High-performance subambient radiative cooling enabled by optically selective and thermally insulating polyethylene aerogel.

Recent progress in passive radiative cooling technologies has substantially improved cooling performance under direct sunlight. Yet, experimental demonstrations of daytime radiative cooling still severely underperform in comparison with the theoretical potential due to considerable solar absorption and poor thermal insulation at the emitter. In this work, we developed polyethylene aerogel (PEA)-a solar-reflecting (92.2% solar weighted reflectance at 6 mm thick), infrared-transparent (79.9% transmittance between 8 and 13 µm at 6 mm thick), and low-thermal-conductivity (k PEA = 28 mW/mK) material that can be integrated with existing emitters to address these challenges. Using an experimental setup that includes the custom-fabricated PEA, we demonstrate a daytime ambient temperature cooling power of 96 W/m2 and passive cooling up to 13°C below ambient temperature around solar noon. This work could greatly improve the performance of existing passive radiative coolers for air conditioning and portable refrigeration applications.

Pumping liquid metal at high temperatures up to 1,673 kelvin.

Heat is fundamental to power generation and many industrial processes, and is most useful at high temperatures because it can be converted more efficiently to other types of energy. However, efficient transportation, storage and conversion of heat at extreme temperatures (more than about 1,300 kelvin) is impractical for many applications. Liquid metals can be very effective media for transferring heat at high temperatures, but liquid-metal pumping has been limited by the corrosion of metal infrastructures. Here we demonstrate a ceramic, mechanical pump that can be used to continuously circulate liquid tin at temperatures of around 1,473-1,673 kelvin. Our approach to liquid-metal pumping is enabled by the use of ceramics for the mechanical and sealing components, but owing to the brittle nature of ceramics their use requires careful engineering. Our set-up enables effective heat transfer using a liquid at previously unattainable temperatures, and could be used for thermal storage and transport, electric power production, and chemical or materials processing.

A new model of peripheral arterial disease: sustained impairment of nutritive microcirculation and its recovery by chronic electrical stimulation.

OBJECTIVES: To develop a model of peripheral arterial disease (PAD) in rat skeletal muscle with sustained impairment of microcirculatory perfusion, and to ascertain whether increased muscle activity can reverse the impairment. METHODS: Three weeks after iliac ligation in rats, the ipsilateral femoral artery was ligated (double ligation, DL), and in some animals, muscle activity was increased by electrical stimulation for 2 weeks (10 Hz, 15 min on, 85 mins off, 7 times per day). Diameter changes of precapillary arterioles to vasoactive agonists and capillary perfusion (flow intermittency, capillary red cell velocity [V(rbc)], and diameters) were measured in extensor digitorum longus muscle and compared with 5 weeks iliac only ligation (single ligation, SL) and controls. Total muscle endothelial nitric oxide synthase (eNOS) was estimated by Western blotting. RESULTS: Whereas single ligation increased intermittency of capillary flow with little effect on V(rbc) and shear stress, DL completely eliminated increases in V(rbc) and shear stress after muscle contractions. Arterial dilation to sodium nitroprusside was attenuated similarly in SL and DL; in SL, acetylcholine induced constriction and bradykinin an attenuated dilation, but in DL vessels were unresponsive to either. Chronic stimulation returned all microcirculatory parameters in DL to normal and increased levels of eNOS protein by 75%. CONCLUSIONS: Femoral artery ligation following iliac ligation impairs arteriolar vasodilator capacity, capillary perfusion, and shear-dependent function of microcirculatory endothelium more than iliac ligation alone and is more representative of long-standing ischemia in PAD. Chronic intermittent electrical stimulation can normalize these derangements.

Arteriolar endothelial dysfunction is restored in ischaemic muscles by chronic electrical stimulation.

Chronic intermittent electrical stimulation (15 min on, 85 min off, seven times per day) eliminated endothelial dysfunction of pre-capillary arterioles in ischaemic rat ankle flexor muscles. Responses to acetylcholine were restored from constriction to dilation, and the reduced dilation to bradykinin was corrected by 1 week of stimulation. Administration of the NOS inhibitor N(omega)-nitro-L-arginine for 1 week impaired arteriolar reactivity in a similar way to ischaemia, and dilator function was likewise restored by chronic stimulation. This suggests that nitric oxide production in the microcirculation is depressed by chronic ischaemia and that chronic electrical stimulation can specifically reverse this deficit. Stimulation applied to ischaemic muscles for 2 weeks also increased the numbers of microvessels immunostained for alpha-smooth muscle actin and the numbers of eNOS-positive microvessels and capillaries. These findings help to elucidate the mechanism of the beneficial effect of exercise in the treatment of peripheral vascular diseases by showing that muscle activity can improve both function and structural capacity of the microvasculature.

Remodeling in the microcirculation of rat skeletal muscle during chronic ischemia.

