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Biomedical subjects

Lei Zheng

Publications and source records attributed to Lei Zheng.

At least 19 recordsLinked to original sources

[Analysis of clinical phenotypes and pathogenicity of a c.4476+5G>T variant of SCN1A gene in a Chinese pedigree affected with Genetic epilepsy with febrile seizures plus].

OBJECTIVE: To explore the pathogenicity and characteristics of a heterozygous splicing variant of SCN1A gene in a Chinese pedigree affected with Genetic epilepsy with febrile seizures plus (GEFS+). METHODS: A retrospective analysis was carried out on the clinical data and results of genetic testing of a GEFS+ pedigree consisting of 5 members who had visited the First Affiliated Hospital of Zhengzhou University on July 1, 2024. Pathogenicity of the splicing variant of the SCN1A gene was validated with a minigene splicing assay. This study was approved by the Medical Ethics Committee of the the First Affiliated Hospital of Zhengzhou University (Ethics No.: KS-2018-KY-36). RESULTS: The proband, a 24-year-old female, presented with FS in conjunct with focal seizures, and both of her younger brothers had Dravet syndrome. All of the three patients had carried a c.4476+5G>T variant of the SCN1A gene, which was unreported previously. Minigene experiment verified that the variant could cause loss of the first 7 bps of exon 24 and 138 bps from exon 23 of the SCN1A gene, resulting in alteration p.V1447_1495delfs*6 and affecting splicing. Based on the guidelines from American College of Medical Genetics and Genomics (ACMG), the variant was predicted as likely pathogenic (PVS1+PM2_Supporting). CONCLUSION: The c.4476+5G>T variant at an intronic site of the SCN1A gene probably underlay the pathogenesis of GEFS+ in this pedigree.

Adult↗

Effects of Time-Based and Distance-Based Repeated Sprint Training on Physical and Physiological Adaptations in Collegiate Basketball Players.

PURPOSE: This study aimed to compare the effects of time-based (TB) and distance-based (DB) repeated-sprint training (RST) on athletic performance adaptations in collegiate basketball players during preseason and to examine whether the 2 training prescriptions produce different levels of homogeneity in the magnitude of individual adaptations. METHODS: Thirty young male basketball players (age = 21.3 [1.4]&#xa0;y) were randomly and equally assigned to 3 groups (n = 10): DB-RST, TB-RST, and an active control group. Participants completed a 7-week RST program performed 3 times per week, consisting of 4 sets of 4 to 9 repetitions per session. The DB-RST group completed each sprint by covering a fixed 35-m distance, whereas the TB-RST group performed each sprint maximally for a fixed 5-second duration. Performance assessments including countermovement vertical jump, 20-m sprint, Illinois change-of-direction speed, reactive strength index, Wingate anaerobic power, and cardiorespiratory fitness were conducted before and after the 7-week training period. RESULTS: Both training groups demonstrated significant performance improvements over the 7-week intervention and relative to the control group (P < .05). Similar gains were observed in the magnitude of adaptations in the countermovement vertical jump, 20-m sprint, Illinois change-of-direction speed, and reactive strength index for the DB-RST and TB-RST groups. Interestingly, the TB-RST group showed more gains than the DB-RST in the magnitude of adaptations in the peak and mean power outputs, as well as cardiorespiratory fitness. Moreover, the TB-RST group showed lower intersubject variability in adaptive responses across the measured performance outcomes following the training intervention. CONCLUSION: Our findings indicate that RST effectively enhances the performance of basketball players, and that implementing a TB-RST protocol is more effective than a DB-RST approach for producing greater adaptations in physiological variables-specifically anaerobic power output and cardiorespiratory fitness-over the 7-week preseason period.

Humans↗

Clinical and molecular characterization of TCF12 variants in an Asian pediatric cohort with craniosynostosis.

