Antibody responses to BSA in dogs: a source of error in diagnostic immunoassays.
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Animals↗
Biomedical subjects
C May
Publications and source records attributed to C May.
Affective neutrality and involvement in nurse-patient relationships: perceptions of appropriate behaviour among nurses in acute medical and surgical wards.
This paper explores ideas about the appropriate basis for nurse-patient relationships which underwrite the nursing practice of experienced staff nurses on the acute surgical and medical wards of a Scottish general hospital. Three central features of involvement with patients are identified, knowledge, reciprocity and investment, and these are related to three general models of the nurse-patient relationship, characterized as primary, demonstrative and associational. The implications of the nursing practice on which these models are based are discussed in the context of issues of quality of care and orientation to work.
Affect↗
Cerebrospinal fluid acetylcholinesterase in progressive supranuclear palsy: reduced activity relative to normal subjects and lack of inhibition by oral physostigmine.
Acetylcholinesterase (AChE) activity was measured in lumbar cerebrospinal fluid (CSF) of 11 patients with progressive supranuclear palsy (PSP) and 18 age-matched healthy control subjects. Mean CSF AChE activity in PSP subjects was significantly reduced by 31% relative to control subjects (p less than 0.002). In the light of evidence of a central cholinergic deficit, physostigmine was administered orally (0.5-2.0 mg every two hours, six times a day for 10 days) to eight of the 11 PSP patients. CSF was sampled when the patients were on placebo and when receiving physostigmine and CSF AChE and butyrylcholinesterase (BChE) activities were measured. There was no significant change in either CSF AChE or BChE activities following physostigmine treatment. These data suggest that the doses of physostigmine used were insufficient to produce marked inhibition of AChE within the central nervous system.
Acetylcholinesterase↗
Cerebrospinal fluid immunoreactive corticotropin-releasing hormone and adrenocorticotropin secretion in Cushing's disease and major depression: potential clinical implications.
To explore whether possible differences in central nervous system neuromodulators contribute to the differential presentation of affective symptomatology in Cushing's disease and major depression, we examined the levels of immunoreactive CRH and ACTH in the cerebrospinal fluid (CSF) of 11 patients with Cushing's disease, a patient with ectopic ACTH secretion, 34 patients with major depression, and 60 healthy subjects. We elected to measure these peptides not only because both are classically involved in pituitary-adrenal regulation, but also because their primarily arousal-producing and anorexigenic behavioral effects in experimental animals suggest that they may play a role in the symptom complex of depressive syndromes. We also explored whether the CSF levels of these peptides were more helpful in determining the often difficult differential diagnosis between major depression and Cushing's disease than the plasma ACTH response to ovine CRH, a currently used but somewhat insensitive laboratory means of distinguishing these disorders. CSF levels of immunoreactive CRH and ACTH were significantly lower in Cushing's disease patients [21.9 +/- 2.7 and 15.4 +/- 1.8 pg/mL, (mean +/- SEM), respectively] compared to patients with major depression [38.4 +/- 2.3 pg/mL (P less than 0.01) and 24.5 +/- 1.6 pg/mL (P less than 0.01), respectively] and controls [38.4 +/- 1.6 pg/mL (P less than 0.001) and 26.3 +/- 1.1 pg/mL (P less than 0.001), respectively]. The coexistence of high plasma ACTH and low CSF ACTH in Cushing's disease yielded a CSF/plasma ACTH ratio consistently less than that in depressed patients, with only 2 of 31 subjects comprising both groups showing values that overlapped. In contrast, 9 of the combined patients showed ACTH responses to ovine CRH that overlapped. These data suggest that differences in centrally directed CRH secretion may account for the differential presentation of the dysphoric syndromes seen in major depression and Cushing's disease. Hence, the classic form of major depression (melancholia), is often associated with evidence of pathological hyperarousal, such as intense anxiety, sleeplessness, and anorexia, while that of Cushing's disease is associated with evidence of pathological hyperarousal, including hyperphagia, fatigue, and inertia. Moreover, measurement of the CSF/plasma ACTH ratio may serve as a clinically useful adjunct to the ovine CRH stimulation test and other laboratory measures in determining the differential diagnosis between major depression and Cushing's disease.
Adolescent↗
Lyme disease in dogs and cats.
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Animals↗
Suramin prevents binding of interleukin 2 to its cell surface receptor: a possible mechanism for immunosuppression.
