Performance improvement and application of copper-based nanomaterials in membrane technology for water treatment: A review.

Membrane fouling, including organic, inorganic, and biological fouling, poses enormous challenges in membrane water treatment. Incorporation of copper-based nanomaterials in polymeric membranes is highly favored due to their exceptional antibacterial properties and capacity to improve membrane hydrophilicity. This review extensively explores the utilization of copper-based nanomaterials in membrane technology for water treatment, with a specific focus on enhancing anti-fouling performance. It elaborates on how copper-based nanomaterials improve the surface properties of membrane materials (such as porosity, hydrophilicity, surface charge, etc.) through physical and chemical processes. It summarizes the properties and potential antibacterial mechanisms of copper-based nanomaterials, primarily by disrupting microbial cell structures through the generation of reactive oxygen species (ROS). Furthermore, recent efforts to enhance the environmental sustainability, cost-effectiveness, and recyclability of copper-based nanomaterials are outlined. The attempts to offer insights for the advancement of anti-fouling practices in water treatment through the use of copper-modified polymer membranes.

Unveiling the overlooked threat: antibiotic resistance in groundwater near an abandoned sulfuric acid plant in Xingyang, China.

Groundwater near a sulfuric acid plant in Xingyang, Henan, China was sampled from seven distinct sites to explore the prevalence of antibiotic resistance genes (ARGs) and mobile genetic elements (MGEs). Results showed that genes aadA, blaCTX-M, tetA, qnrA, and sul1 were detected with 100% frequency followed by aac(6')-Ib (85.71%), ermB (85.71%), and tetX (71.42%). Most abundant ARGs were sul1 in LSA2 (1.15 × 1011 copies/mL), tetA in LSA6 (4.95 × 1010 copies/mL), aadA in LSA2 (4.56 × 109 copies/mL), blaCTX-M in LSA4 (1.19 × 109 copies/mL), and ermB in LSA5 (1.07 × 109 copies/mL). Moreover, in LSA2, intl1 as a marker of class 1 integron emerged as the most abundant gene as part of MGE (2.25 × 1011 copies/mL), trailed by ISCR1 (1.57 × 109 copies/mL). Environmental factors explained 81.34% of ARG variations, with a strong positive correlation between the intl2 and blaCTX-M genes, as well as the ISCR1 gene and qnrA, tetA, intl2, and blaCTX-M. Furthermore, the intI1 gene had a strong positive connection with the aadA, tetA, and sul1 genes. Moreover, the aac(6')-Ib gene was associated with As, Pb, Mg, Ca, and HCO3-. The intl2 gene was also shown to be strongly associated with Cd. Notably, network analysis highlighted blaCTX-M as the most frequently appearing gene across networks of at least five genera. Particularly, Lactobacillus, Plesiomonas, and Ligilactobacillus demonstrated correlations with aadA, qnrA, blaCTX-M, intI2, and ISCR1. Based on 16S rRNA sequencing, the dominant phyla were Proteobacteria, Firmicutes, Bacteroidota, Acidobacteriota, and Actinobacteriota, with dominant genera including Pseudomonas, Ligilactobacillus, Azoarcus, Vogesella, Streptococcus, Plesiomonas, and Ferritrophicum. These findings enhance our understanding of ARG distribution in groundwater, signaling substantial contamination by ARGs and potential risks to public health.

Thyroid Hormone Receptor ß Knockdown Reduces Suppression of Progestins by Activating the mTOR Pathway in Endometrial Cancer Cells.

