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Abstract The antitumor performance of PROteolysis-TArgeting Chimeras (PROTACs) is limited by its insufficient tumor specificity and poor pharmacokinetics. These disadvantages are further compounded by tumor heterogeneity, especially the presence of cancer stem-like cells, which drive tumor growth and relapse. Herein, we design a region-confined PROTAC nanoplatform that integrates both reactive oxygen species (ROS)-activatable and hypoxia-responsive PROTAC prodrugs for the precise manipulation of bromodomain and extraterminal protein 4 expression and tumor eradication. These PROTAC nanoparticles selectively accumulate within and penetrate deep into tumors via response to matrix metalloproteinase-2. Photoactivity is then reactivated in response to the acidic intracellular milieu and the PROTAC is discharged due to the ROS generated via photodynamic therapy specifically within the normoxic microenvironment. Moreover, the latent hypoxia-responsive PROTAC prodrug is restored in hypoxic cancer stem-like cells overexpressing nitroreductase. Here, we show the ability of region-confined PROTAC nanoplatform to effectively degrade BRD4 in both normoxic and hypoxic environments, markedly hindering tumor progression in breast and head-neck tumor models.

Abstract Proteolysis targeting chimeras (PROTACs) have emerged as a promising strategy for drug discovery and exploring protein functions, offering a revolutionary therapeutic modality. Currently, the predominant approach to PROTACs discovery mainly relies on an empirical design–synthesis–evaluation process involving numerous cycles of labor‐intensive synthesis‐purification and bioassay data collection. Therefore, the development of innovative methods to expedite PROTAC synthesis and exploration of chemical space remains highly desired. Here, a direct‐to‐biology strategy is reported to streamline the synthesis of PROTAC libraries on plates, enabling the seamless transfer of reaction products to cell‐based bioassays without the need for additional purification. By integrating amide coupling and light‐induced primary amines and o‐nitrobenzyl alcohols cyclization (PANAC) photoclick chemistry into a plate‐based synthetic process, this strategy produces PROTAC libraries with high efficiency and structural diversity. Moreover, by employing this platform for PROTACs screening, we smoothly found potent PROTACs effectively inhibit triple‐negative breast cancer (TNBC) cell growth and induce rapid, selective targeted degradation of cyclin‐dependent kinase 9 (CDK9). The study introduces a versatile platform for assembling PROTACs on plates, followed by direct biological evaluation. This approach provides a promising opportunity for high‐throughput synthesis of PROTAC libraries, thereby enhancing the efficiency of exploring chemical space and accelerating the discovery of PROTACs.

Introduction Severe septic cardiomyopathy (SCM) is one of the main causes of refractory septic shock (RSS), with a high mortality. The application of venoarterial extracorporeal membrane oxygenation (ECMO) to support the impaired cardiac function in patients with septic shock remains controversial. Moreover, no prospective studies have been taken to address whether venoarterial ECMO treatment could improve the outcome of patients with sepsis-induced cardiogenic shock. The objective of this study is to assess whether venoarterial ECMO treatment can improve the 30-day survival rate of patients with sepsis-induced refractory cardiogenic shock.Methods and analysis ExtraCorporeal Membrane Oxygenation in the therapy for REfractory Septic shock with Cardiac function Under Estimated is a prospective, multicentre, non-randomised, cohort study on the application of ECMO in SCM. At least 64 patients with SCM and RSS will be enrolled in an estimated ratio of 1:1.5. Participants taking venoarterial ECMO during the period of study are referred to as cohort 1, and patients receiving only conventional therapy without ECMO belong to cohort 2. The primary outcome is survival in a 30-day follow-up period. Other end points include survival to intensive care unit (ICU) discharge, hospital survival, 6-month survival, quality of life for long-term survival (EQ-5D score), successful rate of ECMO weaning, long-term survivors’ cardiac function, the number of days alive without continuous renal replacement therapy, mechanical ventilation and vasopressor, ICU and hospital length of stay, the rate of complications potentially related to ECMO treatment.Ethics and dissemination The trial has been approved by the Clinical Research and Application Institutional Review Board of the Second Affiliated Hospital of Guangzhou Medical University (2020-hs-51). Participants will be screened and enrolled from ICU patients with septic shock by clinicians, with no public advertisement for recruitment. Results will be disseminated in research journals and through conference presentations.Trial registration number NCT05184296.

