Biomedical subjects
Publications and source records attributed to N Rawashdeh.
The rate of consanguineous mating in north Jordan was 63.7% with an average inbreeding coefficient of 0.0283. First cousin marriages were the most predominant type (58.5%); villagers showed higher levels than city dwellers. The level of female education did not influence consanguinity rate.
The acetylator phenotype was determined in 31 insulin-dependent (IDDM) and 110 noninsulin-dependent (NIDDM) Jordanian diabetics, and was compared to that of 160 healthy volunteers of the same ethnic group. Dapsone was used as the test drug. The rapid acetylator phenotype was slightly less frequent in IDDM and slightly more frequent in NIDDM. Neither of the differences was significant. When acetylator status in the two types of diabetes mellitus was compared, there was a significant difference among the two groups. Patients with IDDM had a higher percentage of the slow acetylator phenotype when compared to NIDDM patients. The association between acetylator status and IDDM in Jordanians, which agrees with that reported for the Saudi Arabian population, is the reverse of what is found in European populations. The results demonstrate ethnic differences in acetylator status among IDDM patients.
To determine the importance of alpha 1-adrenergic receptors in the endocrine responses of fetal lambs to hemorrhage, eight chronically instrumented fetal lambs were bled of 20% of their measured blood volume after pretreatment with prazosin (24.8 +/- 2.1 days' gestation) or inert vehicle (124.2 +/- 2.2 days' gestation) according to a randomized, crossover protocol. Cortisol levels increased threefold with prazosin injection and remained elevated after hemorrhage but did not change with hemorrhage after vehicle infusion. Plasma renin activity was unaffected by the injection of prazosin but increased in both groups after hemorrhage. Vasopressin levels were unchanged in the control group throughout the experiment but increased tenfold with hemorrhage after pretreatment with prazosin. alpha 1-Adrenergic receptor blockade removes adrenergic inhibition of cortisol secretion and changes the hypotensive threshold for the secretion of vasopressin.
To ascertain if reductions in fetal plasma cortisol cause increases in fetal plasma ACTH, we treated pregnant ewes or their fetuses with aminoglutethimide (10 mg/kg BW) and metyrapone (20 mg/kg BW) and measured the hormonal responses with RIAs. When given to fetuses (n = 9) at 0.90 +/- 0.01 gestation (term-145 days), the steroid synthesis inhibitors reduced fetal plasma cortisol from 35.1 +/- 11.9 to 18.5 +/- 6.2 ng/ml (P less than 0.01) and plasma ACTH increased from 37 +/- 7 to 189 +/- 74 pg/ml (P less than 0.02). Thus, late in gestation cortisol from the fetal adrenal suppresses basal fetal ACTH secretion. Blockade of steroid biosynthesis in pregnant ewes carrying intact fetuses at 0.76 +/- 0.02 gestation (n = 11) or adrenalectomized fetuses at 0.81 +/- 0.01 gestation (n = 6) also reduced cortisol and increased ACTH in fetal plasma. In intact fetuses cortisol declined from 9.4 +/- 2.0 to 3.6 +/- 0.9 ng/ml (P less than 0.05), and ACTH increased from 46 +/- 8 to 183 +/- 67 (P less than 0.01); cortisol declined in adrenalectomized fetuses from 2.1 +/- 0.4 to 1.1 +/- 0.3 ng/ml (P less than 0.01), and ACTH increased from 106 +/- 13 to 400 +/- 104 pg/ml (P less than 0.01). Cortisol infusions into intact and adrenalectomized fetuses prevented both the decline in steroid concentration caused by the biosynthesis inhibitors given to the ewe and the increase in fetal plasma ACTH concentration. These data indicate that reductions in plasma cortisol in adrenalectomized fetuses or intact fetuses at a time in development when the fetal adrenal produces little cortisol cause compensatory increases in fetal plasma ACTH concentration. The simplest explanation for these observations is that from approximately 0.70 gestation, basal fetal ACTH secretion is tonically inhibited by cortisol circulating in fetal plasma. This cortisol can originate from sources other than the fetal adrenal.
A study of 260 Jordanians who became blind or visually impaired (according to World Health Organization standards) before the age of 15 years showed the dominant effects of genetically determined causes in two generations. Genetic causes were responsible for the visual impairment in 122 (77.7%) of 157 subjects in the group born after 1970 and for 69 (67%) of 103 in the group born before 1970. There was a statistically significant change in the overall pattern (genetic and acquired causes) of blindness between the two generations, and there was also a significant change in the pattern of acquired blindness alone. A decrease in corneal infections leading to blindness or visual disability in the younger generation was accompanied by an increase of trauma in the same age group. Parental consanguinity in those with genetically determined causes of visual impairment was high compared with those with nongenetic causes (79% vs 33.3%, P < .05). The autosomal recessive mode of inheritance was the most common pattern encountered (53.9%).