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PubMedDate not supplied

The benefits and challenges of the computerized electronic medical record.

Data from aggregate individual patient records can be gathered to answer many clinical and nursing research questions about quality assurance and resource allocation, assisting in the measurement and evaluation of patient care outcomes. The use of standardized nursing language, large integrated computer databases, and information management processes provide for the use of patient-specific data and information to facilitate patient care. The use of aggregated data can also facilitate the comparison of nursing practice across populations, demonstrate and project nursing care trends, serve as a financial and legal record, aid in clinical research, support decision analysis, and guide professional and organization performance improvement.

Data Collection↗

PubMed2003

City-level gender differentials in the prevalence of dental caries and restorative dental treatment.

This study assesses gender differentials in the distribution of dental caries and restorative treatment at the city level in order to discuss gender inequities in health. We retrieved data for caries prevalence and dental service utilisation by 11- and 12-year-old girls and boys in 131 towns in the state of São Paulo, Brazil, 1998. We also gathered aggregate population data for these towns, and information already held by the health authority regarding the provision of dental services. Results of data analysis indicated that girls presented higher caries indices in permanent teeth than boys of the same age, concurrent with a higher utilisation of dental care. When studying aggregate data at the city level, we gathered evidence reinforcing the hypothesis that the higher prevalence of caries in girls is attributable to their earlier eruption of permanent teeth, with no significant association between this excess and indices of socio-economic status at the city level. However, indices assessing the discrepant incorporation of dental services between genders were higher in towns with a poorer profile of socio-economic status. We also observed that towns whose public health service was more effective in providing dental care presented a more equitable gender distribution of dental services. Public resources destined to dental assistance contributed to reducing inequities in oral health by allowing an incorporation of restorative dental treatment more equitably distributed between girls and boys.

Brazil↗

PubMed2006

Alcohol-related mortality, drinking behavior, and business cycles: are slumps really dry seasons?

This paper explores the connection between alcohol-related mortality, drinking behavior, and macroeconomic conditions in Finland using both aggregate and microlevel data from recent decades. The aggregate data reveal that an improvement in economic conditions produces a decrease in alcohol-related mortality. Microlevel data show that alcohol consumption increases during economic expansion while the probability of being a drinker remains unchanged. This demonstrates that alcohol-related mortality and self-reported alcohol consumption may be delinked in the short-run business cycle context. One explanation for this paradox is that most harmful forms of drinking are not captured in survey-based data used to study the effect of macroeconomic conditions on alcohol consumption. Our evidence does not overwhelmingly support the conclusions reported for the United States that temporary economic downturns are good for health.

Alcohol Drinking↗

PubMed1999

N-ethylmaleimide inhibition of thrombin-induced platelet aggregation.

The data presented in this report show that N-ethylmaleimide (NEM) is a powerful inhibitor of thrombin-induced platelet aggregation. NEM increased guanosine 3', 5'-cyclic monophosphate (cGMP) and adenosine 3', 5'-cyclic monophosphate (cAMP) levels in intact cells. The inhibition of cAMP high-affinity phosphodiesterase and cGMP phosphodiesterase was implicated in the elevation of the cyclic nucleotides. NEM dose dependently blocked the thrombin-stimulated, but not the phorbol myristate acetate-dependent phosphorylation of the protein kinase C substrate pleckstrin. Myosin light chain phosphorylation was also inhibited by NEM. In addition, the sulphydryl reagent inhibited Ca2+ mobilisation induced by thrombin. The data indicate that phospholipase C activation by thrombin is interrupted by NEM at the level of receptor-mediated signal transduction.

Blood Proteins↗

PubMed2004

Pooling of animal experimental data reveals influence of study design and publication bias.

BACKGROUND AND PURPOSE: The extensive neuroprotective literature describing the efficacy of candidate drugs in focal ischemia has yet to lead to the development of effective stroke treatments. Ideally, the choice of drugs taken forward to clinical trial should be based on an unbiased assessment of all available data. Such an assessment might include not only the efficacy of a drug but also the in vivo characteristics and limits--in terms of time window, dose, species, and model of ischemia used--to that efficacy. To our knowledge, such assessments have not been made. Nicotinamide is a candidate neuroprotective drug with efficacy in experimental stroke, but the limits to and characteristics of that efficacy have not been fully described. METHODS: Systematic review and modified meta-analysis of studies of experimental stroke describing the efficacy of nicotinamide. The search strategy ensured ascertainment of studies published in full and those published in abstract only. DerSimonian and Laird random effects meta-analysis was used to account for heterogeneity between studies. RESULTS: Nicotinamide improved outcome by 0.287 (95% confidence interval 0.227 to 0.347); it was more effective in temporary ischemia models, after intravenous administration, in animals without comorbidities, and in studies published in full rather than in abstract. Studies scoring highly on a quality measure gave more precise estimates of the global effect. CONCLUSIONS: Meta-analysis provides an effective technique for the aggregation of data from experimental stroke studies. We propose new standards for reporting such studies and a systematic approach to aggregating data from the neuroprotective literature.

