Effects of Curing Agents on the Adhesion of Epoxy Resin to Copper: A Density Functional Theory Study.

Epoxy resins are widely used adhesives in industrial fields. To use epoxy resin as an adhesive, it is necessary to mix the epoxy resin with a hardener. Hardeners have various functional groups and skeletons, and the properties of epoxy resins vary depending on the hardener. Although the adhesion of epoxy resins has been extensively studied using density functional theory (DFT) calculations, few studies have evaluated the effect of hardener molecules. Therefore, in this study, DFT calculations of adhesion energies and bonding structures on Cu (111) and Cu2O (111) surfaces are performed for model molecules of adducts of epoxy resin with hardeners having various functional groups and skeletons to evaluate the influence of the hardeners on the adhesion of epoxy resin to the metal surface. The adhesion energy to the Cu (111) surface is governed by the energy due to dispersion forces. Hardeners of the thiol type, which contain relatively heavy sulfur atoms, and hardeners with aromatic rings, displaying high planarity, enable the entire molecule to approach the metal surface, resulting in a relatively high adhesion strength. The calculations for the Cu2O (111) surface show the adhesion strength is more strongly influenced by interactions such as hydrogen bonds between the surface and adhesive molecules than by dispersion forces. Therefore, in adhesion to Cu2O (111), the benzylamine-epoxy adduct with hydrogen bonding and OH-π interactions with the surface, in addition to having a relatively flexible framework, shows a high adhesion strength.

Synthesis and Characterization of 1-Hydroxy-4,5-arene-Fused Tropylium Derivatives.

The properties of 1-hydroxy-4,5-arene-fused tropyliums were assessed based on experimental and theoretical investigations. An X-ray crystallographic analysis revealed a decrease of bond alternation in the seven-membered ring of 1-hydroxy-4,5-benzotropylium derivatives compared with that of the parent 4,5-benzotropones, which is indicative of an increase in aromaticity upon protonation. NICS and AICD calculations also supported the increased aromaticity of 1-hydroxy-4,5-arene-fused tropylium. The pKa values for a series of 1-hydroxy-4,5-arene-fused tropylium derivatives were also determined.

Synthesis of 4,5-Benzotropone π Complexes of Iron, Rhodium, and Iridium and Their Potential Use in Catalytic Borrowing-Hydrogen Reactions.

The syntheses of rhodium, iridium, and iron π complexes bearing 4,5-benzotropone ligands are reported. X-ray crystallographic analyses revealed that a tropone core coordinates to a metal center in a η4 manner with a tub-form geometry. Some of the benzotropone π complexes exhibited catalytic activity for N-alkylation of aniline by borrowing hydrogen.

Effect of astaxanthin-rich extract derived from Paracoccus carotinifaciens on the status of stress and sleep in adults.

This study investigated the effect of a dietary supplement containing astaxanthin-rich extract derived from Paracoccus carotinifaciens (astaxanthin supplement) on the status of stress and sleep in individuals aged 20-64 years. Twenty-five subjects orally administered 12 mg astaxanthin/day of astaxanthin supplement for 8 weeks (astaxanthin group) and 29 subjects given a placebo (placebo group) were evaluated with Profile of Mood States 2nd Edition for stress and Oguri-Shirakawa-Azumi Sleep Inventory for Middle-aged and Aged version for sleep. We did not observe any significant intergroup differences in the stress and sleep. A subgroup analysis was performed after dividing the subjects into two groups: those who scored >65 and those who scored ≤65 in the "Depression-Dejection" dimension of Profile of Mood States 2nd Edition. The sleep of subjects who scored >65 ("Depression-Dejection") showed significant improvement in the astaxanthin group compared with the placebo group, whereas no significant improvement was observed in stress and the other subjects. Our results indicate that people who tend to be strongly depressed may experience improved sleep after ingesting astaxanthin supplement. On the basis of the parameters tested, administration of astaxanthin supplement was not associated with any problems related to safety. Clinical registration: This study has been registered at the University Hospital Medical Information Network (https://upload.umin.ac.jp/cgi-open-bin/ctr/ctr_view.cgi?recptno=R000038619) on August 24, 2018 as "A study to evaluate the effect of intake of astaxanthin on the status of stress and sleep in adults," Identification No. UMIN000033863.

Total Synthesis of Polycavernosides A and B, Two Lethal Toxins from Red Alga.

