Effectiveness of a Federal Healthy Start Program in Reducing Infant Mortality

Objective: Infant mortality is an important indicator of the health status of a community. In this analysis, we aimed to evaluate temporal changes in infant mortality rates (IMR) in the Central Hillsborough Healthy Start (CHHS) program service area in Tampa, Florida compared to rates in the rest of Hillsborough County and the state. Method: We conducted a five-year (2010-2014) trends analysis using birth and infant death data extracted from the Florida Community Health Assessment Resource Tool Set (CHARTS). The number of infant deaths and live births were used to calculate and compare IMRs in the CHHS catchment area to those in the rest of Hillsborough County, and the state of Florida. Three-year centered moving averages were directly adjusted to account for differences in the racial/ethnic distribution of mothers across geographic areas. Results: Between 2010 and 2014, the IMR decreased 42.8% in the CHHS service area (from 14.5 to 8.3 per 1,000 live births) compared to decreases of 10.1% and 7.7% in the rest of Hillsborough County and the state of Florida, respectively. Additionally, the infant mortality gap in the CHHS catchment area narrowed from 72% in 2010 to 14% in 2014 compared to the rest of the state, and was eliminated when compared to the rest of Hillsborough County. Discussion: The absolute and relative decreases in IMR in the CHHS catchment area reflect the program’s effectiveness in decreasing disparity in infant mortality. The quality services provided by the CHHS program have had a significant positive impact on the families served

Assessment of quality of life in vitiligo patients in terms of clinical severity and psychological burden in a tertiary care hospital: An observational study

Background: Vitiligo is characterized depigmented macules and patches over the skin. It has a major impact on the quality of life (QoL) of patients, many of whom feel distressed and stigmatized by their condition. Aim: To assess QoL in vitiligo patients in terms of clinical severity and psychological burden. Materials and Methods: An observational study on 60 patients with age ≥16 years was conducted at an outpatient department of a tertiary care hospital. Data were collected in a predesigned pro forma. The QoL of patients and family members was assessed using Dermatology Life Quality Index (DLQI) and Family DLQI (FDLQI), respectively. The clinical severity was measured using Vitiligo Area Severity Index (VASI) and psychological burden by Vitiligo Impact Score-22 (VIS-22) questionnaire. Results: Sixty patients were included in the study. The mean age was 35.27 ± 2.24. Male-to-female ratio was 1.1:1. About 51.7% of patients were married. Majority of patients were students (30%). The time of presentation after disease onset was 5 years. About 20% of subjects had positive family history. The common sites were face (75%), lower limb (71.67%), and upper limb (60%), with leukotrichia in 11.7% of patients. The mean VASI score at baseline and at 1-month of follow-up after starting treatment was 4.11 ± 0.38 and 3.59 ± 0.58, respectively. The mean DLQI, FDLQI and VIS-22 score were 11.73 ± 0.80, 10.58 ± 0.71, and 37.32 ± 1.53, respectively. VIS-22 and VASI score correlated with changes in DLQI (P < 0.059). Conclusion: Vitiligo largely impairs the QoL of patients. The more the clinical severity (high VASI score), the higher the psychological burden, impairing QoL of patients, and family members

Oxidative Stress Induces Club Cell Proliferation and Pulmonary Fibrosis in Atp8b1 Mutant Mice

Atp8b1 (ATPase, aminophospholipid transporter, class I, type 8B, member 1) is a cardiolipin transporter in the apical membrane of lung epithelial cells. While the role of Atp8b1 in pneumonia-induced acute lung injury (ALI) has been well studied, its potential role in oxidative stress-induced ALI is poorly understood. We herein show that Atp8b1G308V/G308V mice under hyperoxic conditions display exacerbated cell apoptosis at alveolar epithelium and aberrant proliferation of club cells at bronchiolar epithelium. This hyperoxia-induced ambivalent response in Atp8b1G308V/G308V lungs was followed by patchy distribution of non-uniform interstitial fibrosis at late recovery phase under normoxia. Since this club cell abnormality is commonly observed between Atp8b1G308V/G308V lungs under hyperoxic conditions and IPF lungs, we characterized this mouse fibrosis model focusing on club cells. Intriguingly, subcellular morphological analysis of IPF lungs, using transmission electron microscopy (TEM), revealed that metaplastic bronchiolar epithelial cells in fibrotic lesions and deformed type II alveolar epithelial cells (AECs) in alveoli with mild fibrosis, have common morphological features including cytoplasmic vacuolation and dysmorphic lamellar bodies. In conclusion, the combination of Atp8b1 mutation and hyperoxic insult serves as a novel platform to study unfocused role of club cells in IPF

Oxidative Stress Induces Club Cell Proliferation and Pulmonary Fibrosis in Atp8b1 Mutant Mice

Atp8b1 (ATPase, aminophospholipid transporter, class I, type 8B, member 1) is a cardiolipin transporter in the apical membrane of lung epithelial cells. While the role of Atp8b1 in pneumonia-induced acute lung injury (ALI) has been well studied, its potential role in oxidative stress-induced ALI is poorly understood. We herein show that Atp8b1G308V/G308V mice under hyperoxic conditions display exacerbated cell apoptosis at alveolar epithelium and aberrant proliferation of club cells at bronchiolar epithelium. This hyperoxia-induced ambivalent response in Atp8b1G308V/G308V lungs was followed by patchy distribution of non-uniform interstitial fibrosis at late recovery phase under normoxia. Since this club cell abnormality is commonly observed between Atp8b1G308V/G308V lungs under hyperoxic conditions and IPF lungs, we characterized this mouse fibrosis model focusing on club cells. Intriguingly, subcellular morphological analysis of IPF lungs, using transmission electron microscopy (TEM), revealed that metaplastic bronchiolar epithelial cells in fibrotic lesions and deformed type II alveolar epithelial cells (AECs) in alveoli with mild fibrosis, have common morphological features including cytoplasmic vacuolation and dysmorphic lamellar bodies. In conclusion, the combination of Atp8b1 mutation and hyperoxic insult serves as a novel platform to study unfocused role of club cells in IPF

The Role of Club Cell Phenoconversion and Migration in Idiopathic Pulmonary Fibrosis

Idiopathic pulmonary fibrosis (IPF) is an age-related multifactorial disease featuring non-uniform lung fibrosis. The decisive cellular events at early stages of IPF are poorly understood. While the involvement of club cells in IPF pathogenesis is unclear, their migration has been associated with lung fibrosis. In this study, we labeled club cells immunohistochemically in IPF lungs using a club cell marker Claudin-10 (Cldn10), a unique protein based on the recent report which demonstrated that the appearance of Cldn10 in developing and repairing lungs precedes other club cell markers including club cell secretory protein (CCSP). Cldn10-positive cells in IPF lungs displayed marked pleomorphism and were found in varied arrangements, suggesting their phenoconversion. These results were corroborated by immunogold labeling for Cldn10. Further, immunohistochemical double-labeling for Cldn10 and α-smooth muscle actin (α-SMA) demonstrated that aberrant α-SMA signals are frequently encountered near disorganized Cldn10-positive cells in hyperplastic bronchiolar epithelium and thickened interstitium of IPF lungs. Collectively, these data indicate that club cells actively participate in the initiation and progression of IPF through phenoconversion involving the acquisition of proliferative and migratory abilities. Thus, our new findings open the possibility for club cell-targeted therapy to become a strategic option for the treatment of IPF