Search PubMed⌕ Search

Biomedical subjects

Xia Li

Publications and source records attributed to Xia Li.

At least 109 records · Page 6Linked to original sources

[Research on gene expression data based on clustering/classification technology].

As the work of sequencing the genome of the human and many model organisms has been partially or fully finished, the "postgenomic era" has begun. Scientists are turning their focus toward identifying gene function from sequencing. Clustering technology, as one of the important tools of analyzing gene expression data and identifying gene function, has been used widely. In this paper we discuss main clustering technology about gene expression data at present, analyze their advantages and disadvantages, present the methods to solve the problems and give new approaches to study gene expression data.

Algorithms↗

[Association of mitochondrial DNA variation with type 2 diabetes mellitus].

OBJECTIVE: To explore the prevalence of mitochondrial DNA (mtDNA) mutations in patients with type 2 diabetes mellitus in Hubei. METHODS: A total of 184 cases of type 2 diabetes mellitus and 210 matched healthy controls with normal glucose tolerance were recruited for the study. The variants of mtDNA, including MIND13316 (G-->A), MIND13394 (T-->C), MTTE14693 (A-->G), MTTL1 3243 (A-->G), MTRNA1310 (C-->T) and 16189 (T-->C), were screened using PCR-restriction fragment length polymorphism (PCR-RFLP) analysis and DNA sequencing. The mutations were analyzed by mfold or tRNAscan-SE softwares. RESULTS: The mutation rates of 3316 (G-->A), 3394 (T-->C), 14693 (A-->G) were 3.26%, 2.72% and 2.17% respectively in type 2 diabetes group, whereas in the control group, the point mutations of 3394 (T-->C) and 14693 (A-->G) were not detected, but two subjects with 3316 (G-->A) were found (0.99%). There were significant differences in mutation rates of 3394 (T-->C) and 14693 (A-->G) between the two groups (P<0.05). In 4 of 184 cases, a T to C transition at nucleotide position 14693 was uncovered for the first time. The prevalence of 16189 variant among type 2 diabetes was significantly higher that of the controls (36.9% vs 26.6%, P=0.03). Moreover, the type 2 diabetes with 16189 variant showed higher fasting serum insulin level and higher HOMA-IR level than those without 16189 variant; stepwise multiple regression analysis showed the 16189 variant was an independent factor contributing to HOMA-IR (R(2)=0.043, P=0.037). Secondary structure prediction revealed that there were differences in 3394 T-->C vs wild-type ND1 protein and in 14693 A-->G vs wild-type tRNA(Glu) protein. CONCLUSION: The mutations of 3394 (T-->C) and 14693 (A-->G) may contribute to the genetic predisposition to type 2 diabetes; 16189 (T-->C) variant is associated with insulin resistance and risk factor of diabetes.

Aged↗

[Study on the postive frequency and distribution of glutamic acid decarboxylase antibody in phenotypic type 2 diabetec patients].

OBJECTIVE: To investigate the positive frequency and distribution of glutamic acid decarboxylase antibody(GAD-Ab) in phenotypic type 2 diabetic(T2DM) patients. METHODS: Sera of 2035 phenotypic T2DM patients were screened for GAD-Ab with radioligand assay. The positive frequency of GAD-Ab and its relation with clinical features were analyzed. RESULTS: (1) The positivity of GAD-Ab in clinic-based, phenotypic T2DM patients was 7.1% (145/2035), comparable to that of data from Caucasians as shown by UKPDS(8.7% vs. 9.8%, P = 0.391) and ADOPT (8.0% vs. 4.2%, P = 0.000) but higher than that of Japanese in Ehime study(7.1% vs. 3.8%, P = 0.000). (2) The positive frequency and distribution of GAD-Ab titer were related to clinical features, including age at onset, body mass index (BMI) and fasting C peptide levels. Patients with younger age at onset (0.33 vs. 0.11, P < 0.05), less BMI (0.34 vs. 0.10, P < 0.05) and lower C peptide levels (0.38 vs. 0.11, P < 0.05) would have higher GAD-Ab titers. CONCLUSION: (1)The positivity of GAD-Ab in adult-onset phenotypic T2DM in Chinese was similar to that of Caucasians but higher than that of the Japanese. (2) The distribution of GAD-Ab titers was associated with clinical features, with high GAD-Ab titers for those having younger age at onset, less BMI and lower C peptide levels.

