An effort was made to identify all patients with polymyositis/dermatomyositis (PM/DM) admitted to hospitals in Israel from 1956-1976. The diagnosis of PM/DM was retrospectively reviewed in 92 (46 definite, 26 probable, and 20 possible) cases. The most common complaints and physical findings in the course of the disease were muscle weakness (86 patients), rash (53 patients), arthritis or arthralgia (39 patients), and dysphagia (35 patients). Elevated serum aldolase levels were found in 64% of the patients for whom data were available; 92% had abnormal electromyogram results, and 60.9% had muscle histopathology consistent with PM/DM. Malignancy was diagnosed in 13 patients. Malignancy, ischemic heart disease, and pulmonary complications were the most common causes of death. The actuarial survival curve was heterogeneous, with an accelerated mortality during the first year after diagnosis and a slower mortality during the following 7 years. Independent unfavorable prognostic signs were: failure to induce remission, leukocytosis, fever, older age, a shorter disease history, and dysphagia.

In previous studies, tungstate and molybdate were found to mimic the biological actions of insulin. It was suggested that these metallooxides initially inhibit vanadate-sensitive protein phosphotyrosine phosphatase (PTPase). This, in turn, stimulates a staurosporine-sensitive cytosolic protein tyrosine kinase (cytPTK), which activates several insulin bioeffects via insulin-independent pathways (Shisheva & Shechter, 1991, 1993; Elberg et al., 1994). Tungstate and molybdate, however, facilitate bioeffects in rat adipocytes only at high (millimolar) concentrations (Goto et al., 1992). We report here that incubations of tungstate or molybdate with hydrogen peroxide (H2O2) result in the formation of pertungstate (pW, peroxide of tungstate) or permolybdate (pMo, peroxide of molybdate). Pertungstate and permolybdate were found to stimulate all or most of the insulin bioeffects in rat adipocytes. Moreover, these permetallooxides are 80-180-fold more potent stimulators than the corresponding metallooxides. This shift in potency resembles that of pervanadate relative to vanadate in stimulating the same effect in rat adipocytes (Fantus et al., 1989). pW and pMo are also active in normalizing blood glucose levels in streptozotocin-induced diabetic rats. Further studies aimed at understanding the higher efficacy of this permetallooxide revealed the following: (a) All three permetallooxides (pV, pW, pMo) are oxidizing agents relative to reduced glutathione (GSH). They oxidize stoichiometric amounts of GSH to GSSG. (b) All three metallooxides do not oxidize GSH to GSSG. (c) Both metallooxides and permetallooxides inhibit rat adipocytic PTPase at micromolar quantities (IC50 = 3-10 microM). Permetallooxides, however, inhibited a larger PTPase fraction (80-100%) compared to metallooxides (40-70% of the total).(ABSTRACT TRUNCATED AT 250 WORDS)

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The Samaritan community, which numbered more than a million in late Roman times and only 146 in 1917, numbers today about 640 people representing four large families. They are culturally different from both Jewish and non-Jewish populations in the Middle East and their origin remains a question of great interest. Genetic differences between the Samaritans and neighboring Jewish and non-Jewish populations are corroborated in the present study of 7,280 bp of nonrecombining Y-chromosome and 5,622 bp of coding and hypervariable segment I (HVS-I) mitochondrial DNA (mtDNA) sequences. Comparative sequence analysis was carried out on 12 Samaritan Y-chromosome, and mtDNA samples from nine male and seven female Samaritans separated by at least two generations. In addition, 18-20 male individuals were analyzed, each representing Ethiopian, Ashkenazi, Iraqi, Libyan, Moroccan, and Yemenite Jews, as well as Druze and Palestinians, all currently living in Israel. The four Samaritan families clustered to four distinct Y-chromosome haplogroups according to their patrilineal identity. Of the 16 Samaritan mtDNA samples, 14 carry either of two mitochondrial haplotypes that are rare or absent among other worldwide ethnic groups. Principal component analysis suggests a common ancestry of Samaritan and Jewish patrilineages. Most of the former may be traced back to a common ancestor in the paternally-inherited Jewish high priesthood (Cohanim) at the time of the Assyrian conquest of the kingdom of Israel.

Glucagon-like peptide 1-(7-37) [GLP-I-(7-37)] is a 31-amino acid hormone which may have an important role in the regulation of insulin secretion, It is processed from preproglucagon and found in the pancreas, brain, and, in highest quantity, intestine. In previous studies we found that GLP-I-(7-37) is a potent insulin secretagogue, and its effect was indistinguishable from that of GLP-I-(7-36) amide at concentrations of 10(-11) M. Herein we report insulinotropic effects of additional GLP-I analogs. GLP-I-(7-34) had no stimulatory effect on insulin release at 10(-10) M, but had a partial effect at 10(-9) M and was as active as GLP-I-(7-37) at 10(-8) M. GLP-I-(7-33) had no effect at any concentration tested. GLP-I-(8-37) caused no significant effect on insulin release at 10(-9) and 10(-8) M, but did have an effect at the high concentration of 10(-7) M. Similar results were found with cAMP formation in the beta TC1 line. In this system GLP-I-(7-34) was less potent than GLP-I-(7-37) at a concentration of 5 x 10(-9) M. GLP-I-(7-33) had only about 0.1% the potency of GLP-I-(7-37); thus, there is good agreement between cAMP formation in the beta-cell line and insulin secretion from the perfused pancreas experiments. We conclude that histidine in the 7 position in the N-terminus of GLP-I-(7-37) is crucial for cAMP formation and insulin secretion, and that removal of the last three C-terminus residues of GLP-I-(7-37) results in only partial loss of activity; the residue in the 34 position is, however, essential for the insulinotropic action.