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Biomedical subjects

E J Nelson

Publications and source records attributed to E J Nelson.

At least 19 recordsLinked to original sources
PubMed2005

Assessing the effectiveness of whole blood-derived platelets stored as a pool: a randomized block noninferiority trial.

BACKGROUND: Prestorage pooling of whole blood-derived platelets (PLTs) would simplify bacterial detection. This study evaluated the in vivo effect of the prestorage pooling of PLTs stored for up to 5 days, by assessing the corrected count increment (CCI) 18 to 24 hours after transfusion of the product. STUDY DESIGN AND METHODS: A randomized block noninferiority design was used. Eligible patients had chemotherapy-induced thrombocytopenia and were considered likely to need at least six PLT transfusions. For every block of two transfusion events, one consisted of PLTs stored individually and then pooled before transfusion, and the other was a product pooled before storage. The primary outcome was categorized as a successful (>4.5) or unsuccessful (<or=4.5) 18- to 24-hour posttransfusion CCI analyzed with a matched pair score test. A mixed-effect linear model estimated the mean difference in CCI between the two types of storage. RESULTS: Twenty-three eligible patients received a total of 189 PLT transfusions. The median number of PLT transfusions was 7 (range, 0-27). Eighty-five complete transfusion pairs were used in the primary analysis. The proportions of transfusions leading to a CCI of greater than 4.5 was identical for both routine and PLTs pooled before storage (45/85=52.9%; relative risk, 1.00; lower limit of the one-sided 95% confidence interval [CI], 0.83). The estimate of the mean difference in CCI between pooled and routine storage (pooled-routine) was -0.45 (95% CI, -2.23 to 1.33; p=0.63). CONCLUSION: These results provide evidence that storage of PLTs as a pool for up to 5 days results in posttransfusion CCIs that are not inferior to PLTs stored individually.

Adult↗
PubMed2005

In vitro evaluation of prestorage pooled leukoreduced whole blood-derived platelets stored for up to 7 days.

BACKGROUND: Advantages to storing whole blood-derived platelets (PLTs) as a pool for 7 days would include operational efficiencies and facilitation of bacterial testing and pathogen inactivation. The in vitro quality of pre-storage pooled PLTs stored for up to 7 days was assessed. STUDY DESIGN AND METHODS: Leukoreduced PLTs were pooled before storage (5 units/pool) and stored for either 5 or 7 days. Samples were collected at the time of pooling and either on Day 5 (n=16-29) or on Day 7 (n=4-30) and tested for biochemical and activation markers and morphology and/or shape change. Control PLTs were stored individually for 5 or 7 days and then tested as indicated above. RESULTS: The mean PLT counts (x10(9)/L) were similar: control PLTs, 1344 (464 SD); and prestorage pooled PLTs, 1327 (220 SD; p=0.93). On Day 5, the pH value was significantly lower (p<or=0.0001) for the prestorage pooled PLTs. Lactate and partial pressure of O2 (pO2) were significantly higher (p<or=0.003). On Day 7 of storage, significant differences were noted with pH, pCO2, and hypotonic shock all being lower with the prestorage pooled product, whereas pO2, lactate, and morphology scores were higher (p values all <0.03). Although significant differences were found, the magnitude of the difference would not be expected to impact on transfusion outcomes. CONCLUSION: These results suggest that prestorage pooled PLTs can be stored for up to 7 days; however, studies are needed to ensure that the clinical benefit of PLTs stored as a pool is not inferior to those stored individually.

Biomarkers↗
PubMed2002

Hybridization and bond-orbital components in site-specific X-ray photoelectron spectra of rutile TiO2.

We have determined the Ti and O components of the rutile TiO2 valence band using the method of site-specific x-ray photoelectron spectroscopy. Comparisons with calculations based on pseudopotentials within the local density approximation reveal the hybridization of the Ti 3d, 4s, and 4p states, and the O 2s and 2p states on each site. These chemical effects are observed due to the large differences between the angular-momentum dependent matrix elements of the photoelectron process.