Progestin resistance is a major obstacle to conservative therapy in patients with endometrial cancer (EC) and endometrial atypical hyperplasia (EAH). However, the related inducing factor is yet unclear. In this study, thyroid hormone and its receptor α (TRα) and ß (TRß) of patients were assayed. THRB-silenced RL95-2 and KLE EC cells were cultured to investigate the response of progestins. Transcriptomics and Western blotting were performed to investigate the changes in signaling pathways. We found that THRB, rather than THRA, knockdown promoted the viability and motilities of RL95-2 cells but not KLE cells. The suppressive effect of progestins on cell growth and motility significantly decreased in THRB-silenced RL95-2 cells. Multiple proliferation-related signaling pathways were enriched, and the activities of mammalian targets of rapamycin (mTOR)/4e-binding protein 1 (4EBP1)/eukaryotic translation initiation factor 4G (eIF4G) rather than phosphorylated protein kinase B (Akt) were remarkably boosted. Progestin treatment enhanced the effects, and the augmentation was partially abated on supplementation with T3. In THRB-knockdown KLE cells, the progestins-activated partial signaling pathway expression (either mTOR or eIF4G), and supplementation with T3 did not induce noticeable alterations. The serum levels of triiodothyronine (T3) were significantly lower in patients with EC compared with healthy women. A strong expression of TRß was observed in most patients with EC and EAH sensitive to progestin treatment. In contrast, TRα positive expression was detected in less than half of the patients sensitive to progestin therapy. In conclusion, THRB knockdown enhanced the viability and motility of type I EC cells and attenuated the suppressive effects of progestins by activating the mTOR-4EBP1/eIF4G pathway. Lower expression of THRB is likely correlated with progesterone resistance.

Global mapping of binding sites for phic31 integrase in transgenic maden-darby bovine kidney cells using ChIP-seq.

BACKGROUND: ΦC31 integrase, a site-specific recombinase, can efficiently target attB-bearing transgenes to endogenous pseudo attP sites within mammalian genomes. The sequence features of endogenous binding sites will help us to fully understand the site-specific recognition function by ΦC31 integrase. The present study was aimed to uncover the global map of ΦC31 integrase binding sites in bovine cells and analysis the features of these binding sites by comprehensive bioinformatics methods. RESULTS: In this study, we constructed a ChIP-seq method that can be used to uncover the global binding sites by phiC31 integrase. 6740 potential ΦC31 integrase binding sites were identified. A sequence motif was found that contains inverted repeats and has similarities to wild-type attP site. Using REPEATMASKER, we identified a total of 20,183 repeat-regions distributed in 50 repeat types for the 6740 binding sites. These sites enriched in "regulation of GTPase activity" of in the GO category of biological process and KEGG pathway of signal transmembrane transporter activity. CONCLUSION: This study is the first time to uncover the global map of binding sites for ΦC31 integrase using ChIP-sequencing method and analysis the features of these binding sites. This method will help us to fully understand the mechanism of the site-specific integration function by phiC31 integrase and will potentially boost its genetic manipulations in both gene therapy and generation of transgenic animals.

Metformin Enhances Nomegestrol Acetate Suppressing Growth of Endometrial Cancer Cells and May Correlate to Downregulating mTOR Activity In Vitro and In Vivo.

This study investigated the effect of a novel progestin and its combination with metformin on the growth of endometrial cancer (EC) cells. Inhibitory effects of four progestins, including nomegestrol acetate (NOMAC), medroxyprogesterone acetate, levonorgestrel, and cyproterone acetate, were evaluated in RL95-2, HEC-1A, and KLE cells using cell counting kit-8 assay. Flow cytometry was performed to detect cell cycle and apoptosis. The activity of Akt (protein kinase B), mTOR (mammalian target of rapamycin) and its downstream substrates 4EBP1 (4E-binding protein 1) and eIF4G (Eukaryotic translation initiation factor 4G) were assayed by Western blotting. Nude mice were used to assess antitumor effects in vivo. NOMAC inhibited the growth of RL95-2 and HEC-1A cells, accompanied by arresting the cell cycle at G0/G1 phase, inducing apoptosis, and markedly down-regulating the level of phosphorylated mTOR/4EBP1/eIF4G in both cell lines (p < 0.05). Metformin significantly increased the inhibitory effect of and apoptosis induced by NOMAC and strengthened the depressive effect of NOMAC on activity of mTOR and its downstream substrates, compared to their treatment alone (p < 0.05). In xenograft tumor tissues, metformin (100 mg/kg) enhanced the suppressive effect of NOMAC (100 mg/kg) on mTOR signaling and increased the average concentration of NOMAC by nearly 1.6 times compared to NOMAC treatment alone. Taken together, NOMAC suppressing the growth of EC cells likely correlates to down-regulating the activity of the mTOR pathway and metformin could strengthen this effect. Our findings open a new window for the selection of progestins in hormone therapy of EC.

