Search PubMed⌕ Search

Biomedical subjects

A S Bloom

Publications and source records attributed to A S Bloom.

At least 37 records · Page 2Linked to original sources
PubMed1988

Differential validity of the K-ABC for lower functioning preschool children versus those of higher ability.

The Kaufman Assessment Battery for Children (K-ABC) and the Stanford-Binet Intelligence Scale, Form L-M, were administered to 93 preschool children at risk for learning problems. Lower and higher functioning groups were determined by a Stanford-Binet IQ median split. Although the Stanford-Binet and K-ABC yielded nearly identical results in the higher group, K-ABC standard scores were significantly higher than Stanford-Binet IQ in the lower group. The Stanford-Binet and K-ABC correlated more strongly in the higher group than in the lower group. These findings question the ability of the K-ABC to discriminate among at-risk preschoolers functioning in the lower ranges of cognitive ability.

Child↗
PubMed1987

Does a supernumerary nipple/renal field defect exist?

In 65 patients evaluated for suspected genetic and/or developmental problems, a roentgenographic study of the kidneys was performed because of the presence of a supernumerary nipple (SNN). Seven of 65 (11%) had a significant renal lesion that included conjoined kidneys in a female with Fanconi's anemia. Four of these patients did not have signs or symptoms suggestive of an underlying urinary tract pathologic condition. These results indicate that an SNN/renal field defect probably exists, although the significance of this association is significantly weaker than that originally proposed by Mehes. One variable influencing this association appears to be racial differences, as evidenced by the absence of renal defects in blacks with an SNN. Based on our findings, the identification of additional minor phenotypic abnormalities may represent an additional mediating variable in this association. However, the discovery of an SNN in an otherwise normal individual, or an individual with a recognizable pattern of human malformation not associated with renal anomalies or central nervous system dysfunction alone, does not appear to be an indication for additional diagnostic studies of the urinary tract.

Breast↗
PubMed1986

Effects of delta 9-tetrahydrocannabinol on glucagon receptor coupling to adenylate cyclase in rat liver plasma membranes.

Delta-Tetrahydrocannabinol (delta 9-THC), the principal psychoactive constituent of Cannabis sativa, was found to increase glucagon activation of liver plasma membrane adenylate cyclase. In the presence of 30 microM delta 9-THC, the EC50 for glucagon was decreased by 60% from 7.6nM to 3.1 nM. 11-OH-delta 9-THC, a psychoactive metabolite of delta 9-THC, also increased glucagon activation of adenylate cyclase while two cannabinoids without marihuana-like psychoactive potency, cannabinol and cannabidiol, did not. At 30 microM, delta 9-THC either slightly decreased or had no effect on the activation of adenylate cyclase by GTP, Gpp(NH)p, fluoride ion, forskolin or ATP alone. Delta 9-THC had no effect on the binding of [125I] glucagon to liver plasma membranes. Arrhenius plots demonstrated that delta 9-THC and 11-OH-delta 9-THC, but not CBD, decreased the activation energy above the break temperature. Therefore, delta 9-THC increased the coupling of the glucagon receptor to adenylate cyclase apparently by removing a constraint on receptor-Ns coupling.

Adenylyl Cyclases↗
PubMed1986

Implications of large WISC/WISC-R Verbal-Performance IQ discrepancies.

Forty children with Verbal-Performance IQ discrepancies on the WISC/WISC-R were studied in regard to clinical findings on psychological, educational, speech-language, and medical evaluations. Significant delays in the development of verbal when compared to performance skills were observed frequently in this referred sample. The verbal deficits were mostly developmental in nature, rather than secondary to emotional or family background factors. These children's developmental difficulties were frequently complex ones that benefitted from multidisciplinary assessment and treatment planning. It was emphasized that future research in regard to these intellectual patterns should be conducted within the confines of more neuropsychologically oriented approaches.

Child↗
PubMed1985

Effects of the cannabinoids on physical properties of brain membranes and phospholipid vesicles: fluorescence studies.

