PTSD malingering detection in damage claim cases: Diagnostic accuracy in cases of personal injury as a result of motor vehicle accidents.

This study aimed to assess the accuracy of post-traumatic stress disorder (PTSD) diagnoses made by mental health experts in people reporting post-traumatic stress symptoms related to traffic accidents. Data were collected from sixty participants: 30 with possible traumatic experiences and 30 who had never experienced this or other types of traumatic events. Six professional diagnosticians examined the participants with Structured Clinical Interview for the Study of Axis I Disorders (SCID-I for DSM-IV-TR) in conditions similar to those typical of judicial cases related to traffic accident damage claims. There was no significant difference in the number of PTSD diagnoses between malingerers and non-malingerers. Some PTSD symptoms were more frequently recognized in malingerers. This study demonstrates that even professional diagnosticians with clinical and jurisprudence experience have significant difficulty identifying PTSD malingering. This difficulty can be linked to the limitations of diagnoses based on introspective reports.

Evidence of Early Emergence of the Primary Dentition in a Northern Plains American Indian Population.

The purposes of this study were to describe primary tooth emergence in an American Indian (AI) population during the first 36 mo of life to compare 1) patterns of emergence between male and female children and 2) tooth emergence between these AI children and other U.S. ethnic groups. Data were derived from a birth cohort of 239 AI children from a Northern Plains tribe participating in a longitudinal study of early childhood caries, with examination data at target ages of 8, 12, 16, 22, 28, and 36 mo of age (±1 mo). Patterns of emergence in AI children were characterized and sex comparisons accomplished with interval-censored survival methodology. Numbers of erupted teeth in AI children at each age were compared via Kruskal-Wallis tests against those in children of the same age, as drawn from a cross-sectional study of dental caries patterns in Arizona; these comparisons were based on the dental examinations of 547 White non-Hispanic and 677 Hispanic children. Characterization of time to achievement of various milestones-including emergence of the anterior teeth, the first molars, and the complete primary dentition-provided no evidence of sex differences among AI children. AI children had significantly more teeth present at 8 mo (median, 3) than either White non-Hispanic (P < 0.0063) or Hispanic (P < 0.0001) children (median, 2 each). This was also true at 12 mo (P < 0.001; medians, 8 vs. 6 and 7, respectively) and 16 mo (P < 0.001; medians, 12 vs. 11 each). Less pronounced differences were seen at 22 mo (P < 0.0001). White non-Hispanic and Hispanic children did not differ at any time considered (P > 0.05). These results provide evidence of earlier tooth emergence in AI children than in the other 2 ethnicities. Although the underlying etiology of the severity of early childhood caries in AI children is likely to be multifactorial, earlier tooth emergence may be a contributing factor. Knowledge Transfer Statement: The findings of this study have practical implications for practitioners providing childhood oral health care to ethnic groups with early tooth emergence. It may be important to provide parents with information on toothbrushing, dentist visits, and other practices supportive of good oral health as early as possible to protect their children's primary dentition.

Streptococcus mutans strains recovered from caries-active or caries-free individuals differ in sensitivity to host antimicrobial peptides.

Antimicrobial peptides (AMPs) are among the repertoire of host innate immune defenses. In the oral cavity, several AMPs are present in saliva and have antimicrobial activities against oral bacteria, including Streptococcus mutans, a primary etiological agent of dental caries. In this study, we hypothesized that unique S. mutans strains, as determined by DNA fingerprinting from sixty 13-year-old subjects with or without experience of caries, would have different susceptibilities to α-defensins-1-3 (HNP-1-3), ß-defensins-2-3 (HBD-2-3) and LL-37. The salivary levels of these peptides in subjects were also measured by enzyme-linked immunosorbent assays. We found that S. mutans strains from children with active caries showed greater resistance to salivary HNP-1-2, HBD-2-3 and LL-37 at varying concentrations than those from caries-free subjects. In addition, combinations of these peptides increased their antimicrobial activity against S. mutans either additively or synergistically. The salivary levels of these peptides were highly variable among subjects with no correlation to host caries experience. However, the levels of a number of these peptides in saliva appeared to be positively correlated within an individual. Our findings suggest that the relative ability of S. mutans to resist host salivary AMPs may be considered a potential virulence factor for this species such that S. mutans strains that are more resistant to these peptides may have an ecological advantage to preferentially colonize within dental plaque and increase the risk of dental caries.

Effects of manganese on Streptococcus mutans planktonic and biofilm growth.

