Search PubMed⌕ Search

Biomedical subjects

S Weiss

Publications and source records attributed to S Weiss.

At least 361 records · Page 20Linked to original sources

Serum IgD elevation is an early marker of B cell activation during infection with the human immunodeficiency viruses.

Serum IgD levels in individuals infected with the human immunodeficiency viruses (HIV) were studied as a means of monitoring the character and timing of B cell activation in individuals with this infection. Significantly increased levels of IgD were characteristic of homosexual men who were HIV seropositive but asymptomatic or mildly symptomatic. The hyper IgD globulinaemia became progressively more pronounced in patients with increasingly severe infection and reached its most marked level in patients with AIDS-related complex (ARC). In ARC patients, IgD levels were increased 8.8-fold above normal which was disproportionately greater than the 2.4-fold increase in IgG, the 1.8-fold increase in IgA and the 1.6-fold increase in IgM. IgD levels declined in AIDS patients (although remained elevated compared to controls). The data suggest that an unusual type of B cell activation is responsible for the unique pattern of hypergammaglobulinaemia seen in this disease and that the B cell activation occurs early in the pathogenesis of HIV infection, often before development of symptoms, and continues throughout the course of infection.

AIDS-Related Complex↗

Serotonin 5-HT1 receptors mediate inhibition of cyclic AMP production in neurons.

In purified striatal and cortical neurons in primary culture, serotonin (5-HT) stimulated basal cyclic AMP production (EC50, 0.5 microM) 2.5- and 1.5-fold, respectively. The 5-HT1 selective agonists, RU 24969 and 8-hydroxy-2-(di-n-propylamino)tetralin (PAT), did not stimulate cyclic AMP production. However, 5-HT, RU 24969 and PAT inhibited VIP-stimulated cyclic AMP formation in a dose-dependent manner. The actions of selective agonists and antagonists at 5-HT receptors mediating attenuation of cyclic AMP production suggest that they may be of the 5-HT1 subtype.

8-Hydroxy-2-(di-n-propylamino)tetralin↗

Increased antidepressant use in patients prescribed beta-blockers.

Little information exists on the epidemiology of central nervous system side effects in patients taking antihypertensive medications. We examined prevalence rates of tricyclic antidepressant (TCA) use among a random sample (N = 143,253) of Medicaid recipients. The TCA use was compared for patients taking any of seven antihypertensive agents and for those prescribed insulin or oral hypoglycemic agents. Use of TCA was significantly higher in patients taking beta-blockers (23% over two years) than for patients taking hydralazine or hypoglycemics (both 15%) or methyldopa or reserpine (both 10%). Prevalence rate ratios revealed a risk of being prescribed a TCA of 1.5 (95% confidence interval, 1.4 to 1.7) for patients receiving beta-blockers relative to patients receiving hydralazine or hypoglycemics. beta-Blocker use may be an important cause of iatrogenic depression among hypertensive patients.

Adrenergic beta-Antagonists↗

The localization of urinary tract infection with 99mTc glucoheptonate scintigraphy.

A retrospective study was performed of 39 children at the Children's Memorial Hospital, Chicago, Illinois, who underwent technetium-99m glucoheptonate (99mTcGH) scintigraphy for evaluation of possible urinary tract infection. Clinical and laboratory criteria classified the children as having pyelonephritis, cystitis, or no urinary tract infection. Of 28 children classified as having pyelonephritis, 24 (86%) children had abnormalities on 99mTcGH scintigraphy. Only 8 of 19 (42%) renal ultrasound scans and 4 of 17 (24%) intravenous pyelography studies performed in these children demonstrated findings consistent with parenchymal disease. Only 9 of 19 (47%) cystograms demonstrated vesicoureteral reflux. Three children who underwent gallium-67 citrate scintigraphy had localization at the sites of focal defects with 99mTcGH scintigraphy. 99mTcGH scintigraphy is a sensitive and specific indicator of renal parenchymal involvement that helps localize urinary tract infection to the kidney.

Child↗

Vasoactive intestinal peptide actions on cyclic AMP levels in cultured striatal neurons.