Identification of New Epididymal Luminal Fluid Proteins Involved in Sperm Maturation in Infertile Rats Treated by Dutasteride Using iTRAQ.

BACKGROUND: Spermatozoa become mature and acquire fertilizing capacity during their passage through the epididymal lumen. In this study, we identified new epididymal luminal fluid proteins involved in sperm maturation in infertile rats by dutasteride, a dual 5α-reductase inhibitor, in order to provide potential epididymal targets for new contraceptives and infertility treatment. METHODS: Male rats were treated with dutasteride for 28 consecutive days. We observed the protein expression profiles in the epididymal luminal fluids in infertile and normal rats using isobaric tags for relative and absolute quantitation (iTRAQ) technique. The confidence of proteome data was validated by enzyme-linked immunosorbent assays. RESULTS: 1045 proteins were tested, and 23 of them presented different expression profiling in the infertile and normal rats. The seven proteins were down-regulated, and 16 proteins were up-regulated. Among the seven proteins which were significantly down-regulated by dutasteride in the epididymal luminal fluids, there were three ß-defensins (Defb2, Defb18 and Defb39), which maybe the key proteins involved in epididymal sperm maturation and male fertility. CONCLUSIONS: We report for the first time that dutasteride influences the protein expression profiling in the epididymal luminal fluids of rats, and this result provides some new epididymal targets for male contraception and infertility therapy.

[Inhibitory effect of dutasteride on the expressions of epididymal Claudin1 and ß-catenin in male rats].

OBJECTIVE: To explore the molecular mechanism of dutasteride inhibiting fertility by studying its effects on the expressions of the epididymal epithelial junction proteins Claudin1 and ß-catenin in rats. METHODS: Sixteen 3-month-old SD male rats were equally divided into an experimental and a negative control group to be treated intragastrically with dutasteride at 40 mg/kg per day and the same dose of solvent, respectively, for 14 consecutive days. Then, the sperm motility and morphology of the rats were detected by computer-assisted sperm analysis, the serum levels of testosterone (T) and dihydrotestosterone (DHT) measured by ELISA, changes in the tight junction of epididymal cells observed under the transmission electron microscope, the protein and gene expressions of Claudin1 and ß-catenin determined by RT-PCR and immunohistochemistry, and the conception rate of the mated female rats calculated. RESULTS: Dutasteride significantly suppressed the serum DHT level, sperm motility, and fertility of the rats (P <0.05). Interspaces between epididymal epithelial cell tight junctions were observed, the volume of epididymal fluid obviously increased, and the expressions of Claudin1 and ß-catenin gene and protein remarkably downregulated in the experimental rats (P <0.05). CONCLUSION: Dutasteride can significantly inhibit the fertility of male rats by reducing the serum DHT level, suppressing Claudin1 and ß-catenin expressions, and damaging epididymal epithelial cell junctions.

Mechanism of enhanced removal of quinonic intermediates during electrochemical oxidation of Orange II under ultraviolet irradiation.

The effect of ultraviolet irradiation on generation of radicals and formation of intermediates was investigated in electrochemical oxidation of the azo-dye Orange II using a TiO2-modified ß-PbO2 electrode. It was found that a characteristic absorbance of quinonic compounds at 255 nm, which is responsible for the rate-determining step during aromatics degradation, was formed only in electrocatalytic oxidation. The dye can be oxidized by either HO radicals or direct electron transfer. Quinonic compounds were produced concurrently. The removal of TOC by photo-assisted electrocatalytic oxidation was 1.56 times that of the sum of the other two processes, indicating a significant synergetic effect. In addition, once the ultraviolet irradiation was introduced into the process of electrocatalytic oxidation, the degradation rate of quinonic compounds was enhanced by as much as a factor of two. The more efficient generation of HO radicals resulted from the introduction of ultraviolet irradiation in electrocatalytic oxidation led to the significant synergetic effect as well as the inhibiting effect on the accumulation of quinonic compounds.

Recent progress and prospects for chain elongation of transforming biomass waste into medium-chain fatty acids.

