A cell line (T17) was derived from C3H 10T1/2 C18 cells after 17 treatments with increasing concentrations of 5-aza-2'-deoxycytidine. The T17 cell line was very resistant to the cytotoxic effects of 5-aza-2'-deoxycytidine, and the 50% lethal dose for 5-aza-2'-deoxycytidine was ca. 3 ,uM, which was 30-fold greater than that of the parental C3H 10T1/2 C18 cells. Increased drug resistance was not due to a failure of the T17 cell line to incorporate 5-aza-2'-deoxycytidine into DNA. The cells were also slightly cross-resistant to 5-azacytidine. The percentage of cytosines modified to 5-methylcytosine in T17 cells was 0.7%, a 78% decrease from the level of 3.22% in C3H 1OT1/2 C18 cells. The DNA cytosine methylation levels in several clones isolated from the treated lines were on the order of 0.7%, and clones with methylation levels lower than 0.45% were not obtained even after further drug treatments. These highly decreased methylation levels appeared to be unstable, and DNA modification increased as the cells divided in the absence of further drug treatment. The results suggest that it may not be possible to derive mouse cells with vanishingly low levels of 5-methylcytosine and that considerable de novo methylation can occur in cultured lines.
Ten episodes of Schonlein-Henoch purpura (SHP) in 8 patients with familial Mediterranean fever (FMF) were observed. Five episodes developed 3-14 days after penicillin injections, suggesting an etiologic association. FMF and SHP have clear clinical similarities, and if the frequency of association of the 2 diseases is indeed high, perhaps a common etiologic factor should be sought. An immune complex mechanism might be the link between these 2 disease entities.Familial Mediterranean fever (FMF) and Schonlein-Henoch purpura (SNP) have a remarkable clinical similarity. This includes episodes of abdominal pains, arthritis, fever, skin eruptions, and transient or permanent renal damage. Little attention has been paid to the simultaneous occurrence of both diseases: only 20 cases have been described, most of them without details (1-3). Ten episodes of typical SHP were observed in 8 of 50 patients who were hospitalized in the Central Emek Hospital between 1966 and 1975 and diagnosed as cases of FMF. The purpose of the present study is to investigate the association of SHP and FMF. PATIENTSHospital charts of all the patients diagnosed as suffering from FMF between 1966 and 1975 were reviewed. Fifty cases fulfilling the following criteria were included in the present study (3); 1) recurrent attacks of fever and abdominal pains lasting 1-3 days, with or without joint pain; 2) an elevated erythrocyte sedimentation rate (ESR) and/or leukocytosis during the attack; 3) absence of other diseases that could explain the clinical picture; and 4) at least a 2-year duration of the disease.The diagnosis of SHP was based on the following criteria: 1) the appearance of nonthrombocytopenic puvura with 1 or several of the following: gastrointestinal tract bleeding, abdominal colicky pains, hematuria, localized edema, and arthritis; and 2) positive results of biopsies from affected skin (4 patients) and kidney biopsies (2 patients). CASE REPORTSRelevant clinical and laboratory data are presented in Table 1.Case 1 involved a 23-year-old Jewish man of Moroccan extraction. Two of his 5 siblings have FMF. At the age of 8 years, he was diagnosed as having FMF and, since then, he has experienced repeated abdominal and synovial attacks. In 1966, at the age of 9 years, he was hospitalized because of migratory polyarthritis (ankles, knees, elbows, hands) and high fever that lasted for more than 2 months and responded to corticosteroid treatment. Antistreptolysin-0 (ASLO) titers ranged between 1 :625-1:2500. The diagnosis was FMF, but the possibility of rheumatic fever could not be ignored. A year later, he was hospitalized once more because of migratory polyarthritis and high fever. One week after admission, he
Kimura’s disease (KD) is an angiolymphoid proliferative disorder of soft tissue with eosinophilia, with a predilection for head and neck regions in young Oriental men. Renal disease is rarely associated with it. We describe a young non-Oriental male with KD and relapsing steroid-responsive minimal-change nephrotic syndrome. This case of KD associated nephrotic syndrome is unique in the relapsing nature of the nephropathy and the non-Oriental origin of the patient. We comment on KD and nephrotic syndrome and on treatment strategy.
Introduction. Although the association of hypertension with established risk factors has been noted in several population studies, the recent redefinition of dyslipidaemia, hypertension and diabetes calls for reassessment of the prevalence and pattern of risk factor clusters in essential hypertension. Objective. To analyse the risk factor profile of Israeli patients with essential hypertension seen by primary care physicians and in hypertension specialty clinics, based on current definitions of dyslipidaemia hypertension and diabetes and JNC-VI guidelines for the assessment of risk factors. Design and Setting. We analysed the risk profile of 324 Israeli hypertensive subjects using the JNC-VI risk table and risk grouping. A total of 122 consecutive patients were recruited from primary care clinics and 212 consecutive patients were recruited from a hospital based hypertension clinic. Results. Amongst hypertensive individuals with no known target organ damage, only 1.5% had no risk factors other than hypertension, whereas all hypertensives with coronary artery disease had additional risk factors. Of the six listed major JNC-VI risk factors (smoking, dyslipidaemia, diabetes, age, sex, family
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