BACKGROUND: Craniosynostosis is a genetically heterogeneous craniofacial disorder caused by the premature fusion of one or more cranial sutures. Pathogenic variants in TCF12, encoding a basic helix-loop-helix (bHLH) transcription factor, represent a major cause of autosomal dominant coronal craniosynostosis and are characterized by incomplete penetrance and marked phenotypic variability. However, clinical and molecular data from Asian pediatric populations remain limited. METHODS: Trio-based whole-exome sequencing was performed on ten pediatric patients with cranial deformities and their parents. The identified TCF12 variants were classified according to the American College of Medical Genetics and Genomics (ACMG) guidelines and validated by Sanger sequencing. Detailed clinical and radiological data were collected. In addition, a comprehensive literature review was conducted to summarize previously reported TCF12 variants and associated phenotypes. RESULTS: Ten distinct heterozygous TCF12 variants were identified in ten unrelated pediatric patients, all of which were classified as pathogenic or likely pathogenic according to ACMG criteria. Six variants were inherited, and four occurred de novo. Seven patients had imaging-confirmed craniosynostosis, predominantly involving the coronal sutures (five bilateral and one unilateral), while one patient presented with multisuture craniosynostosis (left coronal and sagittal sutures). Three patients showed cranial deformities without radiographic evidence of suture fusion. Phenotypic heterogeneity and incomplete penetrance were observed, including a mildly affected parent. Most pathogenic variants were truncating variants distributed mainly across exons 14-19 and predicted to induce loss of function, either through nonsense-mediated mRNA decay or the production of truncated proteins lacking the entire C-terminal bHLH domain. Structural modeling analysis further indicated that the bHLH-domain-located missense variant p.Arg603Trp alters the local DNA-binding conformation of TCF12 and impairs its binding affinity to the E-box DNA motif. CONCLUSIONS: This study provides additional clinical and molecular data on TCF12-related craniosynostosis in a pediatric cohort from an Asian population. Our findings support haploinsufficiency as the central pathogenic mechanism, primarily driven by truncating variants affecting the C-terminal bHLH domain. The marked clinical heterogeneity, the presence of mild or evolving phenotypes, and incomplete penetrance observed in our cohort underscore the importance of early diagnosis and longitudinal clinical surveillance in affected families.

Humans↗

Neoadjuvant Immunotherapy Promotes the Formation of Mature Tertiary Lymphoid Structures in a Remodeled Pancreatic Tumor Microenvironment.

Pancreatic ductal adenocarcinoma (PDAC) is a rapidly progressing cancer that responds poorly to immunotherapies. Intratumoral tertiary lymphoid structures (TLS) have been associated with rare long-term PDAC survivors, but the role of TLS in PDAC and their spatial relationships within the context of the broader tumor microenvironment remain unknown. In this study, we report the generation of a spatial multiomic atlas of PDAC tumors and tumor-adjacent lymph nodes from patients treated with combination neoadjuvant immunotherapies. Using machine learning-enabled hematoxylin and eosin image classification models, imaging mass cytometry, and unsupervised gene expression matrix factorization methods for spatial transcriptomics, we characterized cellular states within and adjacent to TLS spanning distinct spatial niches and pathologic responses. Unsupervised learning identified TLS-specific spatial gene expression signatures that are significantly associated with improved survival in patients with PDAC. We identified spatial features of pathologic immune responses, including intratumoral TLS-associated B-cell maturation colocalizing with IgG dissemination and extracellular matrix remodeling. Our findings offer insights into the cellular and molecular landscape of TLS in PDACs during immunotherapy treatment.

Humans↗

BIWT: a bioinformatics walkthrough for embedding spatial multiomics in agent-based models for virtual cells.

SUMMARY: Whereas transcriptomic and spatial profiling offer static snapshots of tissue structure, mechanistic models use biological rules to predict how tissues evolve. We present the BioInformatics WalkThrough (BIWT) software to directly initialize spatial agent-based models from single-cell and spatial molecular data. We demonstrate how initialization strategies affect tumor-immune dynamics and spatial clustering, positioning BIWT as a software suite to generate data-driven virtual cells representing both experimental and clinical contexts. AVAILABILITY AND IMPLEMENTATION: The BIWT software is available at https://github.com/PhysiCell-Tools/PhysiCell-Studio. The sample dataset for running the BIWT is available at https://zenodo.org/records/16365625. The code and instructions for reproducing the use case example is available at https://github.com/drbergman/BIWT-Paper.