Chain elongation technology utilises microorganisms in anaerobic digestion to transform waste biomass into medium-chain fatty acids that have greater economic value. This innovative technology expands upon traditional anaerobic digestion methods, requiring abundant substrates that serve as electron donors and acceptors, and inoculating microorganisms with chain elongation functions. While this process may result in the production of by-products and elicit competitive responses, toxicity suppression of microorganisms by substrates and products remains a significant obstacle to the industrialisation of chain elongation technology. This study provides a comprehensive overview of existing research on widely employed electron donors and their synthetic reactions, competitive reactions, inoculum selection, toxicity inhibition of substrates and products, and increased chain elongation approaches. Additionally, it presents actionable recommendations for future research and development endeavours in this domain, intending to inspire and guide researchers in advancing the frontiers of chain elongation technology.

Dan'e fukang decoction reduces hemorrhage in a rat model of mifepristone induced incomplete abortion and may correlate with cell adhesion molecule signaling interference.

ETHNOPHARMACOLOGICAL RELEVANCE: Dan'e fukang decoction (DFD) is a traditional Chinese medicine formula. DFD obtains 10 herbs, including Salvia yunnanensis C.H.Wright (Zidanshen), Curcuma zedoaria (Christm.) Roscoe (Ezhu), Angelica sinensis (Oliv.) Diels (Danggui), Cyperus rotundus L. (Xiangfuzi), Corydalis yanhusuo (Y.H.Chou & Chun C. Hsu) W.T.Wang ex Z.Y.Su & C.Y.Wu, Bupleurum marginatum Wall. ex DC. (Yanhusuo), Sparganium stoloniferum (Buch.-Ham. ex Graebn.) Buch.-Ham. ex Juz. (Sanleng), Panax notoginseng (Burkill) F.H.Chen (Sanqi), Paeonia lactiflora Pall. (Shaoyao) and Glycyrrhiza uralensis Fisch. (Gancao). DFD is now clinically used for the treatment of menstrual irregularities, dysmenorrhea and menstrual discomfort caused by blood stasis and easing of endometriosis. Based on this, it is reasonable to presume that DFD may be effective in treating incomplete abortion and reducing postpartum bleeding, but no specific studies have been reported so far. AIM OF THE STUDY: To investigate the efficacy of Dan'e fukang decoction (DFD) in reducing prolonged vaginal bleeding followed by mifepristone induced incomplete abortion and explore the mechanisms of action of DFD in treating incomplete abortion. METHODS: An incomplete abortion model of rat was established by single intragastrically administered 8.5 mg/kg mifepristone on the 7th day of pregnancy. From the 8th day of pregnancy, the abortive rats were administered solvent, a positive control drug, or different doses of DFD, respectively for seven consecutive days. The efficacy of DFD was assessed by measuring the vaginal bleeding volume of the rats. Four coagulation parameters and platelet counts were measured. Hematoxylin and eosin (HE) staining was performed to evaluate pathological changes in the uterine embryos. Serum levels of progesterone and estrogen were measured using ELISA. Network pharmacology and transcriptomics were used to predict potential targets and pathways for DFD to reduce hemorrhage. The levels of mRNA related to cell adhesion molecules (CAMs) were detected by RT-qPCR. The levels of progesterone and estrogen receptors and the proteins associated with CAMs pathway in uterine tissues were detected by Western Blot. RESULTS: DFD significantly reduced the volume of vaginal bleeding of the abortive rats and significantly downgraded the pathological scores of uterine embryos. DFD significantly increased serum levels of E2, and had no impact on serum levels of P4 and the protein expression of ER and PR in the uteri of the abortive rats. Pathways in cancer, lipid, focal adhesion and immune-related signaling were predicted to be influenced by DFD via the analysis of network pharmacology. The CAMs signaling was found the most critical pathway regulated by both mifepristone and DFD via RNA-seq assay, followed by axon guidance, basal cell carcinoma, hippo signaling pathway and neuroactive ligand-receptor interaction. Combining the two analytical methods, ICAM-1 was predicted likely the key targeted gene by DFD. Finally, DFD was validated to decrease the protein expression of ICAM-1, ITGB2, ITGB7 and RASSF5 in the uterine tissues, which correlated to suppress the CAMs signaling pathway. CONCLUSION: DFD significantly reduced hemorrhage. DFD significantly increased the serum levels of E2 and inhibited CAMs signaling pathway, which was likely to be involved in the mechanism of action of DFD facilitating residual uterine embryo expulsion in the rat model of incomplete abortion.