Abstract Protein-modifying enzymes regulate the dynamics of myriad post-translational modification (PTM) substrates. Precise characterization of enzyme-substrate associations is essential for the molecular basis of cellular function and phenotype. Methods for direct capturing global substrates of protein-modifying enzymes in living cells are with many challenges, and yet largely unexplored. Here, we report a strategy to directly capture substrates of lysine-modifying enzymes via PTM-acceptor residue crosslinking in living cells, enabling global profiling of substrates of PTM-enzymes and validation of PTM-sites in a straightforward manner. By integrating enzymatic PTM-mechanisms, and genetically encoding residue-selective photo-crosslinker into PTM-enzymes, our strategy expands the substrate profiles of both bacterial and mammalian lysine acylation enzymes, including bacterial lysine acylases PatZ, YiaC, LplA, TmcA, and YjaB, as well as mammalian acyltransferases GCN5 and Tip60, leading to discovery of distinct yet functionally important substrates and acylation sites. The concept of direct capturing substrates of PTM-enzymes via residue crosslinking may extend to the other types of amino acid residues beyond lysine, which has the potential to facilitate the investigation of diverse types of PTMs and substrate-enzyme interactive proteomics.

Background: Cholangiocarcinoma is characterized by significant cellular heterogeneity and complex intercellular communication, which contribute to its progression and therapeutic resistance. Therefore, unraveling this complexity is essential for the development of effective treatments.Methods: We employed single-cell RNA sequencing (scRNA-seq) to investigate cellular heterogeneity and intercellular communication in cholangiocarcinoma and adjacent normal tissues from two patients. Distinct cell types were identified, and gene ontology analyses were conducted to determine enriched pathways. Moreover, cell-cell communications were analyzed using CellChat, a computational framework. Additionally, we performed sub-clustering analysis of T cells and fibroblasts.Results: The scRNA-seq analysis revealed distinct cell clusters and diverse cellular compositions of cholangiocarcinoma. CellChat analysis underscored an amplified outgoing signal from fibroblasts within the tumor, suggesting their pivotal role in the tumor microenvironment. Furthermore, T cell sub-clustering analysis revealed an active immune response within the tumor and new tumor-specific T cell clonotypes, suggesting scope for targeted immunotherapies. Moreover, fibroblast sub-clustering analysis indicated distinct functional states and highlighted the role of activated fibroblasts in shaping intercellular communication, particularly via CD99 and FN1 signaling.Conclusion: Our findings reveal the intricate cellular heterogeneity and dynamic intercellular communication in cholangiocarcinoma, providing valuable insights into disease progression and potential therapeutic strategies.

Abstract Aging is characterized by inevitable organ function decline over time, with consequent body deterioration and increased susceptibility to death. Astragalus polysaccharide (APS) has been reported to have anti‐oxidative, anti‐apoptotic, and anti‐inflammatory properties. We investigated the potential protective effects of APS on hydrogen peroxide (H2O2) induced hepatocyte senescence and identified related mechanisms in L02, Huh7, and LM3 cell lines. Aged female C57BL/6 mice were given APS for 1 week by intraperitoneal injection, and APS provided the strongest protective effect against H2O2‐induced damage at 100 μM. APS reduced the expression of cell senescence markers and alleviated pathological damage in aged mouse liver. APS treatment decreased oxidative stress, apoptosis, NOD‐like receptor protein‐3‐mediated pyroptosis, and maintained mitochondrial homeostasis. Notably, the protective effect of APS was weakened in the presence of chloroquine. APS might enrich autophagy by activating AMP‐activated protein kinase (AMPK) and inhibiting mammalian target of rapamycin (mTOR). In conclusion, APS reduced reactive oxygen species levels, inhibited apoptosis and pyroptosis, and promoted mitophagy via AMPK/mTOR pathway to alleviate hepatocyte senescence in vitro and in vivo.

