Boosting the Faradaic Efficiency of Br--Mediated Photoelectrochemical Epoxidation by Local Acidity on α-Fe2O3.

The redox mediated photoelectrochemical (PEC) or electrochemical (EC) alkene oxidation process is a promising method to produce high value-added epoxides. However, due to the competitive reaction of water oxidation and overoxidation of the mediator, the utilization of the electricity is far below the ideal value, where the loss of epoxidation's faradaic efficiency (FE) is ≈50%. In this study, a Br-/HOBr-mediated method is developed to achieve a near-quantitative selectivity and ≈100% FE of styrene oxide on α-Fe2O3, in which low concentration of Br- as mediator and locally generated acidic micro-environment work together to produce the higher active HOBr species. A variety of styrene derivatives are investigated with satisfied epoxidation performance. Based on the analysis of local pH-dependent epoxidation FE and products distribution, the study further verified that HOBr serves as the true active mediator to generate the bromohydrin intermediate. It is believed that this strategy can greatly overcome the limitation of epoxidation FE to enable future industrial applications.

NIR-Absorbing B,N-Heteroarene as Photosensitizer for High-Performance NIR-to-Blue Triplet-Triplet Annihilation Upconversion.

Triplet-triplet annihilation upconversion (TTA-UC) with near-infrared (NIR) photosensitizers is highly desirable for a variety of emerging applications. However, the development of NIR-to-blue TTA-UC with a large anti-Stokes shift is extremely challenging because of the energy loss during the intersystem crossing (ISC). Here, we develop the first NIR-absorbing B,N-heteroarene-based sensitizer (BNS) with multi-resonance thermally activated delayed fluorescence (MR-TADF) characters to achieve efficient NIR-to-blue TTA-UC. The small energy gap between the singlet and triplet excited states (0.14 eV) of BNS suppresses the ISC energy loss, and its long-delayed fluorescence lifetime (115 µs) contributes to efficient triplet energy transfer. As a result, the largest anti-Stokes shift (1.03 eV) among all heavy-atom-free NIR-activatable TTA-UC systems is obtained with a high TTA-UC quantum yield of 2.9 % (upper limit 50 %).

Synthesis of Highly Luminescent Chiral Nanographene.

Chiral nanographenes with both high fluorescence quantum yields (ΦF ) and large dissymmetry factors (glum ) are essential to the development of circularly polarized luminescence (CPL) materials. However, most studies have been focused on the improvement of glum , whereas how to design highly emissive chiral nanographenes is still unclear. In this work, we propose a new design strategy to achieve chiral nanographenes with high ΦF by helical π-extension of strongly luminescent chromophores while maintaining the frontier molecular orbital (FMO) distribution pattern. Chiral nanographene with perylene as the core and two dibenzo[6]helicene fragments as the wings has been synthesized, which exhibits a record high ΦF of 93 % among the reported chiral nanographenes and excellent CPL brightness (BCPL ) of 32 M-1 cm-1 .

A Eu(iii) metal-organic framework based on anthracenyl and alkynyl conjugation as a fluorescence probe for the selective monitoring of Fe3+ and TNP.

In this work, a luminescent metal-organic framework (Eu-MOF {[Eu6L6(µ3-OH)8(H2O)3]8·H2O} n ) was constructed by a solvothermal method with a linear organic ligand L (10-[(2-amino-4-carboxyl-phenyl)ethynyl]anthracene-9-carboxylic acid) based on anthracene and alkyne groups and using Eu3+ as the metal center. The MOF exhibits a stable UiO-66 crystal structure, and a six-core cluster twelve-linked secondary structural unit was successfully synthesized using 2-fluorobenzoic acid as a modulator, forming a classical fcu topology. Moreover, it exhibits good chemical stability. Interestingly, Eu-MOF exhibited high selectivity and sensitive fluorescence burst properties towards Fe3+ ions and 2,4,6-trinitrophenol (TNP) in DMF solution. For Fe3+, the K SV value is 5.06 × 105 M-1 and the LOD value is 5.1 × 10-7 M. For TNP, the K SV value is 1.92 × 104 M-1 and the LOD value is 1.93 × 10-6 M. In addition, Eu-MOF showed good anti-interference ability and fast response. This work provides an excellent fluorescent sensor for the detection of Fe3+ and 2,4,6-trinitrophenol (TNP) residues in contaminants.

