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Biomedical subjects

G Ahmad

Publications and source records attributed to G Ahmad.

34 records · Page 2Linked to original sources

Urinary erythrocyte morphology as a diagnostic aid in haematuria.

The value of urinary erythrocyte morphology in diagnosing glomerular and nonglomerular haematuria was studied using phase contrast microscopy in 105 patients with significant haematuria. Fifty-eight (93.6%) out of 62 patients with glomerulonephritis had dysmorphic erythrocytes and 40 (93.1%) out of the 43 patients with nonglomerular disease had isomorphic erythrocytes in the urine. A mixed picture of glomerular and nonglomerular haematuria was seen in 5 patients. The sensitivity was 93.6%, the specificity was 97.7% and the positive predictive value was 98.3% for glomerulonephritis in patients with dysmorphic haematuria. The positive predictive value for a nonglomerular source of bleeding was 96.7% with isomorphic haematuria. It is concluded that phase contrast microscopic examination of erythrocytes in urine is a simple, inexpensive and noninvasive technique that reliably distinguishes between glomerular and nonglomerular bleeding in patients.

Erythrocyte Count↗

Cerebral ornithine decarboxylase levels following gestational exposure to cocaine.

The pre- and postnatal developmental course of cerebral ornithine decarboxylase (ODC) has been studied in infant rats after treatment of pregnant dams with cocaine. Levels of cocaine attained in brains and serum of embryos were not initially increased over corresponding maternal values, but were more persistent. However, cocaine was not longer detectable in these tissues 4 days after administration. The cerebral ODC level of treated pups was initially depressed and subsequently elevated relative to control values. These changes were apparent at times when cocaine was not detected in the developing brain. Results indicate that a transient exposure to cocaine in utero may lead to prolonged developmental abnormality.

Aging↗

Effects of gestational exposure to phencyclidine: distribution and neurochemical alterations in maternal and fetal brain.

Phencyclidine is a widely used drug of abuse and is known to produce a wide variety of psychoactive effects. PCP abuse by pregnant women has been reported to result in the birth of infants exhibiting irritability, jitteriness and hyperactivity with high pitched cries. The present study was designed to evaluate the distribution of PCP in the maternal and fetal brain and the neurochemical effects produced by gestational exposure. Pregnant Sprague-Dawley rats were treated sc with 5 mg/kg PCP on 3 consecutive days (GD 9-11, 12-14, 15-16, or 18-20). On gestational day (GD) 21 all rats were killed by decapitation and maternal and fetal blood was collected for PCP analysis. Brains were dissected from dams and fetuses for PCP and neurochemical analyses. On GD 21 after exposure on GD 18-20, the fetal: maternal ratio of brain PCP concentrations was 11:1. PCP exposure on GD 12-14, 15-17, and 18-20 significantly decreased fetal brain PCP binding sites on GD 21, whereas maternal values were unchanged. Fetal dopaminergic and muscarinic cholinergic receptor binding and neurotransmitter concentrations were unaffected by prenatal PCP exposure. These data demonstrated that maternal PCP exposure resulted in prolonged exposure of the developing CNS and also indicated that gestational exposure to PCP decreased high affinity binding sites of PCP in term fetal brain.

Animals↗

Gestational exposure to phencyclidine (PCP) in rats decreases PCP binding sites in term fetal brain.

Pregnant Sprague-Dawley rats were treated with 5 mg/kg body weight of phencyclidine (PCP) injected at 1 ml/kg subcutaneously on three consecutive days at four different stages of gestation. Within 10-30 min after treatment, dams showed some lack of motor coordination and became lethargic. On gestational day 21, all rats were killed by decapitation and brains were dissected and stored from mother and fetus for neurochemical analysis. PCP, dopamine and muscarinic cholinergic receptor binding was measured in membranes prepared from maternal and fetal whole brain. Neurotransmitter concentrations were also measured in the fetal brain homogenates. There was a significant decrease in PCP binding sites in fetal but not maternal brains after maternal PCP injection at gestational days 12-14, 15-17 and 18-20, but not at 9-11 days. Dopamine and muscarinic cholinergic receptor binding was not significantly altered in fetal or maternal brain when compared with vehicle control animals. The whole brain dopamine, 3,4-dihydroxyphenylacetic acid, serotonin, and 5-hydroxyindoleacetic acid concentrations did not show significant change in any group studied. These data indicate that gestational exposure to PCP decreases high affinity binding of PCP in term fetal brain at doses which do not alter maternal PCP receptor binding.