Developing new click chemistry reactions for robust molecular assembly remains challenging. Here the authors report a light-induced primary amines and o-nitrobenzyl alcohols photoclick cyclization for rapid and modular functionalization of small molecules and native biomolecules, in vitro and in living systems.

In this paper, we investigate the long-time behavior for the nonautonomous semilinear second-order evolution equation ∂2u/∂t2−Δu−Δ∂u/∂t−Δ∂2u/∂t2=ft,ux,t−ρt+gt,x,inτ,∞×Ω with some hereditary characteristics, where Ω is an open-bounded domain of ℝNN≥3 with smooth boundary ∂Ω. Firstly, we establish the existence of solutions for the second-order nonautonomous evolution equation by the standard Faedo–Galerkin method, but without the uniqueness of solutions. Then by proving the pullback asymptotic compactness for the multivalued process Ut,τ on CH01Ω,H01Ω, we obtain the existence of pullback attractors in the Banach spaces CH01Ω,H01Ω for the multivalued process generated by a class of second-order nonautonomous evolution equations with hereditary characteristics and ill-posedness.

We aimed to identify an unique host transcriptional signature in peripheral blood mononuclear cells (PBMCs) in response to Mycobacterium leprae antigens to distinguish between patients with leprosy and non-leprosy controls for early diagnosis of the disease. Sixteen individuals were enrolled in the discovery cohort [eight patients with leprosy, comprising four multibacillary (MB) and four paucibacillary (PB); and eight non-leprosy controls, comprising four healthy house contacts (HHCs) and four endemic controls (ECs)]. The differences in the transcriptome response of PBMCs to M. leprae sonicate antigen were evaluated between leprosy patients and non-leprosy controls, and 12 differentially expressed genes (CCL2/MCP-1, IL-8, JAKM, ATP, ND1, SERP, FLJ10489, LINC00659, LOC34487, LOC101928143, MIR22, and NCF1C) were identified. The accuracy of the 12 differentially expressed genes was further validated for the diagnosis of leprosy using real-time quantitative PCR in 82 individuals (13 MB, 10 PB, 37 HHCs, and 22 ECs) in the validation cohort. We found that a 5 gene signature set IL-8, CCL2/MCP-1, SERP, LINC00659 and FLJ10489 had a suitable performance in discriminating leprosy from ECs. In addition, elevated expression of IL-8, CCL2/MCP-1, SERP and LINC00659 was associated with MB diagnosis compared with ECs, whereas increased expression of IL-8, CCL2/MCP-1, SERP and FLJ10489 was found to be useful biomarkers for PB diagnosis from ECs. Moreover, we found decreased expression of NCF1C among leprosy patients could distinguish leprosy from HHCs, whereas higher expression of CCL2 among MB than PB could distinguish different leprosy patients. In conclusion, among the 12 candidate host genes identified, a three gene signature IL-8, CCL2/MCP-1, and SERP showed the best performance in distinguishing leprosy patients from healthy controls. These findings may have implications for developing a rapid blood-based test for early diagnosis of leprosy.

Background/purpose: Ground section is the only way to study tooth enamel, and the conventional methods of making ground sections, grinding by hand or using a hard tissue microtome are either too time consuming or money costing. This study aimed to develop and assess a novel cutting machine in making ground sections and learning aid for dental students. Materials and methods: By using the novel cutting machine, the students cut the embedding teeth and got 50 μm ground sections efficiently. A series of fine/coarse combination stones were used for grinding the sections to uniform 20 μm thickness. Self-made ground sections were used in the lab class of tooth tissue. Questionnaires were designed to assess the participants’ attitude towards the cutting machine and their knowledge of the tooth tissue before and after making the tooth ground sections. Results: Our findings indicated that the novel cutting machine can act as an efficient tool to make tooth ground sections. Indeed, data indicated that making tooth ground section progress can assist students’ understanding of the structure and function of tooth and their pathology knowledge had improved. From a qualitative point of view, the students described making tooth ground section progress improve their practical ability and study interest in oral pathology. Conclusion: Overall, these findings indicate that our novel cutting machine can act as an efficient tool to make tooth ground sections and support dental students to study the pathology of the tooth hard tissue in a simple and functional way.