B,N-Embedded Double Hetero[7]helicenes with Strong Chiroptical Responses in the Visible Light Region.

The development of helicene molecules with significant chiroptical responses covering a broad range of the visible spectrum is highly desirable for chiral optoelectronic applications; however, their absorption dissymmetry factors (gabs) have been mostly lower than 0.01. In this work, we report unprecedented B,N-embedded double hetero[7]helicenes with nonbonded B and N atoms, which exhibit excellent chiroptical properties, such as strong chiroptical activities from 300 to 700 nm, record high gabs up to 0.033 in the visible spectral range, and tunable circularly polarized luminescence (CPL) from red to near-infrared regions (600-800 nm) with high photoluminescence quantum yields (PLQYs) up to 100%. As revealed by theoretical analyses, the high gabs values are related to the separate molecular orbital distributions owing to the incorporation of nonbonded B and N atoms. The new type of B,N-embedded double heterohelicenes opens up an appealing avenue to the future exploitation of high-performance chiroptical materials.

Erratum: Chlorido-tetra-kis-(imidazole)-copper(II) chloride. Corrigendum.

[This corrects the article DOI: 10.1107/S1600536807044108.].

Let-7a regulates EV secretion and mitochondrial oxidative phosphorylation by targeting SNAP23 in colorectal cancer.

BACKGROUND: MicroRNAs (miRNAs) are abundant in tumor-derived extracellular vesicles (EVs) and the functions of extracellular miRNA to recipient cells have been extensively studied with tumorigenesis. However, the role of miRNA in EV secretion from cancer cells remains unknown. METHODS: qPCR and bioinformatics analysis were applied for determining extracellular let-7a expression from CRC patient serum and cells. Nanosight particle tracking analysis was performed for investigating the effect of let-7a on EV secretion. Luciferase reporter assays was used for identifying targeted genes synaptosome-associated protein 23 (SNAP23). In vitro and in vivo assays were used for exploring the function of let-7a/SNAP23 axis in CRC progression. Bioenergetic assays were performed for investigating the role of let-7a/SNAP23 in cellular metabolic reprogramming. RESULTS: let-7a miRNA was elevated in serum EVs from CRC patients and was enriched in CRC cell-derived EVs. We determined that let-7a could suppress EV secretion directly targeting SNAP23. In turn, SNAP23 promotes EV secretion of let-7a to downregulate the intracellular let-7a expression. In addition, we found a novel mechanism of let-7a/SNAP23 axis by regulating mitochondrial oxidative phosphorylation (OXPHOS) through Lin28a/SDHA signaling pathway. CONCLUSIONS: Let-7a plays an essential role in not only inhibiting EV secretion, but also suppressing OXPHOS through SNAP23, resulting in the suppression of CRC progression, suggesting that let-7a/SNAP23 axis could provide not only effective tumor biomarkers but also novel targets for tumor therapeutic strategies.

Toll-like receptor 2 regulates metabolic reprogramming in gastric cancer via superoxide dismutase 2.

Toll-like receptors (TLRs) play critical roles in host defense after recognition of conserved microbial- and host-derived components, and their dysregulation is a common feature of various inflammation-associated cancers, including gastric cancer (GC). Despite the recent recognition that metabolic reprogramming is a hallmark of cancer, the molecular effectors of altered metabolism during tumorigenesis remain unclear. Here, using bioenergetics function assays on human GC cells, we reveal that ligand-induced activation of TLR2, predominantly through TLR1/2 heterodimer, augments both oxidative phosphorylation (OXPHOS) and glycolysis, with a bias toward glycolytic activity. Notably, DNA microarray-based expression profiling of human cancer cells stimulated with TLR2 ligands demonstrated significant enrichment of gene-sets for oncogenic pathways previously implicated in metabolic regulation, including reactive oxygen species (ROS), p53 and Myc. Moreover, the redox gene encoding the manganese-dependent mitochondrial enzyme, superoxide dismutase (SOD)2, was strongly induced at the mRNA and protein levels by multiple signaling pathways downstream of TLR2, namely JAK-STAT3, JNK MAPK and NF-κB. Furthermore, siRNA-mediated suppression of SOD2 ameliorated the TLR2-induced metabolic shift in human GC cancer cells. Importantly, patient-derived tissue microarrays and bioinformatics interrogation of clinical datasets indicated that upregulated expression of TLR2 and SOD2 were significantly correlated in human GC, and the TLR2-SOD2 axis was associated with multiple clinical parameters of advanced stage disease, including distant metastasis, microvascular invasion and stage, as well as poor survival. Collectively, our findings reveal a novel TLR2-SOD2 axis as a potential biomarker for therapy and prognosis in cancer.

