenes, and canicola. Of the ten hybridoma antibodies to the Shiromizu strain, one reacted specifically to serovar copenhageni, seven reacted to both serovars copenhageni and icterohaemorrhagiae at almost the same titer, and two exhibited intermediate properties. Of the five hybridoma antibodies to the M20 strain, three reacted to both serovars copenhageni and icterohaemorrhagiae at almost the same titer, one reacted to serovar copenhageni at a low titer and serovar icterohaemorrhagiae at a high titer, and one reacted to serovars copenhageni, icterohaemorrhagiae, and pyrogenes. The results revealed that each serovar has its own antigen(s) and their common antigens. In addition, 20 strains of leptospires were recently isolated and tested with three monoclonal antibodies characterized by different reactivities. Twenty strains were clearly identified by their antibodies, i.e., 16 strains were identified as serovar icterohaemorrhagiae and three strains were identified as serovar copenhageni. The remaining strain, which was not agglutinated by three antibodies, was identified as serovar autumnalis by an agglutination test with immune rabbit sera.

Hybridoma cells were produced by fusing P3X63Ag8.653 mouse myeloma cells with spleen cells from BALB/c mice immunized with Japanese encephalitis (JE) virus, Nakayama-RFVL strain. The resulting 26 clones produced hemagglutination inhibition antibodies against the homologous strain. The hemagglutination inhibition reactivity of each clone was tested against six flaviviruses: JE, Murray Valley encephalitis (MVE), Egypt 101 strain of West Nile (WN), St. Louis encephalitis (SLE), Russian spring summer encephalitis, and dengue type 1. The 26 monoclonal antibodies fell into four groups: 14 JE species-specific antibodies, 6 antibodies reactive to JE and MVE viruses, 3 antibodies to three or four viruses in the JE-MVE-WN-SLE subgroup, and 3 antibodies to all six flaviviruses. Furthermore, antigenic comparison of 27 strains of JE virus was carried out by using five JE species-specific monoclonal antibodies. Of these, 24 strains were isolated in various parts of Japan, and 3 strains came from Southeast Asia. In reactivity, the 27 strains were classified into at least four antigenic groups. The results showed that the Nakayama-Yakken strain is a mutant strain which lacks the Nakayama strain-specific antigen and that the recently isolated strains are immunologically different from Nakayama and JaGAr 01 strains. One clone (NARMA 13) produced a JE species-specific antibody which showed almost the same titer against 26 JE virus strains, whereas one clone (NARMA 5) produced a Nakayama strain-specific antibody which reacted only to the Nakayama-RFVL and Nakayama-Yoken strains.

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To examine the mechanism of induction of differentiation in the human malignant T-lymphoblastic cell line, MOLT-3, by 12-O-tetradecanoylphorbol-13-acetate (TPA), the role of receptors for phorbol esters was investigated. Binding of [20–³H]-phorbol-12,13-dibutyrate to TPA-resistant subclones derived from MOLT-3 was less than50 % of that of the parental MOLT-3. Scatchard analysis showed that the concentration of phorbol ester receptors in a TPA-resistant subclone was about 50% of that in the parental MOLT-3, but affinities of binding were similar, indicating that more than a certain number of phorbol ester receptors is required to induce differentiation by TPA in this human T cell line.