Streptococcus mutans, an agent of dental caries, was tested for growth in the presence or absence of manganese (Mn), since studies have linked Mn levels with cariogenic potential. Seven S. mutans serotype c strains were grown in chemically defined medium under different atmospheric conditions: 5% CO2, O2-enriched 5% CO2 (shaking) and anaerobic. There was significant strain variability with respect to Mn requirements under the various conditions tested. Both sucrose-dependent and sucrose-independent biofilm growth by strain UA159 were affected by the absence of Mn. S. mutans strains show highly variable responses to both high and low Mn concentrations.

Manganese affects Streptococcus mutans virulence gene expression.

BACKGROUND/AIMS: Studies of trace metals in drinking water and tooth enamel have suggested a caries-promoting potential for manganese (Mn). Additionally, Mn has been shown to be essential for the expression of mutans streptococci virulence factors such as the glucan-binding lectin (GBL) of Streptococcus sobrinus. The Streptococcus mutans glucan-binding protein (Gbp) GbpC is the functional analogue of the S. sobrinus GBL. S. mutans Gbps have been shown to contribute to biofilm architecture and virulence. This study was undertaken to examine the effects of Mn on the transcription of genes encoding S. mutans Gbps, including gbpC, along with other critical S. mutans virulence genes. METHODS: Microarray analyses suggested the potential for an Mn effect on Gbp genes. Further investigation of the Mn effects on selected genes was undertaken by performing Northern blots, Western blots, and RT-PCR under conditions of planktonic and biofilm growth in Mn-depleted media or in media containing 50 mircoM Mn. RESULTS: Mn resulted in increased expression of gbpC and gtfB, and decreased expression of wapA, in both planktonic and biofilm cultures. The expression levels of gbpA and gbpD were also decreased in the presence of Mn, but only in biofilms. The expression of gtfC was increased in the presence of Mn only in planktonic cultures. The spaP gene was expressed more highly in Mn-supplemented planktonic cultures but less in Mn-supplemented biofilms. CONCLUSION: Mn availability affects the expression of multiple S. mutans genes involved in adhesion and biofilm formation. Furthermore, these effects depend on the growth state of the organism.

Glucan-binding proteins of the oral streptococci.

The synthesis of extracellular glucan is an integral component of the sucrose-dependent colonization of tooth surfaces by species of the mutans streptococci. In investigators' attempts to understand the mechanisms of plaque biofilm development, several glucan-binding proteins (GBPs) have been discovered. Some of these, the glucosyltransferases, catalyze the synthesis of glucan, whereas others, designated only as glucan-binding proteins, have affinities for different forms of glucan and contribute to aspects of the biology of their host organisms. The functions of these latter glucan-binding proteins include dextran-dependent aggregation, dextranase inhibition, plaque cohesion, and perhaps cell wall synthesis. In some instances, their glucan-binding domains share common features, whereas in others the mechanism for glucan binding remains unknown. Recent studies indicate that at least some of the glucan-binding proteins modulate virulence and some can act as protective immunogens within animal models. Overall, the multiplicity of GBPs and their aforementioned properties are testimonies to their importance. Future studies will greatly advance the understanding of the distribution, function, and regulation of the GBPs and place into perspective the facets of their contributions to the biology of the oral streptococci.

Importance of potassium in cardiovascular disease.

The pivotal role of potassium (K+) in cardiovascular disease and the importance of preserving potassium balance have become clinical hot points, particularly as relates to new and emerging cardioprotective and renoprotective therapies that promote potassium retention. Although clinicians may be aware of the critical nature of this relationship, quite frequently there is some uncertainty as to the best way to monitor potassium levels in the face of a host of pathologic states and/or accompanying drug therapies that affect serum levels and/or total body potassium balance. Moreover, guidelines for monitoring of serum potassium levels are at best tentative and oftentimes are translated according to the level of concern of the respective physician. To address these uncertainties, an expert group was convened that included representatives from multiple disciplines. They attempted to reach consensus on the importance of K+ in hypertension, stroke, and arrhythmias as well as practical issues on maintaining K+ balance and avoiding K+ depletion. Because of the complexity of this topic, issues of hyperkalemia will be addressed in a forthcoming manuscript.

Lipoteichoic acid inhibits interleukin-2 (IL-2) function by direct binding to IL-2.