Animals↗

Toxic effects of phencyclidine on developing chick embryo brain.

We studied the effects of Phencyclidine (PCP, Angel Dust) on the developing chick embryo brain. In Group-1, the eggs were injected with PCP on the 7th day of incubation and the embryo brains were studied on the 10th day. In Group-2, eggs were injected twice; first on the 7th day and then on the 10th day of incubation. Group-2 brains were then studied on the 16th day of incubation. PCP significantly depressed the development of embryo brains. Cerebral hemisphere weight, total protein and total DNA were significantly lower on day 10 of incubation in Group-1. Similar results were observed in Group-2. Concomitantly, the concentration of brain serotonin at day 10 was also significantly reduced when PCP was injected into the eggs on the 7th day of incubation. Since serotonin has been reported to influence development of the chick embryo brain, the present finding of the effect of PCP on brain development might be a secondary phenomenon. The possible implications of the effects of PCP on human brain development are also discussed.

Animals↗

Persistence of phencyclidine in fetal brain.

Phencyclidine residues were found in the brains of rat pups of mothers dosed with this drug during pregnancy. These levels were significant at times after dosing when maternal levels of phencyclidine in serum or brain were low or undetectable. The persistence of this compound in fetal serum was also not prolonged. Maternal ingestion of PCP for a relatively brief time may result in an extended exposure of the developing nervous system.

Animals↗

Abuse of phencyclidine (PCP) a laboratory experience.

Emergency Room patients at Riverside General Hospital who are found by the attending physician to have depressed sensorium and altered personality are routinely subjected to urine tests for various drugs of abuse including phencyclidine (PCP). The findings of the laboratory analysis of these patients are presented in this paper. The toxicology laboratory of this hospital performs screening procedures for various drugs on urine specimens by thin layer chromatography. Drugs detected are confirmed by gas chromatography and a homogeneous enzyme immunoassay technique. In 1981, 1.6% of the urine specimens of patients in the above-mentioned category were found to be positive for PCP. This percentage increased sharply during 1982 (5.8%) and 1983 (5.6%). During 1984 and 1985 the percentage dropped to 4.2% and 4.6%. It is implied from data that the abuse of this drug in this area has leveled off. The data also indicated that PCP is predominantly used by young adults with ages ranging from 21 to 30 years. The abuse of this drug in people over 40 years of age is comparatively very small. Among users of this drug, 67.5% are men and 32.5% are women. Out of 68 women found to be abusing PCP, 5 delivered their babies in this hospital. PCP was detected in the urine specimens of each of these babies. Four out of the five infants showed withdrawal symptoms such as extreme irritability, jitteriness, hyperactivity with high pitched cries and a poor ability to take food.

California↗

Correlations between neonatal body weight and adolescent brain development in rats.

Correlations between neonatal body weight, and body weight and several brain parameters at 30 days of age were studied in normal rats. At 30 days ('adolescence') cortex has already reached its final thickness and the rat exhibits long-term memory. Brain parameters included cerebral weight, DNA, protein and cholesterol contents and densities, as well as cortical and cerebral dimensions (cerebral sections). As expected, most of these parameters in 30-day-old animals were significantly correlated with each other. Unexpectedly, neonatal body weight was also significantly correlated with cholesterol content and density at 30 days, as well as with cortical and cerebral dimensions at 30 days. Thus, statistically, neonatal body weight already predetermines the extent of neuronal (cerebral) development at adolescence (30 days). This finding also makes it possible to make at birth statistical predictions about future brain development without having to sacrifice neonatal animals.