Toll-like receptor 2 stimulation promotes colorectal cancer cell growth via PI3K/Akt and NF-κB signaling pathways.

Toll-like receptor (TLR) 2 is a key regulator of innate immune responses and has been shown to play an important role in inflammation-associated cancers. In this study, we aimed to evaluate the role of TLR2 in colorectal cancer (CRC). We demonstrated that TLR2 mRNA and protein expression was significantly upregulated in tumors from CRC patients and indicated poor prognosis. Using the TLR2 agonist Pam3Cys (P3C) to activate TLR2 signaling in human CRC cell lines, we showed that TLR2 drives cellular proliferation, which was dependent upon PI3K/Akt and NF-κB signaling pathways and was associated with the upregulation of anti-apoptotic genes BCL2A1, WISP1 and BIRC3. Likewise, pharmacological blockade of PI3K/Akt and NF-κB pathways mitigated the CRC pro-survival effects of TLR2 stimulation. Furthermore, genetic ablation of TLR2 using CRISPR/Cas9 suppressed CRC cell proliferation, invasion and migration. Taken together, these findings demonstrate that TLR2 plays an important role in colorectal tumorigenesis and may represent a promising therapeutic target in CRC.

Clinical Utility of a STAT3-Regulated miRNA-200 Family Signature with Prognostic Potential in Early Gastric Cancer.

Purpose: The majority of gastric cancer patients are diagnosed with late-stage disease, for which distinct molecular subtypes have been identified that are potentially amenable to targeted therapies. However, there exists no molecular classification system with prognostic power for early-stage gastric cancer (EGC) because the molecular events promoting gastric cancer initiation remain ill-defined.Experimental Design: miRNA microarrays were performed on gastric tissue from the gp130F/F preclinical EGC mouse model, prior to tumor initiation. Computation prediction algorithms were performed on multiple data sets and independent gastric cancer patient cohorts. Quantitative real-time PCR expression profiling was undertaken in gp130F/F-based mouse strains and human gastric cancer cells genetically engineered for suppressed activation of the oncogenic latent transcription factor STAT3. Human gastric cancer cells with modulated expression of the miR-200 family member miR-429 were also assessed for their proliferative response.Results: Increased expression of miR-200 family members is associated with both tumor initiation in a STAT3-dependent manner in gp130F/F mice and EGC (i.e., stage IA) in patient cohorts. Overexpression of miR-429 also elicited contrasting pro- and antiproliferative responses in human gastric cancer cells depending on their cellular histologic subtype. We also identified a miR-200 family-regulated 15-gene signature that integrates multiple key current indicators of EGC, namely tumor invasion depth, differentiation, histology, and stage, and provides superior predictive power for overall survival compared with each EGC indicator alone.Conclusions: Collectively, our discovery of a STAT3-regulated, miR-200 family-associated gene signature specific for EGC, with predictive power, provides a molecular rationale to classify and stratify EGC patients for endoscopic treatment. Clin Cancer Res; 24(6); 1459-72. ©2018 AACR.

TLR Agonists as Adjuvants for Cancer Vaccines.

Toll-like receptors (TLRs) are one of the best characterised families of pattern recognition receptors (PRRs) and play a critical role in the host defence to infection. Accumulating evidence indicates that TLRs also participate in maintaining tissue homeostasis by controlling inflammation and tissue repair, as well as promoting antitumour effects via activation and modulation of adaptive immune responses. TLR agonists have successfully been exploited to ameliorate the efficacy of various cancer therapies. In this chapter, we will discuss the rationales of using TLR agonists as adjuvants to cancer treatments and summarise the recent findings of preclinical and clinical studies of TLR agonist-based cancer therapies.

Molecular Iodine-Mediated α-C-H Oxidation of Pyrrolidines to N,O-Acetals: Synthesis of (±)-Preussin by Late-Stage 2,5-Difunctionalizations of Pyrrolidine.

