Congenital syphilis not an artifact.
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Humans↗
Biomedical subjects
D A Cohen
Publications and source records attributed to D A Cohen.
Parietal area 5 neuronal activity encodes movement kinematics, not movement dynamics.
A previous study reported that proximal-arm related area 5 neurons showed continuously-graded changes in activity during unloaded arm movements in different directions (Kalaska et al. 1983), which resembled the responses of primary motor cortex cells in several respects (Georgopoulos et al. 1982). We report here that loading the arm reveals an important difference between cell activity in the two areas. Loads were continuously applied to the arm in different directions. The loads produced large continuously-graded changes in muscle activity but did not alter the handpath or joint angle changes of the arm during the movements. The activity of most area 5 cells was only weakly affected by the loads, and the overall pattern of population activity was virtually unaltered under all load conditions. This indicates that area 5 activity encodes the invariant spatial parameters (kinematics) of the movements. In contrast, many motor cortex cells showed large changes in activity during loading, and so signal the changing forces, torques or muscle activity (movement dynamics; Kalaska et al. 1989).
Animals↗
The effect of the endophyte (Acremonium coenophialum) and associated toxin(s) of tall fescue on serum titer response to immunization and spleen cell flow cytometry analysis and response to mitogens.
Experiments were conducted with rats and mice to evaluate the effect of the consumption of endophyte (Acremonium coenophialum) and associated toxin(s) infected tall fescue on humoral and cellular aspects of immune function. Treatment diets were: (1) rodent chow (RC) or (2) rodent chow mixed 1:1 (w/w) with endophyte infected (E+) or (3) non-infected (E-) tall fescue seed. Rats fed the E+ diet in experiment 1 (43 days) exhibited a lower (P less than 0.05) serum titer to sheep red blood cell (SRBC) immunization than those fed the E- diet (38.4 vs 131.3). The E+ rats also had lower (P less than 0.01) white cell counts than either RC or E- groups (5225 vs 8959 and 7491/mm3). Spleen cells from mice fed the E+ diet for 37 days exhibited a reduced (P less than 0.05) response to the mitogens Concanavalin A and lipopolysaccharide. Flow cytometric analysis revealed a significant (P less than 0.01) 42% increase in T suppressor cell numbers in spleens of mice fed the E+ vs RC diets.
Acremonium↗
The effects of case definition in maternal screening and reporting criteria on rates of congenital syphilis.
Reports of congenital syphilis in 1987 were reviewed to determine how new national guidelines for defining congenital syphilis would influence reported rates in Los Angeles County. After reviewing all reported reactive serologic tests for syphilis, we found 166 additional cases, resulting in a 426 percent increase in the 1987 reported rate of congenital syphilis. Rates of congenital syphilis are dependent upon surveillance practices, screening policies, and case definition.
Female↗
Monokine-induced lung injury in rats: similarities to monocrotaline-induced pneumotoxicity.
Previous studies have shown that abnormal alveolar macrophages and biological activity resembling the macrophage-derived mediator interleukin-1 (IL-1) can be detected in bronchoalveolar lavage fluid from rats with monocrotaline-induced lung injury and pulmonary hypertension. To determine if monokines might play a pathogenic role in this model, the present study evaluated the effects of a murine monokine preparation enriched in IL-1 bioactivity on selected events characterizing the early pneumotoxic response to monocrotaline, including pulmonary edema and protein extravasation, pulmonary vascular hyperreactivity, and enhanced lung tissue activity of the rate-limiting enzyme in polyamine biosynthesis, ornithine decarboxylase (ODC). Intravenous injection of the monokine preparation containing 200 units/kg IL-1 (quantified by lymphocyte activating factor assay) into intact rats produced pulmonary edema within 3 hr manifested by increases in the lung wet-to-dry weight ratio and in the extent of pulmonary albumin extravasation. The edema had resolved within 24 hr of monokine administration as indicated by a return to control levels of the wet-to-dry weight ratio and albumin extravasation index. The monokine preparation also increased the transfer of albumin across monolayers of cultured porcine pulmonary vascular endothelial cells. While salt solution-perfused rat lungs isolated from animals treated 3 hr previously with the monokine preparation were hyporesponsive to angiotensin II, preparations derived from animals treated 24 hr previously were markedly hyperresponsive to the vasoconstrictor actions of the peptide. Pressor responses to potassium chloride and prostaglandin F2a were unaffected by exposure to the monokine preparation. Lung ODC activity in monokine-exposed animals did not differ from control at 3, 6, or 24 hr after treatment. In contrast, a 24-hr exposure of cultured pulmonary vascular endothelial cells to the monokine preparation increased ODC activity approximately 100-fold. These observations indicate that a monokine preparation containing IL-1 bioactivity causes transient pulmonary edema and pulmonary vascular hyperreactivity and increases ODC activity in pulmonary vascular endothelial cells. Because the monokine preparation mimics certain aspects of monocrotaline-induced pneumotoxicity in the rat, it is reasonable to postulate that monokines could play a pathogenic role in this and similar animal models of lung injury and pulmonary hypertension.
