Excessive body weight is associated with additional loss of quality of life in children with asthma

BACKGROUND: Asthma and excessive body weight frequently coexist, whereas the exact relationship between the 2 diseases is unknown. OBJECTIVE: To study whether asthma combined with excessive body weight has a greater effect on quality of life in children than the separate effects of asthma or excessive body weight alone. METHODS: In a cross-sectional design, 1758 school children (age 7-10 years) participated: 4 study groups were composed of children with asthma and with/without excessive body weight, and healthy controls with/without excessive body weight. Diagnosis of asthma was defined by either a doctor's diagnosis or by core questions of the International Study of Asthma and Allergies in Childhood questionnaire in combination with either reversible airway obstruction or bronchial hyperresponsiveness. Excessive body weight was defined by using international cutoff points for body mass index. Quality of life was evaluated by the Pediatric Asthma Quality of Life Questionnaire. RESULTS: For all domains of quality of life, children with both asthma and excessive body weight had lower scores than children with either asthma alone or excessive body weight alone. Compared with healthy controls, the score was 25% lower in children with asthma and excessive body weight, 14% lower in children with asthma and normal weight, and only 1% lower in overweight controls. CONCLUSION: Excessive body weight is associated with an additional decrease in quality of life in children with asthma. CLINICAL IMPLICATIONS: Clinicians should be aware of the interaction between asthma and excessive body weight and the effect on quality of life and should give extra attention to children with both conditions.     

Direct electrical stimulation of the optic radiation in patients with covered eyes

Direct electrical stimulation (DES) of the optic radiation (OR) during an awake tumor resection has been repeatedly reported. In all cases, visual function monitoring was performed in patients with open eyes which were looking at a picture. We report a new modification of the standard method, OR stimulation in patient with closed and covered eyes. To the best of our knowledge, this method was not presented before. According to our first experience, this methodology may be in some cases a potentially more sensitive form of neuromonitoring than the OR stimulation in patients with open eyes, as the phosphenes elicited by DES may be more distinct in patients with covered eyes. The technique is discussed, and a literature review on intraoperative identification of the OR is presented as well. However, a future prospective study is needed to confirm the relevance of our finding.     

Impaction bone grafting and a cemented cup after acetabular fracture

Purpose

Patients suffering from post traumatic osteoarthritis of the acetabulum often require a total hip arthroplasty at a relatively young age. Long-term data outcome studies for this population are lacking. We report on the long-term outcome of 20 acetabular fractures in 20 patients treated with impaction bone grafting and a cemented cup after a mean follow-up of 18 years (range, 12–26 years).

Methods

The group consisted of 14 males (70 %) and six females (30 %) with an average age of 53.3 years (range, 35–75 years) at time of surgery. No patients were lost to follow-up. Four patients died and three patients underwent a revision; at review 13 patients were still living with their implant in situ. Survivorship analysis was performed at 20 years follow-up for three endpoints.

Results

Survival rate with endpoint revision for any reason at 20 years postoperative was 74.7 % (95 % confidence interval (CI), 40–91 %), 80.0 % (95 % CI, 41–95 %) for endpoint aseptic loosening, and 63.9 % (95 % CI 32–84 %) for endpoint radiographic failure. Three acetabular components were revised at 14.5, 15.3, and 16.7 years postoperative. Two cups failed for aseptic loosening and one cup failed due to septic loosening. The average postoperative Harris hip score was 82 (range, 56–100).

Conclusion

Acetabular reconstruction with impaction bone grafting and the use of a cemented cup after acetabular fracture is an attractive technique with acceptable long-term results and a low complication and re-operation rate.     