Software↗

Polycystic ovarian syndrome (PCOS) and recurrent spontaneous abortion (RSA) are associated with the PI3K-AKT pathway activation.

AIMS: We aimed to elucidate the mechanism leading to polycystic ovarian syndrome (PCOS) and recurrent spontaneous abortion (RSA). BACKGROUND: PCOS is an endocrine disorder. Patients with RSA also have a high incidence rate of PCOS, implying that PCOS and RSA may share the same pathological mechanism. OBJECTIVE: The single-cell RNA-seq datasets of PCOS (GSE168404 and GSE193123) and RSA GSE113790 and GSE178535) were downloaded from the Gene Expression Omnibus (GEO) database. METHODS: Datasets of PSCO and RSA patients were retrieved from the Gene Expression Omnibus (GEO) database. The "WGCNA" package was used to determine the module eigengenes associated with the PCOS and RSA phenotypes and the gene functions were analyzed using the "DAVID" database. The GSEA analysis was performed in "clusterProfiler" package, and key genes in the activated pathways were identified using the Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis. Real-time quantitative PCR (RT-qPCR) was conducted to determine the mRNA level. Cell viability and apoptosis were measured by cell counting kit-8 (CCK-8) and flow cytometry, respectively. RESULTS: The modules related to PCOS and RSA were sectioned by weighted gene co-expression network analysis (WGCNA) and positive correlation modules of PCOS and RSA were all enriched in angiogenesis and Wnt pathways. The GSEA further revealed that these biological processes of angiogenesis, Wnt and regulation of cell cycle were significantly positively correlated with the PCOS and RSA phenotypes. The intersection of the positive correlation modules of PCOS and RSA contained 80 key genes, which were mainly enriched in kinase-related signal pathways and were significant high-expressed in the disease samples. Subsequently, visualization of these genes including PDGFC, GHR, PRLR and ITGA3 showed that these genes were associated with the PI3K-AKT signal pathway. Moreover, the experimental results showed that PRLR had a higher expression in KGN cells, and that knocking PRLR down suppressed cell viability and promoted apoptosis of KGN cells. CONCLUSION: This study revealed the common pathological mechanisms between PCOS and RSA and explored the role of the PI3K-AKT signaling pathway in the two diseases, providing a new direction for the clinical treatment of PCOS and RSA.

Humans↗

An unusual twin-his arrangement in the pore of ammonia channels is essential for substrate conductance.

Amt proteins constitute a class of ubiquitous integral membrane proteins that mediate movement of ammonium across cell membranes. They are homotrimers, in which each subunit contains a narrow pore through which substrate transport occurs. Two conserved histidine residues in the pore have been proposed to be necessary for ammonia conductance. By analyzing 14 engineered polar and non-polar variants of these histidines, in Escherichia coli AmtB, we show that both histidines are absolutely required for optimum substrate conductance. Crystal structures of variants confirm that substitution of the histidine residues does not affect AmtB structure. In a subgroup of Amt proteins, found only in fungi, one of the histidines is replaced by glutamate. The equivalent substitution in E. coli AmtB is partially active, and the structure of this variant suggests that the glutamate side chain can make similar interactions to those made by histidine.

Amino Acid Sequence↗

Targeting N-cadherin through fibroblast growth factor receptor-4: distinct pathogenetic and therapeutic implications.