The purine-carboxylate-containing coordination polymer poly[[µ4-1-(2-carboxylatoethyl)-6-oxo-6,9-dihydro-1H-purin-9-ido]zinc(II)].

The title compound, [Zn(C8H6N4O3)]n or [Zn(L)]n [H2L is 3-(6-oxo-6,9-dihydro-1H-purin-1-yl)propionic acid], crystallized as a nonmerohedral twin. The Zn(II) cation is four-coordinated, ligated by two carboxylate O atoms from two L ligands and two N atoms from another two ligands. Each ligand bridges four Zn(II) centres, extending the structure into a three-dimensional polymer with a 4-connected (6(5),4(1)) topological structure containing two-dimensional homochiral layers constructed from one-dimensional metal-organic helices. Investigation of the thermal stability of the compound shows that the network has very high thermostability and is stable up to 720 K.

catena-Poly[[[diaquazinc]-bis{µ-N2,N6-bis[(pyridin-3-yl)methyl]pyridine-2,6-dicarboxamide}] dinitrate].

In the title compound, {[Zn(C(19)H(17)N(5)O(2))(2)(H(2)O)(2)](NO(3))(2)}(n), the Zn(II) cation is located at an inversion centre within a slightly distorted octahedron, ligated by four N atoms from four N(2),N(6)-bis[(pyridin-3-yl)methyl]pyridine-2,6-dicarboxamide (L) ligands occupying a plane about the Zn(II) atom with the two water O atoms perpendicular to that. In the complex molecule, the bidentate bridging L ligands display helical R and S conformers, and link the Zn(II) cations into a one-dimensional centrosymmetric double-chain structure containing 32-membered rings. The nitrate anions reside in these rings and are involved in multiple N-H...O hydrogen-bond interactions. On excitation at 390 nm, the title compound displays a strong blue emission centred at 449 nm. Investigation of the thermal stability shows that the network structure is stable up to 420 K.

Poly[bis[µ2-3-(pyridin-4-yl)benzoato-κ³N:O,O']lead(II)].

In the title compound, [Pb(C12H8NO2)2]n, the Pb atom sits on a crystallographic C2 axis and is six-coordinate, ligated by two chelating carboxylate groups from two 3-(pyridin-4-yl)benzoate (L) ligands and by two N atoms from another two ligands. Each ligand bridges two PbII centres, extending the structure into a corrugated two-dimensional (4,4) net. The ligand L is conformationally chiral, with a torsion angle of 27.9 (12)° between the planes of its two rings. The torsion angle has the same sense throughout the structure, so that the extended two-dimensional polymer is homochiral. Investigation of the thermal stability shows that the network is stable up to 613 K. In the absence of any stereoselective factor in the preparation of the compound, the enantiomeric purity of the crystal studied, based only on the torsional conformation of the ligand, implies that the bulk sample is a racemic conglomerate.

Nomegestrol acetate ameliorated adipose atrophy in a rat model of cisplatin­induced cachexia.