In this study, 45Si2MnCr2Mo steel was fabricated by casting, hot rolling, and normalizing, followed by tempering at different temperatures from 180 to 520 °C for 2 h. Special attention was paid to the effects of tempering on the microstructure and mechanical properties of the steel. The results indicate that microstructure of tempered steel consists of bainite, martensite, and retained austenite (RA), and it is not sensitive to tempering at temperatures below 320 °C. However, after tempering at temperatures of 420 and 520 °C, bainitic ferrite plates merged and their lath boundaries became vague. In turn, RA decomposed, whereas carbide particles appeared and then coarsened. With increasing tempering temperature, the volume fraction of RA achieved its peak value at 320 °C and carbon concentration within RA attained its peak value at 420 °C. The optimal balance of ultimate tensile strength of 2306 MPa and total elongation of 8.24% in the steel were achieved after being normalized at 950 °C for 0.5 h and subsequent tempering at 220 °C for 2 h. These values are found to exceed those of air-cooled and isothermal bainitic steels. Finally, the correlation between microstructure and mechanical properties of the steel under consideration was discussed.

Abstract Background Identifying gastric heterotopic pancreas and stromal tumors is difficult. Few studies have reported computed tomography (CT) findings for differentiating lesions less than 3 cm in diameter. In this study, we aimed to identify clinical characteristics and CT findings that can differentiate gastric heterotopic pancreatic lesions from stromal tumors less than 3 cm in diameter. Methods A total of 132 patients with pathologically confirmed gastric heterotopic pancreas (n = 66) and stromal tumors (n = 66) were included. Each group was divided into primary (n = 50) and validation cohort (n = 16). Clinical characteristics and CT findings were retrospectively reviewed. CT findings included location, border, contour, growth pattern, enhancement pattern and grade, the enhancement value of tumor, enhancement ratio of tumor, and enhancement ratio of tumor to pancreas in venous phase. The findings in the two groups were compared using the Pearson χ2 test or Student t-test. Receiver operating characteristic curves were used to determine areas under the curve and optimal cut-offs. Results Significant differences were observed between heterotopic pancreas and stromal tumors in the distribution of tumor location, border, contour (all P

Abstract Background Many tripartite motif (TRIM) family proteins have been reported to be of great importance in the initiation and progression in hepatocellular carcinoma (HCC). However, the biological role and regulatory mechanism of tripartite motif containing 52 (TRIM52) in HCC development and progression are poorly defined. Methods Immunohistochemistry (IHC), quantitative real-time PCR (qRT-PCR) or Western blot analysis was used to detect TRIM52, p21, matrix metalloproteinase 2 (MMP2), protein phosphatase, Mg2+/Mn2+ dependent 1A (PPM1A), p-Smad2/3 and Smad2/3 levels in HCC tissues and cell lines. HCC cell proliferation and cell cycle were measured by Cell Counting Kit-8 (CCK-8) and flow cytometry analysis, respectively. HCC cell migration and invasion were measured by Transwell assay. Tumor growth of HCC cells in vivo was measured using the nude mouse xenograft model. The correlation between TRIM52 and PPM1A was measured by co-immunoprecipitation (Co-IP) and ubiquitination analysis in vitro. Results TRIM52 was significantly up-regulated in the HCC tissues in comparison with the adjacent non-tumor hepatic tissues. TRIM52 was also up-regulated in HCC cell lines (MHCC-97H and MHCC-97L cells) compared with normal human liver cell line LO2. TRIM52 down-regulation by RNA interfering in MHCC-97H cells enhanced inhibition of cell proliferation, migration and invasion. TRIM52 down-regulation also induced MHCC-97H cells arrest in G0-G1 phase cell cycle and inhibited MHCC-97H cell growth in the nude mice. However, TRIM52 up-regulation in MHCC-97L cells promoted cell proliferation, migration and invasion. Furthermore, TRIM52 down-regulation significantly increased p21 and PPM1A expression, but inhibited MMP2 expression and induced Smad2/3 dephosphorylation in MHCC-97H cells, which were reversed by TRIM52 up-regulation in MHCC-97L cells. TRIM52 was found interacted with PPM1A and TRIM52 down-regulation inhibited the ubiquitination of PPM1A. Importantly, PPM1A up-regulation in MHCC-97L cells significantly suppressed TRIM52-mediated enhancement on cell proliferation, invasion and migration. Conclusions Our findings suggest that TRIM52 up-regulation promotes proliferation, migration and invasion of HCC cells through the ubiquitination of PPM1A.