Adolescent↗

Changes of adrenomedullin and its receptor components mRNAs expression in the brain stem and hypothalamus-pituitary-adrenal axis of stress-induced hypertensive rats.

In this study, reverse transcription-polymerase chain reaction (RT-PCR) was used to detect the changes in mRNAs levels of preproadrenomedullin (ppADM) gene encoding adrenomedullin (ADM) and the essential receptor components of ADM, calcitonin receptor-like receptor (CRLR), and the receptor activity modifying protein 2 and 3 (RAMP2 and RAMP3) in the medulla oblongata, hypothalamus, midbrain, pituitary gland and adrenal gland of the stress-induced hypertensive rats. It was shown that chronic foot-shock and noise stress for 15 consecutive days induced a significant increase in systolic blood pressure (SBP) and unique changes in ppADM and its receptor components mRNAs in all areas studied. As compared with the control group, the level of ppADM mRNA, normalized against a glyceraldehydes-3-phosphate dehydrogenase (GAPDH) control, was up-regulated in the hypothalamus-pituitary-adrenal (HPA) axis, but down-regulated in the medulla oblongata and midbrain (P<0.01 and P<0.05, respectively). The relative amount of CRLR mRNA was higher in the hypothalamus than that in other areas. The level of CRLR mRNA expression was significantly increased in the medulla oblongata of the stress group (P<0.01), but decreased in the midbrain (P<0.01) as well as hypothalamus(P<0.05), as compared with that of the control group. Chronic stress for 15 consecutive days produced an increase in the level of RAMP2 mRNA expression in the medulla oblongata (P<0.01) and a decrease in the adrenal gland (P<0.01), as compared with the control. No significant stress-related changes in RAMP2 mRNA were observed in the midbrain, hypothalamus and pituitary gland. The amount of RAMP3 mRNA was relatively higher in the midbrain and hypothalamus than that in the medulla oblongata, adrenal gland and adrenal gland. Stress-induced hypertensive rats exhibited an increased RAMP3 mRNA expression in the hypothalamus and pituitary gland (P<0.01 and P<0.05, respectively) and a decrease in the adrenal gland and midbrain (P<0.05). No significant stress-related change in RAMP3 mRAN was observed in the medulla oblongata. Taken together, our results indicate that the significant changes in ppADM and its receptor components mRNAs expression in the HPA axis and autonomic centers may be related to the development of the stress-induced hypertension. Nevertheless, the pathophysiological significance of brain-derived ADM and its receptors in stress and blood pressure regulation and their roles in stress-induced hypertension still await further investigation.

Adrenomedullin↗

Prenatal stress causes gender-dependent neuronal loss and oxidative stress in rat hippocampus.

Our purpose was to investigate the effects of prenatal stress on neuronal changes in the hippocampus and the possible involvement of oxidative stress in female and male rats. Female and male offspring (1-month-old), whose dams were restrained in middle or later pregnant stage (MS or LS), were studied to observe changes in the number of hippocampal neurons and the expression of neuronal nitric oxide synthase (nNOS) in the hippocampus. Both MS and LS induced an increase in the number of nNOS-positive expression in female and male offspring in the hippocampus; however, both MS and LS caused a significant decrease in the number of hippocampal neurons in the female, but not in the male offspring. In addition, significant increases in calcium content and oxidant generation were induced by LS in the hippocampal CA3 region in female rats. These data suggest that prenatal stress can cause oxidative stress and consequent damage to neurons, leading to neuronal loss in the brain of offspring during development.

Animals↗

NDRG2 expression and mutation in human liver and pancreatic cancers.

AIM: To investigate the expression of NDRG2 and mutation of the entire coding region of NDRG2 in human liver and pancreatic cancers, and to further discuss the possible causes of NDRG2 distinct expression patterns. METHODS: Reverse transcription-polymerase chain reaction (RT-PCR) was used to analyze the expression of NDRG2 mRNA in 37 fresh cancer specimens (including 8 cases of pancreatic cancer and 29 cases of liver cancer) and adjacent normal tissues collected from clinical operation. In addition, mutation analysis of the whole coding region of NDRG2 in these cancers was examined by polymerase chain reaction-single strand conformational polymorphism (PCR-SSCP). RESULTS: Compared with adjacent normal tissues, the expression levels of NDRG2 mRNA in corresponding cancer tissues reduced significantly (pancreatic cancer: 0.680+/-0.112 vs 2.089+/-0.214, P<0.01) (liver cancer: 0.894+/-0.098 vs 1.345+/-0.177, P<0.05). Using PCR-SSCP, the mutation of the whole coding region of NDRG2 was not found in those cancer tissues where the expression of NDRG2 mRNA reduced markedly. CONCLUSION: NDRG2 gene might express differently between normal tissues and cancer tissues, and might play an important role in the development of pancreatic cancer and liver cancer. Low expression of NDRG2 might be unrelated to the mutation of coding region of NDRG2.

