Academic Entitlement in Physician Assistant Students.

PURPOSE: The purpose of this study was to identify the prevalence and characteristics of academic entitlement (AE) among physician assistant (PA) students in the United States. METHODS: A cross-sectional survey design was used to assess AE using 2 previously validated AE surveys. Current PA students were recruited via email, and survey data were analyzed using descriptive statistics and cumulative logistic regression. RESULTS: Overall, the 337 PA students who participated in the study reported low levels of AE. Students displayed the highest level of AE on statements related to the role of professors and the lowest level of entitlement on statements pertaining to student responsibility and grade entitlement. Students who struggled academically were more likely to report AE in relation to professors' roles. Older students were more likely to display AE related to provision of necessary resources by the university and less likely to display AE regarding the method of delivery for learning materials. Higher levels of grade-related AE were found in students in the didactic phase, female students, and students who did not identify as White. In addition, students who did not identify as White were more likely to display AE in relation to tests. CONCLUSIONS: Literature shows that AE has increased and is a major concern in higher education. Although the overall study results indicated relatively low AE, we found increased AE in certain student groups. Earlier identification of students at increased risk for AE would allow educators to intervene more effectively in a timely manner.

Acute monoarthritis.

Acute monoarthritis affects a single joint and has many potential underlying causes, including crystal deposition diseases, infection, trauma, and osteoarthritis. A comprehensive health history and physical examination can help narrow the list of differential diagnoses; judicious diagnostic testing can help pinpoint the diagnosis. Clinicians also must be able to recognize which patients require emergency referral to prevent long-term adverse consequences.

Supplementation with antioxidants and folinic acid for children with Down's syndrome: randomised controlled trial.

OBJECTIVES: To assess whether supplementation with antioxidants, folinic acid, or both improves the psychomotor and language development of children with Down's syndrome. DESIGN: Randomised controlled trial with two by two factorial design. SETTING: Children living in the Midlands, Greater London, and the south west of England. PARTICIPANTS: 156 infants aged under 7 months with trisomy 21. INTERVENTION: Daily oral supplementation with antioxidants (selenium 10 mug, zinc 5 mg, vitamin A 0.9 mg, vitamin E 100 mg, and vitamin C 50 mg), folinic acid (0.1 mg), antioxidants and folinic acid combined, or placebo. MAIN OUTCOME MEASURES: Griffiths developmental quotient and an adapted MacArthur communicative development inventory 18 months after starting supplementation; biochemical markers in blood and urine at age 12 months. RESULTS: Children randomised to antioxidant supplements attained similar developmental outcomes to those without antioxidants (mean Griffiths developmental quotient 57.3 v 56.1; adjusted mean difference 1.2 points, 95% confidence interval -2.2 to 4.6). Comparison of children randomised to folinic acid supplements or no folinic acid also showed no significant differences in Griffiths developmental quotient (mean 57.6 v 55.9; adjusted mean difference 1.7, -1.7 to 5.1). No between group differences were seen in the mean numbers of words said or signed: for antioxidants versus none the ratio of means was 0.85 (95% confidence interval 0.6 to 1.2), and for folinic acid versus none it was 1.24 (0.87 to 1.77). No significant differences were found between any of the groups in the biochemical outcomes measured. Adjustment for potential confounders did not appreciably change the results. CONCLUSIONS: This study provides no evidence to support the use of antioxidant or folinic acid supplements in children with Down's syndrome. TRIAL REGISTRATION: Clinical trials NCT00378456.

Inequalities in provision of the Disability Living Allowance for Down syndrome.

OBJECTIVES: To assess factors associated with granting of the Disability Living Allowance (DLA) for Down syndrome. DESIGN: Cross-sectional survey. SETTING: Families with a child with Down syndrome enrolled in a community-based trial of vitamin supplementation. PARTICIPANTS: 156 children with trisomy 21 (59% male, 20% non-white) were enrolled before 7 months of age and 138 completed follow-up. MAIN OUTCOME MEASURES: Before the child was 2 years old, we surveyed parents about applications for the DLA and socioeconomic factors, and assessed the child's development. RESULTS: Application for the DLA was not associated with ethnicity or speaking English. Significantly fewer ethnic minority parents (OR = 0.10; 95% CI 0.03 to 0.35; 69% vs 96%, risk difference 27%) and parents with English as a second language (OR = 0.15: 95% CI 0.04 to 0.62; 67% vs 93%, risk difference 26%) were granted the DLA. Amongst those granted the DLA, ethnic minority families were significantly less likely to be granted a higher monetary award (OR = 0.19; 95% CI 0.06 to 0.55). Severity of disability, reflected by quartile of Griffiths Developmental Quotient or the presence of severe cardiac disease requiring surgery, was not associated with application, granting or level of the DLA award. CONCLUSIONS: Although all children with Down syndrome meet some of the criteria for the DLA, only 80% were receiving this benefit. The decision to award the DLA and the monetary level of the award favoured white, English speaking parents and was not related to severity of disability. Routine monitoring of awards by ethnicity and language spoken is needed. TRIAL REGISTRATION NUMBER: NCT00378456.

Discrimination of human pathogenic subspecies of Francisella tularensis by using restriction fragment length polymorphism.

