Inequality in medical care in Israel: Arabs and Jews in the Jerusalem district of the General Sick Fund

Background: Differences in health and health services use amongdifferent ethnic groups within populations have been alwaysa major concern in democratic societies. Past research has documentedthe gaps both in health and in services utilization betweenthe Israell Arab and Jewish populations. Methods: This paperstudies the 1993 utilization of health services by a sampleof 70,000 Arabs and Jews insured by the General Sick Fund (Clalit),the biggest sick fund in Israel, in the Jerusalem district.The Arab population consists of Palestinian residents of greaterEast Jerusalem and Israell Arabs, offering a unique opportunityto study the health care use of the three population groups.Results: The results show that, while the mean annual cost ofcare per user is the same for Jews and Arabs, Arabs insureesare dramatically less likely to use medical services, controllingfor age, gender, income, chronic conditions and settlement size.This was found true for both ambulatory and in-patient careand, in particular, for elderly persons. The Israell Arabs arethe most intensive users of care compared to the Jews and thePalestinians. Conclusion: The gaps in utilization can be attributedto differences in accessibility, traditionalism and social andcultural assets. Early findings following the implementationof the National Health Insurance Law in 1995 indicate that somedifferences in accessibility to and use of medical servicesbetween Arabs and Jews have been reduced. The founding of thePalestinian Authority Council will hopefully further enhancethe use of medical care and the health state of the Palestinianpopulation.     

Diacylglycerol/protein kinase C signalling: a mechanism for insulin resistance?

Abstract. It is proposed that an intracellular cycle exists to limit or terminate the insulin signal. The cycle involves increased synthesis of sn-1,2-diacylglycerol (DAG) in response to insulin. The DAG activates protein kinase C (PKC) which phosphorylates glycogen synthase either directly or through other protein kinases to render it inactive. Protein kinase C may also inhibit the insulin receptor by phosphorylation of receptor serine residues. Insulin resistance could then arise as a consequence of a persistent increase in DAG levels. Such an increase could occur in three different ways. Chronic hyperinsulinaemia could increase DAG levels by de-novo synthesis from phosphatidic acid, by hydrolysis of phosphatidylcholine, or by hydrolysis of glycosyl-phosphatidylinositol; DAG is also formed by hydrolysis of phosphatidylinositol 4,5-biphosphate (PIP₂). This reaction, known as the ‘PI response,’ may be the connection between hypertension and insulin resistance. A third mechanism for an increase in DAG involves neural abnormalities. Thus, muscle denervation in the rat is characterized both by a profound insulin resistance and a large increase in DAG. It is possible that a similar increase occurs in humans and may explain the association between denervation, inactivity, and insulin resistance.