Gene Expression Regulation, Neoplastic↗

Correlation of three-dimensional structures with the antibacterial activity of a group of peptides designed based on a nontoxic bacterial membrane anchor.

To understand the functional differences between a nontoxic membrane anchor corresponding to the N-terminal sequence of the Escherichia coli enzyme IIA(Glc) and a toxic antimicrobial peptide aurein 1.2 of similar sequence, a series of peptides was designed to bridge the gap between them. An alteration of a single residue of the membrane anchor converted it into an antibacterial peptide. Circular dichroism spectra indicate that all peptides are disordered in water but helical in micelles. Structures of the peptides were determined in membrane-mimetic micelles by solution NMR spectroscopy. The quality of the distance-based structures was improved by including backbone angle restraints derived from a set of chemical shifts ((1)H(alpha), (15)N, (13)C(alpha), and (13)C(beta)) from natural abundance two-dimensional heteronuclear correlated spectroscopy. Different from the membrane anchor, antibacterial peptides possess a broader and longer hydrophobic surface, allowing a deeper penetration into the membrane, as supported by intermolecular nuclear Overhauser effect cross-peaks between the peptide and short chain dioctanoyl phosphatidylglycerol. An attempt was made to correlate the NMR structures of these peptides with their antibacterial activity. The activity of this group of peptides does not correlate exactly with helicity, amphipathicity, charge, the number of charges, the size of the hydrophobic surface, or hydrophobic transfer free energy. However, a correlation is established between the peptide activity and membrane perturbation potential, which is defined by interfacial hydrophobic patches and basic residues in the case of cationic peptides. Indeed, (31)P solid state NMR spectroscopy of lipid bilayers showed that the extent of lipid vesicle disruption by these peptides is proportional to their membrane perturbation potential.

Anti-Bacterial Agents↗

Sem1, the yeast ortholog of a human BRCA2-binding protein, is a component of the proteasome regulatory particle that enhances proteasome stability.

Degradation of polyubiquitinated proteins by the proteasome often requires accessory factors; these include receptor proteins that bind both polyubiquitin chains and the regulatory particle of the proteasome. Overproduction of one such factor, Dsk2, is lethal in Saccharomyces cerevisiae and we show here that this lethality can be suppressed by mutations in SEM1, a gene previously recognized as an ortholog of the human gene encoding DSS1, which binds the BRCA2 DNA repair protein. Yeast sem1 mutants accumulate polyubiquitinated proteins, are defective for proteasome-mediated degradation and cannot grow under various stress conditions. Moreover, sem1 is synthetically lethal with mutations in proteasome subunits. We show that Sem1 is a component of the regulatory particle of the proteasome, specifically the lid subcomplex. Loss of Sem1 impairs the stability of the 26S proteasome and sem1Delta defects are greatly enhanced by simultaneous deletion of RPN10. The Rpn10 proteasome subunit appears to function with Sem1 in maintaining the association of the lid and base subcomplexes of the regulatory particle. Our data suggest a potential mechanism for this protein-protein stabilization and also suggest that an intact proteasomal regulatory particle is required for responses to DNA damage.

BRCA2 Protein↗

[Mechanisms of human glutamic acid decarboxylase 65 DNA vaccine preventing diabetes in non-obese diabetic mice].