Suramin, a polysulfonic naphthalene antihelminthic drug, inhibits proliferation of a variety of T-cell lines in vitro and induces immunosuppression in some human patients and thymic atrophy and splenic depletion in mice. Recent clinical trials indicate that suramin has activity against human tumors, indicating that it will be necessary to understand the mechanism by which suramin induces immunosuppression. The T-cell growth factor, interleukin 2 (IL2), is the major growth factor involved in regulating lymphoid differentiation and proliferation and thus regulates, to a major degree, the magnitude and duration of the immune response. We demonstrate herein that suramin induces a concentration-dependent decrease in binding of 125I-labeled IL2 to its receptor complex on human and murine T-lymphocytes. Binding of 125I-labeled IL2 to both Mr 75,000 and 55,000 IL2 binding molecules was inhibited by suramin. Similar concentrations of suramin were required to inhibit binding of 125I-labeled IL2, IL2-induced tyrosine phosphorylation, and IL2-induced proliferation, suggesting that these processes may be linked. With murine cells, suramin-induced growth inhibition could be overcome completely by increasing the concentration of IL2, suggesting that suramin inhibited growth by competing for the IL2 receptor. With human cells, growth inhibition by suramin could only be partially overcome by increasing the concentration of IL2, suggesting that an additional growth-inhibiting mechanism is present. The ability of suramin to prevent binding of IL2 to its receptor was used to confirm that prolonged interaction of IL2 with its receptor is required to induce cell proliferation. Since IL2 plays a role in lymphocyte proliferation and differentiation, the ability of suramin to inhibit binding of IL2 to its receptor may explain, in part, the in vivo immunosuppressive activities of suramin.
Animals↗
Interleukin 2-induced tyrosine phosphorylation. Interleukin 2 receptor beta is tyrosine phosphorylated.
Interaction of interleukin 2 (IL2) with its high affinity membrane receptor complex (IL2R) is sufficient to induce proliferation of T lymphocytes. However, the biochemical mechanisms by which IL2 induces this process remain unresolved. The IL2R complex consists of at least two distinct polypeptides that bind IL2, a 75-kDa intermediate affinity subunit (IL2R beta) and a 55-kDa low affinity subunit (IL2R alpha). As indicated by Western blotting with anti-phosphotyrosine-specific antibodies and confirmed by phosphoamino acid analysis, we now demonstrate that interaction of the T cell growth factor interleukin 2 (IL2) with its high affinity receptor on IL2-sensitive human peripheral blood lymphoblasts induces tyrosine phosphorylation of proteins of 92, 80, 78, 70-75, and 57 kDa. IL2 induced tyrosine phosphorylation in YT 2C2 cells which express only the 75-kDa intermediate affinity IL2 binding molecule (IL2R beta) but not in cells which either express only the 55-kDa low affinity IL2 receptor molecule (IL2R alpha) or no IL2-binding sites. Therefore, IL2R beta, in the absence of IL2R alpha, appears sufficient to transduce the transmembrane signal leading to tyrosine phosphorylation. Two different antibodies reactive with phosphotyrosine specifically immunoprecipitated IL2R beta cross-linked to radiolabeled IL2. These findings suggest that IL2R beta is a substrate for the tyrosine kinase which is activated by IL2 binding to its receptor. Thus, like several other growth factor receptors, activation of the IL2R results in an increase in tyrosine phosphorylation with the receptor itself serving as one substrate.
Amino Acids↗
Withholding and withdrawal of life support from the critically ill.
We investigated decisions to withhold or withdraw life support from patients in the medical-surgical intensive care units at the Moffitt-Long Hospital of the University of California and San Francisco General Hospital, from July 1987 through June 1988. Among 1719 patients admitted to the two intensive care units, life support was withheld from 22 (1 percent) and withdrawn from 93 (5 percent). The reason for limiting care was poor prognosis. Of these 115 patients (18 of whom were considered brain-dead), 89 died in the intensive care unit (accounting for 45 percent of all deaths there), and all but 1 of the remaining patients died after transfer from the intensive care unit. Thirteen (11 percent) had earlier expressed the wish that their terminal care be limited, but this affected care in only four cases. Only 5 of the 115 patients made the actual decision to limit care; the others were incompetent at the time. Of the latter, 102 had families who participated in the decision; family members of the other 8 incompetent patients could not be found, and the decisions were made by physicians. Only 10 families initially disagreed with the recommendations to limit care, and they later agreed. The median duration of intensive care among the patients from whom life support was withheld or withdrawn was eight days at Moffitt-Long Hospital and four days at San Francisco General, as compared with medians of three and one days, respectively, for other patients who died in the intensive care units. We conclude that although life-sustaining care is withheld or withdrawn relatively infrequently from patients in the intensive care unit, such decisions precipitate about half of all deaths in the intensive care units of the hospitals we studied. In most of these cases the patients are incompetent, but physicians and families usually agree to limit care.
Adult↗
The viral hypothesis of Alzheimer's disease. Absence of antibodies to lentiviruses.
