Patient characteristics of pediatric inpatients with sensorineural hearing loss: Insights from the 2016 KID database.

This study examines how patient demographics impact pediatric sensorineural hearing loss (SNHL) prevalence using the 2016 Kids' Inpatient Database (KID). By analyzing age, gender, race, income, insurance, and region, the study provides insights for early intervention and diagnosis. Multivariate regression analysis reveals associations between these factors and SNHL occurrence. OBJECTIVE: This study aims to assess the influence of patient demographics on pediatric SNHL prevalence, offering guidance for early detection and intervention strategies. STUDY DESIGN: Using 2016 KID data, this retrospective analysis investigates how patient factors like age, gender, race, income, insurance, and region relate to SNHL prevalence. Multivariate regression is employed to control for potential confounders. METHODS: Data from 6,266,285 patient discharges, including 9997 hearing loss cases, are analyzed. SNHL prevalence is calculated, and demographic variables are examined. Weighted odds ratios and multivariate regression are used to assess associations. RESULTS: The study finds an overall SNHL prevalence of 101.67 cases per 100,000 discharges in 2016. Non-Hispanic White patients show the highest prevalence. Black patients are more likely to be diagnosed, while Hispanic patients are less likely. Multivariate analysis highlights race, income, insurance, region, age, and sex as significant confounders. CONCLUSION: This study underscores the impact of patient demographics on pediatric SNHL prevalence. Factors like race, income, insurance, and region play a role. These findings aid in risk assessment, early identification, and tailored interventions. Further research can uncover socioeconomic disparities and underlying mechanisms.

Understanding pediatric inpatient conductive hearing loss: An analysis of patient demographics.

OBJECTIVE: Hearing loss is a common sensory impairment in children that affects quality of life and development. Early intervention, such as hearing aids and communication therapies, can help children overcome these challenges and lessen the impact on their development. The objective of this study was to identify specific patient demographic factors correlated with the prevalence of pediatric conductive hearing loss. STUDY DESIGN: The study utilized the Kids' Inpatient Database (KID) by the Agency for Healthcare Research and Quality which collects inpatient information from hospitals for patients under 21 years old. We included all patients discharged in 2016 diagnosed with conductive hearing loss, and excluded neonatal patients discharged within 28 days of birth. METHODS: Statistical analyses were performed using R Studio and IBM SPSS Statistics. Weighted odds ratios were calculated for conductive hearing loss in relation to race and income, and a multivariate regression analysis examined associations between demographic variables and race categories in conductive hearing loss. RESULTS: The prevalence of conductive hearing loss (CHL) in pediatric patients in 2016 was 51.62 cases per 100,000 patients. Non-Hispanic White patients had the highest prevalence, while Black patients had the highest likelihood of CHL compared to the overall population. Lower income levels were associated with a decreased probability of CHL diagnosis. After adjusting for age, sex, hospital region, insurance, and income on multivariate analysis, White and Black patients were less likely to be diagnosed with CHL. Furthermore, patients in specific income quartiles also had lower CHL likelihood compared to the general population. CONCLUSION: While Black patients had a higher likelihood of being diagnosed with CHL than the general population, socioeconomic factors such as income greatly influenced the likelihood of CHL diagnosis. Other significant factors included income, region of the country, sex, and age. Further research is needed to better understand and address healthcare disparities related to pediatric hearing loss.

Inhibition of MCU forces extramitochondrial adaptations governing physiological and pathological stress responses in heart.

Myocardial mitochondrial Ca(2+) entry enables physiological stress responses but in excess promotes injury and death. However, tissue-specific in vivo systems for testing the role of mitochondrial Ca(2+) are lacking. We developed a mouse model with myocardial delimited transgenic expression of a dominant negative (DN) form of the mitochondrial Ca(2+) uniporter (MCU). DN-MCU mice lack MCU-mediated mitochondrial Ca(2+) entry in myocardium, but, surprisingly, isolated perfused hearts exhibited higher O2 consumption rates (OCR) and impaired pacing induced mechanical performance compared with wild-type (WT) littermate controls. In contrast, OCR in DN-MCU-permeabilized myocardial fibers or isolated mitochondria in low Ca(2+) were not increased compared with WT, suggesting that DN-MCU expression increased OCR by enhanced energetic demands related to extramitochondrial Ca(2+) homeostasis. Consistent with this, we found that DN-MCU ventricular cardiomyocytes exhibited elevated cytoplasmic [Ca(2+)] that was partially reversed by ATP dialysis, suggesting that metabolic defects arising from loss of MCU function impaired physiological intracellular Ca(2+) homeostasis. Mitochondrial Ca(2+) overload is thought to dissipate the inner mitochondrial membrane potential (ΔΨm) and enhance formation of reactive oxygen species (ROS) as a consequence of ischemia-reperfusion injury. Our data show that DN-MCU hearts had preserved ΔΨm and reduced ROS during ischemia reperfusion but were not protected from myocardial death compared with WT. Taken together, our findings show that chronic myocardial MCU inhibition leads to previously unanticipated compensatory changes that affect cytoplasmic Ca(2+) homeostasis, reprogram transcription, increase OCR, reduce performance, and prevent anticipated therapeutic responses to ischemia-reperfusion injury.