Lipoteichoic acid (LTA) is associated with the cell envelope of most gram-positive bacteria. Although previously thought to act mainly as a virulence factor by virtue of its adhesive nature, evidence is now provided that LTA can also suppress the function of interleukin-2 (IL-2), an autocrine growth factor for T cells. LTA from four separate bacterial strains lowered the levels of detectable IL-2 during a peripheral blood mononuclear cell response to the antigen tetanus toxoid (TT). T-cell proliferation in response to TT was similarly inhibited by LTA. In contrast, levels of detectable gamma interferon increased. In addition, LTA inhibited IL-2 detection by enzyme-linked immunosorbent assay (ELISA) and blocked the proliferative response of an IL-2-dependent T-cell line to soluble IL-2. Further studies using ELISA demonstrated that LTA blocks IL-2 detection and function by binding directly to IL-2. Flow cytometric analysis revealed that IL-2 binding to T cells is inhibited in the presence of purified LTA but not LTA plus anti-LTA monoclonal antibody. In summary, these studies demonstrate a novel effect of LTA on the immune response through direct binding to IL-2 and inhibition of IL-2 function. Importantly, gram-positive organisms from which LTA is obtained not only play an important role in the pathology of diseases such as bacterial endocarditis, septic shock, acute respiratory distress syndrome, and multiple organ failure but also comprise a significant portion of commensal populations within the human host. Inhibition of IL-2 function by LTA may represent yet another mechanism by which gram-positive bacteria dampen the host immune response and facilitate survival. Thus, LTA provides a potential target for therapeutic intervention when gram-positive organisms are involved.

Feasibility of photopheresis to reduce the occurrence of restenosis after percutaneous transluminal coronary angioplasty: a clinical pilot study.

BACKGROUND: Photopheresis was evaluated as a means of preventing restenosis on the basis of immune modulation. METHODS: This was a prospective, randomized, controlled clinical trial analyzing clinical restenosis at 6 months after percutaneous transluminal coronary angioplasty (PTCA). Seventy-eight patients with single-vessel angioplasty were randomly assigned to a control group of 41 patients and a treatment group of 37 patients. At 6 months, there were 72 evaluable patients: 39 control patients and 33 treated. Twenty-nine control patients received balloon PTCA only and 10 patients received stents. Twenty treated patients received PTCA only and 13 patients received stents. Baseline clinical characteristics of both groups were similar. The treatment group received photopheresis for a total of 5 treatments. Primary end points were death from any cause, myocardial infarction, ischemia, and repeat revascularization procedures. RESULTS: By intention-to-treat analysis, clinical restenosis occurred in 27% of control patients versus 8% of treated patients (P =.040, relative risk = 0.30). CONCLUSIONS: Photopheresis therapy in patients undergoing balloon PTCA with and without stent deployment has been shown to be effective in reducing restenosis. The use of photopheresis in such patients merits further investigation.

An in vitro model for studying the contributions of the Streptococcus mutans glucan-binding protein A to biofilm structure.

The method described here for analyzing biofilms was sensitive enough to allow the detection of differences formed by pure cultures of S. mutans or a GbpA knockout strain. Other strains have also been tested, and the differences in biofilm structure were sometimes even more extensive (data not shown). The advantages of this method are that it is quick, inexpensive, and adaptable to almost any laboratory setting. The constant rotation of the cultures, which was employed to simulate salivary flow, appears to be a critical element for establishing biofilm differences. An analysis of protein profiles confirmed that the biofilm bacteria were metabolically distinct from the planktonic phase bacteria. For the strains tested, the variations in biofilm architecture could be visualized with or without magnification. Staining of the bacteria was not required, though we typically stained the biofilms with either crystal violet or Schiff's reagent. Altogether, this in vitro method for generating biofilms allowed the evaluation of visual, quantitative (confocal microscopy), and functional (antimicrobial susceptibility) differences. We have employed these methods in a reductionist approach to understanding the contribution of individual proteins to dental plaque development. These methods may also be useful in the screening of mutants that would be of greatest for testing in multispecies biofilms, animal models, or more complex biofilm models.

Predictors and outcomes of networking intensity among unemployed job seekers.

This study examined predictors and outcomes of networking intensity (i.e., individual actions directed toward contacting friends, acquaintances, and referrals to get information, leads, or advice on getting a job) during the job searches of a sample of unemployed individuals. The study used a Big Five framework, in which extraversion and conscientiousness were associated with both higher levels of networking intensity and higher use of other traditional job-search methods. Networking comfort (a procedure-specific constellation of evaluative beliefs depicting attitudes toward using networking as a job-search method) was positively related to networking intensity above and beyond the effects of personality. Networking intensity did not provide incremental prediction of unemployment insurance exhaustion, reemployment or reemployment speed, or job satisfaction when intensity of use of other job-search methods was considered.

Modulation of glucan-binding protein activity in streptococci by fluoride.

