Thermoregulation of Premature Infants during and after Skin-to-Skin Care.

OBJECTIVE: Providing normothermia is an important issue in daily routine care of premature neonates. We recently found with infrared thermography (IRT) a drop in skin temperature of premature babies after they were positioned from skin-to-skin care (SSC) back into the incubator. Since this did not disappear within 10 min, we wanted to find out how long it takes until the baby has fully warmed up after SSC and if the IRT measurements correlate with conventional rectal temperature? STUDY DESIGN: A prospective observational study was undertaken with 5 premature infants [3 male, median gestational age 28 weeks (25-29), median age at study 34 d (28-52), median birth weight 898 g (400-1095), median weight at study 1263 g (790-1465)], temperature was determined with IRT (leg, back, arm, head, upper abdomen; diameter 1 cm, scale 0.00°C), comparison with 2 conventional sensors and rectal temperature. Temperatures were recorded every 2 min and displayed for 4 time points, namely at the beginning and the end of skin-to-skin care (SSC1, SSC2), as well as at the beginning and the end of a subsequent 60 min incubator period (I). RESULTS: A significant rise during SSC occurred while the cooling after SSC persisted during the complete incubator measurement time (I; p<0.05). Rectal temperature remained stable through the whole measuring period. CONCLUSION: While SSC in our setting led to an increase in temperature, the lack of compensation of peripheral heat loss in the incubator after 60 min may express an inadequate peripheral regulation of body temperature. This should be taken into account before routine care after SSC.

Neuronal expression of class 6 semaphorins in zebrafish.

Semaphorins are a large family of guidance molecules identified by an extracellular SEMA domain. Classes 1 and 2 are derived from invertebrates, classes 3-7 are vertebrate and class 8 (v) are viral semaphorins. Class 6 semaphorins are reported to have a wide variety of roles including in axon guidance, transcriptional regulation and cancer. Here we report the identification and expression of four class 6 semaphorins (6A, 6Ba, 6Bb and 6Dl) in three stages of larval development in zebrafish (24, 48 and 72 hours postfertilization). Our data indicate that each of the class 6 semaphorins shows a distinct pattern of expression in the developing nervous system that is dynamic over the first 3 days of embryonic development. These data suggest that the individual class 6 semaphorins have diverse roles in nervous system development.

Ca2+ channel-independent requirement for MAGUK family CACNB4 genes in initiation of zebrafish epiboly.

CACNB genes encode membrane-associated guanylate kinase (MAGUK) proteins once thought to function exclusively as auxiliary beta subunits in assembly and gating of voltage-gated Ca(2+) channels. Here, we report that zygotic deficiency of zebrafish beta4 protein blocks initiation of epiboly, the first morphogenetic movement of teleost embryos. Reduced beta4 function in the yolk syncytial layer (YSL) leads to abnormal division and dispersal of yolk syncytial nuclei, blastoderm retraction, and death, effects highly similar to microtubule disruption by nocodazole. Epiboly is restored by coinjection of human beta4 cRNA or, surprisingly, by mutant cRNA encoding beta4 subunits incapable of binding to Ca(2+) channel alpha1 subunits. This study defines a YSL-driven zygotic mechanism essential for epiboly initiation and reveals a Ca(2+) channel-independent beta4 protein function potentially involving the cytoskeleton.

Calcium extrusion is critical for cardiac morphogenesis and rhythm in embryonic zebrafish hearts.

Calcium entry into myocytes drives contraction of the embryonic heart. To prepare for the next contraction, myocytes must extrude calcium from intracellular space via the Na+/Ca2+ exchanger (NCX1) or sequester it into the sarcoplasmic reticulum, via the sarcoplasmic reticulum Ca2+-ATPase2 (SERCA2). In mammals, defective calcium extrusion correlates with increased intracellular calcium levels and may be relevant to heart failure and sarcoplasmic dysfunction in adults. We report here that mutation of the cardiac-specific NCX1 (NCX1h) gene causes embryonic lethal cardiac arrhythmia in zebrafish tremblor (tre) embryos. The tre ventricle is nearly silent, whereas the atrium manifests a variety of arrhythmias including fibrillation. Calcium extrusion defects in tre mutants correlate with severe disruptions in sarcomere assembly, whereas mutations in the L-type calcium channel that abort calcium entry do not produce this phenotype. Knockdown of SERCA2 activity by morpholino-mediated translational inhibition or pharmacological inhibition causes embryonic lethality due to defects in cardiac contractility and morphology but, in contrast to tre mutation, does not produce arrhythmia. Analysis of intracellular calcium levels indicates that homozygous tre embryos develop calcium overload, which may contribute to the degeneration of cardiac function in this mutant. Thus, the inhibition of NCX1h versus SERCA2 activity differentially affects the pathophysiology of rhythm in the developing heart and suggests that relative levels of NCX1 and SERCA2 function are essential for normal development.