The actions of vasoactive intestinal peptide (VIP) on intracellular cyclic AMP, in primary cultures of striatal neurons, were examined. VIP stimulated cyclic AMP formation five-fold over basal levels in neurons after 6 days in vitro (DIV); half maximal activation (EC50) was obtained with 10 nM of the peptide. VIP stimulation was both more potent and effective than those due to adrenocorticotropin (ACTH), dopamine (DA) or serotonin (5-HT). VIP efficacy was augmented to 15-20-fold in the presence of 0.1 microM forskolin, which had virtually no effect on cyclic AMP production alone; VIP potency was unaffected. At saturating concentrations of VIP (0.1-1.0 microM), no other agonist can further activate cyclic AMP production. Under these conditions, the interaction with opiate, DA D2 and 5-HT1 receptors, whose activation results in the inhibition of cyclic AMP production, was shown. During the differentiation of striatal neurons, VIP stimulation of cyclic AMP over basal levels, in the presence of 0.1 microM forskolin, decreases progressively from 30-fold after 3 DIV to 11-fold after 10-13 DIV.

Animals↗

Mutation affecting the expression of immunoglobulin variable regions in the rabbit.

We have found a variant of the allotype allele a2 in the rabbit, which presumably arose by mutation, that segregates as expected for an allele at the a locus. This allele is called "ali" and the corresponding rabbit strain is called "Alicia." In heterozygous animals (ali/a1 and ali/a3) the concentration of a2 molecules is lower by a factor of 1000 than in standard a2/a2 homozygotes. In homozygous ali/ali individuals the a2 concentration varies with age--i.e., very low in young rabbits and higher in older ones--but it never reaches normal levels. The low level of a2 is compensated by increased amounts of a-negative molecules. Southern blot analysis did not reveal any gross changes in the intron between JH and C mu (joining region of immunoglobulin heavy chain and constant region of immunoglobulin mu chain) or in the number of VH gene segments encoding a locus specificities. We suggest that the ali phenotype is due to a mutation in a control element.

Animals↗

Synaptogenesis of cultured striatal neurons in serum-free medium: a morphological and biochemical study.

Striatal neurons were cultured from the fetal mouse brain and maintained in serum-free medium for 14-21 days in vitro (DIV). Pretreatment of the culture dishes successively with a polycation followed by fetal calf serum resulted in rapid neuron attachment and neurite proliferation. After 9-10 DIV, electron microscope observations revealed the presence of vesicles in axon terminals forming mature synapses with axons and perikarya of adjacent neurons and in varicosities along extended axons. Synapsin I, a synaptic vesicle-specific protein, was present only in neuronal perikarya after 3 DIV, in perikarya and in varicosities along extended axons after 6 DIV, and in varicosities and contact points between axon terminals and adjacent axons or perikarya after 11-14 DIV. Neurotransmitter-stimulated intracellular formation of cAMP decreased markedly during neuronal differentiation. Inositol phosphate formation in response to neurotransmitters, however, increased significantly throughout the period of striatal neuronal development. K+ (56 mM) depolarization resulted in a 2-fold increase in endogenous gamma-aminobutyric acid (GABA) release from striatal neurons, 50% of which was Ca2+-dependent, between 3 and 11 DIV. Between 11 and 14 DIV, subsequent to synapse formation (as revealed by electron microscope observations), GABA release evoked by 56 mM K+ increased up to 5-fold, 75% of which was Ca2+-dependent. It appears that the complete differentiation of striatal neurons in serum-free medium may provide a suitable model for the study of the physiological and regulatory mechanisms involved in nerve cell development.

Animals↗

Release of endogenous amino acids from striatal neurons in primary culture.

Endogenous amino acid release was examined in highly purified striatal neurons obtained from fetal mouse brain, and differentiated in primary culture. This study aimed to determine which amino acids are released from striatal neurons after a brief depolarization period induced by elevated potassium concentration or veratrine. Amino acids released into the extracellular medium, subsequent to a 3-min exposure of striatal neurons, were subjected to HPLC analysis. At 14 days in vitro potassium (56 mM) depolarization elicited a 25-fold increase in gamma-aminobutyric acid release, 85% of which was calcium-dependent. This effect was small but apparent at 7 days in vitro (two-fold increase) and greatly increased between 11 and 14 days in vitro, subsequent to the appearance of synaptic vesicles in nerve terminals. gamma-Aminobutyric acid release was readily reversible within minutes of return to the resting state. Veratrine induced a quantitatively similar but calcium-independent increase in gamma-aminobutyric acid release. Similar results were observed on aspartate and glutamate release, but the increase was very small even after 14 days in vitro (62.2 and 123.3% increase over basal release, respectively). Taurine and hypotaurine release increased during and after depolarization induced by potassium. This effect remained constant between 11 and 18 days in vitro. BAY K 8644, a dihydropyridine-sensitive calcium channel agonist, augmented the effect of 15 mM potassium on gamma-aminobutyric acid release, but this effect remained very small as compared to the potassium (56 mM) or veratrine effects. In addition, nifedipine inhibited this BAY K 8644-induced release. These results demonstrate the high level of differentiation among striatal neurons containing gamma-aminobutyric acid in this in vitro system.

