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Results for “Data Aggregation”

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PubMed2004

Effects of dietary supplementation with arachidonic acid on platelet and renal function in patients with cirrhosis.

Advanced cirrhosis is associated with reduced platelet function and altered renal function and sodium handling. Arachidonic acid (AA) metabolites contribute to platelet aggregation and to maintain the response to diuretics in advanced cirrhosis. In the present study, we tested the effects of a dietary supplementation for 8 weeks with a triacylglycerol (triglyceride) enriched in AA (ARASCO; 4 g/day) or oleic acid (OA) on plasma and membrane fatty acid composition, platelet aggregation and renal prostaglandin (PG) metabolism. At baseline, all patients had reduced platelet aggregation. Patients treated with AA showed a significant increase in the percentage of AA in plasma lipids and membrane phospholipids. These changes were associated with an increased platelet aggregation in response to collagen (from 55.83 +/- 20.63 to 67.67 +/- 14.44%; P<0.05). At baseline, all urinary AA metabolites, including PGE2, 6-keto-PGF1alpha, 8-epi-PGF2alpha and 11-dehydro-thromboxane B2, were elevated in cirrhotic patients when compared with a group of normal subjects. After furosemide treatment, urinary excretion of 11-dehydro-thromboxane B2 increased significantly. Supplementation with AA did not result in any significant change in urinary PG excretion either before or after diuretic administration. The results of the present study show that dietary supplementation with AA effectively increases the levels of this fatty acid in plasma and membrane phospholipids and improves platelet aggregation. These data suggest a possible novel approach to the treatment of the haemostatic defect observed in these patients.

Aged↗

PubMed1990

The autopsy and vital statistics.

Vital statistics in the United States are collected through a decentralized, cooperative system of various levels of government administrated by the National Center for Health Statistics. Although registration of all deaths is virtually complete and demographic items are accurate, the reliability of cause of death data is hampered by the current state of medical knowledge, the incompleteness of information available at the time of death, the way in which physicians complete death certificates, and the system of classification of underlying cause. The need for quality assurance in national cause of death statistics can be met in large part by connecting the autopsy to the mainstream of vital statistics. Through case by case individual linkage of death certificates and autopsies in designated demographic and/or geographic areas, a representative, continuously collected, population-based system of aggregated autopsy data would be created. Demographic and clinical selection bias should be checked and adjusted through traditional methods of epidemiologic standardization. Such a use of autopsy information could further pathology's goals of understanding disease and improving the public health.

Autopsy↗

PubMed2005

Generation and characterization of a recombinant single chain Fv antibody to von Willebrand factor A1 domain from phage display library.

In this study, cDNA of von Willebrand factor domain A1 (VWF-A1) was cloned from human umbilical vein endothelial cells, and expressed in E. coli. The expressed VWF-A1 was used as antigen to immunize Balb/c mice. Reverse transcribed-polymerase chain reaction (RT-PCR) was used to amplify VH and VL gene segment from the RNA isolated from the immunized mouse spleens. Single chain Fv (ScFv) genes were generated by splicing overlap extension and subcloned into a phagemid vector pHEN-1. Phage display library of repertoire single chain antibodies of anti-VWF-A1 was then constructed and screened for ScFvs that interact with VWF-A1. The ScFv gene of phage clone 28 that has best binding activity to VWF-A1 was cloned into pET20b vector for higher expression in E. coli strain BL-21(DE3) pLysS. The recombinant ScFv specifically reacted with VWF, rVWF-A1 and rVWF-A1/A3, but not with rVWF-A3, P-selectin and BSA. It inhibited ristocetin-induced platelet aggregation with an IC50 of 0.75 micromol/l, and its maximal extent of inhibition is 62.5%. The ScFv had no effect on thrombin-induced platelet aggregation. These data show that the ScFv is specific against VWF-A1 and could have a potential to be used as an antithrombotic agent.

Animals↗

PubMed1990

Aurintricarboxylic acid in a canine model of coronary artery thrombosis.