Several molecular aberrations have been implicated in the pathogenesis of pituitary tumors, but few have proven thus far to be of therapeutic value. Pituitary tumor-derived fibroblast growth factor receptor-4 (ptd-FGFR4) is an alternatively transcribed cytoplasmic isoform lacking most of the extracellular domain. This oncogene recapitulates the morphological features of human pituitary tumors in transgenic mice. To investigate the therapeutic potential of targeting ptd-FGFR4, we examined the impact of FGFR4 tyrosine kinase inhibition in xenografted mice. GH4 pituitary cells expressing ptd-FGFR4 develop into invasive tumors. Systemic treatment of mice bearing ptd-FGFR4 tumors with the FGFR-selective inhibitor PD173074 resulted in recovery of membranous N-cadherin staining and a significant reduction in tumor volume with less invasive growth behavior. Mutation of tyrosine Y754F in ptd-FGFR4 abrogated the effect of PD173074-mediated inhibition. The pivotal role of N-cadherin as a mediator of this pituitary cell growth was demonstrated by small interfering RNA mediated down-regulation, which promoted invasive growth in xenografted mice. To validate this model in primary human pituitary tumors, we examined the expression of ptd-FGFR4, N-cadherin, and clinical behavior. Loss of membranous N-cadherin correlated with cytoplasmic FGFR4 expression and with tumor invasiveness in surgically resected human pituitary tumors. Primary human pituitary tumor cells treated with PD173074 showed restoration of N-cadherin to the membrane with dephosphorylation of retinoblastoma protein. These data highlight the pathogenetic significance of N-cadherin misexpression and emphasize the importance of FGFR partnership in mediating its functions.

Adenoma↗

Activation of sterol regulatory element-binding proteins (SREBPs) is critical in IL-8-induced angiogenesis.

Angiogenesis is essential in many physiological and pathological processes and can be stimulated by many different factors. To better understand and to manipulate this process more effectively, it would be beneficial to identify molecules common to the signaling pathways stimulated by different classes of angiogenic factors. Sterol regulatory element-binding proteins (SREBPs) are involved in the metabolism of cholesterol and fatty acids, molecules that are critical in membrane biology, and hence, many of the processes involved in angiogenesis. Here, we show that angiogenic factors of different families, such as basic fibroblast growth factor, thrombin, and interleukin (IL)-8, stimulate SREBP activation, whereas nonangiogenic factors, such as transforming growth factor-beta1, do not. We focused our detailed studies on IL-8 in vitro and in vivo, as this chemokine is also involved in inflammation and hence, has the potential to be critical in inflammation-induced angiogenesis, a process common to many diseases. Using human microvascular endothelial cells, a rabbit skin wound-healing model, and the chorioallantoic membrane assay, we show that IL-8 stimulates the activation of SREBP-1 and -2, and this activation is specific and receptor-mediated. SREBP activation leads to activation of RhoA through 3-hydroxy-3-methylglutaryl CoA reductase. RhoA is a small guanosinetriphosphatase, important in cytoskeletal functions, which in turn, are critical in many of the cellular processes needed for angiogenesis. Given that diverse, angiogenic factors use different cell-surface receptors, identification of this common step in the signal-transduction pathway provides the opportunity for novel approaches for prevention and treatment of diseases involving abnormal angiogenesis.

Cell Movement↗

Fabrication of TiO2/Ti electrode by laser-assisted anodic oxidation and its application on photoelectrocatalytic degradation of methylene blue.

A TiO2/Ti mesh electrode by laser calcination was prepared in this article. The resulting TiO2 film was investigated by X-ray diffraction (XRD), atomic force microscopy (AFM) and electrochemical impedance spectroscopy (EIS), and it illuminated that the prepared electrode mainly consisted of anatase TiO2 nanoparticles on its surface and exhibited a superior photocatalytic activity. The photodegradation of methylene blue (MB) using the proposed electrode under different experimental conditions was investigated in terms of both UV absorbance at 664 nm and chemical oxygen demand (COD) removal. The electrical bias applied in photoelectrocatalytic (PEC) oxidation was also studied. The experimental results showed that under the optimal potential of +0.50 V (versus SCE), UV absorbance and COD removal during the photodegradation of MB by the proposed TiO2/Ti mesh electrode were 97.3% and 87.0%, respectively. Through the comparison between photocatalytic (PC) oxidation and photoelectrocatalytic (PEC) oxidation, it was found that PEC oxidation was a convenient and effective way to mineralize the organic matters and that laser-treated photoelectrode exceeded the oven-treated one.

