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Biomedical subjects

D J Goldstein

Publications and source records attributed to D J Goldstein.

At least 163 records · Page 9Linked to original sources
PubMed1984

Developmental delays in Williams ("Elfin facies") syndrome.

This study reports the results of psychological and physical characteristics of seven children with Williams syndrome. All subjects were found to be borderline to severely mentally retarded. The previously reported pattern of superior verbal abilities over motor abilities was not supported, nor was there any evidence of an "unusual command" of language, usually considered a marker of the syndrome. The early development profiles of these children are important for parental counseling and planning of early intervention stimulation programs.

Aortic Valve Stenosis↗
PubMed1983

Bradykinin reverses the effect of opiates in the gut by enhancing acetylcholine release.

Four naturally occurring peptides of the kinin family, bradykinin, lysylbradykinin, methionyllysylbradykinin, and polisteskinin reverse the inhibitory effect of morphine, metenkephalin, and epinephrine on the electrically stimulated guinea pig ileum longitudinal muscle myenteric plexus preparation. Bradykinin, the most potent kinin, enhances the release of acetylcholine in the gut, and its reversal of the opiate inhibitory effect is blocked by the anticholinergic drug, hyoscine.

Acetylcholine↗
PubMed1983

Abdominal vagotomy does not modify endotoxic shock in rats.

Bilateral subdiaphragmatic vagotomy does not improve the clinical course nor the survival of Sprague-Dawley rats injected intravenously with E. coli lipopolysaccharide. These results show that whatever peripheral signals are elicited by endotoxin to generate the centrally mediated hypotensive response, they are not conveyed to the central nervous system by abdominal vagal afferent fibers.

Animals↗
PubMed1983

A case of episodic flushing and organic psychosis: reversal by opiate antagonists.

A woman had episodic attacks of flushing associated with severe skin, bone, and abdominal pain, accompanied by mood alterations and anxiety, and followed by an organic psychosis. These symptoms and signs could be induced by small doses of clonidine, L-5-hydroxytryptophan, pentagastrin, insulin, epinephrine, compound 48/80, methacholine, morphine, histamine, or d-tubocurarine. Skin testing showed abnormally sensitive mast cells and an exaggerated axon flare. Cimetidine initially prevented the attacks but became less effective after 18 months. Thyrotropin-releasing hormone stopped the skin pain whereas neurotensin reproduced the burning sensation in the skin without inducing the attack. Both the flush and the organic psychosis were reversed entirely by naloxone or naltrexone, and the hallucinosis could be reversed by vasodilators.

Adult↗
PubMed1982

A search for trace expression of placental-like alkaline phosphatase in non-malignant human tissues: demonstration of its occurrence in lung, cervix, testis and thymus.

A search for placental or placental-like human alkaline phosphatase (ALP) was made in human tissues. The tissue extracts were assayed for ALP before and after heating at 65 degrees C for 1 h. Trace amounts of heat-stable ALP activity (greater than 0.01 IU/g) were found in lung, testis, cervix and thymus. The heat-stable ALP in these four tissues gave in Ouchterlony double diffusion plates lines of apparent identity with placental ALP when a rabbit anti-human placental antiserum was used. Inhibition studies with L-phenyl-alanine (Phe), L-homoarginine (Har), L-phenylalanylglycylglycine (Pgg), L-leucine (Leu) and levamisole (Leva), were carried out on the heat-stable ALP and on the total ALP. The heat-stable ALPs from cervix and lung gave [I]50 values with each inhibitor comparable to those of placental ALP. The heat-stable ALPs froM testis and thymus gave [I]50 values for Leu and Pgg which were significantly different from the placental isoenzyme. Electrophoresis of heat-stable lung ALP from different individuals showed polymorphic differences similar to those seen with placental ALPs. Such differences were not seen with heat-stable testis ALP. We conclude that human non-malignant testis, cervix, lung and thymus tissues contain small amounts of placental or placental-like ALPs. The heat-stable ALPs in cervix and lung appear to have the same characteristics as placental ALP and are probably encoded by the same gene locus. The heat stable ALPs in testis and thymus, though immunologically very similar to placental ALP differ from it in inhibition profile and electrophoretically. The significance of the results in relation to the "ectopic' expression of placental and placental-like ALPs in malignancy is discussed.