Platelet thrombus formation occurs at sites of severe arterial narrowing where shear stress is elevated. Shear stress appears to induce platelet aggregation in vitro by means of initiation of von Willebrand factor binding to platelet glycoprotein Ib. Recent in vitro studies have demonstrated that aurintricarboxylic acid can inhibit shear stress-induced platelet aggregation. This effect is mediated by aurintricarboxylic acid binding to von Willebrand factor; this binding results in inhibition of von Willebrand factor interaction with glycoprotein Ib. In this study, we examined the effect of aurintricarboxylic acid on platelet-dependent cyclic flow reductions (CFRs) in a canine coronary stenosis model. In dose-response experiments, six animals received 4 mg/kg aurintricarboxylic acid by bolus infusion, followed by 1 mg/kg every 10 minutes. Total inhibition of CFRs was observed in all animals after 6.7 mg/kg aurintricarboxylic acid; CFRs could not be reinitiated by the thromboxane A2 analogue U46619. Continuous infusion of epinephrine (0.4 micrograms/kg/min) caused CFRs to return; however, 3.7 mg/kg additional aurintricarboxylic acid again induced total inhibition of CFRs. In addition, five animals received a bolus infusion of 10 mg/kg aurintricarboxylic acid, which caused total inhibition of CFRs. The average area of stenosis in the constricted vessels was 83%, and shear stress at the site of constriction averaged 350 dynes/cm2. Aurintricarboxylic acid did not alter hemodynamics, thrombin time, platelet count, or ADP/epinephrine-induced platelet aggregation. These data indicate that platelet glycoprotein Ib-von Willebrand factor interactions are important during coronary occlusion and that aurintricarboxylic acid can inhibit coronary thrombosis associated with coronary constriction.

Animals↗

PubMed1990

Participation of C1q and its receptor in adherence of human diploid fibroblast.

C1q binds through its collagen-like domain to specific surface receptors of fibroblasts and to adhesive elements of extracellular matrix including fibronectin, collagens, proteoglycans, and laminin. To determine whether C1q participates in fibroblast adhesion, cells in serum-free medium were plated on surfaces coated with purified C1q at physiologic ionic strength and pH. Surfaces coated with fibronectin or collagen type I served as positive controls, and those coated with BSA were negative controls. Substratum-adsorbed C1q promoted fibroblast adhesion to a maximum of 73% of available cells within 90 min at 37 degrees C. Adhesion was C1q concentration dependent, saturable, specific, and dependent on the collagen-like domain of the molecule. De novo protein synthesis plays a role in adhesion: pretreatment of fibroblasts with cycloheximide reduced adherence about 50% of controls. Addition of exogenous fibronectin, collagen type I, or C1q as soluble mediators did not affect adhesion of the cycloheximide-treated cells to C1q substrate. Adhesion could be accounted for primarily, although not completely, by the C1q receptors. Antibodies raised against the Raji cell C1q receptors (alpha C1qR Ab) specifically inhibited fibroblast adhesion to C1q substrates about 60% of controls. The binding of fibroblasts to C1q substrates could be inhibited about 24% of controls with the GRGDTP cell recognition peptide. GRGDTP and alpha C1q Ab had an additive effect on adhesion that was inhibited 77 to 80% of controls. We conclude from these data that aggregated rather than monomeric C1q may be the natural ligand of the fibroblast C1q receptor, and the biologic function of the receptor in cells of the connective tissue may be cell adhesion.

Amino Acid Sequence↗

PubMed1985

Inhibition of fibronectin binding to platelets by proteolytic fragments and synthetic peptides which support fibroblast adhesion.

To define regions within fibronectin (Fn) recognized by platelet binding sites, inhibition of Fn binding by an Fn fragment and synthetic peptides has been analyzed. A highly purified 120-kDa chymotryptic fragment, which has cell attachment activity but did not bind to insolubilized heparin or gelatin, inhibited Fn binding to platelets with an ID50 approximately 3 microM. Previous work indicates that fibroblasts attach to an 11.5-kDa subfragment of this 120-kDa fragment, and that one of four 30-residue synthetic peptides containing sequences from this region supports cell attachment. Only the peptide containing the COOH terminus of the 11.5-kDa fragment inhibited Fn binding to platelets, with an ID50 approximately 10 microM and is the peptide which supports fibroblast attachment. Of the smaller peptides studied from this sequence, all peptides containing the Arg-Gly-Asp-Ser sequence, including the tetrapeptide itself, were active in inhibiting Fn binding to platelets (ID50 values approximately 10-20 microM). The same peptides support fibroblast attachment. Those which lacked this sequence including Gly-Asp-Ser-Pro and Thr-Gly-Arg-Gly (immediately adjacent tetrapeptides) lacked both activities. Further evidence for specificity of inhibition was provided by structurally modified peptides in which substitution of a Glu for Asp abolished inhibitory activity and substitution of Lys for Arg or Ala for Gly reduced activity 6- and 8-fold, respectively. In addition, Arg-Gly-Asp-Ser-containing peptides inhibited the rate and extent of thrombin-induced platelet aggregation. These data suggest that the Arg-Gly-Asp-Ser tetrapeptide contains a recognition specificity involved in the binding of Fn to platelets and that platelets share features of this recognition specificity with fibroblasts.