Cachexia, a complex disorder that results in depletion of adipose tissue and skeletal muscle, is driven by anorexia, metabolic abnormalities and inflammation. There are limited therapeutic options for this syndrome. Previous evidence has demonstrated that increasing adipose tissue may improve quality of life and survival outcomes in cachexia. Cisplatin, as a chemotherapy drug, also causes cachexia during antitumor therapy due to its adverse effects. To establish a rat model of cachexia, the animals were intraperitoneally treated with cisplatin at doses of 1, 2 and 3 mg/kg, and the rats that responded to cisplatin at the optimal dose were used to test the effect of nomegestrol acetate (NOMAc). Rats that were assessed to be sensitive to cisplatin were randomly grouped and intragastrically administered vehicle, 5 or 10 mg/kg megestrol acetate (MA) or 2.5, 5 or 10 mg/kg NOMAc. The body weights and food consumption of the rats were assessed. Serum IL-6 and TNF-α levels were assessed using ELISA. The protein expression levels of adipose triglyceride lipase (ATGL), hormone-sensitive lipase (HSL), peroxisome proliferator activated receptor γ (PPARγ), fatty acid synthase (FASN) and sterol regulatory element-binding protein-1 (SREBP-1) from inguinal white adipose tissue (iWAT) and epididymal white adipose tissue (eWAT) were evaluated using western blotting. The optimal way to establish a chemotherapy-induced rat model of cachexia demonstrated in the present study was to intraperitoneally administer the rats with 2 mg/kg cisplatin for 3 consecutive days. NOMAc (2.5, 5 mg/kg) and MA (10 mg/kg) were able to significantly ameliorate the loss of body weight in the cisplatin-induced cachectic rats. NOMAc significantly reduced the serum levels of TNF-α at 10 mg/kg. Morphologically, iWAT atrophy, with a remarkable reduction in adipocyte volume, was observed in the cisplatin-induced cachectic rats, but the effects were reversed by administering 5, 10 mg/kg NOMAc or 10 mg/kg MA. Furthermore, 2.5 mg/kg NOMAc markedly reduced the protein expression levels of the lipolysis genes HSL and ATGL, and 5 mg/kg NOMAc markedly enhanced the protein expression levels of adipogenesis genes, including FASN, SREBP-1 and PPARγ in iWAT but not in eWAT. NOMAc was demonstrated to improve cachexia at lower doses compared with MA. Overall, NOMAc is likely to be a promising candidate drug for ameliorating cancer cachexia induced by cisplatin.

Jinfeng pills ameliorate premature ovarian insufficiency induced by cyclophosphamide in rats and correlate to modulating IL-17A/IL-6 axis and MEK/ERK signals.

ETHNOPHARMACOLOGICAL RELEVANCE: Jinfeng Pill (JFP) is a classical Chinese medicine formula and composed of 9 herbs, including Epimedium brevicornu Maxim (Yinyanghuo), Cervus elaphus Linnaeus (Lurong), Panax ginseng C.A.Mey. (Renshen), Equus asinus (EJiao), Ligustrum lucidum W.T.Aiton (Nvzhenzi), Reynoutria multiflora (Thunb.) Moldenke (Heshouwu), Curculigo orchioides Gaertn (Xianmao), Neolitsea cassia (L.) Kosterm. (Rougui) and Leonurus japonicus Houtt. (Yimucao). The formula is clinically used to regulate menstrual cycle and alleviate polycystic ovarian syndrome due to its capabilities of ovulation induction. It is therefore presumed that JFP could be used for the therapy of premature ovarian insufficiency (POI) but the assumed efficacy has not been fully substantiated in experiment. AIM OF STUDY: To evaluate the effectiveness of JFP on cyclophosphamide (CTX)-induced POI and preliminarily explore its potential mechanisms of action. MATERIAL AND METHODS: An experimental rat model of POI was established by using CTX induction to assess the efficacy of JFP. The potential targets of action for JFP alleviating POI were predicted by the combination of network pharmacology and transcriptomics and finally validating by RT-qPCR and Western blot. RESULTS: JFP alleviated the damages of ovarian tissue induced by CTX in the rat model of POI via significantly decreasing serum levels of FSH and LH and the ratio of FSH/LH and increasing the levels of E2 and AMH, accompanied with promoting ovarian folliculogenesis and follicle maturity and reversing the depletion of follicle pool. With the analysis of network pharmacology, pathways in cancer, proteoglycans in cancer, PI3K-AKT, TNF and FoxO signaling pathways were predicted to be influenced by JFP. The results of RNA-seq further revealed that IL-17 signaling pathway was the most important pathway regulated by both CTX and JFP, following by transcriptional misregulation in cancer and proteoglycans in cancer. Combining the two analytical methods, JFP likely targeted genes associated with immune regulation, including COX-2, HSP90AA1, FOS, MMP3 and MAPK11 and pathways, including IL-17,Th17 cell differentiation and TNF signaling pathway. Finally, JFP was validated to regulate the mRNA expression of FOS, FOSB, FOSL1, MMP3, MMP13 and COX-2 and decrease the release of IL-17A and the protein expression of IL-6 and suppress the phosphorylation of MEK1/2 and ERK1/2 in CTX induced POI rats. CONCLUSION: Jinfeng Pill is effective to ameliorate the symptoms of POI induced by CTX in the model of rats and its action is likely associated with suppressing IL-17A/IL-6 axis and the activity of MEK1/2-ERK1/2 signaling.

