Neutrophils from vasculitis patients exhibit an increased propensity for activation by anti-neutrophil cytoplasmic antibodies.

Anti-neutrophil cytoplasmic antibodies (ANCA) are thought to be pathogenic in ANCA-associated vasculitis (AAV) by stimulating polymorphonuclear leucocytes (PMNs) to degranulate and produce reactive oxygen species (ROS). The aim of this study was to investigate if PMNs from AAV patients are stimulated more readily by ANCA compared with PMNs from healthy controls (HCs). Differences in ANCA characteristics that can account for different stimulation potential were also studied. PMNs from five AAV patients and five HCs were stimulated with 10 different immunoglobulins (Ig)Gs, purified from PR3-ANCA-positive patients, and ROS production, degranulation and neutrophil extracellular trap (NET) formation was measured. ANCA levels, affinity and clinical data of the AAV donors were recorded. The results show that PMNs from AAV patients produce more intracellular ROS (P = 0·019), but degranulate to a similar extent as PMNs from HCs. ROS production correlated with NET formation. Factors that may influence the ability of ANCA to activate PMNs include affinity and specificity for N-terminal epitopes. In conclusion, our results indicate that PMNs from AAV patients in remission behave quite similarly to HC PMNs, with the exception of a greater intracellular ROS production. This could contribute to more extensive NET formation and thus an increased exposure of the ANCA autoantigens to the immune system.

Visual color and doneness indicators and the incidence of premature brown color in beef patties cooked to four end point temperatures.

An interlaboratory study was undertaken to assess the frequency that cooked color of ground beef patties appeared brown at internal temperatures of 52.7 degrees C (135 degrees F), 65.6 degrees C (150 degrees F), 71.1 degrees C (160 degrees F), and 79.4 degrees C (175 degrees F). In general, as internal cooked temperature of the patties increased, the following results were observed in the patties: (i) more brown meat color, (ii) less pink or red juice color, and (iii) more cooked texture. However, brown meat color occurred prematurely at the two lower internal temperatures (57.2 degrees C/135 degrees F and 65.6 degrees C/150 degrees F) that are insufficient to eliminate foodborne pathogens without holding times. The common consumer practice of freezing bulk ground beef, followed by overnight thawing in a refrigerator, led to substantial premature brown color in patties cooked from this product. In addition, at 71.1 degrees C (160 degrees F), recognized to be the lowest temperature for cooking ground beef safely in the home, meat color, juice color, and texture appearance were not fully apparent as doneness indicators. In fact, at no temperature studied did 100% of the patties appear done when evaluated by the criteria of no red or pink in the meat, no red or pink in the juices, or by texture appearance. Patties in this study were evaluated under a set protocol for forming the products, cooking, and viewing under the same lighting conditions. Other preparation conditions are possible and may produce different results. Thus, temperature to which patties have been cooked cannot be judged by color and appearance. This study provided the evidence to support the message to consumers regarding cooking of beef patties of "use an accurate food thermometer and cook beef patties to 160 degrees F (71.1 degrees C)" in place of messages based on consumer judgment of cooked color.

Effect of pH on absorbance of azo dye formed by reaction between nitrite and sulfanilamide/N-(1-naphthyl)ethylenediamine in residual nitrite methods for foods.

Current methods used for determining residual nitrite concentration in foods involve forming an azo dye that is measured spectrophotometrically. Conventional procedures do not specify control of pH for the final colored solution. Because many indicator dyes are pH-dependent, absorbance of the azo dye may vary not only because of nitrite concentration differences, but also because of pH variation. Thus, erroneous results could arise from a standard curve developed at one pH and used for a test sample at a different pH. This would cause an inaccurate concentration conversion from the standard curve. In this study, absorbances at lambda max wavelengths were recorded at 28 pH values (range 1.0-4.5) for each of 5 nitrite concentrations. A mathematical equation was fitted to these data and its plot gives a 3-dimensional response surface showing the relationships between pH, nitrite concentration, and absorbance. A modification for the spectrophotometric measurement of nitrite is proposed.

Kinetics of carbon dioxide during cardiopulmonary resuscitation.

CO2 kinetics during CPR was investigated in 15 anesthetized piglets. BP, blood gases, and acid-base balance were monitored through catheters in the carotid artery and a central vein, as well as in cerebrospinal fluid. Cardiac arrest was induced by a transthoracic direct current shock. CPR was begun immediately by artificial ventilation and simultaneous external chest compressions. Epinephrine was administered after 8 min of CPR. One group (n = 5) of animals received no buffer treatment while another (n = 5) received an infusion of 75 mmol sodium bicarbonate and a third group (n = 5) received an equivalent amount of tris-buffer mixture. The results of these experiments, as well as previously described circulatory variables during CPR, were analyzed using a computer model describing the CO2 kinetics of the pig. Our main finding was that PaCO2 was positively correlated to cardiac output during CPR; improved cardiac output during CPR resulted in more efficient tissue CO2 elimination and was associated with increased survival rates. PaCO2 was also somewhat reduced by efficient alveolar hyperventilation. The arterial PCO2 and pH did not reflect the acid-base balance in peripheral tissues. During CPR, bicarbonate and tris-buffer mixture both quickly passed through the blood-brain barrier. When buffer treatment is indicated during CPR, a buffer which does not increase tissue PCO2 may be the drug of choice.

Carbon dioxide production during mechanical ventilation.

Because of large stores of CO2 in different body tissues, metabolic change cannot be detected by measuring gas exchange until the CO2 stores have adapted to the new situation. Similarly, changes in the CO2 stores not due to metabolic alterations, may lead to error in gas exchange measurements. We studied CO2 production (VCO2) and oxygen consumption (VO2) in mechanically ventilated ICU patients, where CO2 stores were altered by: a) changing minute ventilation by 15%, b) reducing body temperature, and c) changing the level of sedation. Expired gases went through a mixing chamber and were analyzed continuously by a mass spectrometer. Signals from this instrument, together with gas-volume signals from the ventilator, were fed to a computer for calculation of VO2 and VCO2. Twenty to 120 min were required to reach a stable level, depending on the patient's size and circulatory response. Similar results were obtained by computer simulation using a five-compartment model of CO2 stores. These experiments indicate that measuring VO2 (for calculation of metabolic respiratory quotient [RQ]) in ventilated patients should occur after the patients maintain a 60-min period of stable body temperature and awareness. Ventilatory variables should not be changed substantially during the 90-min period before gas sampling. Cardiac output and muscle blood flow should not have changed 2 to 3 h before measuring RQ. If muscle blood flow is low, the stable periods for body temperature and ventilatory variables should be increased.