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗

Primary culture of striatal neurons: a model of choice for pharmacological and biochemical studies of neurotransmitter receptors.

Striatal neurons were cultured from fetal mouse brain and maintained in serum-free medium for 14-21 days in vitro (DIV). A double coating of culture dishes with polyornithine and fetal calf serum was needed in order to obtain synaptic differentiation. Synaptic vesicles were present in axon terminals as well as in varicosities along extended axons. The presence of differentiated synapses was confirmed by the immunostaining of the preparation with synapsin I antibody. After 13 days in vitro synapsin I was present in axonal varicosities and particularly concentrated at contact points between axonal terminals and postsynaptic sites on adjacent axons or perikarya. On a surface of 429 mm2 on which 2211 cells were observed under phase contrast microscopy only 7% were stained with an antibody against GFAP (glial fibrillary acidic protein). One or two days after the formation of differentiated synapses (11 DIV), a Ca2+-dependent liberation of GABA was observed. These cultures are an excellent model for studying the coupling of some neurotransmitter receptors with an adenylate cyclase. In particular using this preparation we were able to demonstrate that dopamine (D2) and serotonin-(5-HT1) receptors are negatively coupled with an adenylate cyclase. These cultures are also an excellent model to study the coupling of some neurotransmitter receptors with inositol phosphate producing enzymes. We demonstrated for the first time that the quisqualate subtype of glutamate receptors is able to increase inositol phosphate production in striatal neurons.

Animals↗

ATP synthesis and hydrolysis by a hybrid system reconstituted from the beta-subunit of Escherichia coli F1-ATPase and beta-less chromatophores of Rhodospirillum rubrum.

Photophosphorylation and ATPase activities were restored to beta-less Rhodospirillum rubrum chromatophores by their reconstitution with purified beta-subunits of either R. rubrum F1-ATPase (Rr beta) or Escherichia coli F1-ATPase (Ec beta). In the homologous reconstituted system both activities were restored to the same extent, whereas in the hybrid system ATP synthesis was restored to about 10% when the hydrolysis was restored to 200%. This difference in rates of synthesis and hydrolysis was not due to any general uncoupling effect of Ec beta leading to an increased membrane permeability to protons, because with both hybrid and homologous systems an identical light-induced quenching of quinacrine fluorescence was observed. They differed, however, in ATP-driven quenching of quinacrine fluorescence, which was much lower in the hybrid system. These results suggest that the hybrid has a decreased capacity for proton-translocation through the membrane-bound Fo channel during ATP hydrolysis, and probably also during ATP synthesis. The very high ATPase activity of the hybrid system indicates that it might enable the released protons to leak to the outside medium rather than to move inside through the Fo channel. The activities restored by Rr beta and Ec beta exhibit a similar sensitivity to dicyclohexylcarbodiimide, but different sensitivities to oligomycin and to an anti-E. coli F1 (EcF1) antibody. Oligomycin inhibited only the homologous R. rubrum system whereas anti-EcF1 was a much more effective inhibitor of the hybrid system. It is therefore concluded that Rr beta plays a role, that the Ec beta cannot fulfill, in conferring oligomycin sensitivity to the RrFo X F1-ATP synthase-ATPase complex.

Adenosine Triphosphate↗

V lambda 2 rearranges with all functional J lambda segments in the mouse.

We have analyzed 210 lambda-producing hybridomas derived from lipopolysaccharide-stimulated spleen cells from a single kappa-suppressed mouse. All were classified as lambda 1, lambda 2 or lambda 3 with the exception of four unusual lines. Two of these were due to V lambda 2 J lambda 1 and the other two to V lambda 2 J lambda 3 rearrangements. The lines were clonally independent since the point of VJ recombination in each one was different. Southern blot analysis of the V lambda 2 C lambda 1-producing lines showed no evidence for an inversion. Under the assumption of a simple deletion model of rearrangement these findings place the V lambda 2 cluster upstream of the V lambda 1 cluster oriented in the same direction.

