Background and Objective The etiology and exact incidence of infantile hemangiomas (IH) are unknown. Prior studies have noted immunohistochemical and biologic characteristics shared by IH and placental tissue. We investigated the possible association between placental anomalies and the development of IH, as well as the demographic characteristics and other risk factors for IH. Methods 578 pregnant women were prospectively enrolled and their offspring followed for 9 months. Placental evaluations were performed and demographic data collected on all mother-infant pairs. Results 594 infants were evaluated: 32 hemangiomas (either IH or congenital (CH)) were identified in 27 infants, yielding an incidence of 4.5% for IH and 0.3% for CH. Placental anomalies were noted in almost 35% of hemangioma-related pregnancies, approximately twice the incidence noted in pregnancies with unaffected infants. (p = 0.025). Other risk factors for IH included prematurity (p = 0.016) and low birth weight (p = 0.028). All IH were present by 3 months of age, and cessation of growth had occurred in all by 9 months of age. Most occurred on the trunk. Of note, 20% of identified IH were abortive/telangiectatic in nature, small focal lesions that did not proliferate beyond 3 months of age. Only one IH required intervention. Conclusions This is the first prospective American study to document the incidence of IH in infants followed from birth to early infancy. The association with placental anomalies was statistically significant. The overall incidence mirrors prior estimates, but the need for treatment was lower than previously reported.
The objective of this study was to evaluate the time-series relationships between stress, sleep duration, and headache pain among patients with chronic headaches. Sleep and stress have long been recognized as potential triggers of episodic headache (< 15 headache days/month), though prospective evidence is inconsistent and absent in patients diagnosed with chronic headaches (≥ 15 days/month). We reanalyzed data from a 28-day observational study of chronic migraine (n = 33) and chronic tension-type headache (n = 22) sufferers. Patients completed the Daily Stress Inventory and recorded headache and sleep variables using a daily sleep/headache diary. Stress ratings, duration of previous nights' sleep, and headache severity were modeled using a series of linear mixed models with random effects to account for individual differences in observed associations. Models were displayed using contour plots. Two consecutive days of either high stress or low sleep were strongly predictive of headache, whereas two days of low stress or adequate sleep were protective. When patterns of stress or sleep were divergent across days, headache risk was increased only when the earlier day was characterized by high stress or poor sleep. As predicted, headache activity in the combined model was highest when high stress and low sleep occurred concurrently during the prior 2 days denoting an additive effect. Future research is needed to expand on current findings among chronic headache patients and to develop individualized models that account for multiple simultaneous influences of headache trigger factors.
Infantile haemangioma is the most common tumour of infancy, yet the origin of these lesions remains controversial and the predictable life cycle is poorly understood. Much new information on infantile haemangiomas has emerged over the past decade, but experts continue to debate fundamental features, including cell of origin, nonrandom distribution, and mechanisms regulating the sometimes explosive growth and slow involution. The development of useful laboratory models has been difficult, in turn restricting the development of treatment options available to the clinician. Despite this, new research and creative thinking has spawned several hypotheses on the origin of these tumours and their interesting clinical behaviour, including suggestions of an intrinsic defect in local endothelial cells, a contribution of circulating endothelial progenitors or haemangioblasts, embolisation of shed placental cells and developmental field defects. While no single hypothesis seems to describe all features of infantile haemangioma, continued research seeks to integrate these ideas, create a better understanding of these important tumours and bring new treatments to the clinic.
Infection by eastern dwarf mistletoe (Arceuthobium pusillum) modifies needle and branch morphology and hastens white spruce (Picea glauca) mortality. We examined potential causal mechanisms and assessed the impacts of infection-induced alterations to host development and performance across scales ranging from needle hormone contents to bole expansion. Needles on infected branches (IBs) possessed higher total cytokinin (CK) and lower abscisic acid contents than needles on uninfected branches (UBs). IBs exhibited greater xylem growth than same-aged UBs, which is consistent with the promotive effect of CKs on vascular differentiation and organ sink strength. Elevated CK content may also explain the dense secondary and tertiary branching observed at the site of infection, i.e. the formation of 'witches' brooms' with significantly lower light capture efficiencies. Observed hormone perturbations were consistent with higher rates of transpiration, lower water use efficiencies (WUEs) and more negative needle carbon isotope ratios observed for IBs. Observed reductions in needle size allowed IBs to compensate for reduced hydraulic conductivity. Severe infections resulted in dramatically decreased diameter growth of the bole. It seems likely that the modifications to host hormone contents by eastern dwarf mistletoe infection led white spruce trees to dedicate a disproportionate fraction of their photoassimilate and other resources to self-shaded branches with low WUE. This would have decreased the potential for fixed carbon accumulation, generating a decline in the whole-tree resource pool. As mistletoe infections grew in size and the number of IBs increased, this burden was manifested as increasingly greater reductions in bole growth.
Background The hemodynamic effects of cardiac resynchronization therapy in patients with left ventricular assist devices (LVADs) are uncharacterized. We aimed to quantify the hemodynamic effects of different ventricular pacing configurations in patients with LVADs, focusing on short‐term changes in load‐independent right ventricular (RV) contractility. Methods and Results Patients with LVADs underwent right heart catheterization during spontaneous respiration without sedation and with pressures recorded at end expiration. Right heart catheterization was performed at different pacemaker configurations (biventricular pacing, left ventricular pacing, RV pacing, and unpaced conduction) in a randomly generated sequence with >3 minutes between configuration change and hemodynamic assessment. The right heart catheterization operator was blinded to the sequence. RV maximal change in pressure over time normalized to instantaneous pressure was calculated from digitized hemodynamic waveforms, consistent with a previously validated protocol. Fifteen patients with LVADs who were in sinus rhythm were included. Load‐independent RV contractility, as assessed by RV maximal change in pressure over time normalized to instantaneous pressure, was higher in biventricular pacing compared with unpaced conduction (15.7±7.6 versus 11.0±4.0 s −1 ; P =0.003). Thermodilution cardiac output was higher in biventricular pacing compared with unpaced conduction (4.48±0.7 versus 4.38±0.8 L/min; P =0.05). There were no significant differences in heart rate, ventricular filling pressures, or atrioventricular valvular regurgitation across all pacing configurations. Conclusions Biventricular pacing acutely improves load‐independent RV contractility in patients with LVADs. Even in these patients with mechanical left ventricular unloading via LVAD who were relative pacing nonresponders (required LVAD support despite cardiac resynchronization therapy), biventricular pacing was acutely beneficial to RV contractility.
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