We previously reported an iterative synthesis of unsymmetrical 2,5-disubstituted pyrrolidines from pyrrolidine by two rounds of redox-triggered α-C-H functionalization. Although this approach can be used to introduce substituents at the 2- and 5-positions, it is lengthy because the redox auxiliary must be removed and then reinstalled. Therefore, we sought to develop a method to oxidize 2-functionalized pyrrolidine to cyclic N,O-acetal which could then react with a nucleophile for introduction of the 5-substituent. In this work, we found that molecular iodine can mediate the preferential oxidation of secondary over tertiary α-C-H bonds of α-substituted pyrrolidines to form cyclic N,O-acetals, improving the step economy of our previously reported method. With this strategy, (±)-preussin and its C(3) epimer were synthesized from (±)-pyrrolidin-3-ol.

Controllable Synthesis of Lindqvist Alkoxopolyoxovanadate Clusters as Heterogeneous Catalysts for Sulfoxidation of Sulfides.

Six alkoxohexavanadate-based Cu- or Co-POVs [Cu(dpa)(acac)(H2O)]2[V6O13(OMe)6] (1), [Cu(phen)(acac)(MeOH)]2[V6O13(OMe)6] (2), [Co(dpa)(acac)2]2[V6O13(OMe)6]·2MeOH (3), [Co(phen)(acac)2]2[V6O13(OMe)6] (4), [Cu(dpa)(acac)]2[VIV2VV4O12(OMe)7] (5), and [Cu(dpa)(acac)(MeOH)]2[VIV2VV4O11(OMe)8] (6) (POV = polyoxovanadate; dpa = 2,2'-dipyridine amine; phen = 1,10-phenanthroline; acac = acetylacetone anion) have been synthesized by controlling the reaction conditions and characterized by single-crystal X-ray diffraction and powder X-ray diffraction analyses, FT-IR spectroscopy, element analyses, and X-ray photoelectron spectroscopy. In compounds 1-4 and 6, Cu or Co complexes and alkoxohexavanadate anions are assembled through electrostatic interactions. Differently, in compound 5, seven-methoxo-substituted Lindqvist-type [V6O12(OMe)7]2- are bridged to Cu complex via terminal O atoms by coordination bonds. All compounds 1-6 exhibit excellent heterogeneous catalytic performance in oxidative desulfurization and CEES ((2-chloroethyl) ethyl sulfide, a sulfur mustard simulant) abatement with H2O2 as oxidant. Among them, the catalytic activity of 6 [conv. of DBT (dibenzothiophene) up to 100% in 6 h; conv. of CEES reached 100% and selectivity of CEESO ((2-chloroethyl) ethyl sulfoxide) up to 85% after 4 h] outperforms others and can be reused without losing its activity.

Four alkoxohexavanadate-based Pd-polyoxovanadates as robust heterogeneous catalysts for oxidation of benzyl-alkanes.

Four alkoxohexavanadate-based Pd-POVs [Pd(dpa)(acac)]2[V6O13(OMe)6] (1), [Pd(dpa)(acac)]2[V6O11(OMe)8] (2), [Pd(dpa)(acac)]2[V6O11(OMe)8]·H2O (3), and [Pd(DMAP)2(acac)]2[V6O11(OMe)8]·H2O (4) (POV = polyoxovanadate; dpa = 2,2'-dipyridine amine; DMAP = 4-dimethylaminopyridine; acac = acetylacetone anion) have been synthesized and fully characterized by single crystal X-ray diffraction and powder X-ray diffraction analyses, Fourier transform infrared spectroscopy, element analyses, and X-ray photoelectron spectroscopy. In 1-4, Pd complexes and hexavanadate anions are assembled through electrostatic interactions. Interestingly, the [V6O11(OMe)8](2-) cores in 2 and 3 are a pair of isomers that can be isolated by controlling crystallization temperature. Moreover, to the best of our knowledge, the {V6} core in 3 represents a new octamethoxyhexavanadates cluster. It is notable that compounds 1-4 exhibit excellent heterogeneous catalytic performance in the oxidation of benzyl-alkanes with t-butylhydroperoxide as oxidant. Among them, the catalytic activity of 1 (conv. and selec. up to 99%, respectively) outperforms others and can be reused without losing its activity.

Significance and prognostic value of Gli-1 and Snail/E-cadherin expression in progressive gastric cancer.

