L S Hurley

University of California, Davis, Davis, California, United States

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Publications (216)1141.55 Total impact

  • L.S. Hurley · B. Lönnerdal ·

    Nutrition Reviews 04/2009; 40(3):65 - 71. DOI:10.1111/j.1753-4887.1982.tb05268.x · 6.08 Impact Factor
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    B L Reis · C L Keen · B Lönnerdal · L S Hurley ·
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    ABSTRACT: We have demonstrated that the zinc (Zn) concentration of mouse milk declines significantly over the lactation period. Pups radiolabeled in utero with 65Zn were forward-fostered (FF) to nonradiolabeled dams at a later stage of lactation to study the effects of early milk deprivation. Other groups of radiolabeled pups were back-fostered at 5, 10 and 15 days of age to a nonradiolabeled dam who had just given birth; this provided additional colostrum during the suckling period. Litters fostered at birth to an unlabeled dam at d 0 of lactation were used as controls. Weight gain of FF litters decreased and signs of Zn deficiency increased as the foster dam's days of lactation increased. The Zn concentration of kidney, brain and plasma tended to decrease with increasing lactation days of the foster dam. Tibia Zn concentration declined progressively as the lactation days of the foster dam increased, and the concentration of calcium also was lower in all three groups of FF litters than in controls, indicating that bone calcification may have been impaired. Kinetic data proved to be a more sensitive index of Zn status than tissue Zn concentration. The biological half-life of whole-body 65Zn for FF suckling mice increased in a linear fashion with increasing lactation days of the foster dam; whole-body retention of 65Zn for back-fostered litters did not differ from that for controls. Brain, small intestine, kidney muscle, plasma and tibia of pups FF to late-lactating dams seemed to have greater retention of Zn than did controls. Thus, deprivation of early milk impaired growth and development of the mouse neonate despite some ability to conserve Zn.
    Journal of Nutrition 06/1991; 121(5):700-10. · 3.88 Impact Factor
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    B L Reis · C L Keen · B Lönnerdal · L S Hurley ·
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    ABSTRACT: We studied changes in the mineral composition of milk of lactating Swiss-Webster mice and the relationship of those changes to mineral metabolism of suckling mouse pups. Concentrations of Zn, Cu, Mg and Ca were analyzed in maternal and neonatal tissues and in milk; Zn metabolism was studied using 65Zn. Although Cu, Ca and Mg concentrations in milk declined during the first 2 d of lactation, only the concentration of Zn decreased progressively throughout 30 d. Various pup tissues were characterized by developmental changes in concentrations of some elements. Turnover of Zn in neonatal tissues was studied by radiolabeling litters in utero and fostering them at birth to nonradiolabeled lactating dams. The turnover of whole-body 65Zn in suckling mice decreased during development, and, at 20 d of age, the biological half-life of 65Zn in the neonate was approximately the same as for a nonpregnant, nonlactating adult female (20 d). The decreased turnover of 65Zn in lactating dams that characterized progressive lactation and was reflected in the Zn concentration of milk is in agreement with changes in whole-body 65Zn turnover observed for the suckling mouse. These findings demonstrate that the metabolism of the suckling neonate is directly related to longitudinal changes in the composition of maternal milk.
    Journal of Nutrition 06/1991; 121(5):687-99. · 3.88 Impact Factor
  • Patricia I. Oteiza · Lucille S. Hurley · Bo Lönnerdal · Carl L. Keen ·
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    ABSTRACT: One of the possible mechanisms that has been proposed to underlie the deleterious effects of zinc deficiency on brain development is an impairment in the normal formation of the cytoskeletal network. In the current study, in vivo microtubule polymerization was characterized in brain supernatant fluids, from 20-d-old pups whose dams were fed diets containing control (50 micrograms zinc/g) or marginal levels of zinc (10 micrograms zinc/g) throughout pregnancy and lactation. Pup brain and body weights were similar between the groups; however, plasma zinc concentrations were lower (27%) in pups fed the marginal zinc diet than in controls. Tubulin concentrations in 100,000 g brain supernates were similar between the groups; however, tubulin polymerization in the brain supernates was significantly lower in pups fed the marginal zinc diet compared to controls. Primarily, the early events of polymerization were affected; the lag period of the reaction was doubled, and the initial velocity was slower (26%) in supernates from pups fed the marginal zinc diet than in controls. These findings support the idea that some of the negative effects of marginal zinc deficiency on brain development and function may be mediated by an alteration in microtubule formation.
