microRNA-181a contributes to gastric hypersensitivity in rats with diabetes by regulating TLR4 expression.

Aim: The aim of this study is to investigate the mechanism and interaction of microRNA-181a (miR-181a), toll-like receptor 4 (TLR4) and nuclear factor-kappa B (NF-κB) in gastric hypersensitivity in diabetic rats. Methods: Diabetes was induced by a single intraperitoneal injection of streptozotocin (STZ; 65 mg/kg) in female SD rats. Gastric balloon distension technique was used to measure diabetic gastric hypersensitivity. Gastric-specific (T7-T10) dorsal root ganglion (DRG) neurons were acutely dissociated to measure excitability with patch-clamp techniques. Western blotting was employed to measure the expressions of TLR4, TRAF6 and NF-κB subunit p65 in T7-T10 DRGs. The expressions of microRNAs in T7-T10 DRGs were measured with quantitative real-time PCR and fluorescence in situ hybridization. Dual-luciferase reporter gene assay was used to detect the targeting regulation of microRNAs on TLR4. Results: (1) Diabetic rats were more sensitive to graded gastric balloon distention at 2 and 4 weeks. (2) The expression of TLR4 was significantly up-regulated in T7-T10 DRGs of diabetic rats. Intrathecal injection of CLI-095 (TLR4-selective inhibitor) attenuated diabetic gastric hypersensitivity, and markedly reversed the hyper-excitability of gastric-specific DRG neurons. (3) The expressions of miR-181a and miR-7a were significantly decreased in diabetic rats. MiR-181a could directly regulate the expression of TLR4, while miR-7a couldn't. (4) Intrathecal injection of miR-181a agomir down-regulated the expression of TLR4, reduced the hyper-excitability of gastric-specific neurons, and alleviated gastric hypersensitivity. (5) p65 and TLR4 were co-expressed in Dil-labeled DRG neurons. (6) Inhibition of p65 attenuated diabetic gastric hypersensitivity and hyper-excitability of gastric-specific DRG neurons. (7) The expression of TRAF6 was significantly up-regulated in diabetic rats. CLI-095 treatment also reduced the expression of TRAF6 and p65. Conclusion: The reduction of microRNA-181a in T7-T10 DRGs might up-regulate TLR4 expression. TLR4 activated NF-κB through MyD88-dependent signaling pathway, increased excitability of gastric-specific DRG neurons, and contributed to diabetic gastric hypersensitivity.

External validation and comparison of two versions of simplified sequential organ failure assessment scores to predict prognosis of septic patients.

BACKGROUND: Evidence shows that simplified SOFA scoring system has better clinical practice. OBJECTIVE: This study aimed to validate and compare the scores acquired with simplified organ dysfunction criteria optimized for electronic health records (eSOFA), and simplified and accurate sequential organ failure assessment (sa-SOFA) for their accuracies in predicting the prognosis of septic patients. METHODS: This retrospective observational study was conducted at three major academic hospitals. Clinical data from 574 patients diagnosed with sepsis following the Third International Consensus Definitions for Sepsis and Septic Shock (Sepsis-3)were retrospectively retrieved and analysed. Scores from the quick sequential organ failure assessment (qSOFA) and sequential organ failure assessment (SOFA) were used as reference scores. The area under the receiver operating characteristic curve (AUROC) was used to assess the performance of eSOFA and sa-SOFA scores in predicting in-hospital mortality. RESULTS: AUROC analysis demonstrated the predictability of the four scoring systems for sepsis surveillance, listed in descending order as: sa-SOFA, 0.790 (95% confidence interval [CI]: 0.754-0.822); SOFA, 0.774 (95% CI: 0.738-0.808); eSOFA, 0.729 (95% CI: 0.691-0.765); and qSOFA, 0.618 (95% CI: 0.577-0.658). Moreover, sa-SOFA and SOFA scores (Z = 1.950, P = .051) did not significantly differ from each other in discriminatory power, but the sa-SOFA score had a higher power than eSOFA score (P values < .001). CONCLUSION: sa-SOFA appeared to have performed better than eSOFA score for predicting in-hospital mortality in patients' sepsis. Further large prospective studies are needed to externally validate.

Clinical characteristics and prognosis in patients with urosepsis from intensive care unit in Shanghai, China: a retrospective bi-centre study.