Poly[[bis{µ2-N2,N6-bis[(pyridin-3-yl)methyl]pyridine-2,6-dicarboxamide}dichloridonickel(II)] N,N-dimethylformamide tetrasolvate].

In the title compound, {[NiCl(2)(C(19)H(17)N(5)O(2))(2)]·4C(3)H(7)NO}(n), the Ni(II) atom is located on an inversion centre and is in a six-coordinated octahedral geometry, formed by four pyridine N atoms from four N(2),N(6)-bis[(pyridin-3-yl)methyl]pyridine-2,6-dicarboxamide (BPDA) ligands occupying the equatorial plane and two chloride anions at the axial sites. The bidentate bridging BPDA ligands link the Ni(II) atoms into a two-dimensional corrugated grid-like flexible layer with a (4,4)-connected topology, which consists of left- and right-handed helical chains sharing the common Ni(II) atoms. Investigation of the thermal stability shows that the network is stable up to 573 K.

catena-Poly[[diaqua-nickel(II)]-bis-(µ-2-{[5-(pyridin-4-yl)-1,3,4-oxadiazol-2-yl]sulfan-yl}acetato)].

In the title compound, [Ni(C(9)H(6)N(3)O(3)S)(2)(H(2)O)(2)](n), the Ni(II) atom, located on an inversion center, is ligated in an octa-hedral geometry by two carboxyl-ate O atoms from two 2-{[5-(pyridin-4-yl)-1,3,4-oxadiazol-2-yl]sulfan-yl}acetate (L) ligands and two O atoms from water mol-ecules in the equatorial plane, and two pyridine N atoms from other two L ligands at the apical sites. Two L ligands bridge pairs of metal atoms in an anti-parallel manner, forming centrosymmetric dinuclear quasi-recta-ngular units which are linked into infinite double-stranded chains parallel to [100]. O-H⋯O hydrogen bonds between the coordinating water mol-ecules and the carboxyl-ate groups of the L ligand as well as interchain S⋯N inter-actions [2.726 (2)-3.363 (2) Å] lead to the formation of a layer structure parallel to (001).

Bis{N(2),N(6)-bis-[(pyridin-3-yl)meth-yl]pyridine-2,6-dicarboxamide-κN}bis-(methanol-κO)bis-(thio-cyanato-κN)cobalt(II).

In the title compound, [Co(NCS)(2)(C(19)H(17)N(5)O(2))(2)(CH(3)OH)(2)], the Co(II) atom lies on an inversion center and is coordinated by two isothio-cyanate N atoms, two O atoms of methanol mol-ecules and two pyridine N atoms in a slightly distorted octa-hedral environment. Inter-molecular O-H⋯O and N-H⋯N hydrogen bonds join the complex mol-ecules into layers parallel to the bc plane.

catena-Poly[[[diaqua-[3-(pyridin-4-yl)benzoato-κ(2)O,O']gadolinium(III)]-bis-[µ-3-(pyridin-4-yl)benzoato-κ(2)O:O']] monohydrate].

In the title coordination polymer, {[Gd(C(12)H(8)NO(2))(3)(H(2)O)(2)]·H(2)O}(n), the Gd(III) ion is ligated by one bidentate carboxyl-ate group, four monodentate bridging carboxyl-ate O atoms and two water mol-ecules. The resulting GdO(8) polyhedron approximates to a square anti-prism. The bridging ligands link the metal ions into a [100] chain, with each pair of adjacent metal ions being bridged by two ligands. Inter-chain O-H⋯O and O-H⋯N hydrogen bonds help to establish the packing.

Tetra-aqua-bis-[3-(pyridin-4-yl)benzoato-κN]manganese(II).

In the title compound, [Mn(C(12)H(8)NO(2))(2)(H(2)O)(4)], the Mn(2+) ion lies on a twofold rotation axis and has a distorted N(2)O(4) octa-hedral coordination geometry formed by four water O atoms in the equatorial plane and two apical pyridyl N atoms. A three-dimensional network is formed in the crystal structure by multiple O-H⋯O hydrogen bonds between the coordin-ating water molecules and the free carboxylate groups.