    Biological Trace Element Research 02/1990; 24(1):13-23. DOI:10.1007/BF02789137 · 1.75 Impact Factor
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    ABSTRACT: Although non-human primates are widely used models of human diseases, often studied for long periods of time, their dietary requirements are not well defined. Over a two—three-year time period, female rhesus macaques were fed either a marginally zinc-deprived diet or a comparable zinc replete purified diet. The purified diets were based on current NRC recommendations. Interestingly poor pregnancy outcome was noted in both the zinc-deprived as well as in the control group. Twenty-eight percent of controls (N=16) and 20% of zinc-deprived animals (N=15) failed to conceive after at least seven matings. Pregnancy loss was also high in both groups of animals including 31% of conceptions in controls (N=11) and 33% of conceptions in zinc deficient animals (N=12). The majority of pregnancy losses occurred after animals had been fed purified diet for over two years. In contrast, normal colony pregnancy loss is estimated at 11%. Furthermore, 3 of 18 live-born infants died prior to 7 months of age and one third of surviving offspring were growth-retarded during the 1st year of life compared to established colony norms. Our data demonstrate the difficulty of constructing adequate purified diets for long-term studies in primates even when based upon available and recommended nutritional information.
    Primates 01/1990; 31(4):579-588. DOI:10.1007/BF02382541 · 1.34 Impact Factor
  • Patricia I. Oteiza · Susana Cuellar · Bo Lönnerdal · Lucille S. Hurley · Carl L. Keen ·
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    ABSTRACT: The hypothesis that one of the biochemical lesions underlying zinc deficiency-induced teratogenicity is altered microtubule formation was tested. Day 19 fetuses from zinc-deficient Sprague-Dawley dams were characterized by low brain supernate zinc concentrations and slow brain tubulin polymerization rates compared to controls. Brain supernate tubulin and protein concentrations were similar in zinc-deficient and control fetuses. In vitro brain tubulin polymerization rates were increased following addition of zinc to either control or zinc-deficient brain supernates; however, the stimulatory effect of added zinc on polymerization was significantly higher in brain supernates obtained from zinc-deficient fetuses compared to controls. These results support the idea that one effect of fetal zinc deficiency is a reduction in tubulin polymerization, which in turn may result in altered microtubule function.
    Teratology 01/1990; 41(1):97-104. DOI:10.1002/tera.1420410110
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    C L Keen · J M Peters · L S Hurley ·
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    ABSTRACT: The effect of valproic acid on the distribution of gavaged 65Zn in maternal and embryonic tissue of Sprague-Dawley rats was examined 24 h after gavaging of the drug on d 13 of pregnancy. Valproic acid treatment resulted in a significantly higher retention of 65Zn in maternal liver and lower amounts in uterus, placenta and embryos than in controls. Compared to controls, gel chromatography of maternal liver from valproic acid-treated dams showed higher 65Zn counts associated with a protein peak of molecular weight of 6,500, the approximate molecular weight of the Zn-binding protein metallothionein. These results support the idea that the teratogenicity of valproic acid is in part due to an induction of embryonic Zn deficiency secondary to a drug-induced sequestering of Zn into maternal liver that results in a decrease in maternal plasma Zn and subsequent reduction in embryonic Zn uptake.