Glucan-binding lectin (GBL) activity of Streptococcus sobrinus was significantly reduced by fluoride in the growth medium. Approximately 1.5 mM fluoride was required for a 50% reduction in GBL activity. In addition to the GBL, several other glucan-binding proteins were reduced when the bacteria were grown in subinhibitory fluoride. Fluoride had no effect on glucosyltransferases (GTFs), enzymes capable of converting sucrose into alpha-1,6-glucans. All the proteins were detected by use of enhanced chemiluminescence (ECL of fluorescein-labeled dextran) and Western blotting of renatured SDS-PAGE gels. The effects of fluoride on the bacteria were abrogated when the manganous ion was included in the growth medium. It thus appears that one mechanism of action of fluoridated water is its effects on glucan-binding proteins. The fluoride may be reducing metabolism of the mangano aquo ion, essential for expression of the glucan-binding proteins.

Coronary angiographic findings and troponin T in patients with unstable angina pectoris.

This study sought to identify differences in coronary anatomic pathology in patients with unstable angina and elevated versus nonelevated serum troponin T values. Previous studies have shown a worse prognosis in unstable angina patients with elevated serum troponin T values. Consecutive patients (n = 117) with Braunwald class IIIB angina were included in the study. Serum samples for troponin T were obtained at admission and every 6 to 8 hours for 18 to 24 hours. Acute myocardial infarction was excluded by routine creatine kinase measurements. All patients underwent coronary angiography before discharge. Cardiac events including cardiac death and myocardial infarction were recorded. Two thirds of the patients with unstable angina had no increase in serum troponin T (<0.1 microg/L) (n = 80). They had a lower incidence of 3-vessel disease (26% vs 46%, p <0.001), left main disease (5% vs 16%, p = 0.04), visible thrombus (4% vs 22%, p = 0.006), and less severe stenosis of the culprit artery (65% vs 84%, p <0.004) than patients with elevated serum troponin T values (> or =0.1 microg/L) (n = 37). The 1-year cardiac event rate was 0% versus 19% in patients with troponin T values <0.1 microg/L compared with patients with serum troponin T values > or =0.1 microg/L (p <0.0001). It was concluded that patients with unstable angina and no release of troponin T have less severe coronary artery disease, and have an excellent prognosis. It is suggested that these patients may be managed more conservatively and without invasive evaluation before discharge.

Predictors and outcomes of openness to changes in a reorganizing workplace.

It is becoming increasingly important for employees to be able to cope with change in the workplace. This longitudinal study examined a set of individual differences and context-specific predictors of employee openness (i.e., change acceptance and positive view of changes) toward a set of workplace changes. Personal resilience (a composite of self-esteem, optimism, and perceived control) was related to higher levels of change acceptance. Three context-specific variables (information received about the changes, self-efficacy for coping with the changes, and participation in the change decision process) were predictive of higher levels of employee openness to the changes. Lower levels of change acceptance were associated with less job satisfaction, more work irritation, and stronger intentions to quit.

Ligand-binding properties of the carboxyl-terminal repeat domain of Streptococcus mutans glucan-binding protein A.

Streptococcus mutans glucan-binding protein A (GbpA) has sequence similarity in its carboxyl-terminal domain with glucosyltransferases (GTFs), the enzymes responsible for catalyzing the synthesis of the glucans to which GbpA and GTFs can bind and which promote S. mutans attachment to and accumulation on the tooth surface. It was predicted that this C-terminal region, comprised of what have been termed YG repeats, represents the GbpA glucan-binding domain (GBD). In an effort to test this hypothesis and to quantitate the ligand-binding specificities of the GbpA GBD, several fusion proteins were generated and tested by affinity electrophoresis or by precipitation of protein-ligand complexes, allowing the determination of binding constants. It was determined that the 16 YG repeats in GbpA comprise its GBD and that GbpA has a greater affinity for dextran (a water-soluble form of glucan) than for mutan (a water-insoluble form of glucan). Placement of the GBD at the carboxyl terminus was necessary for maximum glucan binding, and deletion of as few as two YG repeats from either end of the GBD reduced the affinity for dextran by over 10-fold. Interestingly, the binding constant of GbpA for dextran was 34-fold higher than that calculated for the GBDs of two S. mutans GTFs, one of which catalyzes the synthesis of water-soluble glucan and the other of which catalyzes the synthesis of water-insoluble glucan.

Inactivation of the gbpA gene of Streptococcus mutans alters structural and functional aspects of plaque biofilm which are compensated by recombination of the gtfB and gtfC genes.