Alkaline Phosphatase↗
PubMed1982

Microcystic adnexal carcinoma: a distinct clinicopathologic entity.

Microcystic adnexal carcinoma is an unusual locally aggressive neoplasm that is important to recognize since it may be confused with benign adnexal neoplasms, particularly desmoplastic trichoepithelioma, trichoadenoma, and syringoma. Six cases are described all of which displayed benign histological features on initial biopsy. Most often these neoplasms presented as solitary flesh-colored indurated plaques on the upper lip. All patients were white, five were women, and the average age was 44-years-old. Islands of basaloid keratinocytes, some of which contained horn cysts and abortive follicles, were embedded in a desmoplastic stroma. In other foci, ducts and gland-like structures lined by a two-cell layer predominated. In deep components individual and thin strands of cells dissected collagen bundles and skeletal muscle and invaded perineural spaces. Despite this, cytologic atypia and mitotic figures were rare. The cell of origin is considered to be a pluripotential adnexal keratinocyte which is capable of both follicular and sweat gland differentiation.

Adult↗
PubMed1982

Naloxone attenuates the hypotension induced by Hageman factor.

The hypotension induced in the pentobarbital anesthesized rat by the i.v. administration of an active Hageman factor fragment (Hff) is significantly attenuated by naloxone. This effect is specific because the opiate antagonist does not modify the hypotension elicited by rat urinary kallikrein, bradykinin or nitroglycerin. These results suggest that the contact activation of endogenous Hageman factor could result in the generation of vasoactive opioid peptides derived from circulating large molecular weight precursors.

Animals↗
PubMed1982

Evolution of alkaline phosphatases in primates.

Alkaline phosphatase [orthophosphoric-monoester phosphohydrolase (alkaline optimum), EC 3.1.3.1] in placenta, intestine, liver, kidney, bone, and lung from a variety of primate species has been characterized by quantitative inhibition, thermostability, and immunological studies. Characteristic human placental-type alkaline phosphatase occurs in placentas of great apes (chimpanzee and orangutan) but not in placentas of other primates, including gibbon. It is also present in trace amounts in human lung but not in lung or other tissues of various Old and New World monkeys. However, a distinctive alkaline phosphatase resembling it occurs in substantial amounts in lungs from Old World monkeys but not New World monkeys. It appears that duplication of alkaline phosphatase genes and mutations of genetic elements controlling their tissue expression have occurred relatively recently in mammalian evolution.

Alkaline Phosphatase↗
PubMed1982

A simple quantitative analysis of phase contrast microscopy, not restricted to objects of very low retardation.

A simple vector analysis of the diffraction of light by an ideal, extended phase grating suggests that irrespective of the amount of retardation imposed on the light passing through a transparent microscopic object the diffracted light leaving the object plane is precisely 90 degrees out of phase with the resultant direct (zero-order diffracted) light. In positive phase contrast microscopy, with a 90 degrees phase plate of transmittance T for the direct light, the image and halo respectively have intensities relative to the original illumination of (square root T.cos 1/2 phi - sin 1/2 phi)2 and (square root T.cos 1/2 phi + sin 1/2 phi)w. The empty background has an apparent intensity of T. Zero intensity of the image is seen if T = tan2(1/2 phi), and reversal of contrast if T less than tan2(1/4 phi). The same equations can be used to predict the intensities of the image and halo in negative phase contrast microscopy, if phi is replaced by (360 degrees - phi). Unlike the 'standard' description of phase contrast microscopy, exemplified by Barer's vector method, the present account is consistent with the conservation of energy and is not restricted to very small object retardations. Barer's method is, however, theoretically valid for objects of any shape, and the two approaches may perhaps be regarded as complementary.

Mathematics↗
PubMed1982

Scanning microdensitometry of objects small relative to the wavelength of light.