OBJECTIVE: To establish the time course and extent of remodeling of terminal microcirculation in ischemic rat skeletal muscle during prolonged low flow that does not lead to inflammation. METHODS: One common iliac artery was ligated via laparotomy in adult Sprague-Dawley rats and extensor digitorum longus (EDL) muscles removed at intervals (1, 2, and 5 weeks) postsurgery. Serial frozen EDL sections were stained to show capillaries (alkaline phosphatase), cell proliferation (antibody to proliferating cell nuclear antigen [PCNA]), terminal microvessels (antibodies to alpha-smooth muscle actin (alpha-SMA) or endothelial nitric oxide synthase [eNOS]), and macrophages (antibodies to infiltrating and resident macrophages). Total muscle eNOS protein was quantified by standard Western blotting techniques. RESULTS: Capillary proliferation was very limited in ischemic EDLs, with a modest 12% increase in the capillary/fiber ratio after 5 weeks, preceded at 2 weeks by increased numbers of PCNA-positive nuclei at capillary sites. There was no muscle necrosis or evidence of inflammation, based on macrophage staining. The number of terminal microvessels that were positive for alpha-SMA and <10 microm in diameter was fewer in ischemic EDLs at all time points, whereas the number of larger positive vessels was unchanged. eNOS-positive vessels <10 microm in diameter were stained similarly throughout ischemic muscles as the controls, and showed a similar increase in vessel/fiber ratio as the capillaries. The total eNOS protein level was similar to that in controls in ischemic EDLs after 1 and 2 weeks, but was 28% lower after 5 weeks. CONCLUSIONS: Prolonged, moderate flow reduction to skeletal muscles does not necessarily lead to inflammation or extensive capillary growth. Based on eNOS staining, the terminal microcirculation remains intact, but the loss of alpha-SMA immunoreactivity may indicate remodeling involving the "deinvestment" of microvessels by smooth muscle.

Alterations in reactivity of small arterioles in rat skeletal muscle as a result of chronic ischaemia.

In a model of chronic hind limb ischaemia, we examined whether impaired muscle blood flow, particularly during exercise, is partly due to modification of the reactivity of skeletal muscle resistance vessels by prolonged low blood flow. Two or 5 weeks after unilateral iliac artery ligation, terminal (A4) and preterminal (A3) arterioles of extensor digitorum longus muscle were viewed by intravital microscopy using epi-illumination, and diameter changes to topical application of endothelium-dependent (bradykinin, acetylcholine) and endothelium-independent (adenosine, sodium nitroprusside and noradrenaline) agonists measured. Chronic ischaemia had no effect on resting diameters of A3 or A4 vessels. Two weeks after ligation, dilation to bradykinin was attenuated by 75% for A3 and 50% for A4 arterioles (p < 0.01 vs. control) and responses to acetylcholine were reversed from dilation to constriction (A3: control diameter change +29%, 2-week-ligated -17%; A4: control 18%, 2-week-ligated -13%). Five weeks after ligation, these effects were still apparent and, additionally, dilation to adenosine and sodium nitroprusside and constriction to noradrenaline were reduced. Thus, impaired dilation, most likely due to endothelial dysfunction, is an early manifestation of altered reactivity in the microcirculation of chronically ischaemic muscles, with functional impairment of vascular smooth muscle as a later consequence. These changes occurred despite modest improvements in muscle blood flow and perfusion pressure over the same time. These changes will act to the detriment of blood flow in contracting muscles and could limit the outcome of interventions to restore flow such as angioplasty or surgical bypass.

Native urotensins influence cortisol secretion and plasma cortisol concentration in the euryhaline flounder, platichthys flesus.

Adrenocorticotrophic hormone (ACTH) and flounder urotensins I and II (UI and UII) stimulate cortisol secretion of isolated interrenal/head kidney preparations of seawater (SW)-adapted flounder. UI and UII at concentrations of 10(-6) and 10(-7) M, respectively, increased cortisol secretion when acting on SW-derived interrenal but did not affect cortisol secretion in tissue derived from freshwater (FW) fish. Combined UI and UII had no synergistic or additive steroidogenic action, but either 10(-7) M UI or 10(-7) M UII in combination with ACTH produced a very marked, additive, or synergistic steroidogenic response, most apparent on interrenal derived from FW fish. These results suggest that urotensins enhance the steroidogenic action of ACTH in flounder. In all cases, significant steroidogenesis was apparent within 1 h postperifusion of ligands. In SW-adapted flounder intraarterial infusion of UII in vivo caused a concentration-dependent increase in plasma cortisol concentration within 1 h after infusion, while after 5 x 10(-6) M UI infusion a similar trend was evident but this did not achieve statistical significance. The data suggest that the caudal neurosecretory system may control interrenal cortisol secretion, to modulate cortisol secretion independently of the hypophysial axis, perhaps in response to specific stress-induced or osmoregulatory challenge.