Animals↗

PubMed1982

Occupational injuries: factors associated with frequency and severity.

In recent years, energy exchange has come to be accepted as the causative agent in accidental injuries. This paper focuses on two fundamental characteristics of accidental workplace injuries, their frequency, and their severity. I propose that the frequency of injuries is determined largely by the nature of the interactions between workers and production processes, while the severity of the occurring injuries will be more strongly affected by the maximum possible harm the production process can cause. Other aspects of the design of the production process may also affect the severity of injuries. Using aggregate national data for manufacturing industries in the US for 1972, the rate of injuries per 100 employees per year and the average number of lost work days per injury (a common measure of severity) were regressed against a number of econometric variables. Eighty percent of the variation in injury frequency rates among 61 industries was explained by seven variables. Among them were the rate of new hires, the productivity of energy and of labor, the average hourly wage, and the percentage of the workforce that was unionized. Four variables explained 69% of the variation in the severity of injuries among industries. Nearly half of this effect was caused by just one variable, the amount of energy consumed per worker. These results provide tentative confirmation for the models of injury frequency and severity that were proposed, and suggest the need for another study using less aggregated data.

Accidents, Occupational↗

PubMed2004

Inducible superoxide dismutase 1 aggregation in transgenic amyotrophic lateral sclerosis mouse fibroblasts.

High molecular weight detergent-insoluble complexes of superoxide dismutase 1 (SOD1) enzyme are a biochemical abnormality associated with mutant SOD1-linked familial amyotrophic lateral sclerosis (FALS). In the present study, SOD1 protein from spinal cords of transgenic FALS mice was fractionated according to solubility in saline, zwitterionic, non-ionic or anionic detergents. Both endogenous mouse SOD1 and mutant human SOD1 were least soluble in SDS, followed by NP-40 and CHAPS, with an eight-fold greater detergent resistance of mutant protein overall. Importantly, high molecular weight mutant SOD1 complexes were isolated with SDS-extraction only. To reproduce SOD1 aggregate pathology in vitro, primary fibroblasts were isolated and cultured from neonatal transgenic FALS mice. Fibroblasts expressed abundant mutant SOD1 without spontaneous aggregation over time with passage. Proteasomal inhibition of cultures using lactacystin induced dose-dependent aggregation and increased the SDS-insoluble fraction of mutant SOD1, but not endogenous SOD1. In contrast, paraquat-mediated superoxide stress in fibroblasts promoted aggregation of endogenous SOD1, but not mutant SOD1. Treatment of cultures with peroxynitrite or the copper chelator diethyldithiocarbamate (DDC) alone did not modulate aggregation. However, DDC inhibited lactacystin-induced mutant SOD1 aggregation in transgenic fibroblasts, while exogenous copper slightly augmented aggregation. These data suggest that SOD1 aggregates may derive from proteasomal or oxidation-mediated oligomerisation pathways from mutant and endogenous subunits respectively. Furthermore, these pathways may be affected by copper availability. We propose that non-neural cultures such as these transgenic fibroblasts with inducible SOD1 aggregation may be useful for rapid screening of compounds with anti-aggregation potential in FALS.

Acetylcysteine↗

PubMed2000

Characterization and isolation of intermediates in beta-lactoglobulin heat aggregation at high pH.