BACKGROUND: The purpose of this study was to retrospectively analyze clinical characteristics and prognostic risk factors of urosepsis patients admitted to two intensive care units in Shanghai, China. METHODS: Clinical data from patients diagnosed with urosepsis were retrospectively retrieved and analyzed from ICU in two regional medical centers from January 2015 to December 2019. RESULTS: Two hundred two patients were included in the subsequent analysis eventually, with an average age of 72.02 ± 9.66 years, 79.21% of the patients were female and the mortality rate of 15.84%.The proportion of patients with chronic underlying diseases such as diabetes and hypertension was relatively high (56.44, 49.50%, respectively), and the incidence of shock was also high (41.58%) correspondingly. The most common pathogen isolated was Escherichia coli (79.20%), of which the extended-spectrumß-lactamases (ESBLs)(+) accounted for 42.57%. In multivariate analysis, the strongest predictors for death were mechanical ventilation (OR 7.260, 95% CI 2.200-23.963; P = 0.001),chronic kidney disease (CKD) (OR 5.140, 95% CI 1.596-16.550; P = 0.006), APACHE II score (OR 1.321, 95% CI 1.184-1.473; P < 0.001) and lactate (OR 1.258, 95% CI 1.037-1.527; P = 0.020). Both APACHE II score and lactate had the ideal predictive value, with the area under the ROC curve (AUC) of 0.858 and 0.805 respectively. CONCLUSION: The patients with urosepsis were characterized by a higher proportion of female, older age, more percentage of comorbidities in this region, and patients with ESBLs (+) Escherichia coli infection were more prone to shock. Mechanical ventilation, comorbidity with CKD, APACHE II score and lactate were independent risk factors for death in urosepsis patient, but lactate level and APACHE II score had better predictive value for prognosis.

Downregulation of glucose-6-phosphate dehydrogenase contributes to diabetic neuropathic pain through upregulation of toll-like receptor 4 in rats.

BACKGROUND AND AIM: Diabetic neuropathic pain is a refractory and disabling complication of diabetes mellitus. The pathogenesis of the diabetic neuropathic pain is still unclear, and treatment is insufficient. The aim of this study is to investigate the roles of glucose-6-phosphate dehydrogenase (G6PD) and toll-like receptor 4 (TLR4) in neuropathic pain in rats with diabetes. METHODS: Type 1 diabetes model was induced by intraperitoneal injection of streptozotocin (STZ, 75 mg/kg) in adult female Sprague-Dawley rats. Paw withdrawal threshold and paw withdrawal latency of rats were measured by von Frey filaments and thermal radiation, respectively. The expressions of G6PD and TLR4 in L4-L6 dorsal root ganglions (DRGs) were measured by western blotting and quantitative real-time polymerase chain reaction analysis. Fluorescent immunohistochemistry was employed to detect expressions of G6PD and TLR4 and co-location of G6PD with TLR4. RESULTS: The mRNA and protein expression levels of G6PD in DRGs were significantly decreased in diabetic rats when compared with age-matched control rats. Upregulation of G6PD by intrathecal injection of G6PD overexpression adenovirus markedly attenuated hindpaw pain hypersensitivity of diabetic rats. The mRNA and protein expression levels of TLR4 in DRGs of diabetic rats were significantly increased when compared with control rats. Intrathecal injection of TLR4-selective inhibitor CLI-095 attenuated diabetic pain in dose- and time-dependent manners. Furthermore, G6PD and TLR4 were co-localized in DRG neurons. Intrathecal injection of G6PD overexpression adenovirus greatly reduced TLR4 expression, while intrathecal injection of CLI-095 had no significant effect on G6PD expression in diabetic rats. CONCLUSIONS: Our results suggest that decrease in G6PD expression was involved in diabetic peripheral neuropathic pain, which was most likely through upregulation of TLR4 expression in the DRGs of rats.

Bioactivity and structure-activity relationship of cinnamic acid derivatives and its heteroaromatic ring analogues as potential high-efficient acaricides against Psoroptes cuniculi.

A series of cinnamic acid derivatives and its heteroaromatic ring analogues were synthesized and evaluated for acaricidal activity in vitro against Psoroptes cuniculi, a mange mite. Among them, eight compounds showed the higher activity with median lethal concentrations (LC50) of 0.36-1.07mM (60.4-192.1µg/mL) and great potential for the development of novel acaricidal agent. Compound 40 showed both the lowest LC50 value of 0.36mM (60.4µg/mL) and the smallest median lethal time (LT50) of 2.6h at 4.5mM, comparable with ivermectin [LC50=0.28mM (247.4µg/mL), LT50=8.9h], an acaricidal drug standard. SAR analysis showed that the carbonyl group is crucial for the activity. The type and chain length of the alkoxy in the ester moiety and the steric hindrance near the ester group significantly influence the activity. The esters were more active than the corresponding thiol esters, amides, ketones or acids. Replacement of the phenyl group of cinnamic esters with α-pyridyl or α-furanyl significantly increase the activity. Thus, a series of cinnamic esters and its heteroaromatic ring analogues with excellent acaricidal activity emerged.

A class of promising acaricidal tetrahydroisoquinoline derivatives: synthesis, biological evaluation and structure-activity relationships.

As part of our continuing research on isoquinoline acaricidal drugs, this paper reports the preparation of a series of the 2-aryl-1-cyano-1,2,3,4-tetrahydroisoquinolines with various substituents on the N-phenyl ring, their in vitro acaricidal activities against Psoroptes cuniculi, a mange mite, and discusses their SAR as well. The structures of all compounds, including 12 new ones, were elucidated by analysis of UV, IR, NMR, ESI-MS, HR-MS spectra and X-ray diffraction experiments. All target compounds showed varying degrees of activity at 0.4 mg/mL. Compound 1 showed the strongest activity, with a 50% lethal concentration value (LC50) of 0.2421 µg/mL and 50% lethal time value (LT50) of 7.79 h, comparable to the standard drug ivermectin (LC50 = 0.2474 µg/mL; LT50 = 20.9 h). The SAR showed that the substitution pattern on the N-aromatic ring exerted a significant effect on the activity. The substituents 2'-F, 3'-F, 2'-Cl, 2'-Br and 2'-CF3 remarkably enhanced the activity. Generally, for the isomers with the same substituents at different positions, the order of the activity was ortho > meta > para. It was concluded that the target compounds represent a class of novel promising candidates or lead compounds for the development of new tetrahydroisoquinoline acaricidal agents.