Background/Objective: To compare the curative effect of single-stage and two-stage Fowler–Stephens (F–S) laparoscopic orchidopexy for intraabdominal high testis and explore the appropriate surgical approach. Methods: We performed a prospective analysis of the clinical data of 28 patients who underwent F-S laparoscopic orchidopexy for intraabdominal high testis in our department from May 2012 to April 2015, including 15 cases of the single-stage F-S operation and 13 cases of the two-stage F-S operation. By comparing the two groups preoperative and postoperative (6 months) clinical data of testicular position, testicular volume, and sex hormone levels [testosterone (T), follicle stimulating hormone (FSH), and estradiol (E2)], we analyzed the difference in efficacy between the two procedures. Results: Twenty-eight patients completed laparoscopic surgery, no case was converted, and no testis was excised. All patients were followed up for 9–25 months after the operation, with an average follow-up of 16.2 months. The postoperative testicular volume of the single-stage and two-stage F-S groups was not significantly reduced (p>0.05). In both groups, the postoperative T levels were significantly increased compared to the preoperative levels (p0.05). In the single-stage F-S group, the testes were located in the scrotum in 13 cases and retracted to the lower groin in two cases. In the two-stage F-S group, the testes were located in the scrotum in 12 cases and retracted to the lower groin in one case. The difference in postoperative testicular position between the two groups was not significant (p>0.05). Conclusion: In the case of testis with good collateral circulation, single-stage F-S laparoscopic orchidopexy had the same safety and efficacy as the two-stage F-S procedure. Surgical options should be based on comprehensive consideration of intraoperative testicular location, testicular ischemia test, and collateral circumstances surrounding the testes. Under the appropriate conditions, we propose single-stage F-S laparoscopic orchidopexy be preferred. It may be appropriate to avoid unnecessary application of the two-stage procedure that has a higher cost and causes more pain for patients.

