Neutral particle analyzer measurements on the SSPX spheromak.

A neutral particle analyzer is used to measure the time-resolved energy spectrum of neutral hydrogen leaving a spheromak plasma. A gas cell filled with 10-50 mTorr of helium is used to strip electrons from incoming neutral hydrogen, lowering the minimum detectable energy well below that obtained with thin foils. Effective neutral particle temperature is calculated by fitting a Maxwellian energy distribution to the measured energy spectrum above and below approximately 300 eV. A computational model with approximated profiles of plasma density and neutral density is used with the measured neutral hydrogen flux to estimate the ion temperature. Measurement of the power flux due to neutral hydrogen emitted at the measurement location is extended to the whole plasma surface to estimate the total charge exchange power loss from the plasma. The initial results indicate that the charge exchange power loss represents only 2% of the total input gun power during the sustainment phase of the discharge.

Transitory stimulation of human platelet 12-lipooxygenase by vitamin E supplementation.

Human platelet lipooxygenase converts arachidonic acid to 12-hydroperoxy-eicosatetraenoic acid (12-HPETE), which is rapidly reduced by peroxidases to 12-hydroxy-eicosatetraenoic acid (12-HETE). This study was conducted to examine the effect of vitamin E supplementation on platelet 12-lipooxygenase activity. Sixteen healthy subjects were supplemented with 400 IU/day of either D-alpha-tocopherol (268 mg) or DL-alpha-tocopherol (364 mg) for 4 wk. Supplements elicited a transitory increase of lipooxygenase activity but a suppression of peroxidase activity, as indicated by increased 12-HETE production and 12-HPETE accumulation. Plasma-tocopherol concentration was double the presupplement value and remained stable during supplementation. Neither age, sex, nor isomeric form of tocopherol supplement significantly influenced the pattern of response. Results show that vitamin E exerts a differential effect on platelet lipooxygenase and peroxidase activities.

Managing angry feelings: teaching troubled children to cope.

Children who have a history of physical and emotional abuse present special problems to nurses who attempt to teach them more effective ways of dealing with anger. Since the adults in abused children's lives have not modeled constructive conflict resolution, the social and cultural learning about aggression in such children frequently has been inadequate. The author asserts that because nurses are in close contact with the children and can observe patterns of behavior during their regular daily activities, hospitalization may prove the ideal situation to teach such children appropriate social and assertiveness skills.

"Color Your Life:" an assessment and treatment strategy for children.

The "Color Your Life" technique, a form of play therapy, is designed to help children become aware of the range of feelings possible, to talk about their own feelings and to move from action to verbal forms of expression. In this article, the authors describe the technique and its variations, and provide examples of its application in both assessment and treatment contexts.

A development of the oxyhemoglobin dissociation curve analyzer.

The development and improvement of an oxyhemoglobin dissociation curve analyzer is described. PO2 electrode performance was improved by electrochemical means and circuits are described for processing the PO2 and pH signals from the analyzer. A circuit for automatically correcting the curve for Bohr shifts from pH 7.40 is described, and the performance of the Bohr shift unit is verified by experiment. The analyzer produces curves under standard conditions of PCO2 40 mmHg, pH 7.40, and 37 degrees C.

Coagulation initiated on herpesviruses.

Herpesviruses have been previously correlated to vascular disease and shown to cause thrombogenic and atherogenic changes to host cells. Herein we show that even in the absence of cells, purified cytomegalovirus (CMV) and herpes simplex virus type 1 (HSV-1) and type 2 (HSV-2) can initiate thrombin production. Functional assays demonstrated that purified HSV-1 and HSV-2 provide the necessary phospholipid (proPL) for assembling the coagulation factors Xa and Va into prothrombinase, which is responsible for generating thrombin. These observations are consistent with our earlier studies involving CMV. The presence of proPL on all three herpesviruses was confirmed directly by flow cytometry and electron microscopy by using annexin V and factor Va, respectively, as proPL-specific probes. Of equal importance, we found that CMV, HSV-1, and HSV-2 were also able to facilitate factor Xa generation from the inactive precursor factor X, but only when factor VII/VIIa and Ca2+ were present. Monoclonal antibodies specific for tissue factor (TF), the coagulation initiator, inhibited this factor X activation and, furthermore, enabled identification of TF antigen on each virus type by flow cytometry and electron microscopy. Collectively, these data show that CMV, HSV-1, and HSV-2 can initiate the generation of thrombin by having essential proPL and TF activities on their surface. Unlike the normal cellular source, the viral activity is constitutive and, therefore, not restricted to sites of vascular injury. Thus cell-independent thrombin production may be the earliest event in vascular pathology mediated by herpesviruses.

Annexin II enhances cytomegalovirus binding and fusion to phospholipid membranes.

A number of studies have suggested that the anionic phospholipid (anPL)-binding protein annexin II may play a role in cytomegalovirus (CMV) infection. Since annexin II has been shown to mediate aggregation and fusion of certain membranes, we investigated whether these properties could be exploited by CMV directly. The experiments showed that purified annexin II, but not the homologous protein annexin V (AnV), can mediate the binding of 35S-CMV (strain AD169) to anPL-coated microtiter wells. This association required Ca2+, could be titrated by varying either annexin II (apparent Kd = 4 x 10(-)8 M) or 35S-CMV, was inhibited by unlabeled CMV, and was observed for the heterotetrameric or monomeric form of annexin II. In experiments utilizing the fluorescence dequenching of octadecyl rhodamine incorporated into the CMV envelope, annexin II was furthermore found to enhance the rate of virus-anPL vesicle fusion. The observed fusion was dependent on the concentration of annexin II, Ca2+, and anPL and was mediated principally by the heterotetramer. Interestingly, AnV was observed to inhibit the effects of annexin II on CMV fusion but not binding to anPL, which indicates that annexin II enhances these processes by distinct mechanisms. The results presented here provide the first direct evidence that annexin II has the capacity to bridge CMV to a phospholipid membrane and to enhance virus-membrane fusion. These observations furthermore suggest that AnV may regulate the fusogenic function of annexin II.