Stable Dropwise Condensation of Ethanol and Hexane on Rationally Designed Ultrascalable Nanostructured Lubricant-Infused Surfaces.

Vapor condensation is a widely used industrial process for transferring heat and separating fluids. Despite progress in developing low surface energy hydrophobic and micro/nanostructured superhydrophobic coatings to enhance water vapor condensation, demonstration of stable dropwise condensation of low-surface-tension fluids has not been achieved. Here, we develop rationally designed nanoengineered lubricant-infused surfaces (LISs) having ultralow contact angle hysteresis (<3°) for stable dropwise condensation of ethanol (γ ≈ 23 mN/m) and hexane (γ ≈ 19 mN/m). Using a combination of optical imaging and rigorous heat transfer measurements in a controlled environmental chamber free from noncondensable gases (<4 Pa), we characterize the condensation behavior of ethanol and hexane on ultrascalable nanostructured CuO surfaces impregnated with fluorinated lubricants having varying viscosities (0.496 < µ < 5.216 Pa·s) and chemical structures (branched versus linear, Krytox and Fomblin). We demonstrate stable dropwise condensation of ethanol and hexane on LISs impregnated with Krytox 1525, attaining about 200% enhancement in condensation heat transfer coefficient for both fluids compared to filmwise condensation on hydrophobic surfaces. In contrast to previous studies, we use 7 h of steady dropwise condensation experiments to demonstrate the importance of rational lubricant selection to minimize lubricant drainage and maximize LIS durability. This work not only demonstrates an avenue to achieving stable dropwise condensation of ethanol and hexane, it develops the fundamental design principles for creating durable LISs for enhanced condensation heat transfer of low-surface-tension fluids.

Mechanisms of cold pain.

Avoidance of cold pain is an important survival mechanism. Intriguingly, whilst cooling can cause numbness, damage sensing mechanisms still seem to operate at low temperatures, and pain can be perceived from cooled damaged tissue. Recent studies have identified two cold-activated transient receptor potential (TRP) channels present in sensory neurons as transducers of cold stimuli. TRPM8 seems to mediate responses to cooling whilst TRPA1 is activated, possibly indirectly, by more extreme cold conditions. The existence of cold-responsive neurons that do not express these channels suggests that other transducers of cold stimuli remain to be discovered. Subsequent action potential electrogenesis and probably propagation from sensory neurons innervating cold tissues depends upon the presence of Na(v)1.8, the sole voltage-gated sodium channel that fails to inactivate at low temperatures. This may explain the remarkable specificity of Na(v)1.8 expression in nociceptive neurons, where it plays an important role in pain pathways.

Deletion of annexin 2 light chain p11 in nociceptors causes deficits in somatosensory coding and pain behavior.

The S100 family protein p11 (S100A10, annexin 2 light chain) is involved in the trafficking of the voltage-gated sodium channel Na(V)1.8, TWIK-related acid-sensitive K+ channel (TASK-1), the ligand-gated ion channels acid-sensing ion channel 1a (ASIC1a) and transient receptor potential vanilloid 5/6 (TRPV5/V6), as well as 5-hydroxytryptamine receptor 1B (5-HT1B), a G-protein-coupled receptor. To evaluate the role of p11 in peripheral pain pathways, we generated a loxP-flanked (floxed) p11 mouse and used the Cre-loxP recombinase system to delete p11 exclusively from nociceptive primary sensory neurons in mice. p11-null neurons showed deficits in the expression of Na(V)1.8, but not of annexin 2. Damage-sensing primary neurons from these animals show a reduced tetrodotoxin-resistant sodium current density, consistent with a loss of membrane-associated Na(V)1.8. Noxious coding in wide-dynamic-range neurons in the dorsal horn was markedly compromised. Acute pain behavior was attenuated in certain models, but no deficits in inflammatory pain were observed. A significant deficit in neuropathic pain behavior was also apparent in the conditional-null mice. These results confirm an important role for p11 in nociceptor function.