Animals↗

A monoclonal lambda 1-bearing anti-dextran antibody from a lambda-defective mouse strain.

A hybridoma from the lambda-defective mouse strain SJA has been established. It produces a lambda 1-bearing IgG2b, dextran B 1355-binding antibody. The DNA sequence of the VJ and C gene segment was in complete accordance with the published germ-line sequence. The rate of secretion and the steady state level of cytoplasmic RNA of this line was comparable to that of cell lines from normal mice. The idiotype was closely related to that of MOPC 104E indicating that the lambda 1 light chain is associated with the same VH region and in a similar fashion as in BALB/c mice. This antibody should be useful for further experiments on the lambda defect of SJL or SJA mice.

Animals↗

Scintigraphic localization of bone lesions during surgery.

Nuclear medicine provides several methods for increasing the accuracy of surgical removal of bone lesions with focally increased uptake. In this paper, three intraoperative procedures are discussed: remote control by imaging, intraoperative control by imaging, and intraoperative control by scintillation probe. All techniques require preoperative injection of bone imaging tracer. Remote operative control calls for a gamma camera to mark the skin over the lesion prior to surgery, providing optimal preoperative localization and imaging of the excised lesion to ensure complete removal. Intraoperative control procedures require that a portable camera or a scintillation probe be used in the operating room; these permit direct monitoring of localization and resection. Our experience with 18 procedures performed on 15 patients suggests that these techniques are worthy of continued use.

Adolescent↗

A complete computerized program for nutritional management in the neonatal intensive care nursery.

A computerized program in BASIC, which integrates the infant's fluid and nutritional requirements per gestational age and weight with the infant's postpartum age, was developed using the Apple II Plus microcomputer, dual floppy disks, and an Epson printer. Daily requirements of fluids, proteins, fat, CHO, vitamins, minerals, and trace elements are computed. For reference, the program displays the composition and indications for intravenous and hyperalimentation solutions, mature human milk, and 14 commercial formulas. Safety limits to prevent overload or deficient formulations are strategically displayed, warning the physician about possible complications and gradually orienting him toward achieving adequate nutritional balance in the patient. The nutritional intake, weight, and other important clinical variables are stored and retrieved for future evaluation. The flexibility of the program allows for modifications in intravenous and oral composition according to clinical requirements. The program improves the efficiency of the arduous daily formulation of nutritional needs, reduces the possibility of human error, facilitates the calculation process, diminishes time spent on the calculations, and increases the ease of nutritional data retrieval and the development of output programs.

Birth Weight↗

Corticotropin-peptide regulation of intracellular cyclic AMP production in cortical neurons in primary culture.

Previous studies have provided evidence for adrenocorticotropic hormone (ACTH) effects on a wide variety of behaviors. However, the precise sites of action and the mechanisms by which these effects may be mediated have yet to be clearly elucidated. Although ACTH was shown to augment cyclic AMP levels in glial cells isolated from whole brain, other studies found little or no effect of ACTH peptides on cyclic nucleotide metabolism in slices of cerebral cortex or homogenates of whole brain. In the present study, our objective was to determine whether ACTH peptides regulate intracellular cyclic AMP levels in neurons of the cerebral cortex in primary culture. ACTH peptides stimulated cyclic AMP synthesis up to threefold in a dose-dependent manner; stimulation was complete within 5-10 min of exposure to agonists. Neurohormone efficacy was augmented by 0.1 microM forskolin (which was virtually ineffective alone); potency was unaffected. The order of potency (EC50) for increasing intracellular cyclic AMP levels was as follows: ACTH (1-24), ACTH (1-17) (10 nM) greater than alpha-melanocyte stimulating hormone, beta-melanocyte stimulating hormone (alpha-MSH, beta-MSH) (100 nM) greater than ACTH (1-10) (1 microM) greater than ACTH (4-10) (5 microM). The hexapeptide ACTH (4-9) as well as ACTH (11-24) were inactive at concentrations as high as 10 microM. Other neuropeptides derived from proopiocortin, such as beta-endorphin and Met- and Leu-enkephalin were without effect on basal or hormonally stimulated cyclic AMP synthesis.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenocorticotropic Hormone↗