Amino Acid Sequence↗

PubMed1998

Thermodynamic consequences of an abasic lesion in duplex DNA are strongly dependent on base sequence.

The abasic site in DNA may arise spontaneously, as a result of nucleotide base damage, or as an intermediate in glycosylase-mediated DNA-repair pathways. It is the most common damage found in DNA. We have examined the consequences of this lesion and its sequence context on DNA duplex structure, as well as the thermal and thermodynamic stability of the duplex, including the energetic origins of that stability. To this end, we incorporated a tetrahydrofuran abasic site analogue into a family of 13-mer DNA duplexes, wherein the base opposite the lesion (A, C, G, or T) and the base pairs neighboring the lesion (C.G or G.C) were systematically varied and characterized by a combination of spectroscopic and calorimetric techniques. The resulting data allowed us to reach the following conclusions: (i) the presence of the lesion in all sequence contexts studied does not alter the global B-form conformation characteristic of the parent undamaged duplex; (ii) the presence of the lesion induces a significant enthalpic destabilization of the duplex, with the magnitude of this effect being dependent on the sequence context; (iii) the thermodynamic impact of the lesion is dominated by the identity of the neighboring base pairs, with the cross strand partner base exerting only a secondary thermodynamic effect on duplex properties. In the aggregate, our data reveal that even in the absence of lesion-induced alterations in global structure, the abasic lesion can significantly alter the thermodynamic properties of the host duplex, with the magnitude of this impact being strongly dependent on sequence context.

Base Composition↗

PubMed1985

Elevated glucose in vivo and in vitro adversely alters prostaglandin generation in rat aortas and platelets.

An imbalance in prostacyclin (PGI2) and thromboxane (TXA2) generation from arachidonic acid (AA) may contribute to the marked increase in susceptibility to cardiovascular disease seen in diabetics. Rats made diabetic with streptozocin, and subsequently treated with saline or insulin, yielded aortic rings that synthesized decreasing amounts of PGI2 and platelets that generated increasing amounts of TXA2 in proportion to the degree of hyperglycemia. These alterations in AA metabolism were mimicked by incubating aortic rings or platelets from normal rats in buffer containing elevated glucose concentrations. Platelets incubated in elevated glucose displayed shorter times to maximal aggregation and higher percent maximal aggregation. Incubation of tissue in a buffer made hyperosmotic with mannitol had no effect on PGI2 or TXA2 formation, or platelet aggregation. These data suggest that hyperglycemia is involved in the PGI2/TXA2 imbalance and platelet abnormalities seen in diabetes, and reinforces the importance of rigid control of blood glucose as an approach to minimizing the incidence of diabetic cardiovascular complications.

6-Ketoprostaglandin F1 alpha↗

PubMed2005

Latent class models for use of primary care: evidence from a British panel.

This paper models access to and utilisation of primary care using data from the British Household Panel Survey for the period 1991-2001. A latent class panel data framework is adopted to model individual unobserved heterogeneity in a flexible way. Accounting for the panel structure of the data leads to a substantial improvement in fit, and permits the identification of latent classes of users of health care. Analysis by gender shows that men and women respond differently to some factors, in particular, to age and income. There is evidence of a positive impact of income on the probability of seeking primary care. This effect is especially significant in the case of women. For both genders, the marginal effect of income on the propensity to visit a GP is greater for individuals who are less likely to seek primary care. A latent class aggregated count data model for the number of GP visits classifies individuals in three latent classes and shows a positive income effect particularly amongst those with lower levels of utilisation.

Adolescent↗

PubMed2001

Chaperone-like activity of alpha-crystallin and other small heat shock proteins.

