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Biomedical subjects

O Zinder

Publications and source records attributed to O Zinder.

At least 37 records · Page 2Linked to original sources
PubMed1998

Experimental induction and termination of acute psychological stress in human volunteers: effects on immunological, neuroendocrine, cardiovascular, and psychological parameters.

The present research investigated the effects of controlled experimental manipulations of stress on biological and psychological reactions. Fifty young adult male volunteers were exposed to a 12-min period of stress induced by the threat of an unavoidable, painful electric shock. A 12-min period without this threat preceded or followed the stress period. Blood was drawn during the 4th and the 12th minute of each period. Anticipatory threat led to significant elevations in the proportions and cytotoxic activity of natural killer (NK) lymphocytes, plasma epinephrine levels, pulse rate, and reported level of tension, and to a reduction in the CD4/CD8 ratios. The no-threat period induced a return to baseline values for epinephrine, pulse rate, and tension, and lower than baseline levels for cytotoxic activity of NK lymphocytes, within a similarly short time span. The findings underline the rapidity with which physiological changes may transpire in the course of a brief and acute period of psychological stress, and the rapidity of their reversal upon relief from the stressor.

Acute Disease↗
PubMed1998

New directions in laboratory-clinician communications.

The widespread availability of computer-generated data interpretation of clinical laboratory determinations, as well as computerized patterns of disease progression, has given the laboratory professional a powerful tool to enhance the capability of the laboratory to provide consultation for the clinicians. Additionally, the new advances in technology, and the measurement of disease markers on a molecular basis, has added a whole new dimension to Laboratory Medicine. This explosion of technology is affording the clinical laboratory professional a renewed chance to become a more visible and productive member of the team of health providers. There is a need for clinicians to be educated on the capabilities of these tests and their relative powers of diagnosis. The ability to determine vanishingly small quantities of biological molecules also presents the clinical laboratory with the opportunity to provide knowledge for preventative medicine, and for extremely early detection of onset of a disease or changes in its status. Prediction of genetic predisposition, using sophisticated molecular techniques, is another aspect of the novel expertise which the clinical laboratory professional can use to educate the clinical staff, and allow for earlier counseling and treatment. It is with these tools and knowledge that the clinical laboratory can contribute substantially to overall patient care. This role for the clinical laboratory is all the more urgent since the proliferation of information presents a substantial obstacle to the physician for understanding the molecular basis of a large number of disease processes and how this information can be best used to enhance patient care. The Laboratory Medicine professional of today has the unique opportunity to communicate and exchange knowledge and expertise with clinical counterparts, using a variety of educational and electronic means.

Communication↗
PubMed1998

Catecholamine secretion from bovine adrenal chromaffin cells induced by the dextrorotatory isomer of anatoxin-a.

1. The nicotinic agonist (+)anatoxin-a was studied in acute preparations of adrenal chromaffin cells and was compared with other known stimulants in this system. 2. (+)Anatoxin-a was found to be a potent stimulant of catecholamine secretion with EC50=545.7 nM, which was 5.8 times as strong as nicotine (EC50=3,165 nM). (+)Anatoxin-a action was time dependent and saturable. 3. The pharmacological characteristics of (+)anatoxin-a were tested by using nicotinic and muscarinic antagonists (mecamylamine and atropine, respectively). Mecamylamine (1 microM) and atropine (100 microM) inhibited the secretion induced by (+)anatoxin-a (1 microM), as well as that induced by nicotine (10 microM), acetylcholine (10 microM and 100 microM) and oxotremorine-M (100 microM). 4. The calcium requirement for (+)anatoxin-a action was tested in comparison with the aforementioned stimulants. Addition of the calcium antagonist verapamil (10 microM) or the calcium chelator EGTA (3 mM) reduced all stimulants' action. 5. These results show that the (+)enantiomer of anatoxin-a is both dose and time dependent. Its action is mediated through the classical operation of the nicotinic acetylcholine receptor, by using calcium influx.

Adrenal Medulla↗
PubMed1998

Contributions of hypoxia and respiratory disturbance index to sympathetic activation and blood pressure in obstructive sleep apnea syndrome.

Hypertension is a common finding among obstructive sleep apnea (OSA) patients, and is thought to be caused by sympathetic hyperactivity. The present study compares the contributions of the respiratory disturbance index (RDI) as a reflection of sleep fragmentation, and the magnitude of oxygen desaturation, to sympathetic activation as indexed by urinary norepinephrine concentrations, as well as to morning and evening blood pressure in sleep apnea syndrome patients. Data (polysomnography, blood pressure [BP], and urine catecholamines) of 38 consecutive OSA patients (age, 46+/-14.5 years) were analyzed. Stepwise logistic regression analysis revealed that minimal oxygen saturation level (SaO2min) was a significant predictor of both morning and evening norepinephrine levels, and that 37% of morning systolic BP variance could be accounted for by a combination of age and norepinephrine, while 20% of the diastolic BP variance was accounted for by SaO2min alone. In contrast, RDI entered the prediction equation only when minimal oxygen saturation was rejected first. Our results indicate that the degree of nocturnal hypoxia is more closely associated with the level of sympathetic activation and with daytime level of blood pressure than with sleep fragmentation.