The effects of four cannabinoids on the physical properties of brain synaptic plasma membranes (SPM), lipid extracts of SPM and phospholipid vesicles were evaluated using fluorescence probes. In vitro, the psychoactive cannabinoids, delta 9-tetrahydrocannabinol (delta 9-THC) and 11-hydroxyl-delta 9-tetrahydrocannabinol (11-OH-delta 9-THC) at concentrations of 1 and 3 microM decreased polarization of the fluorescence emission of 1,6-diphenyl-1,3,5-hexatriene (DPH) in SPM. At the same concentrations, cannabidiol (CBD) and cannabinol, cannabinoids devoid of marijuana-like psychoactivity, had no effect on DPH polarization. The effects of 11-OH-delta 9-THC and CBD on vesicles made from lipids extracted from SPM were identical to their effects on intact SPM. These changes in DPH polarization were not due to changes in fluorescence lifetime and indicate that, at low concentrations, the psychoactive cannabinoids increase the rotational mobility of DPH in the membrane core. In contrast, in SPM-extracted lipids, both 11-OH-delta 9-THC and CBD decreased the mobility of stearic acid with an anthroyloxy label at both the second (2-AS) and twelfth (12-AS) carbon atoms. Studies of DPH polarization in various phosphatidylcholines (PC) demonstrated that the actions of the cannabinoids were dependent on initial bilayer fluidity. 11-OH-delta 9-THC was less effective at decreasing polarization of trimethylammonium DPH (TMA-DPH), a probe of the bilayer surface, than of DPH whereas CBD affected mobility of the two probes equally. Neither CBD nor 11-OH-delta 9-THC altered DPH mobility in phosphatidylethanolamine, phosphatidylserine vesicles. These findings indicate that the psychoactive cannabinoids increase fluidity in the hydrophobic core of brain membranes and support a membrane perturbant hypothesis of the mechanism of delta 9-THC action.

Animals↗
PubMed1984

The effects of delta 9-tetrahydrocannabinol on serum thyrotropin levels in the rat.

The effects of acute treatment with delta 9-tetrahydrocannabinol (delta 9-THC) on serum levels of thyrotropin (TSH) and the thyroid hormones triiodothyronine (T3) and thyroxine (T4) were determined in the rat. Intraperitoneal doses of delta 9-THC greater than 3 mg/kg reduced serum TSH levels to less than 10% of control. The ED50 for delta 9-THC was approximately 0.3 mg/kg. After a 10 mg/kg dose of delta 9-THC, the maximum decrease in serum TSH occurred at one hour. Both serum T3 and serum T4 levels were decreased by a single 10 mg/kg delta 9-THC injection with maximal decreases at 6 hr post-injection. The effects of delta 9-THC on the ability of thyrotropin releasing hormone (TRH) to increase serum TSH and T3 were determined. TRH produced a 10-fold increase in serum TSH levels and this increase was unaffected by delta 9-THC pretreatment. Serum T3 levels were slightly increased by TRH and this increase was also unaffected by delta 9-THC. These findings indicate that acute treatment with delta 9-THC results in a decrease in circulating TSH, T3 and T4 levels but has no effect on the pituitary or thyroid response to exogenous TRH.

Animals↗
PubMed1984

Possible noradrenergic involvement in naloxone potentiation of apomorphine-induced stereotypic climbing in mice.

Apomorphine-induced stereotypic climbing behavior in mice was significantly potentiated by pretreatment with the opiate receptor blocker naloxone. In animals additionally pretreated with alpha-methyl-p-tyrosine, brain levels of norepinephrine (NE) and dopamine (DA) were markedly reduced and naloxone potentiation of apomorphine-induced stereotypic climbing was blocked. In mice pretreated with diethyldithiocarbamic acid, brain NE was slightly reduced, brain DA was slightly elevated but naloxone potentiation of apomorphine-induced stereotypic climbing was unaltered. In animals pretreated with reserpine, both brain NE and DA were significantly reduced by naloxone potentiation of apomorphine-induced stereotypic climbing was not affected. In other experiments, pretreatment with low doses of the alpha-adrenergic receptor blocker BE-2254 failed to suppress climbing activity induced by apomorphine alone but did successfully prevent naloxone potentiation of apomorphine-induced stereotypic climbing. These findings suggest the possibility that NE and alpha-adrenergic receptors might play a role in the potentiating influence of naloxone upon apomorphine-induced stereotypic climbing activity in mice.

Animals↗
PubMed1983

Possible role of prostaglandins in the effects of the cannabinoids on adenylate cyclase activity.