Inactivation of the gbpA gene of Streptococcus mutans increases virulence in a gnotobiotic rat model and also promotes in vivo accumulation of organisms in which gtfB and gtfC have recombined to reduce virulence (K. R. O. Hazlett, S. M. Michalek, and J. A. Banas, Infect. Immun. 66:2180-2185, 1998). These changes in virulence were hypothesized to result from changes in plaque structure. We have utilized an in vitro plaque model to test the hypothesis that the absence of GbpA alters S. mutans plaque structure and that the presence of gtfBC recombinant organisms within a gbpA background restores a wild-type (wt)-like plaque structure. When grown in the presence of sucrose within hydroxyapatite-coated wells, the wt S. mutans plaque consisted primarily of large aggregates which did not completely coat the hydroxyapatite surface, whereas the gbpA mutant plaque consisted of a uniform layer of smaller aggregates which almost entirely coated the hydroxyapatite. If 25% of the gbpA mutants used as inoculum were also gtfBC recombinants (gbpA/25%gtfBC), a wt-like plaque was formed. These changes in plaque structure correlated with differences in susceptibility to ampicillin; gbpA plaque organisms were more susceptible than organisms in either the wt or gbpA/25%gtfBC plaques. These data allow the conclusion that GbpA contributes to S. mutans plaque biofilm development. Since the changes in plaque structure detailed in this report correlate well with previously observed changes in virulence, it seems likely that S. mutans biofilm structure influences virulence. A potential model for this influence, which can account for the gtfBC recombination compensating gbpA inactivation, is that the ratio of glucan to glucan-binding protein is a critical factor in plaque development.

Intravenous beta-blockers in acute myocardial infarction: perceived versus actual use by cardiologists and emergency physicians.

This study sought to determine the relationship between perceived and actual use of intravenous beta-blockers by cardiologists and emergency physicians for patients with acute myocardial infarction (AMI). The charts of 35 patients who presented to the emergency department of a community hospital with AMI during a 6-month period were retrospectively reviewed. Members of the departments of cardiology and emergency medicine were mailed a one-page survey pertaining to their use of intravenous beta-blockers in AMI. Of the 35 patients only 4 (11%) received an intravenous beta-blocker. Three of these 4 patients were either hypertensive or tachycardic and none had a contraindication to beta-blockade. A contraindication was present in 15 (48%) of those who did not get intravenous beta-blockade. The survey was completed by 11 (100%) of the emergency physicians and 68 (69%) of the cardiologists. Emergency physicians were significantly less likely to report using intravenous beta-blockers in AMI patients who were normotensive with normal heart rates (P=.007) and most (9 of 11) deferred the decision to the cardiologist. Although the majority of cardiologists reported giving an intravenous beta-blocker to at least 50% of AMI patients with normal blood pressure and pulse rates, the actual frequency was only 8% (1 of 13). In this institution, cardiologists overestimated the frequency of intravenous beta-blocker administration to patients with AMI. Emergency physicians usually deferred the decision on intravenous beta-blockers to cardiologists and reported a frequency of use that was much closer to actual practice.

Inactivation of the gbpA gene of Streptococcus mutans increases virulence and promotes in vivo accumulation of recombinations between the glucosyltransferase B and C genes.

Glucan-binding protein A (GbpA) of Streptococcus mutans has been hypothesized to promote sucrose-dependent adherence and the cohesiveness of plaque and therefore to contribute to caries formation. We have analyzed the adherence properties and virulence of isogenic gbpA mutants relative to those of wild-type S. mutans. Contrary to expectations, the gbpA mutant strains displayed enhanced sucrose-dependent adherence in vitro and enhanced cariogenicity in vivo. In vitro, S. mutans was grown in the presence of [3H] thymidine and sucrose within glass vials. When grown with constant rotation, significantly higher levels of gbpA mutant organisms than of wild type remained adherent to the vial walls. Postgrowth vortexing of rotated cultures significantly decreased adherence of wild-type organisms, whereas the adherence of gbpA mutant organisms was unaffected. In the gnotobiotic rat model, the gbpA mutant strain was hypercariogenic though the colonization levels were not significantly different from those of the wild type. The gbpA mutant strain became enriched in vivo with organisms that had undergone a recombination involving the gtfB and gtfC genes. The incidence of gtfBC recombinant organisms increased as a function of dietary sucrose availability and was inversely correlated with caries development. We propose that the absence of GbpA elevates the cariogenic potential of S. mutans by altering the structure of plaque. However, the hypercariogenic plaque generated by gbpA mutant organisms may be suboptimal for S. mutans, leading to the accumulation of gtfBC recombinants whose reduced glucosyltransferase activity restores a less cariogenic plaque structure.