Some Thermoelectric Phenomena in Copper Chalcogenides Replaced by Lithium and Sodium Alkaline Metals

This review presents thermoelectric phenomena in copper chalcogenides substituted with sodium and lithium alkali metals. The results for other modern thermoelectric materials are presented for comparison. The results of the study of the crystal structure and phase transitions in the ternary systems Na-Cu-S and Li-Cu-S are presented. The main synthesis methods of nanocrystalline copper chalcogenides and its alloys are presented, as well as electrical, thermodynamic, thermal, and thermoelectric properties and practical application. The features of mixed electron–ionic conductors are discussed. In particular, in semiconductor superionic copper chalcogenides, the presence of a “liquid-like phase” inside a “solid” lattice interferes with the normal propagation of phonons; therefore, superionic copper chalcogenides have low lattice thermal conductivity, and this is a favorable factor for the formation of high thermoelectric efficiency in them.

Peristalsis and propulsion of colonic content can occur after blockade of major neuroneuronal and neuromuscular transmitters in isolated guinea pig colon

We recently identified hexamethonium-resistant peristalsis in the guinea pig colon. We showed that, following acute blockade of nicotinic receptors, peristalsis recovers, leading to normal propagation velocities of fecal pellets along the colon. This raises the fundamental question: what mechanisms underlie hexamethonium-resistant peristalsis? We investigated whether blockade of the major receptors that underlie excitatory neuromuscular transmission is required for hexamethonium-resistant peristalsis. Video imaging of colonic wall movements was used to make spatiotemporal maps and determine the velocity of peristalsis. Propagation of artificial fecal pellets in the guinea pig distal colon was studied in hexamethonium, atropine, ω-conotoxin (GVIA), ibodutant (MEN-15596), and TTX. Hexamethonium and ibodutant alone did not retard peristalsis. In contrast, ω-conotoxin abolished peristalsis in some preparations and reduced the velocity of propagation in all remaining specimens. Peristalsis could still occur in some animals in the presence of hexamethonium + atropine + ibodutant + ω-conotoxin. Peristalsis never occurred in the presence of TTX. The major finding of the current study is the unexpected observation that peristalsis can occur after blockade of the major excitatory neuroneuronal and neuromuscular transmitters. Also, the colon retained an intrinsic polarity in the presence of these antagonists and was only able to expel pellets in an aboral direction. The nature of the mechanism(s)/neurotransmitter(s) that generate(s) peristalsis and facilitate(s) natural fecal pellet propulsion, after blockade of major excitatory neurotransmitters, at the neuroneuronal and neuromuscular junction remains to be identified.

Saccharomyces cerevisiae Hsp70 Mutations Affect [PSI+] Prion Propagation and Cell Growth Differently and Implicate Hsp40 and Tetratricopeptide Repeat Cochaperones in Impairment of [PSI+]

We previously described an Hsp70 mutant (Ssa1-21p), altered in a conserved residue (L483W), that dominantly impairs yeast [PSI+] prion propagation without affecting growth. We generated new SSA1 mutations that impaired [PSI+] propagation and second-site mutations in SSA1-21 that restored normal propagation. Effects of mutations on growth did not correlate with [PSI+] phenotype, revealing differences in Hsp70 function required for growth and [PSI+] propagation and suggesting that Hsp70 interacts differently with [PSI+] prion aggregates than with other cellular substrates. Complementary suppression of altered activity between forward and suppressing mutations suggests that mutations that impair [PSI+] affect a similar Hsp70 function and that suppressing mutations similarly overcome this effect. All new mutations that impaired [PSI+] propagation were located in the ATPase domain. Locations and homology of several suppressing substitutions suggest that they weaken Hsp70's substrate-trapping conformation, implying that impairment of [PSI+] by forward mutations is due to altered ability of the ATPase domain to regulate substrate binding. Other suppressing mutations are in residues important for interactions with Hsp40 or TPR-containing cochaperones, suggesting that such interactions are necessary for the impairment of [PSI+] propagation caused by mutant Ssa1p.