Sleep Evaluation in the Assessment of Pediatric Attention Deficit Disorders

Introduction

Examining the impact of appropriate sleep evaluation on diagnosis of attention deficit disorders can improve the standard of care in pediatrics. This quality improvement project examined current practice and subsequent implementation of a validated standardized sleep evaluation tool in the assessment of children with symptoms of attention deficit.

An Analysis of the Morphology of Bony Bicipital Groove Fractures in Proximal Humeral Fractures

Objective

Research on proximal fractures in the humeral bicipital groove (BG), a region in which bones are not commonly fractured, is considered sparse in the literature. The objective of this research was to present the definite characteristics and distribution of BG fractures.

Methods

This retrospective study included and enrolled 119 proximal humeral fractures in adult patients with complete radiography data to identify the fracture distribution in the BG from January 2021 to August 2021. The bicipital region was divided into three parts, i.e. the upper 1/3, middle 1/3, and lower 1/3 of the BG, and the distribution of fracture lines was transcribed on the male or female template, as appropriate. In addition, the normal contralateral humerus was used to calculate the cortical thickness of the supratubercular groove and different parts of the BG (upper, middle, and lower parts). The Mann–Whitney test or one-way ANOVA along with LSD tests were used to determine differences in the fracture distribution and cortical thickness between men and women.

Results

Fractures of the BG in both men and women were mainly located in the upper 2/3 region of the BG, especially in the middle 1/3 of the BG. There were significant differences in the cortical thickness of the BG in men compared with that in women. The cortical thickness was highest in the supratubercular ridge but not the BG in men and women, respectively.

Conclusion

This research concluded that bony BG fractures were always observed in the middle part of the BG and were mainly found in patients with four fractures of the proximal humerus. As a unique fracture pattern, the existence of a bony BG fracture always means that a patient has been injured by a relatively severe mechanism, and more attention should be given to these proximal humeral fractures.     

Lung pathology in response to repeated exposure to Staphylococcus aureus in congenic residual function cystic fibrosis mice does not increase in response to decreased CFTR levels or increased bacterial load.

OBJECTIVE: To establish the role of defects in murine Cftr in the susceptibility to Staphylococcus aureus lung disease using mouse models of cystic fibrosis (CF), congenic or inbred strains. METHODS: We describe the histopathological analyses of CF mice repeatedly exposed by aerosolisation to a CF isolate of S. aureus, using residual function Cftr mice and compound heterozygotes generated by intercrossing these with Cftr 'null' mice, all congenic on the C57Bl6/N background. RESULTS: We demonstrate that mice congenic on the C57Bl/6 background develop significantly more severe lung pathology than non-CF littermates in response to repeated exposure to the most frequent early CF lung pathogen S. aureus. Furthermore, reducing the level of Cftr by half in compound heterozygote mice does not impact upon disease severity, even in response to an increased bacterial dose. CONCLUSIONS: These results are consistent with an airway clearance defect, or abnormal inflammatory response secondary to Cftr mutation. These studies confirm the primary role for Cftr mutation in the development of this lung phenotype. In addition, these results demonstrate that a further 50% decrease in residual wild-type Cftr mRNA levels in this model does not impact the severity of the histopathological response to S. aureus, suggesting a critical threshold level for functional CFTR.     

Tumor proliferative fraction in solid malignant neoplasms. A comparative study of Ki-67 immunostaining and flow cytometric determinations.

Tumor proliferative fraction (TPF) has been shown to correlate with prognosis in some malignancies. A method for its determination that is practical, accurate, and reproducible is still being sought. In this comparative study of techniques, TPF values were determined in mirror-image samples of 126 consecutive solid malignant neoplasms using flow cytometry and immunostaining with Ki-67, a monoclonal antibody that recognizes an unknown nuclear antigen expressed during the entire cell proliferation cycle but not in resting cells. The mean TPF values for all cases were 19.5 +/- 15.6% (percentage of tumor cells stained) by Ki-67 (range, 1-86%) and 15.7 +/- 9.6% (S + G2M) by flow cytometry (range, 3-60%), which correlated significantly at r = 0.53 and P = 0.005. The correlation was less strong in tumors with low S-phase values (less than or equal to 10%, r = 0.28) than in tumors with intermediate and high S-phase values (r = 0.66). Ki-67 staining percentages did not correlate with patient age, sex, or tissue origin of the tumor. Ki-67 staining appears comparable to flow cytometry determination of TPF in solid malignancies with intermediate and high S-phase values. In tumors with low S-phase values, Ki-67 immunostaining shows higher TPF values, which perhaps reflect an increase in the proportion of G1-phase cells or dilutional effect of nonneoplastic cells in the tumors with low proliferative fraction.     

Reduction of acetylcholine sensitivity of chick muscle in culture by myasthenia gravis serum

Sera from seven patients with myasthenia gravis and from six control subjects were tested for the presence of anti-acetylcholine receptor antibodies and for the ability to reduce acetylcholine sensitivity of embryonic chick skeletal muscle cells in culture. Anti-receptor antibodies were found in all but one of the myasthenic samples and in none of the control samples. The average reduction in sensitivity caused by the myasthenic sera was 89±4%, compared with an average reduction of 15±7% caused by the control sera. A sample taken from a patient during myasthenic crisis was found to have less blocking activity and less anti-receptor antibody than a sample from the same patient after recovery.     

Immunological adjuvants promote activated T cell survival via induction of Bcl-3

Injection of soluble protein antigen into animals causes abortive proliferation of the responding T cells. Immunological adjuvants boost T cell responses at least in part by increasing the survival of activated T cells during and after the initial proliferative phase of their clonal expansion. To understand how adjuvants promote T cell survival, we used gene microarrays to analyze gene expression in T cells activated either with antigen alone or in the presence of two different adjuvants. Among the genes whose expression was increased by both adjuvants was the IkappaB family member Bcl-3. Retroviral infection experiments showed that expression of Bcl-3 increased survival of activated T cells in vitro and in vivo. Adjuvants may therefore improve survival of activated T cells via induction of Bcl-3.     

Identification of polymorphisms within Disrupted in Schizophrenia 1 and Disrupted in Schizophrenia 2, and an investigation of their association with schizophrenia and bipolar affective disorder

We have undertaken a search for polymorphic sequence variation within Disrupted in Schizophrenia 1 and Disrupted in Schizophrenia 2 (DISC1 and DISC2), which are both novel genes that span a translocation breakpoint strongly associated with schizophrenia and related psychoses in a large Scottish family. A scan of the coding sequence, intron/exon boundaries, and part of the 5' and 3' untranslated regions of DISC1, plus 2.7 kb at the 3' end of DISC2, has revealed a novel microsatellite and 15 novel single nucleotide polymorphisms (SNPs). We have tracked the inheritance of four of the SNPs through multiply affected families, and carried out case-control association studies using the microsatellite and four common SNPs on populations of patients with schizophrenia or bipolar affective disorder versus normal control subjects. Neither co-segregation with disease status nor significant association was detected; however, we could not detect linkage disequilibrium between all these markers in the control population, arguing that an even greater density of informative markers is required to test rigorously for association in this genomic region.