Modeling the summertime evolution of sea-ice melt ponds

1] We present a mathematical model describing the summer melting of sea ice. We simulate the evolution of melt ponds and determine area coverage and total surface ablation. The model predictions are tested for sensitivity to the melt rate of unponded ice, enhanced melt rate beneath the melt ponds, vertical seepage, and horizontal permeability. The model is initialized with surface topographies derived from laser altimetry corresponding to first-year sea ice and multiyear sea ice. We predict that there are large differences in the depth of melt ponds and the area of coverage between the two types of ice. We also find that the vertical seepage rate and the melt rate of unponded ice are important in determining the total surface ablation and area covered by melt ponds

A model of melt pond evolution on sea ice

A one-dimensional, thermodynamic, and radiative model of a melt pond on sea ice is presented that explicitly treats the melt pond as an extra phase. A two-stream radiation model, which allows albedo to be determined from bulk optical properties, and a parameterization of the summertime evolution of optical properties, is used. Heat transport within the sea ice is described using an equation describing heat transport in a mushy layer of a binary alloy (salt water). The model is tested by comparison of numerical simulations with SHEBA data and previous modeling. The presence of melt ponds on the sea ice surface is demonstrated to have a significant effect on the heat and mass balance. Sensitivity tests indicate that the maximum melt pond depth is highly sensitive to optical parameters and drainage. INDEX TERMS: 4207 Oceanography: General: Arctic and Antarctic oceanography; 4255 Oceanography: General: Numerical modeling; 4299 Oceanography: General: General or miscellaneous; KEYWORDS: sea ice, melt pond, albedo, Arctic Ocean, radiation model, thermodynami

Association of Rewarming Rate on Neonatal Outcomes in Extremely Low Birth Weight Infants with Hypothermia

Objective To explore the possible association between rewarming rate and neonatal outcomes in extremely low birth weight infants (ELBWIs) with hypothermia. Study design All ELBWIs with hypothermia (temperature <36.0\ub0C) on neonatal intensive care unit (NICU) admission were retrospectively evaluated. Rewarming rate was analyzed as both a dichotomous ( 650.5\ub0C/h rapid group; <0.5\ub0C/h slow group) and a continuous variable. Multivariable analysis was performed to explore the relation between rewarming rate and several outcomes, adjusting for clinically relevant confounders. Results Hypothermia on NICU admission was present in 182 out of 744 ELBWIs (24.5%). The rewarming rate was slow in 109 subjects (59.9%) and rapid in 73 subjects (40.1%), with a median rewarming rate of 0.29\ub0C/h (IQR 0.2-0.35) and 0.76\ub0C/h (IQR 0.61-1.09), respectively (P <.0001). The median rewarming time was 340 minutes (IQR 250-480) and 170 minutes (IQR 110-230), respectively (P <.0001). After adjusting for clinically relevant confounders, we did not find significant associations between rewarming rate group ( 650.5\ub0C/h vs <0.5\ub0C/h) and neonatal outcomes. When we considered the rewarming rate as continuous variable, a higher rewarming rate was identified as a protective factor for respiratory distress syndrome (OR 0.39, 95% CI 0.17-0.87; P =.02). Conclusions In ELBWIs with hypothermia upon NICU admission, there were no significant differences between rapid or slow rewarming rate and major neonatal outcomes. A higher rewarming rate was associated with a reduced incidence of respiratory distress syndrome

Associated norepinephrine loss following calcium-induced spinal paralysis

A 10% calcium chloride solution or normal physiological saline was instilled onto the intact dorsal surface of the spinal cord via a specially constructed catheter-canopy system fixed above the T9 level in conscious rats. Within 5 min after calcium instillation rats developed flaccid paralysis of the lower limbs with sensory loss. Sensory loss was accompanied by abnormal or negative evoked potentials. Rats instilled with physiological or 10% sodium chloride remained normal. Rats were sacrificed at 1, 16 and 48 h post-calcium exposure and following full functional recovery from paralysis. Spinal cords were removed for histologic and high-performance liquid chromatography (HPLC) analysis. Histologic examination for catecholamines using SPG histofluorescence showed loss of catecholamine-containing varicosities in gray matter below calcium exposure which returned to normal levels upon sensorimotor recovery of hindlimbs about 14 days pce. Light microscopic examination of vascular permeability and general morphology of cord tissue axons and neurons remained normal in calcium and saline instilled rats. HPLC analysis of spinal cord below calcium exposure, also showed norepinephrine (NE) and 3-methoxy-4-hydroxyphenylglycol (MHPG) tissue level reductions which returned to normal upon sensorimotor recovery of paralysis about 2 weeks later. No significant changes were noted in dopamine or serotonin levels in any group. Our findings suggest an impairment of ascending and descending tract transmitter transport, specifically reflected in the noradrenergic bulbospinal pathway. The results implicate a neurofilament-microtubule disassembly in axonal cytoskeleton triggered by the sudden calcium influx

GENERALIZED PRESENCE OF A PEC-6O-LIKE PEPTIDE IN CATECHOLAMINE NEURONS

PEC-60, a 60-residue intestinal peptide structurally related to the pancreatic secretory type of trypsin inhibitor, has been isolated, characterized and molecularly cloned. It shows biological activity as a hormone in both the gastrointestinal tract and in the immune system. We now report immunohistochemical evidence suggesting its neural localization exclusively within central and peripheral catecholamine (CA) neurones. PEC-60-like immunoreactivity was present in cell bodies, dendrites and nerve terminals of virtually all catecholamine neurones examined and including the noradrenergic gland cells of the adrenal medulla. PEC-60-like immunoreactivity was not seen, however, within the tyrosine hydroxylase-positive but CA-negative arcuate neurones producing growth hormone releasing hormone. The findings open up the possibility that a PEC-60-like peptide may represent a generalized co-transmitter in the peripheral and central CA neurones