The early stages of heat induced aggregation at 67.5 degrees C of beta-lactoglobulin were studied by combined static light scattering and size exclusion chromatography. At all conditions studied (pH 8.7 without salt and pH 6.7 with or without 60 mM NaCl) we observe metastable heat-modified dimers, trimers, and tetramers. These oligomers reach a maximum in concentration at about the time when large aggregates (1000-4000 kg/mol) appear, after which they decline in concentration. By isolating the oligomers it was demonstrated that they rapidly form aggregates upon heating in the absence of monomeric protein, showing that these species are central to the aggregation process. To our knowledge this is the first time that intermediates in protein aggregation have been isolated. At all stages of aggregation the dominant oligomer was the heat-modified dimer. Whereas the heat-modified oligomers are formed at a higher rate at pH 8.7 than at pH 6.7, the opposite is the case for the formation of aggregates from the metastable oligomers indicating cross-linking via disulfide bridges for the oligomers and noncovalent interaction in the formation of the aggregates. The data suggest that an aggregate nucleus is formed from four oligomers. For protein concentrations of 10 or 20 g/l a heat-modified monomer can be observed until about the time when the maximum in concentration appears of the heat-modified dimer. The disappearance of this heat-modified monomer correlates to the formation of dimers (trimers and tetramers).

Dimerization↗

PubMedDate not supplied

An analysis of allegations of sexual abuse in a multi-victim day-care center case.

Sexual abuse in day-care centers is a phenomenon of increasing concern, both in terms of its prevalence and its serious effects on child victims. Legal intervention in this area is problematic because criminal investigations are usually beset with difficulties: Characteristics of children and of the abuse situation affect disclosure rates and credibility. Research on children as witnesses is amassing; however, so far, little systematic analysis has been conducted on multi-victim child sexual abuse cases. The present study concerns a case of sexual abuse in a day-care center with over 100 alleged victims. Criteria derived from Statement Validity Analysis (SVA) protocols were applied to aggregate record review data to assess the veritability of the abuse allegations. Individual children's abuse disclosures were also analyzed, vis-à-vis characteristics of the children (age, gender, recency of attendance) and of the investigation (agency doing the interview, number of interviews, use of anatomically detailed dolls). The use of SVA criteria supported the veritability of allegations in this day-care abuse case. Even acknowledging the limitations of archival data collected for other purposes, the aggregate data analysis reflected consistency, logical structure, and spontaneity; however, little evidence of accommodation was found. Multivariate comparison of disclosing and nondisclosing children found an unexpected inverse relationship of disclosure with age, as well as positive associations with number of interviews and use of dolls. Alternative interpretations of these results are discussed.

Age Factors↗

PubMed2002

Birth cohort effects in New South Wales suicide, 1865-1998.

OBJECTIVE: To examine birth cohort effects in New South Wales (NSW) suicide data (1865-1998). METHOD: Aggregate suicide data were examined after controlling for age and period using descriptive statistics and Poisson regression modelling. Three approaches were applied to address the non-identification of age, period and cohort in age-period-cohort (APC) models of suicide. RESULTS: Apparent cohort effects in male and female suicide using a minimum constraints APC model of age, period and cohort were no longer present in female suicide when a surrogate period APC model was used, and were absent in both male and female suicide when identifiable cohort effects were isolated using a 'drift' adjusted approach to APC modelling. CONCLUSION: Increases in youth suicide rates in NSW occurring since the 1960s cannot be attributed to cohort effects, such as family influences on development. The causes of youth suicide are thus effects operating contemporaneously.

Age Factors↗

PubMed2004

Targeting expression of expanded polyglutamine proteins to the endoplasmic reticulum or mitochondria prevents their aggregation.

Aggregation of misfolded proteins is a characteristic of several neurodegenerative diseases. The huntingtin amino-terminal fragment with extended polyglutamine repeat forms aggregates closely associated with chaperones both in the cytoplasm and the nucleus. Because each cellular compartment contains distinct chaperones and because the molecular mechanisms controlling polyglutamine aggregation are largely unknown, we decided to investigate the influence of different cellular environments on the aggregation of this pathological protein. Here, we show that aggregation of a protein containing a polyglutamine stretch of pathological length is abolished when its expression is targeted to the endoplasmic reticulum. Once retrogradely transported outside the endoplasmic reticulum, the aggregation-prone polyglutamine-containing protein recovers its ability to aggregate. When expressed in the mitochondria, a protein containing 73 glutamines is entirely soluble, whereas the nucleocytosolic equivalent has an extremely high tendency to aggregate. Our data imply that polyglutamine aggregation is a property restricted to the nucleocytosolic compartment and suggest the existence of compartment-specific cofactors promoting or preventing aggregation of pathological proteins.

Cell Line↗

PubMed1975

Physiological role of an endoperoxide in human platelets: hemostatic defect due to platelet cyclo-oxygenase deficiency.