Catalysis↗

Normal mitochondrial dynamics requires rhomboid-7 and affects Drosophila lifespan and neuronal function.

In addition to being energy generators, mitochondria control many cellular processes including apoptosis. They are dynamic organelles, and the machinery of membrane fusion and fission is emerging as a key regulator of mitochondrial biology. We have recently identified a novel and conserved mitochondrial rhomboid intramembrane protease that controls membrane fusion in Saccharomyces cerevisiae by processing the dynamin-like GTPase, Mgm1, thereby releasing it from the membrane. The genetics of mitochondrial membrane dynamics has until now focused primarily on yeast. Here we show that in Drosophila, the mitochondrial rhomboid (Rhomboid-7) is required for mitochondrial fusion during fly spermatogenesis and muscle maturation, both tissues with unusual mitochondrial dynamics. We also find that mutations in Drosophila optic atrophy 1-like (Opa1-like), the ortholog of yeast mgm1, display similar phenotypes, suggesting a shared role for Rhomboid-7 and Opa1-like, as with their yeast orthologs. Loss of human OPA1 leads to dominant optic atrophy, a mitochondrial disease leading to childhood onset blindness. rhomboid-7 mutant flies have severe neurological defects, evidenced by compromised signaling across the first visual synapse, as well as light-induced neurodegeneration of photoreceptors that resembles the human disease. rhomboid-7 mutant flies also have a greatly reduced lifespan.

Animals↗

Effect of Nd3+ ion on carboxylation activity of ribulose-1,5-bisphosphate carboxylase/oxygenase of spinach.

Neodymium (Nd), as a member of rare earth elements, proved to enhance the photosynthesis rate and organic substance accumulation of spinach through the increase in carboxylation activity of Rubisco. Although the oxygenase activity of spinach Rubisco was slightly changed with the Nd(3+) treatment, the specific factor of Rubisco was greatly increased. It was partially due to the promotion of Rubisco activase (R-A) activity but mainly to the formation of Rubisco-Rubisco activase super-complex, a heavier molecular mass protein (about 1200kD) comprising both Rubisco and Rubisco activase. This super-complex was found during the extraction procedure of Rubisco by the gel electrophoresis and Western-blot studies. The formation of Rubisco-R-A super-complex suggested that the secondary structure of the protein purified from the Nd(3+)-treated spinach was different from that of the control. Extended X-ray absorption fine structure study of the 'Rubisco' purified from the Nd(3+)-treated spinach revealed that Nd was bound with four oxygen atoms and two sulfur atoms of amino acid residues at the Nd-O and Nd-S bond lengths of 2.46 and 2.89A, respectively.

Cations↗

Feedback network controls photoreceptor output at the layer of first visual synapses in Drosophila.

At the layer of first visual synapses, information from photoreceptors is processed and transmitted towards the brain. In fly compound eye, output from photoreceptors (R1-R6) that share the same visual field is pooled and transmitted via histaminergic synapses to two classes of interneuron, large monopolar cells (LMCs) and amacrine cells (ACs). The interneurons also feed back to photoreceptor terminals via numerous ligand-gated synapses, yet the significance of these connections has remained a mystery. We investigated the role of feedback synapses by comparing intracellular responses of photoreceptors and LMCs in wild-type Drosophila and in synaptic mutants, to light and current pulses and to naturalistic light stimuli. The recordings were further subjected to rigorous statistical and information-theoretical analysis. We show that the feedback synapses form a negative feedback loop that controls the speed and amplitude of photoreceptor responses and hence the quality of the transmitted signals. These results highlight the benefits of feedback synapses for neural information processing, and suggest that similar coding strategies could be used in other nervous systems.