Animals↗

The effect of progesterone on brain and body growth of chick embryos.

It has been suggested that in the embryo hormonal steroids may act also as control factors for the growth of neural systems. In the present work progesterone was introduced onto the chorioallantoic membrane of the chick embryo on day 7 or days 7 and 10 of incubation. The embryo, dissected at day 10, showed significant increases in body weight and cerebral hemispheres weight. The response at day 13 was less pronounced; male embryos responded to progesterone more than the female embryos. Progesterone is a precursor to other corticosteroids, but corticosterone itself had a significant harmful effect on embryonal growth. Several possible explanations of these results have been offered. It appears that progesterone itself promotes the growth of the early embryo, but the effect depends on its age and sex.

Animals↗

The effects of exogenous nutrients on growth of chick embryo brain.

The effect of an early addition of exogenous nutrients on brain growth has been investigated in chick embryo. The nutrients were introduced onto chorioallantoic membrane at day 6 or 7 of embryonal life, and the cerebral hemispheres examined at the end of neuronal proliferation for the following parameters: weight, DNA content (index of cell number) and protein content. L-Tryptophan produced significant inhibition, probably by creating amino acid imbalance and interference with the transport of other amino acids. D-Tryptophan (slower transport) was inactive. 5-Methyltryptophan produced significant inhibition, probably by causing deficiency of tryptophan utilization and of production of serotonin, which is a growth factor for early brain. Glycine stimulated brain growth, probably by conversion to glucose which is the main energy source for the embryo in this period. Brain weight and DNA were found to be significantly correlated with blood glucose level. It is concluded that, within genetic limits, early brain growth might be manipulated in both directions (inhibition or stimulation) by addition of proper nutrients during sensitive period of neuronal proliferation.

Age Factors↗

Effects of undernutrition and protein malnutrition on brain chemistry of rats.

The present study was undertaken to assess the effects of different degrees of nutritional restrictions during fetal life, suckling, and after weaning on the chemical composition of the brain. At 42 days of age, the rats were killed, and the brains were processed for analyses. The rats exposed to severe protein malnutrition after weaning had lower brain weights than those on controls. The brain seems to be resistant to the effects of moderate protein malnutrition imposed during suckling or after weaning. Thus, the brain is either resistant to the effects of mild nutritional deficiency imposed during suckling, or brain composition is very responsive to nutritional rehabilitation initiated after weaning. The effects of severe undernutrition during suckling were not, however, reversed when adequate nutrition was initiated after weaning. The suckling period seems to be critical during development, as the process of myelination was lowered and the levels of electrolytes were irreversibly disturbed. The brains of the rats born to the mothers protein malnourished during gestation were not significantly different from those of controls. The brain seems to be either preferentially protected from the effects of malnutrition imposed during fetal development, or the brain component are very responsive to nutritional rehabilitation initiated immediately after birth. It is suggested that the mother's nutritional status during gestation does not significantly affect the development of the brain. When the young were born to and nursed by protein-malnourished mothers, the growth and the maturation of the brain in such animals were similar to those in rats moderately undernourished during suckling. Growth and maturation of the brain are affected by a lowered level of protein in the diet. Moderate undernutrition imposed during suckling is not important, but the effect is maximum when undernutrition is severe during this period. The suckling period is therefore, comparatively more critical during development.

Acetylcholinesterase↗

Surdo-cardiac syndrome: incidence among children in schools for the deaf.

This is a report on a survey of 1126 deaf children in three schools for the deaf in the Province of Ontario. One case of the surdo-cardiac syndrome previously reported is included. There were four other children who had a history of syncope but no prolongation of the Q-T interval on the ECG. It is possible that these may represent a variant of the syndrome. Five more children had a prolonged Q-T interval but no fainting spells.

Adams-Stokes Syndrome↗