Diffraction effects may have to be taken into account in microdensitometry when dealing with relatively dark specimens even an order of magnitude larger than the wavelength of light, and become progressively more important with smaller objects. According to geometrical optical theory, when scanning across the straight edge of a uniformly absorbing, semi-infinite object the distribution error per scan line is directly proportional to the diameter of the measuring-spot. Diffraction theory predicts similar results for measuring-spots larger than about 3 times the wavelength of light, but a significant error per scan line with very small or even infinitesimal measuring-spots. Diffraction theory further indicates that point absorbance measurements can be 95 + % accurate in the centers of 6.25, 2.5, and 2.0 microns diameter disks with absorbances respectively up to about 1.0, 0.39, and 0.25, but that this accuracy is unattainable with any object less than 1.25 microns in diameter. Scanning, integrating absorbance measurements are of somewhat lower accuracy than central point measurements with relatively large objects, e.g., they are only about 89% accurate with a 6 micron diameter object of absorbance 1.0. With very small objects, diffraction theory shows distribution error to be almost independent of the size of the scanning spot, and with an object of less than about 0.125 micron diameter the apparent integrated absorbance predicted by diffraction theory is effectively identical with that predicted by geometrical theory for an infinitesimal object scanned with a finite measuring-spot, i.e., it is the product of the object area and 0.4343 (1-It), where It is the true transmission. Scanning microdensitometry of objects of very low true absorbance is effectively free from distribution error. In practice, distribution error can be reduced by using an off-peak wavelength, by reducing the area illuminated, and by routine measurement and offsetting of apparent glare (some of which is actually due to diffraction). Little or nothing is to be gained by using a measuring-spot smaller than about one-quarter the wavelength of light.

Densitometry↗
PubMed1981

Nalidixic acid, oxolinic acid, and novobiocin inhibit yeast glycyl- and leucyl-transfer RNA synthetases.

Nalidixic acid and novobiocin inhibit the aminoacylation and pyrophosphate exchange activities of glycyl- and leucyl-transfer RNA synthetases from bakers' yeast. Similar types of inhibition are observed for both enzymes, suggesting similar mechanisms. The potency of these inhibitors is comparable to that observed for their inhibition of in vivo DNA synthesis in eukaryotic cells.

Amino Acyl-tRNA Synthetases↗
PubMed1981

Errors in microdensitometry.

Microdensitometric errors can originate in the instrument, in the specimen or in the human operator. Instrumental sources of systematic error mostly reduce the apparent integrated absorbance, especially of relatively small and highly absorbing objects. They can be assessed, minimized or eliminated by available techniques, but with modern apparatus are in general important only if results of high accuracy are required. Instrument errors include: (a) distributional error, due to the use of too large a measuring spot or the specimen being out of focus; (b) glare (stray light), due mainly to multiple reflections in the microscope objective; (c) monochromator error (the use of insufficiently pure light); (d) calibration errors; and (e) errors resulting from lack of photometric linearity, or the specimen absorbance exceeding the measuring range of the instrument. Specimen errors, including the problems of specificity and stoichiometry, are now the most important obstacles to a wider use of microdensitometry. The following selected topics are briefly discussed: fading; rate of staining; Beer's law deviations and the microdensitometry of opaque particles. Human errors include faulty logic, and failing to attempt an investigation because of anticipated difficulties which are in fact exaggerated or imaginary. The significance of microdensitometric results should, in general, be assessed by biological criteria rather than merely statistically; the use is urged of appropriate internal biological controls and standards wherever possible.

False Negative Reactions↗
PubMed1981

Recording of chromosome banding with the Vickers M85/M86 scanning microdensitometer.

An electronic interface is described which permits the Vickers M85/M86 microdensitometer to be used with a chart recorder to plot linear distance along a chromosome against (1) the absorbance, (2) the product of the chromosome width and the mean absorbance transverse to the long axis of the chromosome, or (3) the integrated absorbance accumulating during a two-dimensional scan of the specimen.