Animals↗
Increased tumor necrosis factor production by monocytes in alcoholic hepatitis.
Tumor necrosis factor is a cytokine that mediates many of the biologic actions of endotoxin. Recent studies have shown that tumor necrosis factor administration may cause liver injury and that tumor necrosis factor may mediate the lethality of the hepatotoxin galactosamine. One of the most potent inducers of tumor necrosis factor production is endotoxin. Because patients with alcoholic liver disease frequently have endotoxemia and because many of the clinical manifestations of alcoholic hepatitis are known biologic actions of tumor necrosis factor, we thought it would be important to evaluate tumor necrosis factor activity in patients with alcoholic hepatitis. Basal and lipopolysaccharide-stimulated tumor necrosis factor release from peripheral blood monocytes, a major source of tumor necrosis factor production, was determined in 16 patients with alcoholic hepatitis and 16 healthy volunteers. Eight of 16 alcoholic hepatitis patients and only two of 16 healthy volunteers had detectable spontaneous tumor necrosis factor activity (p less than 0.05). After lipopolysaccharide stimulation, mean monocyte tumor necrosis factor release from alcoholic hepatitis patients was significantly increased to over twice that of healthy controls (25.3 +/- 3.7 vs. 10.9 +/- 2.4 units per ml, p less than 0.005). We conclude that monocytes from alcoholic hepatitis patients have significantly increased spontaneous and lipopolysaccharide-stimulated tumor necrosis factor release compared to monocytes from healthy volunteers. We suggest that some of the metabolic abnormalities and possibly some of the liver injury of alcoholic hepatitis may be due to enhanced tumor necrosis factor production.
Adult↗
Odontogenic sinus tracts.
Odontogenic sinus tracts are the most common cause of a chronically draining, fixed, nodulocystic papule of the face and neck. Injury or disease of a tooth may result in a periapical abscess that subsequently dissects along the path of least resistance and erupts through the skin. If recognized early, the sinus tract usually resolves after appropriate endodontic therapy or extraction.
Adult↗
A comparison of movement direction-related versus load direction-related activity in primate motor cortex, using a two-dimensional reaching task.
Shoulder joint-related motor cortex cells show continuously graded changes in activity, centered on a preferred movement direction, during active arm movements in 8 directions away from a central starting position (Georgopoulos et al., 1982). We demonstrate here that many of these cells show similar large continuously graded changes in discharge when the monkey compensates for inertial loads which pull the arm in 8 different directions. These load-dependent discharge variations are typically unimodal, centered on one load direction called the cell's load axis, and are often sufficiently continuous, symmetric, and broad as to show a good fit to a sinusoidal curve. A vectorial representation of cell activity indicates that the pattern of load-dependent activity changes in the population forms a signal whose direction is appropriate to compensate for the loads. The responses of single cells to different combinations of movement and load direction are often complex. Nevertheless, the mean activity of the sample population under any condition of movement direction and load direction can be described reasonably well by a simple linear summation of the movement-related discharge without any loads, and the change in tonic activity of the population caused by the load, measured prior to movement. The strength of the load-dependent discharge variation differs among cells. Cells can be sorted into 2 phasic and 2 tonic groups that show differing degrees of sensitivity to loads. In particular, it was found that the greater the degree of cell discharge variation associated with different actively maintained limb postures, the greater the activity changes caused by loads. No similar correlation was found for the degree of discharge variation during movement. Preliminary evidence suggests that phasic and tonic cell groups may be spatially segregated in the motor cortex. These observations are consistent with the idea that there exists in the motor cortex activity encoding aspects of movement kinematics, as well as movement dynamics. These observations are in agreement with studies of more distal arm joints, showing that the activity of certain motor cortex cells varies with the patterns of muscle activity and output forces required to produce a movement. These experiments extend the description of the control of the direction of movement of a multiple degree-of-freedom joint into the spatial (direction) domain to a greater extent than previously achieved.
Animals↗
Artificial T cell:B cell conjugation. A unique approach to analyze weak cell-cell interactions.