Animals↗

Mechanism of nano-anatase TiO2 on promoting photosynthetic carbon reaction of spinach: inducing complex of rubisco-rubisco activase.

Having a photocatalyzed characteristic, our previous research had proved that nano-anatase TiO2 is closely related to the photosynthesis of spinach. It could not only improve the light absorbance and the transformation from light energy to electron energy and to active chemical energy but also promote carbon dioxide (CO2) assimilation of spinach. However, the mechanism of carbon reaction promoted by nano-anatase TiO2 remains largely unclear. By electrophoresis and Western blot methods, the results of the experiments proved that Rubisco from the nano-anatase TiO2-treated spinach during the extraction procedure of Rubisco was found to consist of Rubisco and a heavier molecular-mass protein (about 1,200 kDa) comprising both Rubisco and Rubisco activase. The Rubisco carboxylase activity was 2.67 times that of Rubisco from the control and it could hydrolyze ATP in the same manner as Rubisco activase. The total sulfhydryl groups and available sulfhydryl groups of the Rubisco were 32 -SH and 21 -SH per mole of enzyme more than those of the Rubisco purified from the control, respectively. The circular dichroism spectra showed that the secondary structure of Rubisco from the nano-anatase TiO2-treated spinach was very different from Rubisco of the control. It suggested that the mechanism of nano-anatase TiO2 activating Rubisco of spinach was that the complex of Rubsico and Rubisco activase was induced in spinach, which promoted Rubsico carboxylation and increased the rate of photosynthetic carbon reaction.

Carbon Dioxide↗

[Identification of effective siRNA sequence for RelB silencing in murine dendritic cells with siRNA cassette].

OBJECTIVE: To construct small interfering RNA (siRNA) expression cassette targeting murine RelB gene and identify the most effective siRNA sequence against RelB gene in murine bone marrow-derived dendritic cells (DCs). METHODS: Three expression cassettes namely R1/siRNA, R2/siRNA and R3/siRNA targeting the sites 1027, 302 and 1121 of RelB gene, respectively, were constructed by PCR approach and transfected into cultured murine myeloid DCs by catione liposome Advant-Gene. After incubation for 24 hours in a incubator containing 5% CO(2) at 37 degrees C, the DCs were stimulated by lipopolysaccharide (LPS), and RelB gene expression in DCs were then detected by RT-PCR and immunofluorescence. RESULTS: RT-PCR and immunofluorescence assay showed that the expression of RelB gene in DCs transfected with R2/siRNA could not be upregulated by LPS stimulation, but transfection with R1/siRNA or R3/siRNA failed to produce such effect. CONCLUSION: R2/siRNA is an effective sequence for RelB silencing, and can be a useful means to construct new tolerogenic DC, RNAi RelB DC, for clinical immunotolerance induction.

Animals↗

[Heart-type fatty acid-binding protein detection for early diagnosis of acute coronary syndrome].

OBJECTIVE: To estimate the reliability of heart-type fatty acid-binding protein (H-FABP) for identifying acute coronary syndrome (ACS) in the early stage of chest pain onset. METHODS: This investigation was conducted based on a small population consisting of 40 healthy individuals, 19 established AMI patients and 20 unstable angina pectoris (UAP) patients. Serum H-FABP concentrations were measured in these subjects by sandwich ELISA, and receiver operating characteristics (ROC) curves for H-FABP for diagnosing AMI and UAP against normal subjects were then generated respectively. The areas under curve (AUCs) were calculated, and 0.5 was defined as the critical value of AUC to evaluate the diagnostic ability. RESULTS: The concentrations of H-FABP in healthy individuals, AMI patients and UAP patients were 1.29+/-0.64, 24.45+/-32.40 and 1.95+/-3.11 ng/ml, respectively; AUC (AMI) and AUC UAP were 0.978 (95%CI: 0.948-1.000) and 0.503 (95% CI: 0.334-0.671) respectively, and the former was significantly greater than 0.5. CONCLUSIONS: In the early stage of chest pain onset H-FABP detection is sufficient in distinguishing AMI patients from healthy individuals, but not capable of distinguishing UAP patients from healthy individuals. H-FABP may be used as a diagnostic biochemical marker in the early stage of AMI.