OBJECTIVE: To investigate the mechanisms of human GAD65 DNA vaccine preventing insulitis and diabetes in NOD mice. METHODS: Female NOD mice at 4 weeks of age were randomly divided into PBS (n = 21), pcDNA (n = 20), and hGAD65 (n = 21) groups. Mice in each group received two intramuscular injections of 0.05 ml PBS alone, 50 microg pcDNA3.1 and 50 microg DNA vaccine emulsified in 0.05 ml PBS 7 days apart respectively. The accumulative diabetes incidence was followed-up to 30 weeks of age in each group of NOD mice. Pancreas was removed from NOD mice at 12 weeks of age in each group (n = 10) to score insulitis severity by routine H-E staining. The apoptotic beta cells in islets were observed with double-labeling technique of TUNEL in situ combined standard sensitive avdin-biotin complex (sABC) immunohistochemical method. Their spleens were for cell culture and total RNA extraction. Spleen IL-4, IFN-gamma, NF-ATc and NF-ATp mRNA levels were tested by RT-PCR. IL-4 and IFN-gamma levels in sera and supernatants of spleen cells were measured by ELISA. RESULTS: (1) At 30 weeks of age, the diabetes incidence was 95.2%, 80.0% and 61.9% in PBS, pcDNA and hGAD65 group respectively. The diabetes incidence in the PBS group was higher than that in hGAD65 group (P = 0.008). (2) At 12 weeks of age, the insulitis scores in hGAD65 group was lower than that in PBS group (P = 0.001) and pcDNA group (P = 0.027) respectively. (3) The apoptotic beta cell rates in hGAD65 group was lower than that in PBS group (P = 0.014) and pcDNA group (P = 0.023). (4) IL-4 levels in sera, spleen IL-4 and NF-ATc mRNA level in hGAD65 group were higher than those in PBS group (all P < 0.05) and pcDNA group (all P < 0.05) respectively, NF-ATp mRNA level in hGAD65 group was lower than that in PBS group (P < 0.05). CONCLUSION: Human GAD65 DNA vaccine via downregulating NF-ATp and upregulating NF-ATc and IL-4, makes Th cells deviate to Th2, and sequently prevents insulitis, beta-cell apoptosis and diabetes onset in NOD mice.

Animals↗

Medullary ventrolateral nitric oxide mediates the cardiac effect of electroacupuncture at "Neiguan" acupoint on acute myocardial ischemia in rats.

Experiments were performed on male Sprague-Dawley (SD) rats anesthetized with a mixture of urethane and chloralose. A rat model of acute myocardial ischemia (AMI) was made by ligation of the left anterior descending branch of the coronary artery (LAD). After the LAD ligation, the ischemia area of the left ventricular wall became somewhat pale immediately. Under a light microscope, the pathological examination revealed that all the cells were swollen and in red color when the cardiac section was stained with hematoxylin basic fuchsin picric acid (HBFP), which indicated a typical change in the myocardial ischemia. In the AMI model, it was found that cardiac functions were markedly attenuated, such as decreases in the heart rate (HR), mean arterial pressure (MAP), left ventricular systolic pressure (LVSP), maximal rate for left ventricular pressure rising and declining (+/-dp/dt(max)), velocity of contractile element (V(CE)) and total area of cardiac force loop (L(0)), and an increase in the left ventricular end diastolic pressure (LVEDP). In such AMI rats, application of electroacupuncture (EA) at "Neiguan" acupoints (Pe 6) for 20 min could obviously improve the above-mentioned cardiac functions. After microinjection of nitro-L-arginine (L-NNA), an inhibitor of nitric oxide synthase (NOS), was made into the rostral ventrolateral medulla (RVLM), the curative effect of EA on myocardial ischemia was reduced significantly or abolished, while after microinjection of normal saline of the same volume was made into the RVLM, the improving effect of EA remained. These results suggest that the effect of EA on myocardial ischemia is possibly mediated by the nitric oxide (NO) in the RVLM.

Acupuncture Points↗

Enhanced corticosterone concentrations and attenuated Fos expression in the medial amygdala of female oxytocin knockout mice exposed to psychogenic stress.