    Journal of Nutrition 05/1989; 119(4):607-11. · 3.88 Impact Factor
  • Kenjie Amemiya · Lucille S. Hurley · Carl L. Keen ·
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    ABSTRACT: The effect of 6-mercaptopurine (6-MP) on the distribution of gavaged 65Zn in maternal and embryonic tissues of Sprague-Dawley rats was examined 24 hr after injection of the drug on day 13 of pregnancy. 6-MP injection resulted in a significantly higher retention of counts of 65Zn in maternal liver and lower counts in maternal plasma, uterus, placenta, and embryo than in controls. Compared to controls, gel chromatography of maternal liver from 6-MP injected dams showed higher counts associated with a protein peak of molecular weight 6,000-8,000, the approximate molecular weight of the zinc-binding protein metallothionein. These results support the idea that the zinc deficiency, which is observed in day 21 fetuses from dams injected with 6-MP during midgestation, may be the result of a drug-induced sequestering of zinc into maternal liver followed by a decrease in maternal plasma zinc and subsequent reduction in fetal zinc uptake. We suggest that this 6-MP-associated redistribution of zinc into maternal liver may be due to induction of maternal metallothionein synthesis by the drug.
    Teratology 04/1989; 39(4):387-93. DOI:10.1002/tera.1420390410
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    ABSTRACT: It has been shown that epileptics have lower mean blood concentration of manganese than do controls but the cause of this abnormality has not been determined. In order to investigate the effects of seizures on manganese distribution in the body, rats were treated with kainic acid to produce spontaneous seizures which were quantitated for number and severity. Manganese, zinc, copper and iron concentrations were determined in blood, brain, liver, heart and kidney. Kainate-treated animals ate more food but gained less weight than controls. Liver and kidney manganese concentrations were significantly higher in kainate-treated animals than in controls. Blood manganese concentration showed a significant negative correlation with seizure index while heart manganese concentration showed a significant positive correlation with seizure index. None of the other trace elements showed a significant correlation between trace element concentration and seizure index in any of the tissues, although iron concentration was lower in brain and copper concentration was lower in kidney of kainate-treated animals than in their appropriate controls. These data show that manganese concentrations are generally elevated in tissues of kainate-treated animals. This increased manganese concentration may be related to the increased energy demand of these animals.
    Neuroscience 02/1989; 33(1):223-7. DOI:10.1016/0306-4522(89)90323-0 · 3.36 Impact Factor
  • M S Mameesh · C L Keen · L S Hurley ·
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    ABSTRACT: The effect of deficiencies of zinc or copper in the rat on the activity of purine nucleoside phosphorylase and pyruvate kinase in erythrocytes, liver and muscle was investigated. The data showed no effect of either zinc or copper deficiencies on the activity of these enzymes in the tissues tested. It is concluded that these enzymes are not useful markers for either zinc or copper deficiency.
    International Journal for Vitamin and Nutrition Research 02/1989; 59(4):390-5. · 0.85 Impact Factor
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    C L Keen · M S Golub · M E Gershwin · B Lönnerdal · L S Hurley ·
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    ABSTRACT: Studies of marginal zinc deficiency in rhesus monkeys have demonstrated that plasma Zn levels are often a poor indication of Zn status. To better assess the Zn status of these animals, we examined their liver concentration of Zn as well as of other minerals, metallothionein (MT), and superoxide dismutase (SOD). Liver-wedge biopsies were obtained from adult rhesus monkeys fed for 15 mo, either a control (100 micrograms Zn/g) or a marginally Zn deficient diet (4 micrograms/g; ZD). Liver Zn and MT concentrations were lower in ZD monkeys than in controls whereas iron concentration was higher in ZD monkeys than in controls. Liver copper, manganese, and magnesium concentrations and activities of CuZnSOD and MnSOD were similar in the two groups. Data from the groups were pooled for regression analysis. Measurement of liver Zn and MT concentrations are useful in the assessment of the effects of long-term Zn deprivation in primates.