Journal Article↗
PubMed2000

Sustained release of silver from periodontal wafers for treatment of periodontitis.

Periodontal wafers intended to treat the underlying infections in patients with periodontitis have been developed. The wafers consist of poly(lactic-co-glycolic acid) as a primary bioerodible polymeric component, poly(ethylene glycol) as a plasticizer and encapsulation aid, and silver nitrate as the antimicrobial agent. The wafers are capable of sustained in vitro release of bioactive silver for at least 4 weeks. The wafers exhibit silver release that follows erosion kinetics, confirming a bulk erosion/release mechanism. In clinical evaluation, sustained release of silver at bactericidal levels for at least 21 days is observed. Staining of hard and soft tissues due to the released silver is minimal and reversible.

Administration, Buccal↗
PubMed2000

Direct measurement of valence-charge asymmetry by x-ray standing waves.

By monitoring valence-photoelectron emission under condition of strong x-ray Bragg reflection, we have determined that a majority of GaAs valence charge resides on the anion sites of this heteropolar crystal, in quantitative agreement with the GaAs bond polarity as calculated from the Hartree-Fock term values. In contrast, the valence-charge distribution in Ge is found to be symmetric. In both cases, the valence emission is found to be closely coupled to the atomic cores.

Journal Article↗
PubMed2000

A comparison of prestorage WBC-reduced whole-blood-derived platelets and bedside-filtered whole-blood-derived platelets in autologous progenitor cell transplant.

BACKGROUND: Prestorage WBC-reduced platelet concentrates (PCs) can be manufactured from platelet-rich plasma (PRP) by in-line filtration of PRP. There are few published data on the clinical use of these products, as compared to bedside-filtered pools of standard PCs (S-PCs) manufactured from PRP. STUDY DESIGN AND METHODS: A prospective, randomized trial was conducted in autologous progenitor cell transplant patients requiring platelet transfusions with each patient as his or her own control who was given a pool of 5 units of WBC-reduced PCs and a pool of 6 units of S-PCs within a 3-hour period. The pools were characterized before transfusion for platelet and WBC content, P-selectin expression, and IL-8. The patients were monitored with platelet counts and vital signs and observed for reactions. Data were analyzed using Mann-Whitney U tests. RESULTS: Thirty-three transfusions were administered to 13 patients. Median platelet content in the WBC-reduced PC pools was lower than that in the S-PC pools (3.3 vs. 4.0 x 10(11), p<0.01). Median WBC content was 4 to 5 log less in the WBC-reduced PC pools (2.5 x 10(4) vs. 4.6 x 10(8), p<0.01). Median IL-8 levels (pg/mL) were lower in the WBC-reduced PC pools (2 vs. 36, p<0.01). No differences were observed in CCI, but the median absolute increase after transfusion of the S-PC pools was higher (25 vs. 19 x 10(9)/L, p<0.01), which reflected the larger size of the S-PC pools. No overall differences in vital signs were recorded. Two reactions were observed, both in temporal association with the transfusion of pools of S-PCs. CONCLUSIONS: A pool consisting of 5 units of WBC-reduced PCs gave a median platelet increment of 19 x 10(9) per L in these thrombocytopenic patients and has a median WBC content 1 to 2 log below the accepted threshold for primary alloimmunization or CMV transmission.

Blood Preservation↗
PubMed1999

Role of protein kinase C in ethanol-induced activation of adenylyl cyclase.