Centrally released oxytocin (OT) is believed to attenuate the response of the hypothalamic-pituitary-adrenal (HPA) axis to psychogenic stress. To test this hypothesis, we measured plasma corticosterone concentrations and Fos-immunoreactive protein in the paraventricular nucleus of the hypothalamus (PVN) and limbic brain areas of female wild-type and OT knockout mice that were exposed to a shaker platform, a predominantly psychogenic stress. Plasma corticosterone concentrations after shaker stress were higher in female OT knockout mice than wild-type mice. Genotypic differences in the corticosterone response after shaker stress persisted across all stages of the estrous cycle and when mice were conditioned to repeated shaker stress. Shaker stress activated Fos in OT-positive neurons of wild-type mice and corticotropin-releasing hormone-positive, but not vasopressin-positive, neurons within the PVN of wild-type and OT knockout mice. Fos expression was also increased after shaker stress in the bed nucleus of the stria terminalis, medial and central nuclei of the amygdala, medial preoptic area, and the paraventricular nucleus of the thalamus of wild-type and OT knockout mice. However, Fos expression in the medial amygdala was significantly lower in female OT knockout mice than wild-type mice. Our findings indicate heightened stress-induced corticosterone release in female OT knockout mice. Therefore, the results suggest that OT pathways play a role in attenuating the HPA axis response to psychogenic stress in female mice.

Amygdala↗

Cross-regulation between the renin-angiotensin system and inflammatory mediators in cardiac hypertrophy and failure.

One of the major conceptual advances in our understanding of the pathogenesis of heart failure has been the insight that heart failure may progress as the result of the sustained overexpression of biologically active "neurohormones", such as norepinephrine and angiotensin II, which by virtue of their deleterious effects are sufficient to contribute to disease progression by provoking worsening left ventricular (LV) remodeling and progressive LV dysfunction. Recently, a second class of biologically active molecules, termed cytokines, has also been identified in the setting of heart failure. Analogous to the situation with neurohormones, the overexpression of cytokines is sufficient to contribute to disease progression in heart failure phenotype. Although important interactions between proinflammatory cytokines and the adrenergic system have been recognized in the heart for over a decade, the nature of the important interactions between proinflammatory cytokines and the renin-angiotensin system has become apparent only recently. Accordingly, in the present review, we will discuss the evidence which suggests that there is a functionally significant cross-talk between neurohormonal and inflammatory cytokine signaling in cardiac hypertrophy and failure.

Angiotensin II↗

Gene mining: a novel and powerful ensemble decision approach to hunting for disease genes using microarray expression profiling.

Current applications of microarrays focus on precise classification or discovery of biological types, for example tumor versus normal phenotypes in cancer research. Several challenging scientific tasks in the post-genomic epoch, like hunting for the genes underlying complex diseases from genome-wide gene expression profiles and thereby building the corresponding gene networks, are largely overlooked because of the lack of an efficient analysis approach. We have thus developed an innovative ensemble decision approach, which can efficiently perform multiple gene mining tasks. An application of this approach to analyze two publicly available data sets (colon data and leukemia data) identified 20 highly significant colon cancer genes and 23 highly significant molecular signatures for refining the acute leukemia phenotype, most of which have been verified either by biological experiments or by alternative analysis approaches. Furthermore, the globally optimal gene subsets identified by the novel approach have so far achieved the highest accuracy for classification of colon cancer tissue types. Establishment of this analysis strategy has offered the promise of advancing microarray technology as a means of deciphering the involved genetic complexities of complex diseases.

Acute Disease↗

catena-Poly[europium(III)-tri-micro-2,3-dimethoxybenzoato].

The title compound, [Eu(C(9)H(9)O(4))(3)](n) or [Eu(2,3-DMOBA)(3)](n), where 2,3-DMOBA is 2,3-dimethoxybenzoate, is an infinite one-dimensional non-centrosymmetric coordination polymer. The unique Eu(III) atom is bridged by six carboxylate ligands; it is ennea-coordinated and has a distorted tricapped trigonal prism geometry. The Eu-O distances are in the range 2.315 (3)-2.959 (5) A.

Journal Article↗

Allelic variation of the Tas1r3 taste receptor gene selectively affects behavioral and neural taste responses to sweeteners in the F2 hybrids between C57BL/6ByJ and 129P3/J mice.