The endoperoxide prostaglandin G2 (PGG2) induced platelet aggregation as well as the platelet release reaction (release of ADP and serotonin) when added to human platelet-rich plasma. Formation of a metabolite of PGG2 [8-(l-hydroxy-3-oxopropyl)-9,12L-dihydroxy-5,10-heptadecadienoic acid] and a lipoxygenase product [12L-hydroxy-5,8,10,14-eicosatetraenoic acid] accompanied the release reaction caused by aggregating agents such as collagen, ADP, epinephrine, and thrombin. Indomethacin inhibited the release reaction and PGG2 formation induced by these agents but had no effect on PGG2-induced release reaction. The aggregating effect of PGG2 was abolished by furosemide, which is a competitive inhibitor of ADP-induced primary aggregation. These data indicate that the aggregating effect of PGG2 is due to release of ADP and that PGG2 synthesis is required for induction of the release reaction by various aggregating agents. A subject with a hemostatic defect due to abnormal release mechanism [decreased aggregation with epinephrine (second wave) and collagen and normal platelet ADP] had a deficiency of the cyclo-oxygenase that catalyzes formation of PGG2. Normal aggregation and release reaction were obtained with added PGG2. Ii is concluded that the endoperoxide (PGG2) is essential in normal hemostasis because of its role in initiating the release reaction required for aggregation by collagen and the second wave of aggregation caused by, e.g., ADP.

Adenosine Diphosphate↗

PubMed1992

The mechanisms of Eikenella corrodens aggregation by salivary glycoprotein and the effect of the glycoprotein on oral bacterial aggregation.

The mechanism of aggregation of Eikenella corrodens 1073 with E. corrodens aggregating factor (EcAF) which was purified from submandibular-sublingual (SM-SL) saliva was investigated. Heating (100 degrees C, 10 minutes) or protease treatment of E. corrodens cells abolished the aggregating activity. The aggregation was inhibited by adding N-acetyl-D-galactosamine (GalNAc) and saccharides which contain a galactose residue at the non-reducing end. The aggregating activity was sensitive to EDTA and was restored by Ca2+ but not by Mn2+ or Mg2+. Neuraminidase treatment of EcAF increased their ability to aggregate. E. corrodens, suggesting that the sialic acids on EcAF interfere with aggregation. These data suggest that the aggregation of E. corrodens 1073 with EcAF is mediated by specific interactions between a bacterial cell surface lectin-like substance and a complementary GalNAc-like receptor. EcAF also aggregated 16 strains of oral bacteria including periodontopathic bacteria such as Porphyromonas (Bacteroides) gingivalis 381 and Actinobacillus actinomycetemcomitans ATCC29522; however, those aggregations were not inhibited by GalNAc. Therefore, EcAF appears to have more than two types of bacterial binding site and plays important roles in accumulation of dental plaque by forming a complex network of plaque bacteria including periodontopathic strains.

Acetylgalactosamine↗

PubMed2003

Follow-up of deaths among U.S. Postal Service workers potentially exposed to Bacillus anthracis--District of Columbia, 2001-2002.

In October 2001, two letters contaminated with Bacillus anthracis spores were processed by mechanical and manual methods at the U.S. Postal Service (USPS) Brentwood Mail Processing and Distribution Center in the District of Columbia. Four postal workers at the Brentwood facility became ill with what was diagnosed eventually as inhalational anthrax; two died. The facility was closed on October 21, and postexposure prophylaxis was recommended for approximately 2,500 workers and business visitors. Subsequent reports of deaths of facility workers prompted concern about whether mortality was unusually high among workers, perhaps related to the anthrax attacks. To evaluate the rates and causes of death among workers at the Brentwood facility during October 12, 2001-October 11, 2002, CDC, in collaboration with state and local health departments, analyzed death certificate data. In addition, these data were compared with aggregate mortality data from the five USPS facilities contaminated with B. anthracis during the fall 2001 anthrax attacks. This report summarizes the results of that analysis, which indicate that rates and causes of death among Brentwood workers during the 12 months after the anthrax attacks of 2001 were not different from rates and causes of deaths that occurred during the preceding 5 years.

Anthrax↗

PubMed1989

Heparin-associated thrombocytopenia: observations on the mechanism of platelet aggregation.