Polycavernosides A and B are glycosidic macrolide natural products isolated as the toxins causing fatal human poisoning by the edible red alga Gracilaria edulis (Polycavernosa tsudai). Total synthesis of polycavernosides A and B has been achieved via a convergent approach. The synthesis of the macrolactone core structure is highlighted by the catalytic asymmetric syntheses of the two key fragments using hetero-Diels-Alder reaction and Kiyooka aldol reaction as the key steps, their union through Suzuki-Miyaura coupling, and Keck macrolactonization. Finally, glycosylation with the l-fucosyl-d-xylose unit and construction of the polyene side chain through Stille coupling completed the total synthesis of polycavernosides A and B.

Progress toward the Total Synthesis of Goniodomin A: Stereocontrolled, Convergent Synthesis of the C12-C36 Fragment.

Goniodomin A is a marine polyether macrolide natural product isolated from the dinoflagellate Alexandrium hiranoi. In this paper, we report stereocontrolled, convergent synthesis of a fully functionalized C12-C36 fragment of goniodomin A. The synthesis of the C12-C25 vinylstannane involved a Wittig reaction and a reductive cycloetherification for the construction of the dihydropyran ring. The C26-C36 thioester was synthesized via a Nozaki-Hiyama-Kishi reaction of an aldehyde and an iodoalkyne, the former of which was easily prepared from (R)-malic acid as a chiral source by taking advantage of substrate-controlled diastereoselective reactions. Finally, a palladium-catalyzed coupling of the C12-C25 vinylstannane and the C26-C36 thioester completed the synthesis of the target compound.

Contrast adaptation to luminance and brightness modulations.

Perceptual brightness and color contrast decrease after seeing a light temporally modulating along a certain direction in a color space, a phenomenon known as contrast adaptation. We investigated whether contrast adaptation along the luminance direction arises from modulation of luminance signals or apparent brightness signals. The stimulus consisted of two circles on a gray background presented on a CRT monitor. In the adaptation phase, the luminance and chromaticity of one circle were temporally modulated, while the other circle was kept at a constant luminance and color metameric with an equal-energy white. We employed two types of temporal modulations, namely, in luminance and brightness. Chromaticity was sinusoidally modulated along the L-M axis, leading to dissociation between luminance and brightness (the Helmholtz-Kohlrausch effect). In addition, luminance modulation was minimized in the brightness modulation, while brightness modulation was minimized in the luminance modulation. In the test phase, an asymmetric matching method was used to measure the magnitude of contrast adaptation for both modulations. Our results showed that, although contrast adaptation along the luminance direction occurred for both modulations, contrast adaptation for luminance modulation was significantly stronger than that for the brightness modulation regardless of the temporal frequency of the adaptation modulation. These results suggest that luminance modulation is more influential in contrast adaptation than brightness modulation.

Graphene oxide-Li(+)@C60 donor-acceptor composites for photoenergy conversion.

An ionic endohedral metallofullerene (Li(+)@C60) with mild hydrophilic nature was combined with graphene oxide (GO) to construct a donor-acceptor composite in neat water. The resulting composite was characterised by UV-Vis and Raman spectroscopy, powder X-ray diffraction, dynamic light scattering measurements and transmission electron microscopy. Theoretical calculations (DFT at the B3LYP/6-31(d) level) were also utilized to gain further insight into the composite formation. As detected by electron paramagnetic resonance spectroscopy, photoexcitation of the GO-Li(+)@C60 composite results in electron transfer from GO to the triplet excited state of Li(+)@C60, leading to photocurrent generation at the OTE/SnO2 electrode.

A rare CYP 21 mutation (p.E431K) induced deactivation of CYP 21A2 and resulted in congenital adrenal hyperplasia.