Recent studies have shown that the T1R3 receptor protein encoded by the Tas1r3 gene is involved in transduction of sweet taste. To assess ligand specificity of the T1R3 receptor, we analyzed the association of Tas1r3 allelic variants with taste responses in mice. In the F2 hybrids between the C57BL/6ByJ (B6) and 129P3/J (129) inbred mouse strains, we determined genotypes of markers on chromosome 4, where Tas1r3 resides, measured consumption of taste solutions presented in two-bottle preference tests, and recorded integrated responses of the chorda tympani gustatory nerve to lingual application of taste stimuli. For intakes and preferences, significant linkages to Tas1r3 were found for the sweeteners sucrose, saccharin, and D-phenylalanine but not glycine. For chorda tympani responses, significant linkages to Tas1r3 were found for the sweeteners sucrose, saccharin, D-phenylalanine, D-tryptophan, and SC-45647 but not glycine, L-proline, L-alanine, or L-glutamine. No linkages to distal chromosome 4 were detected for behavioral or neural responses to non-sweet quinine, citric acid, HCl, NaCl, KCl, monosodium glutamate, inosine 5'-monophosphate, or ammonium glutamate. These results demonstrate that allelic variation of the Tas1r3 gene affects gustatory neural and behavioral responses to some, but not all, sweeteners. This study describes the range of ligand sensitivity of the T1R3 receptor using an in vivo approach and, to our knowledge, is the first genetic mapping study of activity in gustatory nerves.

Alleles↗

[Preventive effects of pioglitazone on diabetes and relevant mechanisms, experimental study on non-obese diabetic mice].

OBJECTIVE: To explore the effects of pioglitazone on insulitis and diabetes and relevant mechanism. METHODS: Seventy-three female non-obese diabetic (NOD)/Lt mice aged 4 weeks were randomly divided into 3 groups, control group (n = 25, fed with regular diet), low dosage pioglitazone group (n = 23, pioglitazone of the concentration of 0.01% was added into the feed) and high dosage pioglitazone group (n = 25, pioglitazone of the concentration of 0.04% was added into the feed). The mice were killed when diabetes developed or they reached the age of 30 weeks. The body weight and amount of food intake were measured every week and the amount of drug intake was calculated. Urine glucose was checked weekly from week 10 to week 30. When urine glucose was positive and relevant symptoms appeared, blood glucose was measured. The criterion of diagnosis of diabetes was the consecutive blood glucose level > or = 16.7 mmol/L for 2 times. At the 12th week 4-7 mice from the 3 groups respectively were killed and their pancreases were removed to be scored on insulitis by HE staining, the spleen cells were cultured. The IL-4 and IFN-r levels in serum and supernatants of spleen cell cultures were measured by ELISA. The pancreatic IFN-r mRNA level was tested using RT-PCR method. RESULTS: (1) At the age of 30 weeks, the diabetes incidence rates was 80% (20/25) in the control group, 60.9% (14/23) in the low dose group, and 60% (15/25) in the high dose group (P > 0.05). At the following time points the diabetes incidence rates of the 2 treated groups were lower than that of the control group (all P < 0.05): (1) 0% in the low dose group vs 16%: of the control group at the age of 100 days, and 39% vs 68% at the age of 185 days; and (2) 0% in the high dose group vs 16% in the control group at the age of 110 days, 4% vs 24% at the age of 120 days, and 12%vs 36% at the age of 135 days. (2) There was no difference in insulitis scores between the control group and low dose or high dose groups at the age of 12 weeks (1.99 +/- 0.75 vs 1.01 +/- 0.68 and 1.19 +/- 0.84, both P > 0.05), however, the score of the combined pioglitazone group (low dose group + high dos group) was significantly higher than that of the control group (1.12 +/- 0.75 vs 1.99 +/- 0.75, P < 0.05). (3) There was no differences in the IL-4/IFN-r ratios in serum and splenocyte culture supernatant and pancreatic IFN-r mRNA levels among the three groups (all P > 0.05). CONCLUSION: Pioglitazone, to some extent, lessens the insulitis severity and delays the diabetes onset. Its mechanism may be unrelated to immune deviation of Th1 to a Th2.

Animals↗

Tetra-mu-2-fluorobenzoato-bis[aqua(4,4'-bipyridine)(2-fluorobenzoato)lanthanum(III)].

Each La3+ ion in the title complex, tetra-micro-2-fluorobenzoato-kappa10 O:O';O:O,O';O:O';O,O':O'-bis[aqua(4,4'-bipyridine-kappaN)(2-fluorobenzoato-kappaO)lanthanum(II)], [La(C7H4FO2)6(C10H8N2)2(H2O)2], is coordinated by six O atoms from the carboxylate groups of five 2-fluorobenzoate ligands, one O atom from a water molecule and one N atom from a 4,4'-bipyridine molecule, thus forming a dimeric molecule. An infinite one-dimensional dimeric supramolecular chain is formed via intermolecular hydrogen bonds.

Journal Article↗