Imprecise information, Variable information, Imprecision aversion,

The following five antimony(V) tetraphenylporphyrins with sigma-bonded antimony-carbon bonds were synthesized: [(TPP)Sb(CH(3))(2)](+)PF(6)(-), [(TPP)Sb(OCH(3))(OH)](+)PF(6)(-), [(TPP)Sb(CH(3))(OH)](+)ClO(4)(-), [(TPP)Sb(CH(3))(OCH(3))](+)ClO(4)(-), and [(TPP)Sb(CH(3))(F)](+)PF(6)(-). Each compound is stable toward air and moisture and has a high melting point (>250 degrees C). The electrochemistry and spectroelectrochemistry of these sigma-bonded porphyrins were examined in benzonitrile or dichloromethane containing 0.1 M tetrabutylammonium perchlorate as supporting electrolyte and the data compared to those for three previously synthesized OEP derivatives containing similar sigma-bonded and/or anionic axial ligands. Each porphyrin shows two reversible reductions and up to a maximun of one oxidation within the potential window of the solvent. Spectroelectrochemical data indicate formation of a porphyrin pi anion radical upon the first reduction as do ESR spectra of the singly reduced species. However, a small amount of the Sb(III) porphyrin products may be generated via a chemical reaction following electron tranfer. An X-ray crystallographic analysis of [(TPP)Sb(CH(3))(F)](+)PF(6)(-) is also presented: monoclinic, space group C2/c, Z = 8, a = 24.068(5) Å, b = 19.456(4) Å, c = 18.745(3) Å, beta = 94.69(2) degrees, R = 0.056.

Adiponectin (APN) is a multi-functional adipokine which sensitizes the insulin signals, stimulates mitochondria biogenesis, and suppresses inflammation. By virtue of these beneficial properties, APN may protect against metabolic syndrome, including obesity and type II diabetes mellitus. Since these diseases are associated with hypoadiponectinemia, it is suggested that loss of function of APN might be involved. In contrast, despite beneficial properties for cardiovascular cells, APN is detrimental in circulatory diseases, including chronic heart failure (CHF) and chronic kidney disease (CKD). Notably, such an APN paradox might also be applicable to neurodegeneration. Although APN is neuroprotective in various experimental systems, APN was shown to be associated with the severity of amyloid accumulation and cognitive decline in a recent prospective cohort study in elderly. Furthermore, Alzheimer's disease (AD) was associated with hyperadiponectinemia in many studies. Moreover, APN was sequestered by phospho-tau into the neurofibrillary tangle in the postmortem AD brains. These results collectively indicate that APN might increase the risk of AD. In this context, the objective of the present study is to elucidate the mechanism of the APN paradox in AD. Hypothetically, APN might be involved in the stimulation of the amyloidogenic evolvability in reproductive stage, which may later manifest as AD by the antagonistic pleiotropy mechanism during aging. Given the accumulating evidence that AD and CHF are mechanistically overlapped, it is further proposed that the APN paradox of AD might be converged with those of other diseases, such as CHF and CKD.

Lewy body diseases, such as Parkinson's disease (PD), dementia with Lewy bodies (DLB), and multiple system atrophy (MSA), are associated with a wide range of nonmotor symptoms (NMS), including cognitive impairment, depression and anxiety, sleep disorders, gastrointestinal symptoms, and autonomic failure. The reason why such diverse and disabling NMS have not been weeded out but have persisted across evolution is unknown. As such, one possibility would be that the NMS might be somehow beneficial during development and/or reproductive stages, a possibility consistent with our recent view as to the evolvability of amyloidogenic proteins (APs) such as α-synuclein (αS) and amyloid-β (Aβ) in the brain. Based on the heterogeneity of protofibrillar AP forms in terms of structure and cytotoxicity, we recently proposed that APs might act as vehicles to deliver information regarding diverse internal and environmental stressors. Also, we defined evolvability to be an epigenetic phenomenon whereby APs are transgenerationally transmitted from parents to offspring to cope with future brain stressors in the offspring, likely benefitting the offspring. In this context, the main objective is to discuss whether NMS might be relevant to evolvability. According to this view, information regarding NMS may be transgenerationally transmitted by heterogeneous APs to offspring, preventing or attenuating the stresses related to such symptoms. On the other hand, NMS associated with Lewy body pathology might manifest through an aging-associated antagonistic pleiotropy mechanism. Given that NMS are not only specific to Lewy body diseases but also displayed in other disorders, including amyotrophic lateral sclerosis (ALS) and Huntington's disease (HD), these conditions might share common mechanisms related to evolvability. This might give insight into novel therapy strategies based on antagonistic pleiotropy rather than on individual NMS from which to develop disease-modifying therapies.