Congenital adrenal hyperplasia (CAH) due to 21-hydroxylase deficiency is caused by mutations in the CYP21A2 gene. The residual enzyme activity is strongly associated with the phenotype. We describe a rare case of CAH with a rare CYP21A2 mutation. The patient was a one-year-old Japanese boy. At 16 days old, he was referred to our hospital because of elevated serum 17-OH-progesterone (17-OHP) levels in neonatal screening. The compound heterozygous mutations (IVS2-13 A/C>G, and p.E431K) in CYP21A2 were identified at 2 months old, and we diagnosed non-classical CAH, since he did not have significant physical signs (pigmentation and salt-wasting). However, his body weight decreased, and his serum 17-OHP level (99.5 ng/mL) was elevated at 3 months old. Steroid replacement therapy was started at 3 months old. Our patient's clinical course resembled simple virilizing (SV) CAH, but classification was difficult because the patient showed increased renin activity indicating an aldosterone deficiency, and late onset of symptoms. While the IVS 2-13 A/C>G mutation is common in the classical form of CAH, p.E431K is a rare point mutation. Functional analysis revealed that the residual enzyme activity of p.E431L was 5.08±2.55% for 17-OHP and 4.12±2.37% for progesterone, which is consistent with SV CAH. p.E431 is localized in the L-helix near the heme-binding site. The mutation might interfere with heme binding, leading to deactivation of CYP21A2. This report showed that CYP21A2 p.E431 has an important effect on enzyme activity.

Robust inclusion complexes of crown ether fused tetrathiafulvalenes with Li⁺@C60 to afford efficient photodriven charge separation.

Inclusion complexes of benzo- and dithiabenzo-crown ether functionalized monopyrrolotetrathiafulvalene (MPTTF) molecules were formed with Li(+)@C60(1⋅Li(+)@C60 and 2⋅Li(+)@C60). The strong complexation has been quantified by high binding constants that exceed 10(6) M(-1) obtained by UV/Vis titrations in benzonitrile (PhCN) at room temperature. On the basis of DFT studies at the B3LYP/6-311G(d,p) level, the orbital interactions between the crown ether moieties and the π surface of the fullerene together with the endohedral Li(+) have a crucial role in robust complex formation. Interestingly, complexation of Li(+)@C60 with crown ethers accelerates the intersystem crossing upon photoexcitation of the complex, thereby yielding (3)(Li(+)@C60)*, when no charge separation by means of (1)Li(+)@C60* occurs. Photoinduced charge separation by means of (3)Li(+)@C60* with lifetimes of 135 and 120 µs for 1⋅Li(+)@C60 and 2⋅Li(+)@C60, respectively, and quantum yields of 0.82 in PhCN have been observed by utilizing time-resolved transient absorption spectroscopy and then confirmed by electron paramagnetic resonance measurements at 4 K. The difference in crown ether structures affects the binding constant and the rates of photoinduced electron-transfer events in the corresponding complex.

Supramolecular formation of Li(+) @PCBM fullerene with sulfonated porphyrins and long-lived charge separation.

Lithium-ion-encapsulated [6,6]-phenyl-C61 -butyric acid methyl ester fullerene (Li(+) @PCBM) was utilized to construct supramolecules with sulfonated meso-tetraphenylporphyrins (MTPPS(4-) ; M=Zn, H2 ) in polar benzonitrile. The association constants were determined to be 1.8×10(5) M(-1) for ZnTPPS(4-) /Li(+) @PCBM and 6.2×10(4) M(-1) for H2 TPPS(4-) /Li(+) @PCBM. From the electrochemical analyses, the energies of the charge-separated (CS) states were estimated to be 0.69 eV for ZnTPPS(4-) /Li(+) @PCBM and 1.00 eV for H2 TPPS(4-) /Li(+) @PCBM. Upon photoexcitation of the porphyrin moieties of MTPPS(4-) /Li(+) @PCBM, photoinduced electron transfer occurred to produce the CS states. The lifetimes of the CS states were 560 µs for ZnTPPS(4-) /Li(+) @PCBM and 450 µs for H2 TPPS(4-) /Li(+) @PCBM. The spin states of the CS states were determined to be triplet by electron paramagnetic resonance spectroscopy measurements at 4 K. The reorganization energies (λ) and electronic coupling term (V) for back electron transfer (BET) were determined from the temperature dependence of kBET to be λ=0.36 eV and V=8.5×10(-3) cm(-1) for ZnTPPS(4-) /Li(+) @PCBM and λ=0.62 eV and V=7.9×10(-3) cm(-1) for H2 TPPS(4-) /Li(+) @PCBM based on the Marcus theory of nonadiabatic electron transfer. Such small V values are the result of a small orbital interaction between the MTPPS(4-) and Li(+) @PCBM moieties. These small V values and spin-forbidden charge recombination afford a long-lived CS state.