Background: Amyloid-β deposition and accumulation of autophagic vacuoles are pathologic features of Alzheimer's disease (AD). Dysregulation of the endosomal–autophagic–lysosomal (EAL) pathway, which impairs amyloid precursor protein processing, is one of the earliest changes in AD. However, the precise role of EAL pathway in neurodegeneration remains unclear. This study aimed to investigate the role of EAL pathway in AD and further study the mechanism of EAL dysfunction. Methods: We used 3-, 7-, and 12-month-old APPswe/PSEN1dE9 (APP/PS1) mice to model different stages of AD with age- and gender-matched wild-type littermates as controls (4–7 mice per group) and detected the changes of EAL markers, endosomal organizers Rab5 and Rab7, autophagosome marker LC3B, and lysosomal proteins Lamp1/2 in cortex and hippocampus by immunohistochemistry and Western blotting analysis. To further explore the mechanism of EAL dysregulation in AD, components of the class III phosphatidylinositol 3-kinase (PI3KC3) complex, activators of Rab7 (Beclin1 and UVRAG), and the negative regulator of Rab7 (Rubicon) were also measured in this two brain regions. Results: In 7-month-old APP/PS1 brain that amyloid beta initiated to accumulate intracellularly, EAL pathway, and related PI3KC3 members, UVRAG and Beclin1 were upregulated both in cortex and hippocampus (all P < 0.05). By the age of 12 months old, when abundant amyloid plaques formed, EAL markers, UVRAG, and Beclin1 were also upregulated in the cortex (all P < 0.05). However, Rab7 was decreased significantly (P = 0.0447), accompanied by a reduction of its activating PI3KC complex component Beclin1 (P = 0.0215) and enhancement of its inhibiting component Rubicon (P = 0.0055) in the hippocampus. Conclusions: Our study implies that EAL pathway, represented as Rab7 and its PI3KC3 regulators' expressions, showed temporal and spatial variation in brains at different stages of AD. It provides new insights into the role of EAL pathway in pathogenesis and indicates potential therapeutic targets in neurodegenerative diseases.

Deep Candida infections commonly occur in immunosuppressed patients. A rare case of a multiple deep organ infection with Candida albicans and spinal tuberculosis was reported in a healthy young man. The 19-year-old man complained of month-long fever and lower back pain. He also had a history of scalded mouth syndrome. Coinfection with Mycobacterium tuberculosis and Candida albicans was diagnosed using the culture of aspirates from different regions. Symptoms improved considerably after antifungal and antituberculous therapy. This case illustrates that infection with tuberculosis might impair the host's immune system and increase the risk of invasive candidiasis in an immunocompetent patient.

In the title complex, [V(C15H12N2O4)(C2H5O)O], the VV ion is coordinated by an oxide O atom, an ethanolate anion and two O atoms and one N atom from the tridentate benzohydrazidate dianion in a distorted square-pyramidal geometry; the V atom is displaced by 0.4748 (8) Å from the basal plane towards the axial oxide O atom. An intramolecular O—H...N hydrogen bond occurs in the benzohydrazidate ligand. Weak intermolecular C—H...O hydrogen bonding is present in the crystal.

In the title compound, [Cd2(C7H3NO4)2(C13H8N4)2(H2O)2], the CdII ion is six-coordinated by two N atoms from a 1H-imidazo[4,5-f][1,10]phenanthroline (IP) ligand, one N atom and one O atom from a pyridine-2,3-dicarboxylate (pdc) ligand, one O atom from another pdc ligand and one water molecule in a distorted octahedral geometry. Two CdII ions are bridged by a pair of pdc ligands, forming a centrosymmetric dinuclear structure. Neighboring dinuclear units are linked by the coordinated water molecules through O—H...N and O—H...O hydrogen bonds, forming a layer parallel to (011). The layers are further linked into a three-dimensional network through N—H...O hydrogen bonds. π–π interactions between the IP ligands further stabilize the supramolecular structure [centroid–centroid distances = 3.579 (3), 3.686 (3), 3.710 (3), 3.766 (3) and 3.841 (3) Å].

The asymmetric unit of the title trinuclear NiII compound, [Ni3(C11H11N2O3)(C5H5N)4], contains two independent molecules which are located on individual inversion centres. The central Ni atom, located on an inversion centre, is coordinated by two pyridine N atoms and is further N,O-chelated by two N-(2-methylpropanoyl)salicyloylhydrazidate anions in an elongated octahedral coordination geometry. The terminal Ni atom is coordinated by a pyridine ligand and is further N,N′,O-chelated by an N-(2-methylpropanoyl)salicyloylhydrazidate anion in a distorted square-planar coordination geometry. Weak intramolecular C—H...O hydrogen bonding is observed in the structure.

In the title complex, [Co(C15H12N3O4)2Cl(C6H7N)], the CoIII ion is coordinated by two N atoms and two O atoms from two deprotonated Schiff base ligands, one N atom from a 4-methylpyridine ligand and one Cl atom, forming a distorted octahedral geometry. The CoIII ion is displaced by 0.038 (2) Å from the equatorial plane towards the axial Cl atom.