We investigated the mechanism of heparin-mediated platelet aggregation in 11 patients with heparin-associated thrombocytopenia. Severe thrombocytopenia (16,000 to 66,000 platelets/microliters) developed in each patient during heparin therapy, and platelet aggregation occurred in vitro when heparin was added to mixtures of patient plasma and normal platelet-rich plasma. In 10 patients, heparin-initiated platelet aggregation was inhibited by preincubation of mixtures of normal platelet-rich plasma and heparin-associated thrombocytopenia plasma with monoclonal antiglycoprotein Ib antibodies 6D1 or LJ-Ib1. Both antibodies are directed against the von Willebrand factor binding site on glycoprotein Ib and inhibit only ristocetin-induced platelet agglutination. Purified immunoglobulin G (IgG) from patients with heparin-associated thrombocytopenia also supported heparin-induced aggregation, but equivalent amounts of antigen-binding fragments [F(ab')2] did not. We also found that F(ab')2 of LJ-Lb1 did not inhibit heparin-induced platelet aggregation but retained inhibitory activity against ristocetin-induced platelet agglutination. The monoclonal antibody 3G6, directed against the alpha-chain of glycoprotein Ib but not inhibitory of ristocetin-induced platelet agglutination, had no effect on heparin-induced platelet aggregation. Antibodies to von Willebrand factor that inhibit ristocetin-induced platelet agglutination did not inhibit heparin-mediated platelet aggregation, but antibodies to glycoprotein IIb-IIIa blocked aggregation. These data suggest that platelet aggregation in heparin-associated thrombocytopenia may be initiated by an interaction between patient IgG, heparin, and the platelet surface. Platelet activation appears to be mediated by a platelet surface crystallizable fragment (Fc) receptor.(ABSTRACT TRUNCATED AT 250 WORDS)

Heparin↗

PubMed1982

Spontaneous aggregation of native immunoglobulins in hypoalbuminemic serum.

We have previously demonstrated that isolated IgG, when added to buffer or serum, undergoes aggregation during incubation at 37 degrees C. The addition of albumin inhibits aggregation. The present studies were designed to determine whether endogenous immunoglobulins in normal serum, present in low-normal concentration, would likewise aggregate in the presence of hypoalbuminemia. Albumin was removed from normal serum by absorption with Affi-gel Blue. Following incubation at 37 degrees C, high molecular weight IgG, IgM and IgA were detectable by density gradient ultracentrifugation. Reconstituting the samples with albumin prior to incubation prevented the formation of immunoglobulin aggregates. These data suggest that immunoglobulin aggregation might also occur in vivo in a variety of pathological conditions associated with hypoalbuminemia and/or hypergammaglobulinemia and might be incorrectly assumed to represent antigen-antibody complexes.

Antigen-Antibody Complex↗

PubMed1999

Effects of pituitary adenylate cyclase-activating polypeptide on the cyclooxygenase pathway of rat platelets and on platelet aggregation.

Several data suggest that pituitary adenylate cyclase-activating polypeptide (PACAP) is involved in the regulation of local circulation. One possible role of PACAP in the regulation of circulation is that, it may modify the cyclooxygenase pathway of the arachidonate cascade in platelets. Our study was designed to study the effect of PACAP on the cyclooxygenase pathway of rat platelets and on platelet aggregation. PACAP (10(-7) and 10(-6) M) significantly inhibited the cyclooxygenase pathway of platelets, mostly the thromboxane synthesis. Pretreatment with a PACAP receptor antagonist, PACAP(6-38), or with an inhibitor of protein kinase A, H-89, shows that the effects of PACAP on the cyclooxygenase pathway were diminished. In the aggregation studies, PACAP inhibited both the arachidonic acid-induced and the thrombin-induced platelet aggregation. It can be concluded that PACAP inhibits the cyclooxygenase pathway of rat platelets via a specific PACAP receptor-activated, cAMP-dependent pathway, and these effects of PACAP are involved in the inhibition of platelet aggregation.

Animals↗

PubMed2006

Protein activity in bacterial inclusion bodies correlates with predicted aggregation rates.

Recent data show that protein aggregation as bacterial inclusion bodies does not necessarily imply loss of biological activity. Here, we investigate the effect of a large set of single-point mutants of an aggregation-prone protein on its specific activity once deposited in inclusion bodies. The activity of such aggregates significantly correlates with the predicted aggregation rates for each mutant, suggesting that rationally tuning the kinetic competition between folding and aggregation might result in highly active, inclusion bodies. The exploration of this technology during recombinant protein production would have a significant biotechnological value.

Bacterial Proteins↗