Alström Syndrome: A Review Focusing on Its Diverse Clinical Manifestations and Their Etiology as a Ciliopathy.

Alström syndrome is a form of inherited obesity caused by a single gene abnormality and is inherited as an autosomal recessive trait. It is characterised by a variety of clinical manifestations, including progressive visual and hearing impairment, type 2 diabetes mellitus, dilated cardiomyopathy, and hepatic and renal dysfunction, in addition to obesity. Recent insights underline the pivotal involvement of the disease-associated gene (ALMS1) in cilia formation and function, leading to the classification of its clinical manifestations as a ciliopathy. This review delineates the diverse clinical indicators defining the syndrome and elucidates its pathological underpinnings.

Small reorganization energies of photoinduced electron transfer between spherical fullerenes.

Rate constants of photoinduced electron transfer between spherical fullerenes were determined using triscandium nitride encapsulated C80 fullerene (Sc3N@C80) as an electron donor and the triplet excited state of lithium ion-encapsulated C60 fullerene (Li(+)@C60) as an electron acceptor in polar and less polar solvents by laser flash photolysis measurements. Upon nanosecond laser excitation at 355 nm of a benzonitrile (PhCN) solution of Li(+)@C60 and Sc3N@C80, electron transfer from Sc3N@C80 to the triplet excited state [(3)(Li(+)@C60)*] occurred to produce Sc3N@C80(•+) and Li(+)@C60(•-) (λ(max) = 1035 nm). The rates of the photoinduced electron transfer were monitored by the decay of absorption at λ(max) = 750 nm due to (3)(Li(+)@C60)*. The second-order rate constant of electron transfer from Sc3N@C80 to (3)(Li(+)@C60)* was determined to be k(et) = 1.5 × 10(9) M(-1) s(-1) from dependence of decay rate constant of (3)(Li(+)@C60)* on the Sc3N@C80 concentration. The rate constant of back electron transfer from Li(+)@C60(•-) to Sc3N@C80(•+) was also determined to be k(bet) = 1.9 × 10(9) M(-1) s(-1), which is close to be the diffusion limited value in PhCN. Similarly, the rate constants of photoinduced electron transfer from C60 to (3)(Li(+)@C60)* and from Sc3N@C80 to (3)C60* were determined together with the back electron-transfer reactions. The driving force dependence of log k(et) and log k(bet) was well fitted by using the Marcus theory of outer-sphere electron transfer, in which the internal (bond) reorganization energy (λi) was estimated by DFT calculations and the solvent reorganization energy (λs) was calculated by the Marcus equation. When PhCN was replaced by o-dichlorobenzene (o-DCB), the λ value was decreased because of the smaller solvation changes of highly spherical fullerenes upon electron transfer in a less polar solvent.

Leprechaunism (Donohue syndrome): a case bearing novel compound heterozygous mutations in the insulin receptor gene.

Leprechaunism (Donohue syndrome) is the most severe type of insulin receptor (INSR) gene anomaly with the majority of patients surviving for only 2 years. We report a surviving 2 -year-old male with leprechaunism, bearing novel compound heterozygous mutations in the INSR. The patient is a Japanese boy with acanthosis nigricans, lack of subcutaneous fat, hirsutism, thick lips, gum hypertrophy and extremely high insulin levels (6702 mU/mL). He was as having identified novel compound heterozygous mutations in INSR (p.T910M and p. E1047K). At 24 day-old, recombinant human insulin-like growth factor 1 (rh-IGF1) treatment was started because of poor weight gain. At 2 years old, the patient's serum glucose level and HbA1C value had worsened, and both a bolus of rh-IGF-1 and a subcutaneous injection of a rapid-acting insulin analog after meals, in addition to α-glycosidase inhibitor, were initiated from 2 years onward. Oxygen administration and biphasic positive airway pressure treatment were also initiated from 2 years old due to upper airway obstruction with adenoidal hypertrophy. In the experiments conducted using COS7 cells homozygously transfected with the INSR mutation, T910M INSR failed to process the proreceptor and decreased insulin-stimulated tyrosine phosphorylation. E1047K INSR resulted in a complete absence of insulin-stimulated tyrosine phosphorylation. These findings suggest the near absence of INSR in this patient. We consider that the rhIGF1 treatment contributed to his long survival, but it was not able to prevent his diabetic condition. Our report provides important insights into the function of INSR, and for the treatment of leprechaunism.