An antibody response against a thymic-dependent Ag requires cognate recognition of the Ag by B and T cells. Functional T-B cell (T-B) interaction involves binding of Ag by B cell surface Ig, internalization and processing of Ag, expression of an Ag fragment in the context of Ia, binding of Ag/Ia by the TCR and binding of T cell-derived lymphokines by B cell lymphokine receptors. It is becoming increasingly evident that B and T cell accessory molecules also are involved in T-B interactions. To determine the role of accessory molecules in T-B collaboration, we have designed a system in which T-B interaction was artificially induced in the absence of carrier protein. TNP-modified, turkey gamma-globulin-specific, Th cells were allowed to form conjugates with TNP-specific B cells in the absence of hapten-carrier complex. Both B and T cells were induced to proliferate and B cells partially differentiated into antibody-secreting cells when B cells were cultured with TNP-modified but not unmodified T cells. The activation of B cells by TNP-modified T cells was not MHC restricted but was blocked by anti-Ia antibodies, suggesting a role for Ia distinct from Ag presentation. Furthermore, B cell proliferation was also inhibited by antibodies to L3T4 and LFA-1, suggesting a functional accessory role for these molecules in induction of B cell proliferation/differentiation.
Animals↗
The requirement for surface Ig signaling as a prerequisite for T cell:B cell interactions. A possible role for desialylation.
Models for T cell:B cell collaboration suggest that activated B cells process and present Ag to Th cells which subsequently induce B cell proliferation and differentiation. In contrast to activated B cells, resting B cells have generally been shown to be less efficient APC. If this model of T:B collaboration is physiologically correct, then resting B cells must undergo a phenotypic change that permits effective interaction with T cells. In this report, the requirement for rapid signaling through surface Ig on resting B cells for the induction of T:B interaction was investigated with an in vitro clustering assay. Resting splenic B cells were unable to form specific conjugates with T cell clones, unless the B cells were first treated with neuraminidase to remove sialic acid. In contrast, LPS-activated B cells were able to form conjugates without prior treatment. The ability of antibody against LFA-1 or L3T4 to inhibit cluster formation depended on the state of B cell activation in that anti-LFA-1 and anti-L3T4 mAb inhibited cluster formation by neuraminidase-treated resting B cells, but not by LPS-activated B cells. In addition, Ag-specific B cells which were isolated by their capacity to bind specific Ag were able to form clusters without any additional treatment. Moreover, treatment of resting splenic B cells with anti-mu-antibody induced clustering potential in B cells in as little as 10 min, suggesting that signaling through surface Ig was sufficient to induce this phenotypic change in B cells. Furthermore, activation of protein kinase C and Ca2+ mobilization were shown to be involved in that PMA and ionomycin treatment were also able to induce clustering potential in resting B cells. The rapid induction of clustering potential in resting B cells after signaling through surface Ig may represent a fundamental change in B cell physiology which occurs after recognition of specific Ag and may be required for effective cognate recognition between resting hapten-specific B cells and carrier-specific T cells. The potential role of desialylation for the induction of T:B interaction is discussed.
Animals↗
Characterization of cell surface molecules involved in the recognition of antigen-presenting cells by cloned helper T-cell lines.
The recognition of antigen-presenting cells (APCs) by T helper (TH) cells occurs in an antigen (Ag)-specific, MHC-restricted manner. Recent evidence, however, suggests that other interaction molecules may also be involved in TH:APC interaction in addition to the T-cell receptor (Ti) and class II or la antigens. We chose, therefore, to examine the role of various interaction molecules (Ia, Ti, L3T4, and LFA-1) in Ag presentation using several TH clones with distinct recognition patterns (self-Ia, self-Ia/Ag, and allogenic Ia). We describe here the use of a rapid clustering assay to study the initial binding events that occur between TH cells and APCs of various types. In all combinations of TH cells and APCs, conjugate formation was both Ag-specific and MHC-restricted. Moreover, with one exception cell clustering was prevented by the addition of monoclonal antibodies (mAb) against either the T-cell receptor or class II MHC molecules. In contrast, mAb to L3T4 and LFA-1 generally failed to inhibit cluster formation even though T-cell proliferation was profoundly inhibited. The relative importance of these interaction molecules in conjugate formation appeared to depend on the APC type as well as on the T-cell clone used. The implications of these findings for the mechanisms of Ag presentation and T-cell activation are discussed.
Animals↗
Provocation of pulmonary vascular endothelial injury in rabbits by human recombinant interleukin-1 beta.