Small heat shock proteins (sHsps) are a large family of proteins with monomeric molecular weight of 12-43 kDa, present within the prokaryotic and eukariotic cell as large oligomeric complexes, ranging in size from 200-800 kDa. Unlike the high molecular weight Hsps, which are involved in protein folding in vivo, under normal conditions, sHsps play an important role in protecting organism from stress. SHsps share an evolutionarily conserved sequence of 80-100 amino acids, located in the C-terminal region, and called "alpha-crystallin domain"; its role in subunits interactions has been recently underlined by site-directed spin labeling studies and by fluorescence resonance energy transfer data. The N-terminal region, preceding the alpha-crystallin domain, is variable in length and amino acid sequence, contributing to structural diversity between different sHsps and having a role in multimerization. The alpha-Crystallin domain is followed by C-terminal extension, a polar structure, involved in protein solubility, which share no sequence homology. Expression of sHsps is induced in response to various kinds of stress including heat shock, oxidative stress, osmostress, or ischemia, but some sHsps are expressed constitutively under physiological conditions. In vitro, sHsps selectively bind and stabilize proteins and prevent their aggregation at elevated temperatures in an ATP-independent way and protect enzymes against heat-induced inactivation. Our own studies focused on the chaperone-like activity of alpha-crystallin, the major protein component of vertebrate lens, using another system than heat-induced aggregation. Our data demonstrated that alpha-crystallin specifically protects enzymes against inactivation by different posttranslational modifications such as glycation, carbamylation and aldehyde binding, and also reactivates GuHCl-denatured enzymes. Complex formation between alpha-crystallin and the denatured enzymes, was suggested as a mechanism of protection.

Animals↗

PubMed1981

9 alpha-homo-9,11-epoxy-5,13-prostadienoic acid analogues: specific stable agonist (SQ 26, 538) and antagonist (SQ 26, 536) of the human platelet thromboxane receptor.

A newly synthesized 9 alpha-homo-9,11-epoxy-5,13-prostadienoic acid analogue, SQ 26, 536, (8(R)9(S)11(R)12(S)-9 alpha-homo-9,11-epoxy-5(Z), 13(E)-15S-hydroxyprostadienoic acid) inhibited arachidonic acid (AA)-induced platelet aggregation with an I50 value of 1.7 microM. SQ 26,536 did not inhibit prostaglandin (PG) synthetase activity of bovine seminal vesicle microsomes or thromboxane (Tx) synthetase activity of lysed human blood platelets. SQ 26,536 also inhibited platelet aggregation induced by epinephrine (secondary phase), 9,11-azoPGH2 and collagen but did not inhibit the primary phase of epinephrine-induced aggregation or ADP-induced platelet aggregation. SQ 26,538 (8(R)9(S)11(R)12(S)-9 alpha-homo-9,11-epoxy-5(Z),13(E)-15R-hydroxyprostadienoic acid), a 15-epimer of SQ 26,536, induced platelet aggregation with an A50 value of 2.5 microM. SQ 26,536 competitively inhibited SQ 26,538-induced platelet aggregation with a Ki value of 3 microM. Neither indomethacin, a PG synthetase inhibitor, nor SQ 80,338 (1-(3-phenyl-2-propenyl)-1H-imidazole), a Tx synthetase inhibitor, inhibited SQ 26,538- or 9,11-azoPGH2-induced platelet aggregation. These data indicate that SQ 26,536 and SQ 26,538 are stable antagonist and agonist, respectively, of the human blood platelet thromboxane receptor.

Adenosine Diphosphate↗

PubMed2006

Incidence trend and risk factors for campylobacter infections in humans in Norway.

BACKGROUND: The objectives of the study were to evaluate whether the increase in incidence of campylobacteriosis observed in humans in Norway from 1995 to 2001 was statistically significant and whether different biologically plausible risk factors were associated with the incidence of campylobacteriosis in the different counties in Norway. METHODS: To model the incidence of domestically acquired campylobacteriosis from 1995 to 2001, a population average random effect poisson model was applied (the trend model). To case data and assumed risk-factor/protective data such as sale of chicken, receiving treated drinking water, density of dogs and grazing animals, occupation of people in the municipalities and climatic factors from 2000 and 2001, an equivalent model accounting for geographical clustering was applied (the ecological model). RESULTS: The increase in incidence of campylobacteriosis in humans in Norway from 1995 to 2001 was statistically significant from 1998. Treated water was a protective factor against Campylobacter infections in humans with an IRR of 0.78 per percentage increase in people supplied. The two-level modelling technique showed no evidence of clustering of campylobacteriosis in any particular county. Aggregation of data on municipality level makes interpretation of the results at the individual level difficult. CONCLUSION: The increase in incidence of Campylobacter infections in humans from 1995 to 2001 was statistically significant from 1998. Treated water was a protective factor against Campylobacter infections in humans with an IRR of 0.78 per percentage increase in people supplied. Campylobacter infections did not appear to be clustered in any particular county in Norway.