    American Journal of Clinical Nutrition 07/1988; 47(6):1041-5. · 6.77 Impact Factor
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    ABSTRACT: Rats fed a magnesium (Mg) deficient diet have a lower endurance capacity than rats fed Mg adequate diets. The current study evaluates the effects of marginal, moderate, and severe Mg deficiencies on physiological and biochemical changes that may contribute to the reduced endurance capacity of Mg deficient rats. Variable levels of dietary Mg (400, 200, 100, 50 micrograms/g) were fed for 23 d to 5-wk-old male Osborne-Mendel rats. Indirect blood pressure and heart rate were measured during dietary treatment. Forty-eight hours after an endurance test, rats were killed and sampled for plasma glucose, insulin, and triglyceride levels. Organ weights, mineral and trace element concentrations, and carcass composition were determined. Blood pressure was lower in rats fed 50 and 100 ppm Mg during the first half of the study than in controls (400 ppm Mg). There were no significant differences in blood pressure among groups at the end of the study. Heart rate was not affected by dietary Mg intake. Plasma insulin was lowered by decreasing dietary Mg; however, plasma glucose and triglyceride concentrations were not affected by dietary Mg intake. Rats fed 100 and 50 ppm Mg diets had significantly higher calcium concentrations in plasma and gastrocnemius muscle than controls. Dietary Mg variably affected tissue trace element (iron, zinc, copper, and manganese) concentrations but did not affect Mg concentrations in any organ studied. Body composition was significantly altered by dietary Mg intake. In conclusion, variable Mg intake differentially affects the parameters evaluated. Thus, the decreased endurance capacity of the Mg deficient rat is apparently not the result of a single biochemical lesion but is likely to be multifactorial.
    Biological Trace Element Research 07/1988; 16(1):1-18. DOI:10.1007/BF02795329 · 1.75 Impact Factor
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    P I Oteiza · L S Hurley · B Lönnerdal · C L Keen ·
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    ABSTRACT: The possible physiological role of Zn in tubulin polymerization was studied. Tubulin assembly in vitro was characterized in brain supernatants from rats fed a marginally Zn-deficient diet (10 micrograms Zn/g) during pregnancy and lactation. The initial rate of tubulin polymerization was significantly lower (27%) in brain supernatants from the marginally Zn-deficient animals than from controls. This was associated with a lower Zn concentration in the brain supernatants from the marginally deficient rats. Total protein and tubulin concentrations were the same in the supernatants from both groups. These data show that Zn is necessary for normal tubulin assembly and indicate that one biochemical defect underlying brain alterations in Zn deficiency could be abnormal microtubule function.
    Journal of Nutrition 07/1988; 118(6):735-8. · 3.88 Impact Factor
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    M S Golub · M E Gershwin · L S Hurley · A G Hendrickx ·
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    ABSTRACT: Arrested adolescent growth and sexual maturation are striking symptoms of severe dietary zinc deprivation. More general implications of mild or marginal Zn deficiency during adolescence are not known. Five marginally Zn-deprived (ZD) male monkeys (4 mg Zn/kg diet) were compared with five controls pair fed a diet containing 100 mg Zn/kg during early adolescence. Mean plasma Zn levels were 38% lower in ZD group than in controls when evaluations began. During rapid growth plasma Zn decreased in controls but not ZD animals. ZD animals had delayed onset of accelerated weight gain and linear growth; loss of subcutaneous fat typical of early adolescence did not occur. ZD monkeys required two to three times more trials for both learning and reversal a visual discrimination task. Immune function was depressed 20-30% as reflected in early reduced proliferative response of peripheral lymphocytes and later lower immunoglobulin levels. Marginal dietary Zn deprivation affects growth and function in adolescence without producing frank developmental retardation.