Use of EEG to Diagnose ADHD

Electroencephalography (EEG) has, historically, played a focal role in the assessment of neural function in children with attention deficit hyperactivity disorder (ADHD). We review here the most recent developments in the utility of EEG in the diagnosis of ADHD, with emphasis on the most commonly used and emerging EEG metrics and their reliability in diagnostic classification. Considering the clinical heterogeneity of ADHD and the complexity of information available from the EEG signals, we suggest that considerable benefits are to be gained from multivariate analyses and a focus towards understanding of the neural generators of EEG. We conclude that while EEG cannot currently be used as a diagnostic tool, vast developments in analytical and technological tools in its domain anticipate future progress in its utility in the clinical setting.     

Pro-inflammatory cytokines favor the emergence of ETV6-RUNX1-positive pre-leukemic cells in a model of mesenchymal niche

ETV6-RUNX1 (E/R) fusion gene, arising in utero from translocation t(12;21)(p13:q22), is the most frequent alteration in childhood acute lymphoblastic leukemia (ALL). However, E/R is insufficient to cause overt leukemia since it generates a clinically silent pre-leukemic clone which persists in the bone marrow but fails to out-compete normal progenitors. Conversely, pre-leukemic cells show increased susceptibility to transformation following additional genetic insults. Infections/inflammation are the most accredited triggers for mutations accumulation and leukemic transformation in E/R⁺ pre-leukemic cells. However, precisely how E/R and inflammation interact in promoting leukemia is still poorly understood. Here we demonstrate that IL6/TNFα/ILβ pro-inflammatory cytokines cooperate with BM-MSC in promoting the emergence of E/R⁺ Ba/F3 over their normal counterparts by differentially affecting their proliferation and survival. Moreover, IL6/TNFα/ILβ-stimulated BM-MSC strongly attract E/R⁺ Ba/F3 in a CXCR2-dependent manner. Interestingly, E/R-expressing human CD34⁺IL7R⁺ progenitors, a putative population for leukemia initiation during development, were preserved in the presence of BM-MSC and IL6/TNFα/ILβ compared to their normal counterparts. Finally, the extent of DNA damage increases within the inflamed niche in both control and E/R-expressing Ba/F3, potentially leading to transformation in the apoptosis-resistant pre-leukemic clone. Overall, our data provide new mechanistic insights into childhood ALL pathogenesis.     

Angiotensin II induces mitochondrial dysfunction and promotes apoptosis via JNK signalling pathway in primary mouse calvaria osteoblast

Objectives

This present study was designed to investigate the effects of Angiotensin II on mitochondrial functions, ROS generation and c-jun N-terminal kinases (JNK) signalling pathway-mediated cell apoptosis in mouse calvaria osteoblasts.

Methods

Calvaria osteoblast were isolated and cultured. The cells were separated into two groups—control and treated groups—where the latter was stimulated with angiotensin II (Ang II). Mitochondrial reactive oxygen species (ROS) and superoxide production were measured. Intracellular ATP levels were also detected. The cell proliferation rate was determined for the two groups. Protein production such as Anti-Bax, Bcl-2, COX IV and activation of c-jun N-terminal kinases signal (JNK) pathway was measured by enzyme-linked immunosorbent assay (ELISA) methods and Western blotting in this study.

Results

Ang II treated cells showed significantly higher levels of superoxide production compared to the control group (p < 0.05). Conversely, Ang II induced inhibitory effects on mitochondrial respiratory enzyme complexes, cause membrane potential dissipation, ATP loss and promote ROS generation, cell apoptosis in cultured osteoblasts. In addition, JNK phosphorylations were involved in activating the mitochondria-dependent apoptotic pathway following Ang II stimulation, as pre-treatment of JNK-specific inhibitor SP600125 could rescue osteoblast cells from apoptosis by enhancing the anti-apoptotic protein Bcl-2 expressions, suppressing the translocation of Bax from cytosol into mitochondria, blocking cytochrome C release and caspase-3 activation.

Conclusions

Ang II stimulates osteoblast apoptosis via suppression of the mitochondrial respiratory enzymes, membrane potential and cellular ATP productions. Clinical application with Ang II-stimulated osteoblast could be used for modelling or bone resorption in the oral region.