Congenital cytomegalovirus infection and the risk of hearing loss in childhood: A PRISMA-compliant meta-analysis.

BACKGROUND: Congenital cytomegalovirus (cCMV) infection is the most common cause of childhood hearing loss (HL), although the strength of this association remains limited and inconclusive. Thus, the purpose of this study was to summarize evidence regarding the strength of the relationship between cCMV and childhood HL and to determine whether this relationship differs according to patient characteristics. METHODS: The PubMed, EmBase, and Cochrane Library databases were searched for studies evaluating the relationship between cCMV and HL from inception to September 2019. Odds ratios (ORs) and corresponding 95% confidence intervals (CIs) were used to calculate the investigated outcomes in a random-effects model. Sensitivity, subgroup, and publication bias analyses were also performed. RESULTS: A total of 15 studies involving 235,026 children met the inclusion criteria and were included in the final analysis. The summary results indicated that cCMV infection was associated with an increased risk of HL (odds ratio [OR]: 8.45; 95% confidence interval [CI]: 3.95-18.10; P < .001), irrespective of whether studies reported sensorineural HL (OR: 5.42; 95% CI: 1.98-14.88; P = .001), or did not evaluate HL types among their patients (OR: 11.04; 95% CI: 3.91-31.16; P < .001). However, in studies conducted in the United States (P < 0.001) and published in or after 2000 (P = 0.026), the study populations included <60% males (P < 0.001). Moreover, studies of high quality (P < .001) demonstrated a significantly greater risk of HL with cCMV infection than that in the corresponding subgroups. CONCLUSIONS: The study results suggest that cCMV infection increases the risk of HL. Further studies are required to investigate the association of cCMV infection with the risk of specific subtypes of HL.

The role of peroxisome proliferator-activated receptor gamma and adiponectin in children with Kawasaki disease.

OBJECTIVE: To investigate the relationship between peroxisome proliferator-activated receptor gamma (PPARγ) mRNA, serum adiponectin (ADP) and lipids in paediatric patients with Kawasaki disease (KD). METHODS: This prospective study enrolled paediatric patients with KD and grouped them according to the presence or absence of coronary artery lesions (CAL). A group of healthy age-matched children were recruited as the control group. The levels of PPARγ mRNA, serum ADP and lipids were compared between the groups. Receiver operating characteristic (ROC) curve analysis was undertaken to determine if the PPARγ mRNA level could be used as a predictive biomarker of CAL prognosis. RESULTS: The study enrolled 42 patients with KD (18 with CAL [CAL group] and 24 without CAL [NCAL group]) and 20 age-matched controls. PPARγ mRNA levels in patients with KD were significantly higher than those in the controls; but significantly lower in the CAL group than the NCAL group. ROC curve analysis demonstrated that the PPARγ mRNA level provided good predictive accuracy for the prognosis of CAL. There was no association between PPARγ, ADP and lipid levels. CONCLUSION: There was dyslipidaemia in children with KD, but there was no correlation with PPARγ and ADP. PPARγ may be a predictor of CAL in patients with KD with good predictive accuracy.

Association between Alzheimer's disease pathogenesis and early demyelination and oligodendrocyte dysfunction.

The APPSwe/PSEN1dE9 (APP/PS1) transgenic mouse model is an Alzheimer's disease mouse model exhibiting symptoms of dementia, and is commonly used to explore pathological changes in the development of Alzheimer's disease. Previous clinical autopsy and imaging studies suggest that Alzheimer's disease patients have white matter and oligodendrocyte damage, but the underlying mechanisms of these have not been revealed. Therefore, the present study used APP/PS1 mice to assess cognitive change, myelin loss, and corresponding changes in oligodendrocytes, and to explore the underlying mechanisms. Morris water maze tests were performed to evaluate cognitive change in APP/PS1 mice and normal C57BL/6 mice aged 3 and 6 months. Luxol fast blue staining of the corpus callosum and quantitative reverse transcription-polymerase chain reaction (qRT-PCR) for myelin basic protein (MBP) mRNA were carried out to quantify myelin damage. Immunohistochemistry staining for NG2 and qRT-PCR for monocarboxylic acid transporter 1 (MCT1) mRNA were conducted to assess corresponding changes in oligodendrocytes. Our results demonstrate that compared with C57BL/6 mice, there was a downregulation of MBP mRNA in APP/PS1 mice aged 3 months. This became more obvious in APP/PS1 mice aged 6 months accompanied by other abnormalities such as prolonged escape latency in the Morris water maze test, shrinkage of the corpus callosum, upregulation of NG2-immunoreactive cells, and downregulation of MCT1 mRNA. These findings indicate that the involvement of early demyelination at 3 months and the oligodendrocyte dysfunction at 6 months in APP/PS1 mice are in association with Alzheimer's disease pathogenesis.