    American Journal of Clinical Nutrition 07/1988; 47(6):1046-51. · 6.77 Impact Factor
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    ABSTRACT: Skeletal maturation was evaluated from ages 1 to 3 y in rhesus monkeys that had been subjected to a diet marginally deficient in zinc (4 micrograms/g Zn) from conception through age 3 y. Skeletal development was assessed at 18, 24, 30, and 36 mo of age and compared with that of controls fed ad libitum. Skeletal maturation was determined by the presence of epiphyseal ossification centers. To evaluate endochondral bone mineralization the appearance of the zone of provisional calcification on the metaphyseal side of the growth plate and the width of the growth plate were observed. Marginal Zn deprivation was associated with delayed skeletal maturation in monkeys up to age 3 y. Defective mineralization of bone was evident in these monkeys up to age 6 mo. Between ages 6 mo and 3 y bone mineralization increased in some of the marginal-Zn monkeys to values that were only slightly below those for control monkeys.
    American Journal of Clinical Nutrition 06/1988; 47(5):889-95. · 6.77 Impact Factor
  • K G Vruwink · L S Hurley · M E Gershwin · C L Keen ·
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    ABSTRACT: To determine if prenatal zinc deficiency has a persistent effect on metallothionein (MT) regulation, Swiss-Webster mice were mated and fed a diet containing either control (100 micrograms Zn/g) or low levels of zinc (5 micrograms Zn/g) from Day 7 of gestation to parturition. After birth all mice were given the control diet. Liver zinc and MT levels were 50% lower in newborn pups from dams fed the low zinc diets than in control pups. In control pups, liver zinc and MT concentrations were relatively stable during the first week of postnatal life. In contrast, in pups prenatally deprived of zinc, liver levels of zinc and MT increased such that by Day 3 of postnatal life, the levels were not significantly different from controls. At Day 56, serum IgM concentrations were significantly lower in the low zinc offspring. Liver zinc concentrations in the two groups of mice were similar at Day 70 postnatal, and in both groups liver MT levels were below detection limits. However, when Day 70 mice were given zinc injections to stimulate MT synthesis, the prenatally zinc deprived offspring showed markedly higher liver MT levels than did control mice given similar injections, despite similar liver zinc concentrations in the two groups. These results show that prenatal zinc deficiency has pronounced effects on postnatal MT metabolism which can persist into adulthood.
    Proceedings of The Society for Experimental Biology and Medicine 06/1988; 188(1):30-4. DOI:10.3181/00379727-188-42702
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    B L Reis · C L Keen · B Lönnerdal · L S Hurley ·
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    ABSTRACT: Zinc metabolism of adult female C57BL/6J mice varying in age and reproductive status was studied using 65Zn. Animals were injected intraperitoneally with isotope, and whole-body and tissue turnover of 65Zn was measured. Biological half-life of whole-body 65Zn for pregnant females was 129% of that for nonpregnant, nonlactating females of similar age (25.7 and 20.0 d, respectively). Conversely, the half-life of zinc was less for lactating (11.1 d) and aged (15.3 d) females than for either pregnant or nonpregnant, nonlactating young adult females. Retention of 65Zn was generally lower for all tissues of pregnant and lactating dams than for nonpregnant, nonlactating females except for brain and tibia. In aged females, specific activity at 20 d postinjection did not differ from that of nonpregnant, nonlactating young adult females for any tissue except bone. While specific activity of tibia increased during pregnancy and lactation, it was lower in aged females than in nonpregnant, nonlactating young adult females. Increased organ content of zinc resulted from changes in zinc concentration or in organ mass or both, and was supported by increased food intake. Thus, greater food intake for these groups than for young adult females contributed to the higher turnover of tissue 65Zn. Differences in concentrations of Cu, Ca and Mg were also observed among groups for some tissues; the significance of these differences and their relationship to zinc metabolism are not clear.