Animals↗
PubMed1981

Mammalian brain alkaline phosphatase: expression of liver/bone/kidney locus. Comparison of fetal and adult activities.

The alkaline phosphatases (EC 3.1.3.1) are determined by at least three gene loci, which can be sharply distinguished one from another by their sensitivity to inhibition with various amino acids and peptides and by thermostability. Alkaline phosphatase is present in the brains of guinea pig, rat, mouse, hamster, squirrel, rabbit, cat, sheep, cow, tamarin, baboon, and man. The gene locus coding for alkaline phosphatase in all these brains is the liver/bone/kidney locus, as indicated by thermostability studies and by inhibition studies with L-phenylalanine, L-homoarginine, and L-phenylalanylglycylglycine. The average brain alkaline phosphatase activity is about 35% of the average for the livers and only 7.2% and 4.4% of the average kidney and placental activities, respectively. During growth and development, brain alkaline phosphatase activity decreases in the mammals studied. The amount of change is tissue- and species-dependent.

Age Factors↗
PubMed1980

Expression of alkaline phosphatase loci in mammalian tissues.

Alkaline phosphatases [orthophosphoric-monoester phosphohydrolase (alkaline optimum), EC 3.1.3.1] have been examined in liver, bone, kidney, intestine, and placenta from nine mammalian species by quantitative inhibition and thermostability studies and compared with alkaline phosphatases in the corresponding human tissues. In humans, three kinds of alkaline phosphatase can be sharply differentiated by these methods, one occurring in liver, bone, and kidney, one in intestine, and one in placenta. They are evidently determined by separate gene loci. In the mammals only two sorts of alkaline phosphatase were found: one, which occurs in liver, bone, kidney, and also placenta, corresponds to the human liver/bone/kidney enzyme and the other corresponds to the human intestinal enzyme. The findings support our earlier proposal that the expression of a distinctive type of alkaline phosphatase in human placenta is the consequence of a late evolutionary event which occurred subsequent to the divergence of the evolutionary lineage leading to humans from the various lineages leading to other mammalian species. The concentrations of the inhibitors, phenylalanine, homoarginine, phenylalanylglycylglycine, and levamisole, required to give 50% inhibition, [I(50)], of the liver/bone/kidney/placental (nonhuman) alkaline phosphatases showed no significant variation among the species. However, the [I(50)] values for the intestinal enzyme varied among species to a much greater extent. This implies that in the liver/bone/kidney/placental (nonhuman) alkaline phosphatase the structures of the binding sites for these inhibitors have been highly conserved during mammalian evolution, but there has been much greater divergence of these structures in the evolution of intestinal alkaline phosphatases.

Alkaline Phosphatase↗
PubMed1980

Placental alkaline phosphatase in nonmalignant human cervix.

At least three loci determine human alkaline phosphatases [orthophosphoric-monoester phosphohydrolase (alkaline optimum), EC 3.1.3.1]: one coding for the placental form of the enzyme; at least one coding for the intestinal forms; and at least one for the liver, bone, and kidney forms. It is generally believed that the locus determining the placental form is, in the normal individual, expressed only in placenta. However, ectopic or aberrant expression of this locus occurs in certain malignancies of other tissues and in cell lines, such as HeLa, derived from malignancies. We have examined by thermostability, inhibition, and immunologic studies the alkaline phosphatases in endocervix, cervical mucus, and endometrium from nonpregnant women with no evidence of malignancy. It was found that on the average about 18% of the alkaline phosphatase activity in endocervix and in cervical mucus is placental in type, the remainder being of the liver/bone/kidney type. The quantity of the placental enzyme is, however, low and amounts to only about 0.5% of the amount in normal term placenta. In endometrium all the alkaline phosphatase activity was of the liver/bone/kidney type. Thus the placental alkaline phosphatase locus is expressed in nonmalignant endocervix. The result is of some significance in connection with the widely held view that the expression of placental alkaline phosphatase in certain malignancies (including cervical malignancy) is due to derepression of a locus for a fetal enzyme protein normally repressed in adult tissues.

Adult↗