Ethanol is known to enhance the activity of adenylyl cyclase (AC) in a number of cells and tissues. Recent work has suggested that the various isoforms of AC show differential sensitivity to ethanol, with Type VII AC being most sensitive. However, the mechanism of action of ethanol is unclear. In the present work, we investigated the effect of ethanol on AC activity in the human erythroleukemia (HEL) cell line, platelets, and AC VII-transfected HEK 293 cells. The HEL cells contain abundant amounts of mRNA for Type VII AC. We found that both ethanol and phorbol dibutyrate (PDBu) treatment enhanced agonist (prostaglandin E1; PGE1)-stimulated AC activity in HEL cells, as well as in platelets and HEK 293 cells transfected with AC VII. Inhibitors of protein kinase C (PKC) blocked the stimulatory effects of both ethanol and PDBu. However, the effects of ethanol and PDBu on AC activity were additive, suggesting that the mechanisms of action of ethanol and PDBu were not identical. Furthermore, a 30-min exposure of HEL cells to ethanol attenuated (desensitized) the ability of ethanol, but not PDBu, to enhance agonist-activated AC activity. On the other hand, a 30-min pretreatment with PDBu attenuated the AC response to the phorbol ester, but not to ethanol; but, after a 20 hr preincubation with phorbol ester, the ability of both PDBu and ethanol to enhance prostaglandin E1-stimulated AC activity was completely eliminated. Finally, pretreatment of HEL cells with pertussis toxin blocked the effect of PDBu, but not ethanol, on AC activity. The results support the involvement of phorbol ester-sensitive PKC(s) in ethanol's enhancement of agonist-activated activity of AC in HEL cells, but suggest that the mechanism of ethanol's action is different from that of PDBu. The findings with pertussis toxin suggest that PDBu activation of PKC(s) may affect AC activity through phosphorylation of a G1 protein, whereas ethanol may act by promoting phosphorylation of a different substrate (e.g., AC VII).

Adenylate Cyclase Toxin↗
PubMed1998

Fluorescence methods to assess multidrug resistance in individual cells.

PURPOSE: Microscopic methods to measure the activity of drug extrusion systems important in multidrug resistance in individual cells were developed. METHODS: Multidrug-resistant (MDR) and parental lines of hamster CHO and pituitary GH3 cells were incubated with the acetoxymethylester (AM) forms of several fluorescent calcium-sensing dyes, fura2, indo1 and fluo3. The AM forms of these compounds are hydrolyzed by intracellular esterases and then trapped in cells, and the AM forms of the dyes are excellent substrates for P-glycoprotein (Pgp). RESULTS: The fluorescent free acid forms of fura2, indol and fluo3 did not accumulate in MDR lines unless a chemosensitizer such as cyclosporin A, R(+)verapamil, quinidine, or progesterone was included during loading to prevent the cells from extruding the AM forms of the dyes before they could be hydrolyzed. Cyclosporin A increased the fluorescence due to intracellularly trapped fura2 free acid from 8- to 20-fold and was maximally effective at < 5 microM. Fluorescence microscopy was employed to measure fura2 free acid accumulation by parental and MDR cell lines using excitation at the Ca2+-insensitive wavelength. When MDR cells were incubated with rhodamine 123 and fura2/AM, no fluorescence was detectable. Cellular fluorescence was dramatically increased by inclusion of cyclosporin A, quinidine, progesterone, or R(+)verapamil. There was no measurable decline in the fura2 free acid fluorescence in 1 h while the fluorescence due to rhodamine 123 diminished rapidly in cells overexpressing Pgp. CONCLUSIONS: These fluorescence methods detect drug-extruding activity in individual cells and therefore have the potential to provide complementary information to studies quantifying protein or mRNA levels of Pgp or other efflux pumps. In addition, they provide a rapid and quantifiable method for screening multidrug resistance reversing agents.

ATP Binding Cassette Transporter, Subfamily B, Mem↗
PubMed1996

Continuous gastric suctioning decreases measured esophageal temperature during general anesthesia.

