Activism and Legitimation in Israel's Jurisprudence of Occupation

Colonial law need not exclude the colonized in order to subordinate them, and ‘activist’ courts can advance the effect of subordination no less than ‘passive’ courts. As a case study, this article examines the jurisprudential legacy of the Israeli Supreme Court in the context of the prolonged Israeli occupation of Palestine. Applying insights from legal realist, law and society, and critical legal studies scholarship, the article questions the utility of using the activist and passive labels. It illustrates how the Israeli activist court, through multiple legal and discursive moves, has advanced and legitimated the colonization of Palestine; that the court is aware of its role; and that arguments that focus on the court’s informal role do not mitigate this legitimating effect. Unlike other scholars, the article shows that the Israeli court’s role—by extending the power of judicial review to the military’s actions in the occupied areas—is neither novel nor unique or benevolent, as the British colonization of India and the US colonization of Puerto Rico show

FACTORS INFLUENCING THE DISTRIBUTION OF PENTOSES IN THE ISOLATED RAT DIAPHRAGM

The addition of insulin, or of various enzyme inhibitors, to the intact isolated rat diaphragm causes an increase in pentose space, without causing a corresponding increase in inulin space or in total water. It is suggested that there is a relationship between cellular metabolism and permeability to pentoses. If pentose permeability and glucose permeability are governed by similar mechanisms, this means the glucose permeability might depend on cellular metabolism. However, phenethylbiguanide and pyruvate do not increase the permeability to pentoses, though they do increase glucose uptake. This means that glucose uptake might be increased without a corresponding increase in glucose permeability. Glucose utilization therefore may be governed by several factors of which the cellular permeability is only one.</jats:p

FACTORS INFLUENCING THE DISTRIBUTION OF PENTOSES IN THE ISOLATED RAT DIAPHRAGM

The addition of insulin, or of various enzyme inhibitors, to the intact isolated rat diaphragm causes an increase in pentose space, without causing a corresponding increase in inulin space or in total water. It is suggested that there is a relationship between cellular metabolism and permeability to pentoses. If pentose permeability and glucose permeability are governed by similar mechanisms, this means the glucose permeability might depend on cellular metabolism. However, phenethylbiguanide and pyruvate do not increase the permeability to pentoses, though they do increase glucose uptake. This means that glucose uptake might be increased without a corresponding increase in glucose permeability. Glucose utilization therefore may be governed by several factors of which the cellular permeability is only one.</jats:p

THE EFFECT OF PHENETHYLBIGUANIDE UPON THE METABOLISM OF THE ISOLATED RAT DIAPHRAGM

Some of the effects of phenethylbiguanide (DBI) upon carbohydrate metabolism in the isolated rat diaphragm have been studied. The addition of this compound to an incubation medium stimulates the uptake of sugars, the breakdown of glycogen, and the output of lactic acid and inorganic phosphate. Free sugar does not accumulate in the diaphragm treated with DBI.</jats:p

THE EFFECT OF PHENETHYLBIGUANIDE UPON THE METABOLISM OF THE ISOLATED RAT DIAPHRAGM

Some of the effects of phenethylbiguanide (DBI) upon carbohydrate metabolism in the isolated rat diaphragm have been studied. The addition of this compound to an incubation medium stimulates the uptake of sugars, the breakdown of glycogen, and the output of lactic acid and inorganic phosphate. Free sugar does not accumulate in the diaphragm treated with DBI.</jats:p

Metabolic interrelations of glucose and lactate in unanesthetized normal and diabetic dogs

Uniformly labelled 14C-glucose infusions were given to normal and pancreatectomized dogs. Plasma glucose and lactate specific activities were measured by appropriate methods. In normal dogs 14–28% of plasma lactate was found to originate from circulating glucose, and in diabetic dogs 11–18%. This fraction was markedly increased in normal but not significantly so in diabetic dogs during a 2-h infusion of a 6.7–11 mg/kg min glucose load. Uniformly labelled 14C-L(+)-lactate and glucose-6-3H were infused simultaneously for 5 h in normal and pancreatectomized dogs. The glucose turnover rate and incorporation of lactate carbon into glucose were calculated. Of the utilized lactate carbon, 41–49% was incorporated into plasma glucose. The recycling rate of glucose carbon via lactate was estimated to be 3–8% of the glucose turnover rate in the normal dog in the postabsorptive state. The absolute rate of gluconeogenesis from lactate was found to be increased in diabetes. </jats:p