Objective Persistent pulmonary hypertension of the newborn (PPHN) is a critical condition with high mortality and morbidity rates in neonatal intensive care unit (NICU) admitted neonates due to severe hypoxemia. The aim of this study was to evaluate red cell distribution width (RDW) as a biomarker of hypoxemia and determine the optimal cutoff point of RDW for identifying neonates with PPHN. Study Design All PPHN diagnosed, NICU admitted term infants with hypoxemia after birth from May 2014 to September 2016 were enrolled as case control and healthy term infants with nonhemolytic jaundice who were admitted for phototherapy on the second or third day of birth were the control group. Blood samples were collected. Multiple logistic regression modeling was used to examine the association between PPHN and RDW. Results Receiver-operating characteristics (ROC) curve analysis was used to determine the optimal cutoff point of RDW for identifying neonates with PPHN. RDW was higher in the PPHN group compared with the control group (p < 0.001). Significant predictors of PPHN were mother's underlying disease (p = 0.01) and RDW (p < 0.001). The optimal RDW cut point for prediction of PPHN by the ROC curve analysis was 17.9 (sensitivity = 85.71%). RDW's area under the curve was 0.9197 (p < 0.001). Conclusion RDW may be a simple, valuable, accessible marker for predicting PPHN before performing echocardiography in hypoxemic NICU admitted neonates.

Background To identify a standard protocol for managing extravasation injuries in neonates. Methods We recruited all the neonates with extravasation wounds from the neonatal intensive care unit of Shariati hospital, Tehran, Iran, between October 2018 and October 2020. Sixteen patients with grade 3–4 extravasation were evaluated in this retrospective study. All grade 3 and 4 extravasation wounds were injected with hyaluronidase at 5 points of the wound circle; the procedure was repeated every 5 min at different points in a smaller circle to the core. The wound was then covered with a warm compress for 24 h. Twenty-four hours after injection, the cover was changed twice a day with normal saline irrigation. Fibrinolysin ointment was applied on top of the wound. The ulcer was then dressed with phenytoin ointment until healing. Results Out of 16 neonates who were followed up, 10 of them were male, with the average birth weight being 1.37 (range 1.05–3.75) kg. The mean (± SD) wound healing duration was 13.12 (± 6) (range: 7–29) days. Factors including the cannulation duration before the appearance of the lesion (R:0.2, P = 0.2), birth weight (R = -.37, P = 015), and extravasated substances (p = 0.2) were not associated with the duration of hospital stay. The only exception to this trend is the wound size factor of 7.31(± 7.45) (R = .83, P < 0.001). Continuous and categorical variables were summarized as mean (SD) and proportions, respectively, and the Kruskal–Wallis test and Spearman correlation coefficients were used. Conclusions Limited evidence exists on the effects of different protocols on extravasation management in neonates in the NICU. We recommend our method as a standard protocol in NICU for high-stage extravasated lesions because of the shorter duration of healing, non-invasive nature of this procedure, and lack of side effects or surgical involvement.

Vargas KJ, Schrod N, Davis T, et al. Synucleins have multiple effects on presynaptic architecture. Cell Rep 2017;18(1):161-173.Point mutations in a-synuclein can reproduce symptoms resembling sporadic Parkinson's disease in both humans and mice. The strategic distribution of the small-sized ubiquitous alpha, beta, and gamma isoforms of this protein is known to alter synaptic membrane trafficking and interfere with synaptic vesicles' exocytosis. This happens as a result of synuclein's unique ability to induce, detect, and respond to synaptic membrane conformational changes and regulate phospholipase D2 and the amount of SNARE complex in synaptic terminals. 1 Through immunoelectron microscopy and cryoelectron tomography on wild-type, synuclein-null, and overexpressing mutant a-synuclein synaptic terminals, Vargas and colleagues 2 were able to provide novel insights into the crucial architectural alterations in the synaptic terminal and the presynaptic cytomatrix in PD associated with the synuclein molecule. Surprisingly, they revealed that the majority of a-synuclein particles (74.2%) were natively localized on synaptic vesicle membranes rather than the synaptic membrane alone. Synuclein deletion reduced the synaptic span and vesicle size while increasing the density of active zone vesicles. Axial distribution of synaptic vesicles was unaltered and signs of release defect, reduced number of "docked" vesicles (zone 1 from the synaptic surface, 0-45 nm), were not identified in synuclein-null slices compared to the wild type.Furthermore, synuclein-null synapses had more tethers in total and in proximal synaptic vesicles and a significantly shortened length of tethers (<5 nm) in cryoelectron tomography. When addressing changes in the readily releasable pool (RRP) of neurotransmitters in the docked synaptic vesicles of mice, they found that the fraction of multiply tethered synaptic vesicles (RRP) was increased by 3-to 4fold in synuclein-free synapses. Protein linkages between synaptic vesicles that form them into clusters(connectors) were decreased in the proximal and intermediate zone, but not in the distal pool of the synaptosome, where the synaptic vesicle clusters belonged to the RRP pool. Together these denote a distal shift in the active synaptic vesicles pool in abg Syn-null mice, a phenomenon reversed by the introduction of wild-type human a-synuclein.Vargas et al also revealed that the point mutation of PARK1/hA30P increased a-synuclein synaptic expression, induced shorter tethers and more synaptic vesicles aggregated by tethers resembling mirror synuclein-null properties. The PARK4/ha-syn mutation, however, affected the synaptic cytomatrix and interfered with neurotransmitter release. Through this final step they validate their results, underscoring synucleins as crucial players in synaptic pathophysiology in Parkinson's disease from structural and functional standpoints.

Background: Neurologic dysfunctions, specifically hearing impairments due to hyperbilirubinemia are ranked among the main concerns in medicine. Objectives: This study evaluates the prevalence of acute auditory neuropathy (AN) disorders in term neonates with mild to moderate hyperbilirubinemia and low bilirubin-induced neurological dysfunction (BIND) score and the roll of early treatment on reducing their incidence.Methods: Fifty one term jaundice neonates with normal newborn exam and total serum bilirubin (TSB) ≥ 15 mg/dL after the third day of birth with normal otoacoustic emission (OAE) test were enrolled. The BIND score assessment for severity of neurologic dysfunction was done. Neonates with low BIND score were divided into two groups based on their TSB levels at the time of admission (15 -18 mg/dL: Mild-moderate hyperbilirubinemia and ≥ 19 mg/dL: Severe hyperbilirubinemia). ABR was performed within the first 12 hours of their admission and the second ABR was performed before discharge. Results: The 30.60% of neonates with TSB < 19 mg/dl had abnormal ABR. Latency of V, III waves and interpeak interval latency of I-III, I-V waves were detected. Mean latency of wave V and I-V interpeak latency after phototherapy were significantly decreased compared to pre-treatment (P < 0.001). Conclusions:With the prevalence of auditory neuropathy (AN) at lower TSB concentrations (that have traditionally been considered safe) it can be concluded that more attention should be given to this group despite the absence of neurologic signs, and it also shows the sensitivity of early phototherapy to lower bilirubin level.