Highly-purified rapidly expanding clones, RECs, are superior for functional-mitochondrial transfer.

BACKGROUND: Mitochondrial dysfunction caused by mutations in mitochondrial DNA (mtDNA) or nuclear DNA, which codes for mitochondrial components, are known to be associated with various genetic and congenital disorders. These mitochondrial disorders not only impair energy production but also affect mitochondrial functions and have no effective treatment. Mesenchymal stem cells (MSCs) are known to migrate to damaged sites and carry out mitochondrial transfer. MSCs grown using conventional culture methods exhibit heterogeneous cellular characteristics. In contrast, highly purified MSCs, namely the rapidly expanding clones (RECs) isolated by single-cell sorting, display uniform MSCs functionality. Therefore, we examined the differences between RECs and MSCs to assess the efficacy of mitochondrial transfer. METHODS: We established mitochondria-deficient cell lines (ρ0 A549 and ρ0 HeLa cell lines) using ethidium bromide. Mitochondrial transfer from RECs/MSCs to ρ0 cells was confirmed by PCR and flow cytometry analysis. We examined several mitochondrial functions including ATP, reactive oxygen species, mitochondrial membrane potential, and oxygen consumption rate (OCR). The route of mitochondrial transfer was identified using inhibition assays for microtubules/tunneling nanotubes, gap junctions, or microvesicles using transwell assay and molecular inhibitors. RESULTS: Co-culture of ρ0 cells with MSCs or RECs led to restoration of the mtDNA content. RECs transferred more mitochondria to ρ0 cells compared to that by MSCs. The recovery of mitochondrial function, including ATP, OCR, mitochondrial membrane potential, and mitochondrial swelling in ρ0 cells co-cultured with RECs was superior than that in cells co-cultured with MSCs. Inhibition assays for each pathway revealed that RECs were sensitive to endocytosis inhibitor, dynasore. CONCLUSIONS: RECs might serve as a potential therapeutic strategy for diseases linked to mitochondrial dysfunction by donating healthy mitochondria.

Novel missense mutation in the IGF-I receptor L2 domain results in intrauterine and postnatal growth retardation.

BACKGROUND: IGFs play key roles in intrauterine and postnatal growth through the IGF-I receptor (IGF-IR). We identified a family bearing a new heterozygous missense mutation at the L2 domain of IGF-IR (R431L). METHOD: We analysed the nucleotide sequences of the IGF1R gene of the family. We prepared R(-) cells (fibroblasts with targeted disruption of the IGF-IR gene) expressing wild-type or R431L IGF-IR and performed functional analyses by evaluating IGF-I binding, IGF-I-stimulated DNA synthesis, tyrosine phosphorylation of IGF-IR and its substrates, and internalization by measuring [(125) I]IGF-I internalization. We also performed confocal microscopy analysis. RESULTS: We identified a family bearing a new heterozygous missense mutation at the L2 domain of IGF-IR (R431L) through an 8-year-old girl and her mother, both born with intrauterine growth retardation. In experiments conducted using cells homozygously transfected with the IGF-IR R431L mutation; (i) IGF-I binding was not affected; (ii) DNA synthesis induced by IGF-I was decreased; (iii) IGF-IR internalization stimulated by IGF-I was decreased and (iv) IGF-I-stimulated tyrosine phosphorylation was reduced IGF-IR by low concentrations of IGF-I and on insulin receptor substrate (IRS)-1 and IRS-2. CONCLUSION: A missense mutation (R431L) leads to the inhibition of cell proliferation, attenuation of IGF signalling and decrease in internalization of IGF-IR. The results of this study suggest a novel link between a mutation at the IGF-IR L2 domain and intrauterine and postnatal growth retardation.

Enhanced photoinduced electron-transfer reduction of Li(+)@C60 in comparison with C60.