Adolescent↗

PubMed1986

Behavior of intracellular glutathione during platelet thromboxane synthesis in diabetes.

The time-dependent relationship between the levels of the reduced form of glutathione (GSH) and thromboxane A2 (TXA2) synthesis, as measured by the accumulation of TXB2, in platelets from human diabetic and control subjects was investigated during aggregation. In platelets from control subjects, the GSH level decreased to 21% of the initial level within 30 sec in response to arachidonic acid (1.65 mM) and rapidly recovered to 91% by 1 min. In platelets from diabetic subjects, the GSH level decreased to 3% of the initial level within 30 sec and recovered to only 41% by 1 min. During collagen (20 ug/ml) aggregation, platelets from control subjects had a 15 sec lag phase which was followed by a decrease in the GSH level to 21% of the initial level within 1 min and a recovery to 74% by 2 min. Platelets from diabetic subjects in response to collagen showed no lag phase and decreased to 10% of the initial level within 1 min which was followed by a recovery to 34% by 2 min. In all aggregations, the initial GSH level was significantly (p less than .001) lower in platelets from diabetic subjects and remained significantly (p less than .01) lower than GSH in platelets from control subjects throughout the aggregation. The amount of TXB2 formed by platelets from control subjects reached a maximum in response to arachidonic acid and collagen by 1 min and 2 min, respectively, whereas, the TXB2 continued to increase up to 4 min when platelets from diabetic subjects were aggregated. These data indicate that TXA2 synthesis occurs during the decrease in GSH and ceases when the GSH level recovers. The continued synthesis of TXA2 by platelets from diabetic subjects coincides with the gradual recovery of the GSH level.

Arachidonic Acids↗

PubMed2006

Increase of Fas-induced apoptosis by inhibition of extracellular phosphorylation of Fas receptor in Jurkat cell line.

Apoptosis signalling through the Fas pathway requires several steps of aggregation of the Fas receptor in the membrane, including aggregation that may occur in the absence of Fas ligand. Association of Fas domains is determinant to signal transmission following Fas ligand binding to a specific domain. The domains involved in Fas aggregation are located in its extracellular region and contain three potential protein kinase C-binding motifs. We therefore studied the possibility that phosphorylation of the extracellular region of Fas might be implicated in the regulation of Fas-mediated apoptosis. Inhibition experiments of extracellular phosphorylation were performed in human Jurkat T leukemia cells with K252b, an impermeant protein-kinase inhibitor. Extracellular phosphorylation of Fas receptor was related to ecto-kinase, as assessed by the [gamma-(32)P] ATP labelling of Fas-116 kDa aggregates, suppressed by K252b inhibitor which significantly increased the sensitivity to Fas-mediated apoptosis. Ecto-PKC involvement was demonstrated by bisindolylmaleimide VIII, a selective inhibitor of protein kinase C which significantly increased both Fas aggregation in the membrane and Fas-mediated apoptosis and by the addition of the PKC pseudo-substrate 19-36 which inhibited the phosphorylation of 116 kDa Fas aggregates. These data support a role for Fas phosphorylation in the decreased sensitivity to apoptosis in the Jurkat T leukemia cell line.

Adenosine Triphosphate↗

PubMed2005

Stimulatory roles of nitric-oxide synthase 3 and guanylyl cyclase in platelet activation.

Nitric oxide (NO) stimulates soluble guanylyl cyclase and, thus, enhances cyclic guanosine monophosphate (cGMP) levels. It is a currently prevailing concept that NO inhibits platelet activation. This concept, however, does not fully explain why platelet agonists stimulate NO production. Here we show that a major platelet NO synthase (NOS) isoform, NOS3, plays a stimulatory role in platelet secretion and aggregation induced by low doses of platelet agonists. Furthermore, we show that NOS3 promotes thrombosis in vivo. The stimulatory role of NOS is mediated by soluble guanylyl cyclase and results from a cGMP-dependent stimulation of platelet granule secretion. These findings delineate a novel signaling pathway in which agonists sequentially activate NOS3, elevate cGMP, and induce platelet secretion and aggregation. Our data also suggest that NO plays a biphasic role in platelet activation, a stimulatory role at low NO concentrations and an inhibitory role at high NO concentrations.