To evaluate the possible role of lentiviruses in Alzheimer's disease we searched for cross-reactive antibodies to human immunodeficiency virus type 1, caprine arthritis encephalitis virus, and equine infectious anemia virus in Alzheimer's disease, Down's syndrome, and related dementing illnesses in serum samples and cerebrospinal fluid samples and in healthy age-matched control subjects. No cross-reactive antibodies were detected.
Aged↗
Lumbar cerebrospinal fluid choline in healthy aging and in Down's syndrome.
Choline concentrations were measured in lumbar cerebrospinal fluid (CSF) and plasma of 37 healthy normal subjects and 13 young (age range, 21 to 34 years) and 6 older (age, greater than or equal to 45 years) healthy adults with Down's syndrome (DS). All subjects with DS had a trisomy 21 karyotype, and 3 of the 6 older subjects were demented as judged from a history of mental deterioration, disorientation, and memory loss. In healthy normal subjects, there was a significant correlation between age and CSF choline concentrations. Compared with age-matched controls, in young subjects with DS, CSF, but not plasma, choline concentrations were elevated (by 49%), whereas in older subjects with DS, CSF and plasma choline concentrations were similar to control values. The CSF choline concentrations were unrelated to body height in the DS and control groups, and rostrocaudal CSF choline gradients did not differ between either the control and DS groups or the young and old subjects with DS, suggesting that the elevation in the CSF choline concentration in young subjects with DS was not related to their shorter stature. Since increased CSF choline concentrations in young adult subjects with DS were accompanied by normal plasma choline concentrations, these results suggest that young adults with DS have either an increased release of choline from the brain or a reduced rate of clearance of choline from CSF.
Adult↗
Interrelationship between signals transduced by phytohemagglutinin and interleukin 1.
In the murine cell line LBRM-331A5, phytohemagglutinin (PHA) induces secretion of the T cell growth factor interleukin 2 (IL2). IL1 augments PHA-induced IL2 production. In this cell line, PHA stimulates a number of biochemical changes including phospholipid hydrolysis, increases in cytosolic free calcium [( Ca2+]i), membrane hyperpolarization, cytosolic alkalinization, and tyrosine phosphorylation of specific substrates. Using LBRM cells, we have studied the interrelationship between these events and the secretion of IL2. Increases in [Ca2+]i triggered by PHA or following addition of ionomycin result in membrane hyperpolarization but are not required for PHA-induced cytosolic alkalinization or tyrosine phosphorylation. Addition of IL1 to PHA-stimulated cells did not affect any of the biochemical parameters, although it significantly augmented PHA-induced IL2 secretion. Increasing [Ca2+]i with ionomycin did not trigger IL2 secretion, increases in cytosolic pH, or tyrosine phosphorylation in the presence or absence of IL1. Preventing increases in cytosolic pH did not alter PHA-induced changes in [Ca2+]i or membrane potential. These data are compatible with PHA including activation of phospholipase C and production of inositol phosphates resulting in both release of Ca2+ from internal stores and transmembrane uptake of Ca2+ as well as activation of protein kinase C. However, unlike other growth factor or mitogen-stimulated systems, the changes stimulated by PHA and IL1 in LBRM cells including IL2 secretion are not regulated by a pertussis toxin-sensitive G protein.
Adenosine Diphosphate Ribose↗
Research on nurse-patient relationships: problems of theory, problems of practice.
Research, theoretical and educational literature on interpersonal relations between nurses and patients has proliferated since the 1960s. This has generated a range of divergent accounts of what the nurse-patient relationship (NPR) ought to be; how this should be achieved; and how the NPR is constituted in practice. In this paper--through a selective review of the literature--the development of two contending perspectives on NPR and on nurse-patient interaction (NPI) characterized as technocratic and contextual, is discussed, and related to the increasingly problematic status of the relationship between nurses and patients in nursing theory and research.
Communication↗
Ascitic fluid from human ovarian cancer patients contains growth factors necessary for intraperitoneal growth of human ovarian adenocarcinoma cells.
Human ovarian cancer, the leading cause of death from gynecologic malignancy, tends to remain localized to the peritoneal cavity until late in the disease. In established disease, ascitic fluid accumulates in the peritoneal cavity. We have previously demonstrated that this ascitic fluid is a potent source of in vitro mitogenic activity including at least one unique growth factor. We now report that the human ovarian adenocarcinoma line, HEY, can be induced to grow intraperitoneally in immunodeficient nude mice in the presence (23/28 mice), but not absence (0/21 mice) of ascitic fluid from ovarian cancer patients. Ascitic fluid from patients with benign disease did not have similar effects on intraperitoneal growth of HEY cells (1/15 mice). Once tumors were established by injections of exogenous ascitic fluid, they could progress in the absence of additional injections of ascitic fluid. The mice eventually developed ascitic fluid which contained potent growth factor activity, suggesting that the tumors eventually produced autologous growth factors. This nude mouse model provides a system to study the action of ovarian cancer growth factors on tumor growth in vivo and to evaluate preclinically, therapeutic approaches designed to counteract the activity of these growth factors.