Abnormal activation of the hedgehog (Hh) signaling pathway has been found to be involved in the occurrence, invasion, and metastasis of cancers. Epithelial-mesenchymal transition (EMT) also plays an important role in the invasion and metastasis of cancers. However, the significance of the Hh signaling pathway and EMT in the invasion and metastasis of gastric cancer is still unclear. This study aimed to investigate the significance and prognostic value of the Hh signaling pathway and EMT in progressive gastric cancer. Immunohistochemistry was performed to detect the expression of the Hh-induced transcriptional factor Gli-1 and the EMT-related molecules Snail and E-cadherin in 121 patients with progressive gastric cancer. Histological type, depth of invasion, lymph node metastasis, and pTNM stage were also recorded. In progressive gastric cancer, Gli-1 expression increased markedly, and was closely associated with increased Snail expression and decreased E-cadherin expression. Diffuse type cancer, lymph node metastasis, and abnormal expression of E-cadherin were independent factors influencing the prognosis of patients with progressive gastric cancer. These findings suggest that abnormal activation of the Hh signaling pathway is closely related to the presence of EMT and is an important factor influencing the prognosis of patients with diffuse progressive gastric cancer.

microRNA-148a suppresses human gastric cancer cell metastasis by reversing epithelial-to-mesenchymal transition.

MicroRNAs (miRNAs) are important regulators of gastric cancer development and progression. miR-148a is one of the most frequently and highly downregulated miRNAs in gastric cancer and is associated with advanced clinical stage and poor prognosis. In this study, we investigated the role of miR-148a in gastric cancer metastasis. Levels of miR-148a were determined by qRT-PCR in 60 gastric cancer samples. Cell migration and invasion assays were performed in a stably expressing miRNA-148a gastric cancer cell line established using a lentivirus expression system. Epithelial-mesenchymal transition (EMT) was evaluated using qRT-PCR and Western Blots to detect epithelial marker E-cadherin and mesenchymal marker, vimentin. Luciferase reporter assays were used to identify downstream targets and biological function of miR-148a. Gastric cancer tissue had significantly lower expression of miR-148a compared to non-tumor tissue. Low miR-148a levels were associated with lymph node metastasis, N stage, and blood vessel invasion. miR-148a overexpression inhibited metastasis of gastric cancer cells. miR-148a overexpression also downregulated vimentin expression and upregulated E-cadherin expression, suggesting that miR-148a inhibited EMT. Finally, the SMAD2 gene was identified as the direct and functional target of miR-148a. MiR-148a suppresses gastric cancer metastasis and EMT, likely via SMAD2. Restoration of miR-148a expression could have important implications in gastric cancer therapy.

The synthesis, crystal structure and enhanced blue fluorescence emission of novel antipyrine derivatives.

Four new antipyrine derivatives were synthesized and characterized by elemental analysis, FT-IR, (1)H NMR, (13)C NMR spectroscopy, and a representative compound 1b was confirmed based on the X-ray crystallographic analysis. The antipyrine-phenylboronic acid 1b crystallizes in the monoclinic space group P2(1)/c, and displays an E configuration about the CN double bond. The absorption and fluorescence spectra of these compounds were investigated. Replacement of a six-membered phenyl group with a five-membered thienyl unit in the antipyrine derivatives resulted in a bathochromic shift approximately 21 nm, while the bithienyl system caused a strong bathochromic effect of 53 nm relative to the substituted phenyl groups. The bithienyl-antipyrine hybrid 1c displayed a turn-on fluorescence response to water, acetic acid (HOAc) and sulfuric acid (H(2)SO(4)) in ethanol solution, but no fluorescence response toward alkali. Whereas the free compound was very weakly fluorescent in ethanol, the addition of water, HOAc and H(2)SO(4) leads to an appearance of strong blue fluorescence and a dramatic increase of emission intensity.

15-PGDH is reduced and induces apoptosis and cell cycle arrest in gastric carcinoma.