We describe the use of two insertion sequence elements (ISFtu1 and ISFtu2) in Francisella tularensis to type strains by restriction fragment length polymorphism (RFLP). The RFLP profiles of 17 epidemiologically unrelated isolates were determined and compared. Our results showed that RFLP profiles can be used to assign F. tularensis strains into five main groups corresponding to strains of F. tularensis subsp. tularensis, F. tularensis strain ATCC 6223, strains of F. tularensis subsp. holarctica, strains of F. tularensis subsp. holarctica from Japan, and F. tularensis subsp. mediaasiatica. The results confirm the genetic identities of these subspecies and also support the suggestion that strains of F. tularensis subsp. holarctica from Japan should be considered members of a separate biovar. These findings should support future studies to determine the genetic differences between strains of F. tularensis at the whole-genome level.

A possible pitfall in the identification of Burkholderia mallei using molecular identification systems based on the sequence of the flagellin fliC gene.

Amotile Burkholderia mallei and motile Burkholderia pseudomallei display a high similarity with regard to phenotype and clinical syndromes, glanders and melioidosis. The aim of this study was to establish a fast and reliable molecular method for identification and differentiation. Despite amotility, the gene of the filament forming flagellin (fliC) could be completely sequenced in two B. mallei strains. Only one mutation was identified discriminating between B. mallei and B. pseudomallei. A polymerase chain reaction-restriction fragment length polymorphism assay was designed making use of the absence of an AvaII recognition site in B. mallei. All seven B. mallei, 12 out of 15 B. pseudomallei and 36 closely related apathogenic Burkholderia thailandensis strains were identified correctly. However, in three B. pseudomallei strains a point mutation at gene position 798 (G to C) disrupted the AvaII site. Therefore, molecular systems based on the fliC sequence can be used for a reliable proof of strains of the three species but not for the differentiation of B. mallei and B. pseudomallei isolates.

Tularemia.

Francisella tularensis is the etiological agent of tularemia, a serious and occasionally fatal disease of humans and animals. In humans, ulceroglandular tularemia is the most common form of the disease and is usually a consequence of a bite from an arthropod vector which has previously fed on an infected animal. The pneumonic form of the disease occurs rarely but is the likely form of the disease should this bacterium be used as a bioterrorism agent. The diagnosis of disease is not straightforward. F. tularensis is difficult to culture, and the handling of this bacterium poses a significant risk of infection to laboratory personnel. Enzyme-linked immunosorbent assay- and PCR-based methods have been used to detect bacteria in clinical samples, but these methods have not been adequately evaluated for the diagnosis of pneumonic tularemia. Little is known about the virulence mechanisms of F. tularensis, though there is a large body of evidence indicating that it is an intracellular pathogen, surviving mainly in macrophages. An unlicensed live attenuated vaccine is available, which does appear to offer protection against ulceroglandular and pneumonic tularemia. Although an improved vaccine against tularemia is highly desirable, attempts to devise such a vaccine have been limited by the inability to construct defined allelic replacement mutants and by the lack of information on the mechanisms of virulence of F. tularensis. In the absence of a licensed vaccine, aminoglycoside antibiotics play a key role in the prevention and treatment of tularemia.

Characterisation of an acapsular mutant of Burkholderia pseudomallei identified by signature tagged mutagenesis.

A Burkholderia pseudomallei mutant which was attenuated in a mouse model of melioidosis was identified by a signature tagged mutagenesis approach. The transposon was shown to be inserted into a gene within the capsular biosynthetic operon. Compared with the wild-type bacteria this mutant demonstrated a 10(5)-fold increase in the median lethal dose in a mouse model and it did not react with a monoclonal antibody against high mol. wt polysaccharide of B. pseudomallei. To determine the kinetics of infection, mice were dosed intraperitoneally (i.p.) and intravenously (i.v.) with mutant and wild-type bacteria. After i.p challenge, the number of mutant bacteria in the peritoneal cavity declined, whereas wild-type bacteria proliferated. When administered by the i.v. route, the mutant was able to cause disease but the time to death was increased compared with the wild type. Mice were dosed with the mutant and subsequently challenged with wild-type B. pseudomallei, but the mutant failed to induce a protective immune response.

In vivo plasminogen deficiency reduces fat accumulation.

Obesity and non-insulin dependent diabetes are associated with a decrease in fibrinolysis, which is mediated by the plasminogen system. The purpose of the current study was to investigate the role of the plasminogen system in the reduced body weight of the plasminogen deficient (Plg-/-) mice. In this study we have found that the reduced body weight in Plg-/- mice is due to a reduced rate of the adipose tissue (25% less) and whole body fat (30% less) accumulation during growth in Plg-/- compared to wild-type (WT) littermates. When the mice are fed a high fat-lipogenic diet, adipose tissue accumulation increases in the Plg-/- mice indicating that the capacity for lipid filling of cells was not blocked. In addition, glycerol phosphate dehydrogenase, a marker of late differentiation, was not different in the depots from WT and Plg-/- mice. The number of stromal cells (number x 10(5)/g adipose tissue), isolated from inguinal (Plg-/- 3.4 +/- 1.2. n = 6; WT 0.17 +/- 0.07, n = 7, p < 0.02) and gonadal (Plg-/- 11.0 +/- 0.4, n = 6; WT 3.1 +/- 0.7, n = 7, p < 0.05) fat depots. was markedly higher in the depots from the Plg-/- mice than WT mice. Differentiation of stromal cells in culture from the Plg-/- mice was reduced compared to cells from WT mice. These results suggest that differences in the stromal cell population are responsible for the reduced adipose tissue accumulation in the Plg-/- mice, and that the plasminogen system plays an important role in adipose tissue accumulation.