Animals↗

PubMed2003

Patient Safety Leadership WalkRounds.

BACKGROUND: In the WalkRounds concept, a core group, which includes the senior executives and/or vice presidents, conducts weekly visits to different areas of the hospital. The group, joined by one or two nurses in the area and other available staff, asks specific questions about adverse events or near misses and about the factors or systems issues that led to these events. ANALYSIS OF EVENTS: Events in the Walkrounds are entered into a database and classified according to the contributing factors. The data are aggregated by contributing factors and priority scores to highlight the root issues. The priority scores are used to determine QI pilots and make best use of limited resources. Executives are surveyed quarterly about actions they have taken as a direct result of WalkRounds and are asked what they have learned from the rounds. RESULTS: As of September 2002, 47 Patient Safety Leadership WalkRounds visited a total of 48 different areas of the hospital, with 432 individual comments. DISCUSSION: The WalkRounds require not only knowledgeable and invested senior leadership but also a well-organized support structure. Quality and safety personnel are needed to collect data and maintain a database of confidential information, evaluate the data from a systems approach, and delineate systems-based actions to improve care delivery. Comments of frontline clinicians and executives suggested that WalkRounds helps educate leadership and frontline staff in patient safety concepts and will lead to cultural changes, as manifested in more open discussion of adverse events and an improved rate of safety-based changes.

Boston↗

PubMedDate not supplied

Inhibition of platelet retention on artificial microvascular grafts with monoclonal antibodies and a high-affinity peptide directed against platelet membrane glycoproteins.

Rapid occlusion of artificial microvascular grafts (AMGs; less than or equal to 2-mm diameter) by platelet-rich thrombi prevents the clinical use of AMGs in cardiac, vascular, and plastic surgery. Since present antiplatelet agents are unable to assure AMG patency, we have studied the role of specific platelet membrane-glycoprotein blockade on platelet retention by AMGs. In a customized in vitro perfusion chamber, retention on polytetrafluoroethylene (PTFE) AMGs (1.0-mm i.d.) of indium-111-labeled platelets in human whole blood was measured in the presence and absence of inhibitors. Specific blockade of platelet membrane glycoprotein (Gp) IIb/IIIa was achieved using monoclonal antibody 10E5 (10 micrograms/ml) and the peptide GRGDS (Gly-Arg-Gly-Asp-Ser, 0.75 mM). These inhibited 98% and 35%, respectively, of platelet retention under circumstances in which aspirin (7 mM) and dextran (4 mg/ml) inhibited 19% and 18%, respectively, of platelet retention. Nonspecific immunoglobulin G F(ab')2 (10 micrograms/ml) and nonspecific peptide (GGDA; Gly-Gly-Asp-Ala, 0.75 mM), used as control reagents, were ineffective in this setting. Monoclonal antibody 6D1 (10 micrograms/ml), which blocks platelet membrane GpIb, prevented 82% of platelet retention on PTFE. These doses of 10E5 and GRGDS completely inhibited platelet aggregation in response to 20 microM ADP, and the dose of 6D1 completely inhibited ristocetin-induced platelet agglutination. The aspirin dose prevented the second phase of ADP-induced aggregation. These data indicate that not only does initial platelet adhesion to PTFE require GpIIb/IIIa but also that GpIb plays a significant role in the early stages of platelet retention on PTFE AMGs.

Adenosine Diphosphate↗

PubMed2006

Standardizing laboratory data by mapping to LOINC.

The authors describe a pilot project to standardize local laboratory data at five Indian Health Service (IHS) medical facilities by mapping laboratory test names to Logical Observation Identifier Names and Codes (LOINC). An automated mapping tool was developed to assign LOINC codes. At these sites, they were able to map from 63% to 76% of the local active laboratory tests to LOINC using the mapping tool. Eleven percent to 27% of the tests were mapped manually. They could not assign LOINC codes to 6% to 19% of the laboratory tests due to incomplete or incorrect information about these tests. The results achieved approximate other similar efforts. Mapping of laboratory test names to LOINC codes will allow IHS to aggregate laboratory data more easily for disease surveillance and clinical and administrative reporting efforts. This project may provide a model for standardization efforts in other health systems.

Clinical Laboratory Techniques↗