Acute Coronary Syndrome↗

[RelB gene expression in murine bone marrow-derived mature and immature dendritic cells].

AIM: To explore the expression of avian reticuloendotheliosis viral(v-rel) oncogene-related B (RelB) mRNA in vitro in murine mature and immature myeloid dendritic cells (DCs). METHODS: The bone marrow was collected from the femur and tibias of C57BL/6 mice in sterile condition. Bone marrow precursors were cultured with recombinant mouse granulocyte-macrophage colony-stimulating factor (rmGM-CSF) and interleukin-4 (rmIL-4) to produce immature DCs. Immature DCs were stimulated by LPS 18 h before the end of culture to become mature. DCs' phenotype was detected by flow cytometry (FCM). RelB expression and protein level were determined by RT-PCR and immunofluorescence staining. RESULTS: The expression level of co-stimulatory molecules (CD86 and CD40) and MHC-II class molecule were low in immature DCs, whereas high in mature DCs. RelB expression was significantly higher in mature DCs than in immature DCs (P<0.01). CONCLUSION: RelB expression is closely associated with the maturative situation of DCs. Inhibition of RelB expression in DCs may induce tolerogenic DCs.

Actins↗

Assembly of azido- or cyano-bridged binuclear complexes containing the bulky [Mn(phen)2]2+ building block: syntheses, crystal structures, and magnetic properties.

Two new cyano-bridged heterobinuclear complexes, [Mn(II)(phen)2Cl][Fe(III)(bpb)(CN)2] x 0.5CH3CH2OH x 1.5H2O (1) and [Mn(II)(phen)2Cl][Cr(III)(bpb)(CN)2] x 2H2O (2) [phen = 1,10-phenanthroline; bpb(2-) = 1,2-bis(pyridine-2-carboxamido)benzenate], and four novel azido-bridged Mn(II) dimeric complexes, [Mn2(phen)4(mu(1,1)-N3)2][M(III)(bpb)(CN)2]2 x H2O [M = Fe (3), Cr (4), Co (5)] and [Mn2(phen)4(mu(1,3)-N3)(N3)2]BPh4 x 0.5H2O (6), have been synthesized and characterized by single-crystal X-ray diffraction analysis and magnetic studies. Complexes 1 and 2 comprise [Mn(phen)2Cl]+ and [M(bpb)(CN)2]- units connected by one cyano ligand of [M(bpb)(CN)2]-. Complexes 3-5 are doubly end-on (EO) azido-bridged Mn(II) binuclear complexes with two [M(bpb)(CN)2]- molecules acting as charge-compensating anions. However, the Mn(II) ions in complex 6 are linked by a single end-to-end (EE) azido bridging ligand with one large free BPh4(-) group as the charge-balancing anion. The magnetic coupling between Mn(II) and Fe(III) or Cr(III) in complexes 1 and 2 was found to be antiferromagnetic with J(MnFe) = -2.68(3) cm(-1) and J(MnCr) = -4.55(1) cm(-1) on the basis of the Hamiltonian H = -JS(Mn)S(M) (M = Fe or Cr). The magnetic interactions between two Mn(II) ions in 3-5 are ferromagnetic in nature with the magnetic coupling constants of 1.15(3), 1.05(2), and 1.27(2) cm(-1) (H = -JS(Mn1)S(Mn2)), respectively. The single EE azido-bridged dimeric complex 6 manifests antiferromagnetic interaction with J = -2.29(4) cm(-1) (H = -JS(Mn1)S(Mn2)). Magneto-structural correlationship on the EO azido-bridged Mn(II) dimers has been investigated.

Journal Article↗