Interleukin-1 (IL-1) mediates components of the acute-phase response, stimulates granulocyte metabolism, and induces endothelial cell surface changes. We studied the effects of human recombinant IL-1 beta (rIL-1 beta) or rIL-1 alpha on circulating granulocytes, their sequestration within the pulmonary microvasculature, pulmonary edema formation, and changes in pulmonary vascular permeability to 125I-labeled albumin. rIL-1 beta administration induced significant (P less than 0.03) but transient granulocytopenia followed by significant (P less than 0.04) neutrophilia and significant (P less than 0.04) pulmonary leukostasis compared with saline-infused rabbits. Rabbits preinfused with 125I-labeled rabbit serum albumin and administered saline, rIL-1 beta, or rIL-1 alpha were sacrificed, and lung wet/dry weight ratios and bronchoalveolar lavage fluid and plasma 125I activities determined. Both rIL-1 beta and rIL-1 alpha increased lung wet/dry weight ratios (P less than 0.025 and P less than 0.01, respectively) compared with saline controls. rIL-1 beta increased bronchoalveolar lavage fluid/plasma 125I radioactivity ratios (P less than 0.025). Electron microscopic analysis of lung sections obtained from rIL-1 beta-infused animals demonstrated endothelial injury, perivascular edema, and extravasation of an ultrastructural permeability tracer. The observation that human rIL-1 can evoke acute pulmonary vascular endothelial injury and lung edema in rabbits supports the hypothesis that IL-1 may play a role in the pathogenesis of the adult respiratory distress syndrome.
Animals↗
Interleukin 1 bioactivity in the lungs of rats with monocrotaline-induced pulmonary hypertension.
A single subcutaneous injection of monocrotaline in rats provokes lung injury, inflammation, and progressive pulmonary hypertension. The specific mediators of the lung injury and inflammation and the relation of these events to the ensuing hypertensive pulmonary vascular disease are not understood. Since the monokine interleukin 1 (IL-1) has been implicated in acute inflammatory reactions, the present study tested the hypotheses that monocrotaline promotes the appearance of IL-1 in the bronchoalveolar spaces of treated rats and that accumulation of the monokine coincides temporally with development of lung injury, inflammation, and/or pulmonary hypertension. As expected, monocrotaline administration was associated with an early phase of pulmonary edema, manifest at Day 7 post-treatment as an increase in the lung wet-to-dry weight ratio, followed at Day 14 post-treatment by development of pulmonary hypertension as evidenced by progressive right ventricular hypertrophy. Lung inflammation also was present at Days 14 and 21 after monocrotaline as indicated by the accumulation of leukocytes in the bronchoalveolar lavage fluid and by an increase in the lung tissue activity of the granulocyte-specific enzyme myeloperoxidase. Interleukin 1, bioassayed in bronchoalveolar lavage fluid using the standard D10 T-cell assay system, was increased slightly at Day 4 postmonocrotaline, returned to baseline at Day 7, and was markedly elevated at Days 14 and 21 after monocrotaline treatment. These observations indicate that increases in the bronchoalveolar lavage fluid content of IL-1 bioactivity are temporally related to the evolution of monocrotaline-induced lung injury, inflammation, and pulmonary hypertension and suggest that the monokine may play a pathogenetic role in these events.
Animals↗
Interleukin-1 (IL-1) depresses cytochrome P450 levels and activities in mice.
Endotoxin depresses cytochrome P450 levels when injected into animals. The purpose of this study was to determine whether endotoxin itself, or monokine(s) released in response to endotoxin administration are responsible for this effect. Cytochrome P450 levels and drug metabolizing activities were measured in endotoxin resistant C3H/HeJ mice 24h after single intraperitoneal injections of either lipopolysaccharide (LPS), a semipurified murine monokine preparation containing interleukin-1 (IL-1), or murine recombinant IL-1. In endotoxin sensitive C3H/HeN mice, LPS (0.5 mg/Kg) decreased total cytochrome P450 levels, benzphetamine demethylase activities, and ethoxyresorufin-0-deethylase activities. This dose of LPS did not alter cytochrome P450 levels or activities in the C3H/HeJ mice. However, after injection of the semipurified monokine preparation or the recombinant IL-1, there were significant decreases in cytochrome P450 levels and activities similar to the decreases observed with LPS in the C3H/HeN mice. These findings suggest that the alterations in hepatic cytochrome P450 seen with endotoxin injection are mediated, at least in part, by IL-1.
Animals↗
Physicians' attitudes toward patient education on nuclear war.