Kinetics of photoinduced electron transfer from a series of electron donors to the triplet excited state of lithium ion-encapsulated C60 (Li(+)@C60) was investigated in comparison with the corresponding kinetics of the photoinduced electron transfer to the triplet excited state of pristine C60. Femtosecond laser flash photolysis measurements of Li(+)@C60 revealed that singlet excited state of Li(+)@C60 (λmax = 960 nm) underwent intersystem crossing to the triplet excited state [(3)(Li(+)@C60)*: λmax = 750 nm] with a rate constant of 8.9 × 10(8) s(-1) in deaerated benzonitrile (PhCN). The lifetime of (3)(Li(+)@C60)* was determined by nanosecond laser flash photolysis measurements to be 48 µs, which is comparable to that of C60. Efficient photoinduced electron transfer from a series of electron donors to (3)(Li(+)@C60)* occurred to produce the radical cations and Li(+)@C60(•-). The rate constants of photoinduced electron transfer of Li(+)@C60(•-) are significantly larger than those of C60 when the rate constants are less than the diffusion-limited value in PhCN. The enhanced reactivity of (3)(Li(+)@C60)* as compared with (3)C60* results from the much higher one-electron reduction potential of Li(+)@C60 (0.14 V vs SCE) than that of C60 (-0.43 V vs SCE). The rate constants of photoinduced electron transfer reactions of Li(+)@C60 and C60 were evaluated in light of the Marcus theory of electron transfer to determine the reorganization energies of electron transfer. The reorganization energy of electron transfer of Li(+)@C60 was determined from the driving force dependence of electron transfer rate to be 1.01 eV, which is by 0.28 eV larger than that of C60 (0.73 eV), probably because of the change in electrostatic interaction of encapsulated Li(+) upon electron transfer in PhCN.

Familial short stature with IGF-I receptor gene anomaly.

Type I insulin-like growth factor receptor (IGF-IR) is widely expressed across many cell types in fetal and postnatal tissues. The activation of this receptor after the binding of secreted IGF-I and IGF-II promotes cell differentiation and proliferation. IGF-IR has an important role in normal fetal and postnatal growth and development. IGF-IR gene anomalies presenting with intrauterine and postnatal growth retardation have recently been reported in some families. Familial short stature with IGF-IR gene anomaly is considered rare, and the clinical condition and features remain unknown. IGF-IR gene anomaly such as heterozygous IGF-IR mutation or haploinsufficiency of the IGF-IR gene should be investigated in those patients presenting with 1) low birth weight and birth height (< -1.5 SD), 2) a familial history of low birth weight, 3) a normal or increased IGF-I level, 4) a normal or increased GH response to the GH stimulation test, and/or 5) less response to GH treatment than common small for gestational age (SGA) short-stature patients. In this review, we provide an overview of current knowledge of familial short stature with IGF-IR gene anomaly.

The insulin-like growth factor-1 binding protein acid-labile subunit alters mesenchymal stromal cell fate.

Age-related osteoporosis is accompanied by an increase in marrow adiposity and a reduction in serum insulin-like growth factor-1 (IGF-1) and the binding proteins that stabilize IGF-1. To determine the relationship between these proteins and bone marrow adiposity, we evaluated the adipogenic potential of marrow-derived mesenchymal stromal cells (MSCs) from mice with decreased serum IGF-1 due to knockdown of IGF-1 production by the liver or knock-out of the binding proteins. We employed 10-16-week-old, liver-specific IGF-1-deficient, IGFBP-3 knock-out (BP3KO) and acid-labile subunit knock-out (ALSKO) mice. We found that expression of the late adipocyte differentiation marker peroxisome proliferator-activated receptor gamma was increased in marrow isolated from ALSKO mice. When induced with adipogenic media, MSC cultures from ALSKO mice revealed a significantly greater number of differentiated adipocytes compared with controls. MSCs from ALSKO mice also exhibited decreased alkaline-phosphatase positive colony size in cultures that were stimulated with osteoblast differentiation media. These osteoblast-like cells from ALSKO mice failed to induce osteoclastogenesis of control cells in co-culture assays, indicating that impairment of IGF-1 complex formation with ALS in bone marrow alters cell fate, leading to increased adipogenesis.

Ion-controlled on-off switch of electron transfer from tetrathiafulvalene calix[4]pyrroles to Li+@C60.

Binding of chloride anion to a tetrathiafulvalene calix[4]pyrrole (TTF-C4P) donor results in ET to Li(+)@C(60) to produce the radical pair (TTF-C4P(•+)/Li(+)@C(60)(•-)), the structure of which was characterized by X-ray crystallographic analysis. The addition of tetraethylammonium cation, which binds more effectively than Li(+)@C(60)(•-) as a guest within the TTF-C4P cavity, leads to electron back-transfer, restoring the initial oxidation states of the donor and acceptor pair.