In the title centrosymmetric dinuclear compound, [Mn2(SO4)2(C13H8N4)2(H2O)4]·2H2O, the MnII atom is octahedrally coordinated by two N atoms from a 1H-imidazo[4,5-f][1,10]phenanthroline (ip) ligand, two O atoms belonging to two bridging sulfate anions and two water O atoms. In the crystal structure, the complex molecules and the uncoodinated water molecules are connected by O—H...O, O—H...N and N—H...O hydrogen bonds into a three-dimensional network. A π–π stacking interaction between the pyridyl ring of the ip ligand and the benzene ring of the neighboring ligand [centroid–centroid distance = 3.579 (2) Å] is also observed.

In the title complex, [V(C15H12N2O4)(CH3O)O], the VV ion exhibits a distorted square-pyramidal coordination geometry; three donor atoms from a hydrazone ligand and one O atom of the deprotonated methanol define the coordination basal plane. The VV ion is displaced by 0.464 (1) Å from the basal plane towards the axial oxide O atom. Intramolecular O—H...N hydrogen bonding occurs. Intermolecular C—H...O hydrogen bonding is also observed in the crystal structure.

The reaction of MoO3 with 2-(3-pyridyl)benzoimidazole and water in the presence of MnSO4·5H2O at 453 K under hydrothermal conditions afforded the title compound, {(C12H11N2)[Mo4O13]}n, in which infinite molybdenum oxide anionic chains are charge-balanced by diprotonated 2-(3-pyridyl)benzoimidazole (H23-PBIM2+) cations. Eight [MoO6] octahedra are edge-shared, forming compact octamolybdate subunits which are connected through pairs of Mo—O—Mo bridges into extended one-dimensional arrays propagating along the a-axis direction. The asymmetric unit of the metal oxide chain contains one half of the octamolybdate unit, denoted [Mo4O13], the other half being generated by an inversion center. These molybdenum oxide chains are further connected through the 2-(3-pyridinio)benzoimidazolium cations into a three-dimensional network via N—H...O hydrogen bonds. In addition, neighbouring diprotonated cations are arranged in a head-to-tail fashion with a plane-to-plane separation of 3.63 (10) Å, indicating the existence of weak aromatic π–π stacking interactions.

In the title compound, [Zn(C10H11N2O2)2(C5H5N)2], the ZnII atom lies on an inversion centre, and is coordinated in a distorted octahedral geometry by two carbonyl O atoms and two imino N atoms from two anionic bidentate acetone (2-hydroxybenzoyl)hydrazone ligands and by two N atoms from two pyridine molecules. The hydroxyl group acts as a donor, forming an intramolecular O—H...N hydrogen bond.

In the title complex, [Ni(C15H11ClN2O3)(C3H4N2)], the NiII ion is coordinated by a phenolate O, hydrazine N and carbonyl O atom from the hydrazone ligand and by an N atom from the imidazole molecule, forming a distorted square-planar geometry. Intermolecular N—H...N hydrogen bonds link neighboring molecules into extended chains parallel to [100].

The title compound, [ZnCl2(C12H8N4S)]n, was obtained by crystallization of 2,5-di-4-pyridyl-1,3,4-thiadiazole with ZnCl2 in an MeOH/CHCl3 solvent system. The structure contains infinite chains of ZnCl2 units connected by the bifunctional thiadiazole ligands, with ZnII adopting a distorted tetrahedral coordination geometry. The dihedral angle between the two pyridyl rings in each ligand is 34.3 (1)°, and the dihedral angles between the thiadiazole ring and the two pyridyl rings are 18.3 (2) and 16.1 (2)°. The shortest Zn...Zn distance within each polymeric chain is 11.862 (3) Å, while the shortest interchain Zn...Zn distance is 7.057 (3) Å.