Adult↗
PubMed1998

Specificity of polyclonal anti-p53 IgG for isolation of the soluble p53 antigen from human serum.

The possibility to use anti-p53 IgG for isolation of the soluble p53 antigen as a serological tumor marker has been shown in our previous studies. In order to prove the specificity of such IgG, we compared the effectiveness of columns with anti-p53 IgG and IgG isolated from non-treated rabbits (regular IgG). The gel fiberglass (GFG) columns for affinity chromatography were prepared separately with both types of IgG. The same serum was percolated simultaneously through both columns and the results of elution were compared. The total concentration of tumor-associated antigens (TAA) eluted from the serum of cancer patients was similar in both TAA mixtures isolated either with anti-p53 IgG or with the regular IgG. Differences are manifest in the content of total proteins and amount of each eluted protein: a mixture eluted with the regular IgG contains several proteins whereas the anti-p53 IgG isolated only two proteins, p64 and p53. The amount of the soluble p53 antigen isolated from the cancer serum was significantly higher when it was isolated with anti-p53 IgG. The method developed in our laboratory was shown to be highly specific both to isolate proteins related to cancer (p53) and non-cancer disorders (p64). Data presented in this report show that such specificity can be achieved only if the anti-p53 IgG is used: the regular IgG obtained from non-treated animals isolate many proteins among which the concentration of specific p53 protein is lost.

Animals↗
PubMed1995

Antisense knockout of a neuropeptide gene reduces fibroblast proliferation.

The opioid peptides enkephalins are widely expressed throughout the body. While their role in the nervous system is well characterized, their function in other tissues is unclear. The antisense knockout approach was used to investigate the involvement of proenkephalin A gene in proliferation of cultured embryonic fibroblasts. Transfection of fibroblasts with enkephalin antisense vectors reduced [3H] thymidine incorporation and fibroblast colony growth. Moreover, FACS analysis indicated that transient or stable transfection with the enkephalin antisense vectors shifted fibroblasts from their normal G1 restriction point to one in the S-phase.

Animals↗
PubMed1995

Strychnine affects catecholamine secretion from bovine adrenal medulla chromaffin cells.

The effect of strychnine on evoked release of catecholamines from a primary culture of bovine adrenal medullary cells was investigated. Strychnine at > 1 microM inhibited catecholamine release stimulated by 10 microM acetylcholine, or 10 microM nicotine, but not by excess K+ (59 mM), the sodium ionophore veratridine (100 microM) or the calcium ionophore A-23187 (10 microM). The inhibitory response elicited by exposure of the cells to strychnine was rapid (< 3 min) and competitive with acetylcholine. High concentrations of acetylcholine (1 mM) completely overcame this inhibition. Strychnine might be acting on a regulatory site of the nicotinic-cholinergic receptor, which is genetically similar to the strychnine-binding 48 KD subunit of the glycine receptor.

Acetylcholine↗
PubMed1995

Clinical similarity and biological diversity in the response to alprazolam in patients with panic disorder and generalized anxiety disorder.

Thirty-six patients with panic disorder (PD) and 35 patients with generalized anxiety disorder (GAD) participated in an open alprazolam treatment phase that preceded controlled withdrawal from alprazolam. Clinical ratings, blood pressure and heart rate were obtained along with plasma measurements of cortisol, ACTH, growth hormone and catecholamines. A similar clinical response profile was evident in both groups with rapid onset of improvement within the first week. The two diagnostic groups differed in their biological response to alprazolam. PD patients had a significant reduction in blood pressure, plasma cortisol and a trend toward significant reduction in plasma epinephrine, which were not seen in the GAD patients. GAD patients showed a significant reduction in plasma norepinephrine. These findings provide further evidence that PD and GAD are biologically distinct syndromes.

Adrenocorticotropic Hormone↗
PubMed1993

Autoradiographic localization of strychnine-sensitive glycine receptor in bovine adrenal medulla.

The presence of an uptake system and a functional glycine receptor in adrenal medulla chromaffin cells was investigated using an autoradiographic technique in adrenal gland slices. Specific 3[H]glycine binding was observed in both adrenal cortex and medulla slices, while only specific binding of [3H]strychnine was seen only in chromaffin cells and was not associated with cortical cells. [3H]Glycine binding sites in the cortex are apparently different from those of [3H]strychnine binding sites in the medulla since excess strychnine does not displace [3H]glycine from adrenal cortex but does so from medulla. This difference supports biochemical evidence for glycine transport into medulla cells and glycine receptor sites on the chromaffin cell membrane.

Adrenal Cortex↗
PubMed1993

Uptake and receptor sites for glycine in isolated bovine adrenal medulla chromaffin cells.