OBJECTIVE: This study sought to determine whether continuous gastric suctioning influences esophageal temperature measurements. METHODS: This study evaluated 21 patients scheduled for extremity or lower abdominal surgery. After induction of general endotracheal anesthesia, an orogastric tube, and esophageal and nasopharyngeal temperature probes were placed in functional positions. Baseline esophageal (Tes) and nasopharyngeal (Tnas) temperatures were recorded and the orogastric tube was placed on continuous suction. After the first 11 patients (Group I) were studied, 10 additional patients (Group II) were studied with more frequent data collection to improve the time resolution of temperature changes. Temperatures were recorded for patients in Group I at 2 and 10 min with suctioning and 10 min after cessation of suctioning. In Group II, temperatures were recorded at 1, 2, 5 and 10 min with suctioning and 10 min after cessation of suctioning. Analysis of data was performed using repeated measures analysis of variance and paired t-tests with the Bonferroni correction. RESULTS: In Group I, Tes decreased significantly from 35.9 +/- 0.2 degrees C (mean +/- SE) to 35.1 +/- 0.4 degrees C at 2 min and 34.8 +/- 0.3 degrees C at 10 min of suctioning (p < 0.01). Ten minutes after cessation of suctioning, Tes was not significantly different from the baseline measurement. Tnas did not change significantly over the 20 min observation period. In Group II, Tes continually decreased from 36.2 +/- 0.1 degrees C to 34.8 +/- 0.3 degrees C after 10 min of suctioning (p < 0.006) and returned to near baseline 10 min after cessation of suctioning. There was no significant change in Tnas over the 20 min observation period. CONCLUSION: We conclude that continuous gastric suctioning decreases esophageal temperature measurements. This phenomenon should be recognized as an artifactual change in esophageal temperature and not a reflection of core temperature.

Adolescent↗
PubMed1995

Visualization of the thyrotropin-releasing hormone receptor and its ligand during endocytosis and recycling.

Endocytosis and recycling of both thyrotropin-releasing hormone (TRH) and its G-protein-coupled receptor were visualized by conventional and confocal fluorescence microscopy in pituitary cells using a rhodamine-labeled TRH analog (Rhod-TRH) and indirect immunofluorescent staining of cells stably transfected with an epitope-tagged TRH receptor (TRHR). The epitope-tagged TRHR was confined to the cell surface prior to agonist treatment. Both Rhod-TRH and TRHR were also localized on the plasma membrane after agonist binding at 0 degrees C. Ligand binding at 37 degrees C resulted in rapid endocytosis, and both Rhod-TRH and the epitope-tagged TRHR appeared in cytoplasmic vesicles within 5 min. Fluorescently labeled TRH and transferrin colocalized in the same endocytotic vesicles, and internalization of Rhod-TRH and TRHR was inhibited by hypertonic medium, suggesting that endocytosis occurred by a clathrin-dependent mechanism. Internalized TRHRs returned to the membrane within 20 min after removal of TRH, and cycloheximide did not block receptor recycling. A mutant TRHR truncated at Cys335 signaled but did not internalize Rhod-TRH, confirming the importance of the carboxyl terminus of the TRHR in receptor-mediated endocytosis. Thus, the TRH-TRHR complex is endocytosed via clathrin-coated vesicles and the receptor is recycled to the plasma membrane.

Amino Acid Sequence↗
PubMed1994

Thyrotropin-releasing hormone activates Ca2+ efflux. Evidence suggesting that a plasma membrane Ca2+ pump is an effector for a G-protein-coupled Ca(2+)-mobilizing receptor.