    Journal of Nutrition 04/1988; 118(3):349-61. · 3.88 Impact Factor
  • S Zidenberg-Cherr · P A Benak · L S Hurley · C L Keen ·
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    ABSTRACT: Excessive ethanol intake during pregnancy can cause birth defects in humans and is referred to as fetal alcohol syndrome (FAS). Because of the characteristic changes that are similar in FAS and zinc (Zn) deficiency, we have examined the role of Zn nutriture in the teratogenicity of ethanol in Sprague-Dawley rats. Female Sprague-Dawley rats were adapted to liquid diets containing Zn at 2 micrograms/ml (LZn), 30 micrograms/ml (AZn), or 300 micrograms/ml (HZn); ethanol contributed either 0% or 36% of kilocalories. Ethanol consumption resulted in reduced fetal growth and retarded skeletal development. Ethanol had no effect on whole body fetal Zn concentrations; however, copper (Cu) deficiency was induced in the HZn fetuses. Ethanol consumption resulted in higher than normal fetal liver CuZnSOD activity in the LZn and AZn groups. Fetuses from HZn dams showed no ethanol effect on CuZnSOD activity, suggesting that the low availability of Cu to the fetus prevented the increase in CuZnSOD activity in response to ethanol. The increase in the activity of fetal CuZnSOD in LZn and AZn groups is consistent with the concept that the metabolism of ethanol results in free radical generation in fetal tissue. Because excessive free radical levels may result in tissue damage, this may be one mechanism contributing to the expression of FAS.
    Drug-nutrient interactions 02/1988; 5(4):257-74.
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    J M Rogers · B Lönnerdal · L S Hurley · C L Keen ·
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    ABSTRACT: Because disturbances in iron metabolism might contribute to the teratogenicity of zinc deficiency, we examined the effect of zinc deficiency on fetal iron accumulation and maternal and fetal retention of 59Fe. Pregnant rats were fed from mating a purified diet containing 0.5, 4.5 or 100 micrograms Zn/g. Laparotomies were performed on d 12, 16, 19 and 21 of gestation. Maternal blood and concepti were analyzed for zinc and iron. Additional groups of dams fed 0.5 or 100 micrograms Zn/g diet were gavaged on d 19 with a diet containing 59Fe. Six hours later maternal blood and tissues, fetuses and placentas were counted for 59Fe. Maternal plasma zinc, but not iron, concentration was affected by zinc deficiency on d 12. Embryo zinc concentration on d 12 increased with increasing maternal dietary zinc, whereas iron concentration was not different among groups. On d 16-21 plasma iron was higher in dams fed 0.5 micrograms Zn/g diet than in those fed 4.5 or 100 micrograms/g, whereas plasma zinc was lower in dams fed 0.5 or 4.5 micrograms Zn/g than in those fed 100 micrograms Zn/g diet. On d 19 zinc concentration in fetuses from dams fed 0.5 micrograms/g zinc was not different from that of those fed 4.5 micrograms/g zinc, and iron concentration was higher in the 0.5 microgram Zn/g diet group. The increase in iron concentration in zinc-deficient fetuses thus occurs too late to be involved in major structural teratogenesis. Although whole blood concentration of 59Fe was not different in zinc-deficient and control dams, zinc-deficient dams had more 59Fe in the plasma fraction.(ABSTRACT TRUNCATED AT 250 WORDS)
    Journal of Nutrition 12/1987; 117(11):1875-82. · 3.88 Impact Factor
  • G. F. Carl · Carl L. Keen · B. B. Gallagher · L. S. Hurley ·

    10/1987: pages 105-111;

Publication Stats

6k Citations
1,141.55 Total Impact Points


  • 1959-2009
    • University of California, Davis
      • • Department of Nutrition
      • • Division of Rheumatology/Allergy/Clinical Immunology
      • • California National Primate Research Center
      • • Department of Economics
      Davis, California, United States
  • 1989
    • Kuwait University
      • Department of Biochemistry
      Kuwait, Muhafazat al `Asimah, Kuwait
  • 1987
    • University of California, Los Angeles
      Los Ángeles, California, United States
  • 1961-1963
    • University of California, Berkeley
      Berkeley, California, United States