In vitro, the cannabinoids delta 9-tetrahydrocannabinol (delta 9-THC), 11-OH-delta 9-THC, cannabidiol and cannabinol all increased adenylate cyclase activity in mouse cerebral cortical homogenates. Levonantradol, a synthetic cannabinoid analog, also increased adenylate cyclase activity while its optical isomer dextronantradol did not. The increases in enzyme activity produced by the active compounds were biphasic with significant increases at 10 microM and/or 30 microM concentrations with return to control levels at 100 microM. The increases did not occur in the absence of added GTP nor did delta 9-THC have any effect on fluoride-stimulation of adenylate cyclase activity. The prostaglandin synthetase inhibitors acetyl salicylic acid and indomethacin and the phospholipase A2 inhibitor quinacrine all abolished the increase in adenylate cyclase activity produced by delta 9-THC, suggesting the involvement of prostaglandins in this cannabinoid action.

Adenosine Triphosphate↗
PubMed1983

IQ discrepancies between the Binet and WISC-R in children with developmental problems.

Administered the Stanford-Binet and WISC-R to 121 children with developmental problems. Twenty-eight of the children received absolute differences of 12 points or greater between the Binet and WISC-R FSIQs, with a mean difference of 16.8 and range of 12 to 28 points. While most of these discrepancies were attributable to expected differences between the tests, there were 10 instances of complete incongruence between the Binet and all the WISC-R IQs. Clinical interpretations of four Binet/WISC-R discrepancy patterns were discussed.

Adolescent↗
PubMed1983

Cognition in cerebral gigantism: are the estimates of mental retardation too high?

The psychological findings on 10 children with cerebral gigantism are reviewed. Infants with cerebral gigantism showed a consistent pattern of psychomotor delay. Preschool age children demonstrated signs of a primary language disorder, and school-age patients had learning disabilities. The incidence of mental retardation was significantly lower than previously reported in the literature. The possibility that some children with cerebral gigantism can be easily misdiagnosed as mentally retarded is discussed.

Child↗
PubMed1982

delta 9-Tetrahydrocannabinol-induced changes in beta-adrenergic receptor binding in mouse cerebral cortex.

The effects of 3 cannabinoids, delta 9-tetrahydrocannabinol (delta 9-THC), 11-OH-delta 9-tetrahydrocannabinol (11-OH-delta 9-THC) and cannabidiol (CBD) on the binding of [3H]dihydroalprenolol [( 3H]DHA) to mouse brain beta-adrenergic receptors were determined. In vitro, delta 9-THC and 11-OH-delta 9-THC increased the specific binding of [3H]DHA. The increased specific binding of [3H]DHA was due to an increase in receptor affinity as indicated by a decrease in the dissociation constant (Kd). CBD had no effect on binding. Chronic administration of delta 9-THC in vivo caused a decrease in the number of [3H]DHA binding sites with no change in Kd.

Animals↗
PubMed1982

Effect of delta9-tetrahydrocannabinol on the synthesis of dopamine and norepinephrine in mouse brain synaptosomes.

The effects of delta 9-tetrahydrocannabinol (THC) on the conversion of [3H]tyrosine (TYR) to [3H]dopamine (DA) and [3H]norepinephrine (NE) by mouse brain synaptosomes were studied. The active uptake of TYR and its conversion to DA and NE were found to be concentrated in a synaptosomal subfraction prepared by using differential and density gradient centrifugation. Therefore, drug studies were performed by using the less pure P2 fraction. THC was administered in vitro by using a polyvinylpyrrolidone vehicle. DA synthesis was examined both in synaptosomes prepared from whole brain and from corpus striatum. THC produced increases in the conversion of TYR to DA in both preparations. Synthesis was stimulated maximally by 10 microns THC in both preparations. Higher concentrations produced either no further increase (whole brain) or a decrease in the synthesis of DA. NE synthesis was measured in synaptosomes prepared from whole brain and from brainstem. A concentration-dependent biphasic response was observed in both preparations. Peak increases in NE synthesis were observed with a 10 micron concentration of THC in synaptosomes from whole brain and a 3 micro concentration in the brainstem. THC also inhibited the active uptake of TYR into synaptosomes in all preparations studied. The lC50 in whole brain was 12.2 microns. The decrease in precursor uptake may be the cause of the decreased DA and NE synthesis observed at the higher concentrations of THC. The data from these studies suggest that delta 9-THC can have a direct effect upon catecholamine-containing neurons in the brain.

Animals↗
PubMed1981

Effects of beta-endorphin on body temperature in mice at different ambient temperatures.