These studies characterize the mechanisms involved in terminating the initial Ca2+ transient stimulated by thyrotropin-releasing hormone (TRH). When TRH was added to GH3 pituitary cells that had been treated with thapsigargin to block any agonist-stimulated increase in [Ca2+]i, TRH caused a decrease in [Ca2+]i. The Ca2+ clearing response was seen in pituitary GH3 cells and in nonexcitable HEK 293 cells transfected with TRH receptor cDNA, was evident at basal or elevated [Ca2+]i, and was mediated by the TRH receptor. The Ca2+ clearing response to TRH was not prevented by thapsigargin, Ca2+ ionophores, nimodipine, or replacement of extracellular Na+ but was inhibited by La3+. La3+ also increased the duration of the TRH-evoked [Ca2+]i transient. TRH-stimulated Ca2+ extrusion was directly demonstrated using extracellular fluo-3 free acid. TRH produced a 5-20-fold increase in Ca2+ efflux that was independent of extracellular Na+ and inhibited by vanadate. TRH stimulation of Ca2+ efflux was not reproduced by phorbol esters or inhibited by down-regulation of protein kinase C or staurosporine. The results suggest that agonist-activated Ca2+ efflux may be a universal component of an agonist-activated Ca2+ response and further suggest that a plasma membrane Ca2+ pump may be an effector for G-protein-coupled receptors linked to Ca2+ mobilization.

Animals↗
PubMed1994

Inhibition of L-type calcium-channel activity by thapsigargin and 2,5-t-butylhydroquinone, but not by cyclopiazonic acid.

Thapsigargin (TG), 2,5-t-butylhydroquinone (tBHQ) and cyclopiazonic acid (CPA) all inhibit the initial Ca(2+)-response to thyrotropin-releasing hormone (TRH) by depleting intracellular Ca2+ pools sensitive to inositol 1,4,5-trisphosphate (IP3). Treatment of GH3 pituitary cells for 30 min with 5 nM TG, 500 nM tBHQ or 50 nM CPA completely eliminated the TRH-induced spike in intracellular free Ca2+ ([Ca2+]i). Higher concentrations of TG and tBHQ, but not CPA, were also found to inhibit strongly the activity of L-type calcium channels, as measured by the increase in [Ca2+]i or 45Ca2+ influx stimulated by depolarization. TG and tBHQ blocked high-K(+)-stimulated 45Ca2+ uptake, with IC50 values of 10 and 1 microM respectively. Maximal inhibition of L-channel activity was achieved 15-30 min after drug addition. Inhibition by tBHQ was reversible, whereas inhibition by TG was not. TG and CPA did not affect spontaneous [Ca2+]i oscillations when tested at concentrations adequate to deplete the IP3-sensitive Ca2+ pool. However, 20 microM TG and 10 microM tBHQ blocked [Ca2+]i oscillations completely. The effect of drugs on calcium currents was measured directly by using the patch-clamp technique. When added to the external bath, 10 microM CPA caused a sustained increase in the calcium-channel current amplitude over 8 min, 10 microM tBHQ caused a progressive inhibition, and 10 microM TG caused an enhancement followed by a sustained block of the calcium current over 8 min. In summary, CPA depletes IP3-sensitive Ca2+ stores and does not inhibit voltage-operated calcium channels. At sufficiently low concentrations, TG depletes IP3-sensitive stores without inhibiting L-channel activity, but, for tBHQ, inhibition of calcium channels occurs at concentrations close to those needed to block agonist mobilization of intracellular Ca2+.

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗
PubMed1994

Characteristics of white cell-reduced red cells stored in tri-(2-ethylhexyl)trimellitate plastic.

BACKGROUND: Standard blood storage containers contain extractable plasticizers that accumulate in blood during storage and are an unintended transfusion product. However, extractable plasticizers have a protective effect on the red cell membrane and improve red cell storage variables. Prestorage white cell reduction also improves selected red cell storage variables. STUDY DESIGN AND METHODS: The study evaluated whether the beneficial effect of prestorage white cell reduction would offset the negative effect of the absence of extractable plasticizer in red cells stored in AS-3 for 42 days at 4 degrees C. Filtered red cells stored in polyvinylchloride containers with the nonextracting plasticizer, tri-(2-ethylhexyl)trimellitate (TEHTM), were compared to unfiltered red cells stored in polyvinylchloride containers with the extractable plasticizer di-(2-ethylhexyl)phthalate (DEHP). RESULTS: Poststorage supernatant potassium and red cell osmotic fragility were significantly higher in white cell-reduced TEHTM units than in unfiltered DEHP units. The mean 24-hour recovery of the filtered TEHTM red cells was significantly lower than that of the unfiltered DEHP red cells (69.1 +/- 7.4% vs. 77.1 +/- 5.1%, p < 0.05, n = 8). CONCLUSION: These data demonstrate that white cell reduction before 42-day storage in TEHTM containers with currently approved preservatives does not yield an acceptable red cell component.