A pilot survey was conducted to determine self-reported knowledge, attitudes, and behavior of physicians with regard to educating patients on the medical consequences of nuclear war. Two groups were sampled: a group of physicians who had expressed interest in patient education on nuclear issues, and a group of randomly selected family practitioners. The majority of respondents from both groups felt that patient education on this subject was important, yet only 37 and 8% of the respective groups had done anything to inform their patients. Physicians require more information and motivation as to the importance and appropriateness in the clinical setting of raising their concerns about the threat of nuclear war.
Attitude of Health Personnel↗
Interleukin 1-induced depression of iron and zinc: role of granulocytes and lactoferrin.
The mechanism(s) of stress-induced hypoferremia and hypozincemia remains unclear. We studied the role of granulocytes and lactoferrin (LF) in endotoxin and murine interleukin 1 (IL-1)-induced depression of serum Fe and Zn concentrations in both rabbits and rats. Both endotoxin and IL-1 administration induced significant hypoferremia (P less than 0.01) and hypozincemia (P less than 0.01) after 6 h in both species. Granulocyte depletion before IL-1 infusion significantly (P less than 0.01) diminished the hypoferremia but not the hypozincemia. Moreover, infusion of 5 or 15 mg of human LF into rabbits caused significant hypoferremia (P less than 0.005) without hypozincemia. Significant hypozincemia (P less than 0.01) could only be demonstrated after a 75-mg infusion. In contrast, infusions of human transferrin at equivalent doses (5, 15, and 75 mg) induced neither hypoferremia nor hypozincemia. Therefore endotoxin and IL-1-induced hypoferremia and, to a much lesser degree, hypozincemia are granulocyte dependent. Granulocyte released LF is a specific carrier molecule for transport and removal of Fe from the circulation during the acute phase response. The data suggest a mechanistic dissociation of IL-1-induced hypoferremia and hypozincemia with LF-independent mechanisms for Zn.
Animals↗
Interleukin-1-induced granulocytopenia and pulmonary leukostasis in rabbits.
Pulmonary leukostasis is a postulated prerequisite lesion for acute lung injury. Interleukin-1 (IL-1) mediates components of the acute-phase response, stimulates granulocyte metabolism and secretion, and augments endothelial adhesiveness. We studied the effects of murine IL-1 infusion on circulating granulocytes, their sequestration within the pulmonary microvasculature, lung water, and bronchoalveolar lavage fluid (BALF) protein concentration in rabbits at 3 and 24 h after infusion. IL-1 administration induced significant (P less than 0.01) granulocytopenia compared with saline-injected controls and at 3 h induced significant increases in both mean alveolar septal wall granulocytes per high power field (HPF) (P less than 0.001) and mean myeloperoxidase (MPO) activity per gram lung tissue (P less than 0.001). At 24 h, IL-1 induced a marked granulocytosis and again significantly increased both mean alveolar septal wall granulocytes per HPF (P less than 0.001) and lung MPO (P less than 0.01). Increased lung water or BALF protein concentration could not be demonstrated in animals killed at either 3 or 24 h after IL-1 administration. Therefore, IL-1 can induce an early profound granulocytopenia followed by later granulocytosis, as well as sustained pulmonary leukostasis in the absence of detectable pulmonary edema formation or an alveolar-capillary leak.
Agranulocytosis↗
Monokine-induced acute lung injury in rabbits.
Interleukin-1 (IL-1) mediates components of the acute phase response, stimulates granulocyte metabolism, and induces endothelial cell surface changes. We studied in unanesthetized rabbits the effects of intravenous divided dose infusions of a murine monokine preparation containing IL-1 activity, on circulating granulocytes, their sequestration within the pulmonary microvasculature, pulmonary edema formation, and changes in pulmonary vascular permeability. Monokine administration induced significant (P less than 0.01) granulocytopenia as well as a significant (P less than 0.001) increase in mean alveolar septal wall granulocytes per high power field (HPF) compared with saline-injected controls. Infusions of the monokine preparation significantly (P less than 0.005) increased lung wet-to-dry weight ratios as well as significantly (P less than 0.025) increased pulmonary extravasation of radiolabeled albumin. Electron microscopic analysis of lung sections obtained from monokine-infused animals demonstrated endothelial injury, perivascular edema, and extravasation of an ultrastructural tracer. We conclude that a monokine preparation containing IL-1 activity can induce profound granulocytopenia, pulmonary leukostasis, and acute pulmonary vascular endothelial injury.
Agranulocytosis↗