Risk of urinary tract infection in infants and children with acute bronchiolitis

OBJECTIVES:

To estimate the prevalence of urinary tract infection in infants and children with bronchiolitis.

METHODS:

A retrospective cross-sectional study involving patients zero to 24 months of age who were hospitalized with acute bronchiolitis was conducted.

RESULTS:

A total of 835 paediatric patients with acute bronchiolitis were admitted to the paediatric ward between January 2010 and December 2012. The mean (± SD) age at diagnosis was 3.47±2.99 months. There were 325 (39%) girls and 510 (61%) boys. For the purpose of data analysis, the patient population was divided into three groups: group 1 included children hospitalized with respiratory syncytial virus (RSV) bronchiolitis; group 2 included children hospitalized with clinical bronchiolitis with no virus detected; and group 3 included children hospitalized with clinical bronchiolitis due to a respiratory virus other than RSV. Results revealed that urinary tract infection was present in 10% of patients, and was most common in group 3 (13.4%) followed by group 2 (9.7%), and was least common in group 1 (6%) (P=0.030).

CONCLUSIONS:

The possibility of a urinary tract infection should be considered in a febrile child with a diagnosis of bronchiolitis, particularly if the trigger is a respiratory virus other than RSV.     

Genetic System of Artemisia maritima L.: An Overexploited Medicinal Species Under Stress

Proceedings of the National Academy of Sciences, India Section B: Biological Sciences - Artemisia maritima L., a potent source of Santonin (a drug used to expel roundworms), forms isolated...     

Utility of the neutrophil to lymphocyte ratio in predicting long-term outcomes in acute decompensated heart failure

Neutrophil-to-lymphocyte ratio (NLR) has been associated with poor outcomes in patients with acute coronary syndromes. However, its role for risk stratification in acute decompensated heart failure (ADHF) has not been well described. In this study, 1,212 consecutive patients admitted with ADHF who had total white blood cell and differential counts measured at admission were analyzed. The patients were divided into tertiles according to NLR. The association between NLR and white blood cell types with all-cause mortality was assessed using Cox regression analysis. During a median follow-up period of 26 months, a total of 284 patients (23.4%) had died, and a positive trend between death and NLR was observed; 32.8%, 23.2%, and 14.2% of deaths occurred in the higher, middle, and lower tertiles, respectively (p <0.001). After adjusting for confounding factors, multivariate analysis demonstrated that patients in the higher NLR tertile had the highest mortality (adjusted hazard ratio 2.23, 95% confidence interval (CI) 1.63 to 3.02, p <0.001), followed by those in the middle tertile (adjusted hazard ratio 1.62, 95% CI 1.16 to 2.23, p = 0.001). Furthermore, tertiles of NLR were superior in predicting long-term mortality compared with white blood cell, neutrophil, and relative lymphocyte counts. Patients in the higher NLR tertile (adjusted odds ratio 3.46, 95% CI 2.11 to 5.68, p <0.001) had a significantly higher 30-day readmission rate. In conclusion, higher NLR, an emerging marker of inflammation, is associated with an increased risk for long-term mortality in patients admitted with ADHF. NLR is a readily available inexpensive marker to aid in the risk stratification of patients with ADHF.     

Glial S100B Protein Modulates Mutant Ataxin-1 Aggregation and Toxicity: TRTK12 Peptide, a Potential Candidate for SCA1 Therapy

Non-cell autonomous involvement of glial cells in the pathogenesis of polyglutamine diseases is gaining recognition in the ataxia field. We previously demonstrated that Purkinje cells (PCs) in polyglutamine disease spinocerebellar ataxia-1 (SCA1) contain cytoplasmic vacuoles rich in Bergmann glial protein S100B. The vacuolar formation in SCA1 PCs is accompanied with an abnormal morphology of dendritic spines. In addition, S100B messenger RNA (mRNA) expression levels are significantly high in the cerebella of asymptomatic SCA1 transgenic (Tg) mice and increase further with age when compared with the age-matched wild-type animals. This higher S100B mRNA expression positively correlates with an increase in the number of vacuoles. To further characterize the function of S100B in SCA1 pathology, we explored the effects of S100B protein on GFP-ataxin-1 (ATXN1) with expanded polyglutamines [82Q] in HEK stable cell line. Externally added S100B protein to these cells induced S100B-positive vacuoles similar to those seen in SCA1 PCs in vivo. Further, we found that both externally added and internally expressed S100B significantly reduced GFP-ATXN1[82Q] inclusion body formation. In contrast, the addition of S100B inhibitory peptide TRTK12 reversed S100B-mediated effects. Interestingly, in SCA1 Tg mice, PCs containing S100B vacuoles also showed the lack of nuclear inclusions, whereas PCs without vacuoles contained nuclear inclusions. Additionally, TRTK12 treatment reduced abnormal dendritic growth and morphology of PCs in cerebellar slice cultures prepared from SCA1 Tg mice. Moreover, intranasal administration of TRTK12 to SCA1 Tg mice reduced cerebellar S100B levels in the particulate fractions, and these mice displayed a significant improvement in their performance deficit on the Rotarod test. Taken together, our results suggest that glial S100B may augment degenerative changes in SCA1 PCs by modulating mutant ataxin-1 toxicity/solubility through an unknown signaling pathway.     

Elevated augmentation index derived from peripheral arterial tonometry is associated with abnormal ventricular–vascular coupling

Background: Although typically derived from the contour of arterial pressure waveform, augmentation index (AIx) may also be derived from the digital pulse volume waveform using finger plethysmography (peripheral arterial tonometry, PAT). Little is known regarding the physiologic correlates of AIx derived from PAT. In this study, we investigated the relation of PAT‐AIx with measures of ventricular–vascular coupling. Methods: Pulse volume waves were measured via PAT and used to derive AIx. Using 2‐dimensional echocardiography, effective arterial elastance index (EaI) was estimated as end‐systolic pressure/stroke volume index. Left ventricular (LV) end‐systolic elastance index (E_LVI) was calculated as end‐systolic pressure/end‐systolic volume index. Ventricular–vascular coupling ratio was defined as EaI/E_LVI. Results: Given the bi‐directional nature of ventricular–vascular uncoupling as measured by echocardiography, patients were separated into three groups: low EaI/E_LVI (<0·6, n = 21), optimal EaI/E_LVI (mean 0·6–1·2, n = 16) and high EaI/E_LVI (>1·2, n = 10). Adjusting for potential confounders (age, mean arterial pressure, height and heart rate), patients with optimal EaI/E_LVI had lower AIx (1 ± 4%, P<0·05) compared to those with low EaI/E_LVI (13 ± 4%) and high EaI/E_LVI (19 ± 5%). Conclusions: Abnormal ventricular–vascular coupling, arising from either increased effective arterial elastance or increased ventricular elastance, is associated with increased AIx as measured by PAT. Additional research is needed to examine other vascular correlates of PAT‐AIx.