AIM: To investigate the expression of 15-hydroxyprostaglandin dehydrogenase (15-PGDH) in human gastric cancer and it's mechanism in apoptosis and cell cycle arrest. METHODS: Expression of 15-PGDH mRNA and protein was examined by immunohistochemistry, immunocytochemistry, reverse transcriptase polymerase chain reaction (RT-PCR) and Western blotting in tissue from human gastric cancer, gastric precancerous state (gastric polyps and atrophic gastritis), normal stomach, and gastric cancer cell lines. The relationship between gastric cancer, gastric precancerous state and 15-PGDH expression was determined. The association between expression of 15-PGDH and various clinicopathological parameters in gastric cancer was evaluated. Human gastric cancer cell line SGC-7901 was transfected with 15-PGDH expression plasmids. The effect of 15-PGDH on the cell cycle was examined by flow cytometry. The effect of 15-PGDH on apoptosis was examined by transmission electron microscopy, flow cytometry and transferase mediated nick end labeling (TUNEL) assay. Expression of cell cycle (p21, p27, p16 and p53) and apoptosis (Survivin, BCL-2, BCL-X(L), BAK and BAX) genes was analyzed by RT-PCR. RESULTS: Expression of 15-PGDH mRNA and protein in human gastric cancer tissues was significantly lower than in normal gastric tissues (P < 0.01). Expression in human gastric cancer cell lines MKN-28 and MKN-45 was reduced, and absent in SGC-7901 cells (P < 0.05). Reduction of 15-PGDH expression was also found in precancerous tissues, such as gastric polyps and atrophic gastritis (P < 0.01). There was a significant difference in expression of 15-PGDH among various gastric cancer pathological types (P < 0.05), with or without distant metastasis (P < 0.05) and different TNM stage (P < 0.01). Flow cytometry demonstrated a significant increase in apoptotic cells in SGC-7901 cells transfected with pcDNA3/15-PGDH plasmid for 24 h and 48 h (P < 0.01), and an increased fraction of sub-G1 phase after transfection (P < 0.05). TUNEL assay showed an increased apoptotic index in cells overexpressing 15-PGDH (P < 0.01). After transfection, expression of proapoptotic genes, such as BAK (P < 0.05), BAX and p53 (P < 0.01), was increased. Expression of antiapoptotic genes was decreased, such as Survivin, BCL-2 and BCL-X(L) (P < 0.01). Expression of cyclin-dependent kinase inhibitors p21 and p16 (P < 0.01) was significantly upregulated in cells overexpressing 15-PGDH. CONCLUSION: Reduction of 15-PGDH is associated with carcinogenesis and development of gastric carcinoma. 15-PGDH induces apoptosis and cell cycle arrest in SGC-7901 cells.

Synthesis, single-crystal characterization and preliminary biological evaluation of novel ferrocenyl pyrazolo[1,5-a]pyrazin-4(5H)-one derivatives.

A series of novel ferrocenyl pyrazolo[1,5-a]pyrazin-4(5H)-one derivatives was synthesized and characterized by 1H NMR, 13C NMR, IR, HRMS and X-ray diffraction analysis. Preliminary evaluation of biological applications showed that the compounds 6c and 6f inhibit the growth of A549 cells in dosage-dependent manners through cell cycle arrest.

1:1 Adducts of 2,2'-[isopropylidenebis(p-phenyleneoxy)]diacetic acid with dimethylammonium and 4,4'-bipyridine.

The title compounds, dimethylammonium 2-{4-[1-(4-carboxymethoxyphenyl)-1-methylethyl]phenoxy}acetate, C(2)H(8)N(+).C(19)H(19)O(6)(-), (I), and 2,2'-[isopropylidenebis(p-phenyleneoxy)]diacetic acid-4,4'-bipyridine (1/1), C(19)H(20)O(6).C(10)H(8)N(2), (II), are 1:1 adducts of 2,2'-[isopropylidenebis(p-phenyleneoxy)]diacetic acid (H(2)L) with dimethylammonium or 4,4'-bipyridine. The component ions in (I) are linked by N-H...O, O-H...O and C-H...O hydrogen bonds into continuous two-dimensional layers parallel to the (001) plane. Adjacent layers are stacked via C-H...O hydrogen bonds into a three-dimensional network with an -ABAB- alternation of the two-dimensional layers. In (II), two H(2)L molecules, one bipy molecule and two half bipy molecules are linked by O-H...N hydrogen bonds into one-dimensional chains and rectanglar-shaped rings. They are assembled via pi-pi stacking interactions and C-H...O hydrogen bonds into an intriguing zero-dimensional plus one-dimensional poly(pseudo)rotaxane motif.