[3H]Glycine is actively taken up into bovine isolated adrenal medulla chromaffin cells with the subsequent catecholamine release. [3H]Glycine uptake has two interaction sites based on relative Km measurements. These sites are inherently distinct since the effects of strychnine and temperature on glycine binding are significantly different. The high affinity site (Km = 6 x 10(-7) M) is strychnine-sensitive and its activity is unaltered at 4 degrees C. These results point to a receptor-like function. The low-affinity site (Km = 1.4 x 10(-3) is strychnine-insensitive and is significantly inhibited (75%) by low temperature (4 degrees C), by low Na+ concentration and 50% by ouabain (10(-4) M). Compounds structurally similar to glycine and known to antagonize its uptake to neuronal cells, such as beta-alanine, N-methyl-d,l-alanine and sarcosine, also inhibit the low affinity site which indicate a glycine uptake function for this site. The relative activity of the uptake inhibitors indicate that in the adrenal chromaffin cell, glycine uptake is carried out by a System A amino acid transporter mechanism. GABA does not affect glycine binding or uptake in the chromaffin cells, suggesting that these two inhibitory amino acid neurotransmitters act via different mechanisms in the adrenal medulla. The results for glycine activity in adrenal medulla chromaffin cells are remarkably similar to those seen in CNS neuronal cells, and thus support the use of chromaffin cells as a model system for studying the mechanism of action of glycine in the central nervous system.

Acetamides↗
PubMed1992

Preferential release of epinephrine by glycine from adrenal chromaffin cells.

Isolated adrenal chromaffin cells were used as a model for the release of catecholamines from adrenergic nerve endings. In this study we used an HPLC technique to determine the effects of acetylcholine and glycine on norepinephrine and epinephrine release. The amount of catecholamine released in response to glycine was 22% less than that released by acetylcholine. However, while the norepinephrine-to-epinephrine ratio was 1.6 after stimulation with acetylcholine, it was 0.6 after stimulation with glycine. This suggests that glycine preferentially affects epinephrine secretion as compared to acetylcholine, which preferentially releases norepinephrine. This differential effect could be of physiological importance considering our recent demonstration of a functional high-affinity chloride-gated glycine receptor on adrenal chromaffin cells.

Acetylcholine↗
PubMed1991

Effects of the glycine prodrug milacemide (2-N-pentylaminoacetamide) on catecholamine secretion from isolated adrenal medulla chromaffin cells.

1. Milacemide (2-n-pentylaminoacetamide) is a glycine prodrug which readily crosses the blood brain barrier and increases brain glycine and glycineamide. In vitro and in vivo studies, with numerous tissues, including adrenal chromaffin cells, have clearly shown that the formation of the latter metabolites is exclusively mediated by monoamine oxidase B for which milacemide is a substrate. 2. Milacemide, glycineamide and glycine caused a time- and dose-dependent release of catecholamines from bovine isolated chromaffin cells. 3. Milacemide (10(-4) M) induced catecholamine release was roughly 30% of that initiated by acetylcholine (10(-4) M), the natural secretagogue. 4. The combined effects of milacemide (10(-4) M) and acetycholine (10(-4) M) on catecholamine secretion from chromaffin cells is additive, suggesting that milacemide does not act through the normal nicotinic receptor release mechanism. 5. The release of catecholamines from chromaffin cells in response to milacemide (10(-4) M) was partially inhibited by the selective MAO-B inhibitors (-)-deprenyl (10(-7) M) and AGN 1135 (10(-6) M). This indicates that the MAO-B derived metabolites, glycineamide and glycine, contribute to the secretion of catecholamines as does milacemide itself. 6. It is apparent that release of catecholamines by glycine is mediated by its uptake into the cells since [3H]-glycine uptake and catecholamine release showed a highly significant correlation (r = 0.96).

Acetamides↗
PubMed1991

Catecholamine determination in sequential urine voiding: a method for detecting pheochromocytoma in patients without elevated urinary catecholamines.

The biochemical diagnosis of pheochromocytoma is based on the demonstration of increased amounts of catecholamines, or catecholamine metabolites, in 24-h urine samples. In patients whose 24-h urine catecholamines are within normal limits, and in whom short duration catecholamine elevations are suspected, timed urine collections have been used to detect these elevations. In this study, determination of catecholamines in sequential urine voidings and consideration of their relative values are suggested as a further method to detect pheochromocytomas, especially in cases without extended elevation of urinary catecholamine levels. The use of this method is demonstrated in three cases in which pheochromocytoma would not otherwise have been proven by laboratory determination.

Adrenal Gland Neoplasms↗
PubMed1989

Guidelines (1988) for training in clinical laboratory management. International Federation of Clinical Chemistry (IFCC) Education Division and International Union of Pure and Applied Chemistry (IUPAC) Clinical Chemistry Division Commission on Teaching of Clinical Chemistry.

Trainees in laboratory medicine must develop skills in laboratory management. Guidelines are detailed for laboratory staff in training, directors responsible for staff development and professional bodies wishing to generate material appropriate to their needs. The syllabus delineates the knowledge base required and includes laboratory planning and organisation, control of operations, methodology and instrumentation, data management and statistics, financial management, clinical use of tests, communication, personnel management and training, and research and development. Methods for achievement of the skills required are suggested. A bibliography of IFCC publications and other material is provided to assist in training in laboratory management.

Administrative Personnel↗