Normative data for certain vocal fold biomarkers among young normophonic adults using ultrasonography.

PURPOSE: The current study aimed to profile vocal fold morphology, vocal fold symmetry, gender and task-specific data for vocal fold length (VFL) and vocal fold displacement velocity (VFDV) in young normophonic adults in the age range of 18-30 years using ultrasonography (USG). METHODS: Participants underwent USG across quiet breathing, /a/ phonation and /i/ phonation tasks, and acoustic analysis was conducted to explore the relationship between USG and acoustic measures. RESULTS: The study found that males have longer vocal folds than females, and overall greater velocities were observed in /a/ phonation, followed by /i/ phonation, with the lowest velocity observed in the quiet breathing task. CONCLUSIONS: The obtained norms can be used as a quantitative benchmark for analyzing the vocal fold behavior in young adults.

Effects of Infant Driven Feeding Program on Provision of Breast Milk in Very Low Birth Weight Infants.

Background: The ability to complete nipple feedings is one of the discharge criteria for most premature neonates. The Infant Driven Feeding (IDF) program suggests a system of objective promotion of oral feeds in premature infants. There is a lack of studies systematically studying the effects of IDF on the provision of breast milk. Methods: This was a retrospective study of all premature infants born before 33 weeks and birth weight of <1,500 g admitted to a level IV neonatal intensive care unit. Infants on IDF were compared with those not on IDF. Results: A total of 46 infants in the IDF group and 52 in the non-IDF group met the inclusion criteria. A higher number of infants in the IDF group breastfed at first oral attempt (54% versus 12%). Forty-five percent of IDF mothers completed a full 72 hours of protected breastfeeding at the start of oral feeds, and IDF infants had earlier removal of nasogastric (NG) tube. There was no difference in the provision of breast milk and/or breastfeeding on discharge between the two groups. There was no difference in the length of stay between the two groups. Conclusion: The IDF program attempts to streamline the promotion of oral feeds in very low birth weight infants. Higher incidence of breastfeeding at the start of oral feeds and earlier removal of NG tube did not translate into higher provision of breast milk on discharge in very low birth weight infants in the IDF group. Prospective randomized trials are needed to validate cue-based infant driven feeding programs and their effects on the provision of breast milk.

HJC0416 Attenuates Fibrogenesis in Activated Hepatic Stellate Cells via STAT3 and NF-κB Pathways.

BACKGROUND: Hepatic fibrosis is wound-healing response that is the result of hepatic stellate cell (HSC) activation and subsequent excess extracellular matrix deposition. HSCs can be activated by a variety of inflammatory stimuli as well as through the signal transducer and activator of transcription 3 (STAT3) pathway. HJC0416 is a novel, orally bioavailable small-molecule inhibitor of STAT3 that was developed by our team using a fragment-based drug design approach. Previously, our team has shown that HJC0416 has antifibrogenic effects in activated HSCs. Recently, increasing evidence suggests that nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) plays an important role in the activation of HSCs. In the present study, we examined the role of NF-κB inhibition of HSC activation by HJC0416. METHODS: LX-2 (human) and HSC-T6 (rat) cell lines were used. Expression levels of extracellular proteins, NF-κB and STAT3 expression and DNA binding, and inflammatory cytokine levels were determined using western blot, ELISA, and immunofluorescence assay. RESULTS: HJC0416 decreased cell viability in a dose-dependent manner in both cell lines and arrested the cell cycle at the S phase. Increased apoptosis was seen in LX-2 cells through Yo-Pro-1 and propidium iodide immunofluorescent stating. HJC0416 significantly decreased expression of fibronectin and collagen I as well as markedly decreased α-SMA and laminin. HJC0416 inhibited the STAT3 pathway by decreasing phosphorylation of STAT3, as well as signal transduction pathway activation. Notably, HJC0416 also inhibited the classic and alternative pathways of NF-κB activation. HJC0416 inhibited LPS-induced p65 nuclear translocation and DNA binding, as well as prevented phosphorylation and degradation of inhibitory protein IκBα. HJC0416 also prevented phosphorylation of serine residue 536 on p65. CONCLUSIONS: HJC0416, an inhibitor of STAT3, was found to have antifibrogenic properties in activated hepatic stellate cell lines. In addition, HJC0416 was found to inhibit the NF-κB pathway. Owing to this double effect, HJC0416 demonstrates promise for in vivo experimentation as an antifibrosis treatment.