The effect of intracerebroventricular injection of beta-endorphin (beta-END) on body temperature of mice was studied at ambient temperatures (Ta) of 10 degrees, 20 degrees and 31 degrees C. Doses between 0.1 and 10.0 microgram/mouse were studied. The lower (less than 1 microgram) doses of beta-END produced a hyperthermia at all Ta's studied. The higher doses of beta-END produced hyper- or hypothermia depending on the Ta. The subcutaneous injection of naloxone (1 mg/kg) antagonized the high dose hypothermic effects, but not the hyperthermic effect of beta-END. These data suggest that there may be different receptors and/or sites of action for high and low doses of beta-END.

Animals↗
PubMed1981

Behavioral correlates in the happy puppet syndrome: a characteristic profile?

Nine children with the "happy puppet" syndrome are presented here and 19 previously reported cases are reviewed. A characteristic psychological profile is suggested by the children's "unfocused" activities and inconsistent responsiveness to their surroundings. Behavioral characteristics are atypical for mental age and do not appear to represent unusual seizure equivalents. Recognition of such non-adaptive behavior may be of importance in selecting specific treatment and management techniques to modify the characteristics of this syndrome at an early age.

Child Behavior Disorders↗
PubMed1981

Endogenous norepinephrine release induced by tyramine modulates intestinal ion transport.

To study the effects of endogenous norepinephrine on intestinal ion transport, we tested the actions of an indirect sympathomimetic agent, tyramine, on electrolyte fluxes in the short-circuited rabbit ileum in vitro. Tyramine (10(-5) M) alone had no effect on short-circuit current or Na transport but increased Cl absorption. Tyramine decreased the short-circuit current, stimulated both Na and Cl absorption, and increased tissue conductance when its breakdown by endogenous monoamine oxidase enzymes was inhibited by pretreatment with pargyline (10(-4) M). Pargyline alone had no effect on short-circuit current and NaCl transport. The effect of norepinephrine on NaCl transport was inhibited by the alpha-adrenergic receptor antagonist, phentolamine (10(-7) M). This response was also prevented when animals were chemically sympathectomized with 6-hydroxydopamine. Although sympathectomy decreased measurable tissue norepinephrine by 80%, it did not alter basal short-circuit current, Na and Cl absorption, and the short-circuit current response to glucose-stimulated Na transport and to exogenous norepinephrine. Thus, a pool of norepinephrine in intestinal adrenergic neurons released by tyramine affects intestinal ion transport but does not alter basal ion transport. These data suggest close neuropharmacologic similarities between the adrenergic nervous system in the intestine and other organs.

Animals↗
PubMed1981

Effect of intraventricular beta-endorphin and morphine on hypothalamic-pituitary-adrenal activity and the release of pituitary beta-endorphin.

The effects of intraventricular (i.v.t.) morphine sulfate (MS) and beta-endorphin (beta-EP) on pituitary-adrenal activity and the release of pituitary beta-EP were studied in rats. Pituitary-adrenal activity was monitored by measuring plasma corticosterone (CS) levels. 45 min after i.v.t. injection, both MS and beta-EP caused dose-related increases in plasma CS, with beta-EP being approximately ten times more potent on a molar basis. MS injected i.v.t. at 0.3, 1.0, 3.0 and 10.0 microgram did not cause a significant reduction in pituitary immunoreactive (i.r.) beta-EP, but did cause an increase in plasma i.r. beta-EP at 3 microgram of MS. beta-EP injected i.v.t. at 1.5 microgram caused a reduction of pituitary i.r. beta-EP. Since i.v.t.-injected beta-EP may have contributed to the measured plasma i.r. beta-EP, a nonimmunoreactive analog (Des-Asn20-beta c-EP) was used to assess the change in plasma i.r. beta-EP. 5 microgram of DES-Asn20-beta c-EP injected i.v.t. caused increases in plasma i.r. beta-EP and CS, as well as a 40% reduction in pituitary i.r. beta-EP. The concomitant intraperitoneal (i.p.) injection of naloxone HCl (10 mg/kg) significantly blocked the increase in plasma CS induced by 5 microgram of beta-EP. When naloxone HCl, 10 mg/kg was injected alone, a significant increase in plasma CS was found. The results indicate that i.v.t. beta-EP is more potent than MS in causing the release of pituitary ACTH and beta-EP. These findings are consistent with a role for brain endorphins in the regulation of CRF release.

Animals↗