Appointment Factors Contributing to Children with Speech Disorders Missing Speech and Language Pathology Appointments.

This study explores missed pediatric speech and language pathology (SLP) appointments to identify barriers for patients with speech disorders. Data from 839 referrals at Boston Medical Center, including demographics, appointment details, COVID-19 lockdown, and number of items on patient problem lists, were analyzed using chi-square tests and logistic regression. The findings revealed that lockdown status, appointment timing, appointment type (in-person vs telemedicine), referral department (ear, nose, and throat [ENT] vs non-ENT), sex, race, primary language, birthplace, and primary care provider presence had no significant impact on attendance. However, the number of patient-listed problems, prior cancelations, and missed appointments were significant predictors of patients who did not keep appointments. In conclusion, this research emphasizes the patient's problem list and past appointment behavior as critical factors in predicting missed SLP appointments for pediatric speech disorder patients. These insights can guide targeted interventions to improve attendance and enhance SLP engagement.

An Analysis of Laryngomalacia and Its Interplay With Obesity and Obstructive Sleep Apnea in Pediatric Inpatients.

Objective  This study aimed to investigate the potential relationship between laryngomalacia and obesity as well as explore the interplay between laryngomalacia and obstructive sleep apnea using the Kids' Inpatient Database (KID) for the year 2016. Methods The Healthcare Cost and Utilization Project (HCUP) KID for 2016 provided a dataset for analysis. Patient demographics, diagnoses, and hospital characteristics were considered. Patients less than three years old were included due to the high prevalence of laryngomalacia in this age group. Results Among 4,512,196 neonatal admissions, 1,341 obesity cases and 11,642 laryngomalacia cases were analyzed. The frequency of laryngomalacia in patients with obesity was 578.1% higher than in the general population. Patients with obstructive sleep apnea (OSA) exhibited a 5,243.2% increase in laryngomalacia frequency compared to the overall population. Combining obesity and laryngomalacia resulted in a 6,738.5% increase in OSA frequency. Conclusions This study identified a significant correlation between obesity and increased laryngomalacia risk. The findings have important clinical implications for pediatric care, emphasizing the need to prevent childhood obesity to reduce laryngomalacia risk. Additionally, understanding these risk factors enables better risk stratification for laryngomalacia and potential OSA development.

Mitochondrial CaMKII causes adverse metabolic reprogramming and dilated cardiomyopathy.

Despite the clear association between myocardial injury, heart failure and depressed myocardial energetics, little is known about upstream signals responsible for remodeling myocardial metabolism after pathological stress. Here, we report increased mitochondrial calmodulin kinase II (CaMKII) activation and left ventricular dilation in mice one week after myocardial infarction (MI) surgery. By contrast, mice with genetic mitochondrial CaMKII inhibition are protected from left ventricular dilation and dysfunction after MI. Mice with myocardial and mitochondrial CaMKII overexpression (mtCaMKII) have severe dilated cardiomyopathy and decreased ATP that causes elevated cytoplasmic resting (diastolic) Ca2+ concentration and reduced mechanical performance. We map a metabolic pathway that rescues disease phenotypes in mtCaMKII mice, providing insights into physiological and pathological metabolic consequences of CaMKII signaling in mitochondria. Our findings suggest myocardial dilation, a disease phenotype lacking specific therapies, can be prevented by targeted replacement of mitochondrial creatine kinase or mitochondrial-targeted CaMKII inhibition.

What Neuroscientific Studies Tell Us about Inhibition of Return.

An inhibitory aftermath of orienting, inhibition of return (IOR), has intrigued scholars since its discovery about 40 years ago. Since then, the phenomenon has been subjected to a wide range of neuroscientific methods and the results of these are reviewed in this paper. These include direct manipulations of brain structures (which occur naturally in brain damage and disease or experimentally as in TMS and lesion studies) and measurements of brain activity (in humans using EEG and fMRI and in animals using single unit recording). A variety of less direct methods (e.g., computational modeling, developmental studies, etc.) have also been used. The findings from this wide range of methods support the critical role of subcortical and cortical oculomotor pathways in the generation and nature of IOR.

A motivationally-based simulation of performance degradation under pressure.

The CLARION cognitive architecture has been shown to be capable of simulating and explaining a wide range of psychological tasks and data. Currently, two theories exist to explain the psychological phenomenon of performance degradation under pressure: the distraction theory and the explicit-monitoring theory. However, neither provides a detailed mechanistic explanation of the exact processes involved. We propose such a detailed theory within the CLARION cognitive architecture that takes into account motivation and the interaction between explicit and implicit processes. We then use our theory to provide a plausible explanation of some existing data. The data are simulated using the theory within the CLARION cognitive architecture.