The role of challenging incentives in feedback-assisted heart rate reduction for coronary-prone adult males

Three experiments were performed to study the influence of challenging incentives on feedback-assisted heart rate reduction for coronary-prone (Type A) and non-coronary-prone (Type B) males. In the first experiment, when subjects were given a competitive instructional set, Type As were significantly more successful relative to Type Bs in reducing their heart rate; with a noncompetitive set, Type Bs were significantly more successful than were Type As. In the second experiment, when told that heart rate reduction was a scarce ability, Type As reduced heart rate significantly better than did Type Bs; when told that heart rate reduction was a common ability, Type Bs achieved significantly greater heart rate reduction than did Type As. In the third experiment, when heart rate reduction was described as being instrumental to time-urgency (i.e., getting more done in less time), Type As reduced heart rate significantly bettern than did Type Bs; when heart rate reduction was described as being instrumental to relaxation, Type Bs were significantly better able to reduce heart rate. In all three studies, the incentives had no effect on heart rate when feedback was not provided. The results are discussed as support for the notion that Type A behavioral pattern characteristics can be exploited to reduce Type A symptoms. Implications for how coronary-prone individuals may be challenged to modify symptoms within the clinical setting are discussed.     

Structure of the abdominal receptor responsive to internally applied pressure in the blood-feeding insect,Rhodnius prolixus

Summary The sensory receptor responsive to pressure applied internally to the ventral abdominal body wall of the blood-feeding insects, Rhodnius prolixus, is a single sense cell containing, at its distal end, a cilium enclosed within a scolopale, a densely staining structure characteristic of insect scolopidial sensilla. A small spherical structure lies within a dilation near the midregion of the cilium, and contains nine heavily staining bodies, the position of each corresponding to a pair of microtubules in the cilium. Proximal to the dilation, the microtubules are organized in a ring of nine pairs with one microtubule of each pair associated with dyneinlike arms. Dastal to the dilation a central pair of microtubules is present, but dyneinlike arms are absent. The scolopale cell, which gives risc to the scolopale, has cytoplasmic invaginations that form an elaborate array of extracellular compartments surrounding the body wall of the sense cell. These compartments may serve to dampen high frequency vibrations permitting the receptor to respond to pressure exerted by touch, an attribute in keeping with the receptor's proposed function of detecting abdominal distension related to the size and movement of the stomach.     

Catalysis by dienelactone hydrolase: A variation on the protease mechanism

Dienelactone hydrolase (DLH), an enzyme from the β-ketoadipate pathway, catalyzes the hydrolysis of dienelactone to maleylacetate. Our inhibitor binding studies suggest that its substrate, dienelactone, is held in the active site by hydrophobic interactions around the lactone ring and by the ion pairs between its carboxylate and Arg-81 and Arg-206. Like the cysteine/serine proteases, DLH has a catalytic triad (Cys-123, His-202, Asp-171) and its mechanism probably involves the formation of covalently bound acyl intermediate via a tetrahedral intermediate. Unlike the proteases, DLH seems to protonate the incipient leaving group only after the collapse of the first tetrahedral intermediate, rendering DLH incapable of hydrolyzing amide analogues of its ester substrate. In addition, the triad His probably does not protonate the leaving group (enolate) or deprotonate the water for deacylation; rather, the enolate anion abstracts a proton from water and, in doing so, supplies the hydroxyl for deacylation. © 1993 Wiley-Liss, Inc.     

Phospholipid membrane stabilization by dimethylsulfoxide and other inducers of friend leukemic cell differentiation

A large number of low molecular weight polar cryoprotective agents have recently been found to induce erythroid differentiation of Friend leukemic cells in vitro. The effect of these agents on membrane fluidity in phospholipid vesicles was studied by determining the solid-to-liquid crystalline phase transition using differential scanning calorimetry. Some of the inducing agents studies were found to raise the normal transition temperature ($\text{T}{}_{\mathrm{<mtext>c</mtext>}}$ by a few degrees. All of these agents were found to produce a separate transition at a much higher temperature. Changes in the head group of the phospholipid, the pH, the presence of divalent cations, and the addition of other membrane-active compounds were found to significantly influence the inducing agent's effects on the $\text{T}{}_{\mathrm{<mtext>c</mtext>}}$ of phospholipid membranes.The ability of the different agents to produce a new transition at a high temperature was found to correlate well with their ability to incude Friend leukemic cell differentiation. The possible mechanisms of action of the chemical inducers, and the significance of the observed membrane effects on differentiation and malignancy are discussed. It is concluded that inducing agents decrease the fluidity and stabilize phospholipid membranes, and that their effects in cell differentiation might be initiated by a similar change in the properties of cell membranes.     

Induction of competence and progression signals in human T lymphocytes by phorbol esters and calcium ionophores

We have investigated the induction of competence (IL-2 responsiveness) and progression in human T lymphocyte proliferation triggered by phorbol ester and calcium ionophore. The degree of proliferation induced with the phorbol ester, phorbol 12,13-dibutyrate (PDB) and the calcium ionophore ionomycin was dependent on the duration of exposure to these agents, with more than 6 h required for obtaining maximum proliferation. Following brief exposure to both agents for 30 min, which did not cause significant proliferation, T cells became competent to proliferate in response to exogenous interleukin 2 (IL-2). These competent T cells also progressed to DNA synthesis following incubation with PDB in the absence of ionomycin. Induction of competence to proliferate in response to either PDB or IL-2 was blocked by EGTA, suggesting that transmembrane Ca2+ flux was obligatory at this stage. Since other phorbol esters and synthetic diacylglycerols also stimulated DNA synthesis in competent cells, it is likely that progression was triggered by activation of protein kinase C. Following a brief exposure to PDB and ionomycin, subsequent incubation with PDB induced gene expression and secretion of IL-2 and augmented the expression of IL-2 receptors in the competent cells. Thus, we have demonstrated that Ca2+ mobilization is required for rendering T cells competent to express functional IL-2 receptors, to produce IL-2 in response to subsequent incubation with PDB, and that sustained activation of protein kinase C seems necessary for IL-2 production and subsequent progression of competent T cells to DNA synthesis.