Adenosine Triphosphate↗
PubMed1994

Characteristics of the Ca2+ spike and oscillations induced by different doses of thyrotropin-releasing hormone (TRH) in individual pituitary cells and nonexcitable cells transfected with TRH receptor complementary deoxyribonucleic acid.

The Ca2+ response of individual cells to TRH was investigated in excitable pituitary GH3 and in nonexcitable Hela cells transfected with the TRH receptor complementary DNA (HelaR cells). GH3 cells typically responded to 1 microM TRH with an immediate transient [Ca2+]i spike (mean peak [Ca2+]i = 1.5 microM) followed by a period of inactivity of approximately 100 sec long and then a secondary increase in [Ca2+]i with oscillations. At 10-100 nM TRH, the initial [Ca2+]i spike was more prolonged and immediately followed by a sustained elevation of [Ca2+]i. At 0.5-1 nM TRH, there was a variable lag before any response; the initial [Ca2+]i spike was absent or small, but the sustained phase was still present. The second phase of elevated [Ca2+]i, which could be eliminated with nimodipine or chelation of extracellular Ca2+, gave a bell-shaped TRH dose response curve. The effect of TRH on Ca2+ oscillations depended both on TRH concentration and the basal oscillation frequency. HelaR cells responded to 1 microM TRH with a rapid [Ca2+]i spike, and at less than or equal to 10 nM TRH, up to 50% of HelaR cells displayed agonist-induced sinusoidal [Ca2+]i oscillations independent of extracellular Ca2+. TRH never caused a sustained elevation of [Ca2+]i in HelaR cells. For GH3 and HelaR cells, the peak [Ca2+]i response increased with TRH concentration up to 1 microM. In contrast, the duration of the initial [Ca2+]i spike was shorter at higher TRH concentrations, decreasing from 16 to 6.3 s (GH3) or 92 to 35 s (HelaR) between 0.5 nM and 1 microM TRH. This shortening of the spike duration was caused by rapid clearing of cytoplasmic Ca2+ that depended primarily on agonist concentration. In summary, TRH stimulates a complex [Ca2+]i response pattern dependent upon both the agonist concentration and cell context. The initial burst of Ca2+ is cleared in part by agonist dependent Ca2+ clearing.

Animals↗
PubMed1993

Regulation of L-type voltage-gated calcium channels by epidermal growth factor.

GH3 rat pituitary cells have L-type voltage-gated calcium channels, and both the rate of uptake of 45Ca2+ and the concentration of intracellular free calcium ion ([Ca2+]i) are increased by depolarization with high potassium. Cells incubated for several days with 10 nM epidermal growth factor (EGF) responded to depolarization with a 30-65% smaller increase in 45Ca2+ uptake than untreated cells. The inhibitory response to EGF developed slowly, with a maximal effect requiring 24-48 h. EGF exerted a half-maximal reduction in depolarization-stimulated 45Ca2+ uptake at 0.1 nM and a maximal effect at 1-10 nM. 45Ca2+ uptake was reduced by EGF at strongly depolarized potentials (added K+, > 25 mM) with or without the calcium channel agonist BAY K8644. [Ca2+]i was measured using fura-2 before and after depolarization in control cells and cells incubated for 48 h with 10 nM EGF. EGF-treated cells responded to the addition of 30-50 mM KCl with a smaller increase in [Ca2+]i than control cells. Digital fluorescence imaging of individual fura-2-loaded cells confirmed that the average [Ca2+]i response to depolarization was lower in cells that had been incubated with EGF for 36 h. EGF treatment increased the amount of PRL secreted basally, but inhibited the acute PRL secretory response to depolarization with 50 mM KCl and 1 microM BAY K8644 from 2.6- to 1.5-fold. The results indicate that EGF reduces the activity of voltage-gated dihydropyridine-sensitive calcium channels on pituitary cells, and that this reduction in L-channel activity is accompanied by a smaller secretory response to depolarization.