Animals↗
Cerebrospinal fluid production is reduced in healthy aging.
In order to study age-related differences in cerebrospinal fluid (CSF) production in humans, we measured the rate of CSF production in 7 young (age 21 to 36 years) and 7 elderly (age 67 to 84 years) healthy volunteers, using a modified Masserman method. In addition, we evaluated CSF protein gradients by collecting CSF in serial fractions up to the 30th ml and assaying for total protein concentration. The mean rate of CSF production was significantly less in the elderly than in the young subjects. Mean CSF total protein concentrations were higher in the elderly than in the young, and significant rostrocaudal protein gradients with similar slopes were present in both groups. However, there was no correlation between CSF production and CSF total protein concentrations or protein gradient slopes. Age-related reductions in CSF production, together with the ventricular dilatation that occurs with aging, should presumably result in reduced CSF turnover and therefore influence measured concentrations of lumbar CSF constituents.
Adult↗
Quantitative analysis of polyols in human plasma and cerebrospinal fluid.
We used gas chromatography in conjunction with flame ionization detection to quantitate nine polyols and aldo and keto sugars (as silyl derivatives) in human plasma and cerebrospinal fluid (CSF). Rhamnose, not found in CSF or plasma, was used as an internal standard with a lower limit of quantitation of 0.4 mg/l. CSF polyol and sugar concentrations (mean +/- S.D.) in fourteen healthy subjects (age range 27.1-85.9 years) were: anhydroglucitol, 19.9 +/- 5.3 mg/l; arabitol, 4.8 +/- 0.9 mg/l; erythritol, 2.4 +/- 0.5 mg/l; myoinositol, 28.6 +/- 8.3 mg/l; ribitol, 1.6 +/- 0.1 mg/l; fructose, 25.5 +/- 11.1 mg/l; glucose, 587 +/- 70 mg/l; glucitol, 7.7 +/- 1.5 mg/l; and mannose, 10.6 +/- 2.4 mg/l. The respective plasma concentrations were 30.6 +/- 11.5, less than 0.4, 0.4 +/- 0.2, 6.3 +/- 2.6, less than 0.4, 23.4 +/- 21.4, 897 +/- 214, less than 0.4 and 13.7 +/- 6.3 mg/l. Polyol CSF-to-plasma concentration ratios greater than 2 were observed for myoinositol, erythritol, arabitol, glucitol and ribitol, indicative of active accumulation or synthesis of these polyols within the central nervous system.
Adult↗
Physiologic activation of protein kinase C limits IL-2 secretion.
Interaction of Ag, antibodies against the T cell receptor complex, or mitogenic lectins with T lymphocytes induces hydrolysis of membrane phospholipids leading to the production of diacylglycerol (DAG). DAG then activates the Ca2+- and phospholipid-dependent phosphotransferase, protein kinase C (PKC). Increases in DAG concentrations are transient as is the increase in PKC activity. Phorbol esters, which induce potent, prolonged activation of PKC, augment many T lymphocyte responses, including cell proliferation and secretion of the T cell growth factor IL-2. Therefore, it has been suggested that activation of PKC is a positive regulatory signal in T lymphocytes. We have determined the consequences of transient stimulation of PKC, and of depletion of PKC, on early cell activation signals and on production of IL-2 by the murine lymphoma line LBRM 331A5. When this cell line is depleted of PKC overnight incubation in high concentrations of phorbol esters, lectin-induced IL-2 secretion is augmented. Similarly, mitogen-induced changes in [Ca2+]i and phosphoinositide metabolism were augmented in these cells. In contrast, a short preactivation of PKC abrogated these early transmembrane signaling events. This suggested that normal physiologic activation of PKC may limit cell activation and decrease IL-2 production. We compared the effects of phorbol esters and mezerein, which produce prolonged activation of PKC, with those of diacylglycerol analogs, which induce transient activation of PKC. At concentrations that give similar levels of PKC activation, phorbol esters and mezerein, but not DAG analogs, increased IL-2 secretion. This suggests that prolonged, nonphysiologic activation of PKC is required to augment IL-2 secretion. Therefore, physiologic activation of PKC may not augment T cell activation but instead may function to decrease cell activation and limit IL-2 secretion.
Animals↗