1-Methyl-3-isobutylxanthine↗
PubMed1992

Measurement of intracellular cadmium with fluorescent dyes. Further evidence for the role of calcium channels in cadmium uptake.

Cellular uptake of Cd2+ has been monitored using intracellularly trapped dyes, Fura 2 and Quin 2, which bind Cd2+ with extremely high affinity, and digital fluorescence imaging has been used to visualize intracellular free Cd2+. The excitation spectrum of the Cd2+ complex of Fura 2 is similar to that of the Ca2+ complex, whereas Cd2+ displaces Ca2+ from Quin 2 and reduces fluorescence. Fluorescence of Fura 2-loaded cells increased when 50 microM extracellular Cd2+ was added and fluorescence of Quin 2-loaded cells decreased. Cd2+ uptake by GH3 pituitary cells, which occurs in part via voltage-sensitive L-type calcium channels, was increased by BAY K8644 and depolarization and decreased by nimodipine. When Fura 2 and Quin 2 were used to measure Cd2+ uptake by glial C6 cells, which have no L-channel activity, high K+ and BAY K8644 did not change the apparent rate of Cd2+ uptake. GH3 and C6 cells were incubated with Cd2+ for 24 h and loaded with Fura 2, and fluorescence was measured before and after addition of tetrakis-(2-pyridylmethyl)ethylenediamine (TPEN), a membrane permeant chelator with extremely high affinity for metals. TPEN had little effect on fluorescence of Fura 2-loaded GH3 and C6 cells not exposed to Cd2+ but decreased fluorescence of cells that had been incubated with 1-10 microM Cd2+. Fluorescence ratio imaging of Fura 2-loaded cells was used to image intracellular free Cd2+ for both GH3 and C6 cells. Cd2+ uptake over 30-180 min could be followed by the increase in 340/380 fluorescence ratio and the increase in fluorescence ratio was reversed within 5 min by TPEN. The results provide further evidence for the importance of voltage-gated calcium channels to Cd2+ uptake of certain cells.

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗
PubMed1992

Prestorage removal of Yersinia enterocolitica from red cells with white cell-reduction filters.

Prestorage removal of phagocytic white cells (WBCs) may increase the survivability of contaminating bacteria in units of stored red cells. Fourteen units of whole blood were inoculated with 65 colony-forming units per mL of Yersinia enterocolitica (serotype O:3) and processed into AS-3-preserved red cells. Five red cell units were filtered with a prototype third-generation filter and five red cell units with a second generation filter. WBC reduction was performed on the day of collection. Four red cell units were not filtered. Three noninoculated whole blood units served as negative controls; two were filtered (one with each type of WBC-reduction filter) and one remained unfiltered. All red cell units were then stored at 4 degrees C for 42 days. One of the five filtered red cell units (20%) in each filter group supported growth of Y. enterocolitica. In contrast, 4 (100%) of 4 unfiltered inoculated red cell units had growth (p = 0.04). Overall, 2 (20%) of 10 units of WBC-reduced red cells supported the growth of Y. enterocolitica, as compared to 100 percent of unfiltered red cell units after inoculation (p = 0.015). Bacterial contamination was not detected in any of the three noninoculated units. It can be concluded that prestorage WBC filtration significantly reduces the potential for growth of Y. enterocolitica in red cells stored at 4 degrees C for 42 days.

Endotoxins↗