[Clinical and biological characteristics of childhood acute myeloid leukemia with EVI1 gene positive expression].

OBJECTIVE: To study the expression of ecotropic viral integration site (EVI1) gene in childhood acute myeloid leukemia (AML) and the clinical features of EVI1-positive children with AML. METHODS: The clinical data of EVI1-positive children with AML were collected and analyzed. RT-PCR and real-time quantitative PCR were used for qualitative and quantitative analysis of expression of EVI1. Flow cytometry (FCM) was used for determining the immunophenotypes of bone marrow cells. Multiparameter FCM was used for monitoring minimal residual disease. The karyotypes were determined. RESULTS: Of 241 children with AML, 33 (13.7%) were positive for EVI1 expression. There were no significant differences in age at first visit as well as the white blood cell count, hemoglobin level, and platelet count in peripheral blood between EVI1-positive and EVI1-negative children with AML (P>0.05), but EVI1-positive children had a significantly increased proportion of females compared with EVI1-negative children (P<0.05). The change in EVI1 expression was not synchronous with clinical remission and the change of MRD: some children had clinical remission or negative conversion of MRD before negative conversion of EVI1, while some had negative conversion of EVI1 before clinical remission or while MRD showed positive. EVI1 gene was usually co-expressed with other fusion genes. CD33 (100%), CD38 (88%), and HLADR (76%) were highly expressed in EVI1-positive children with AML. Abnormal chromosome structure or number was found in 15 patients. Compared with EVI1-negative children, EVI1-positive children had significantly lower complete remission rates after the first course of treatment (P<0.05). CONCLUSIONS: EVI1-positive children with AML have a poor short-term prognosis. In the development of AML, the activation of EVI1 gene is not isolated, but the result of interactions with other genes or chromosome abnormalities, and the mechanism of activation and its function need further study.

Proliferation and tenogenic differentiation of bone marrow mesenchymal stem cells in a porous collagen sponge scaffold.

BACKGROUND: Collagen is one of the most commonly used natural biomaterials for tendon tissue engineering. One of the possible practical ways to further enhance tendon repair is to combine a porous collagen sponge scaffold with a suitable growth factor or cytokine that has an inherent ability to promote the recruitment, proliferation, and tenogenic differentiation of cells. However, there is an incomplete understanding of which growth factors are sufficient and optimal for the tenogenic differentiation of rat bone marrow mesenchymal stem cells (BMSCs) in a collagen sponge-based 3D culture system. AIM: To identify one or more ideal growth factors that benefit the proliferation and tenogenic differentiation of rat BMSCs in a porous collagen sponge scaffold. METHODS: We constructed a 3D culture system based on a type I collagen sponge scaffold. The surface topography of the collagen sponge scaffold was observed by scanning electron microscopy. Primary BMSCs were isolated from Sprague-Dawley rats. Cell survival on the surfaces of the scaffolds with different growth factors was assessed by live/dead assay and CCK-8 assay. The mRNA and protein expression levels were confirmed by quantitative real-time polymerase chain reaction and Western blot, respectively. The deposited collagen was assessed by Sirius Red staining. RESULTS: Transforming growth factor ß1 (TGF-ß1) showed great promise in the tenogenic differentiation of BMSCs compared to growth differentiation factor 7 (GDF-7) and insulin-like growth factor 1 (IGF-1) in both the 2D and 3D cultures, and the 3D culture enhanced the differentiation of BMSCs into tenocytes well beyond the level of induction in the 2D culture after TGF-ß1 treatment. In the 2D culture, the proliferation of the BMSCs showed no significant changes compared to the control group after TGF-ß1, IGF-1, or GDF-7 treatment. However, TGF-ß1 and GDF-7 could increase the cell proliferation in the 3D culture. Strangely, we also found more dead cells in the BMSC-collagen sponge constructs that were treated with TGF-ß1. Moreover, TGF-ß1 promoted more collagen deposition in both the 2D and 3D cultures. CONCLUSION: Collagen sponge-based 3D culture with TGF-ß1 enhances the responsiveness of the proliferation and tenogenic differentiation of rat BMSCs.

Poly[[tris-(µ(3)-2-oxidopyridinium-3-carboxyl-ato)manganese(II)sodium(I)] monohydrate].

In the crystal structure of the title compound, {[MnNa(C(6)H(4)NO(3))(3)]·H(2)O}(n), the Mn(II) cation is located on a threefold rotation axis and is chelated by three 2-oxidopyridinium-3-carboxyl-ate (opc) anions in an octa-hedal coordination. The Na(I) cation is located on a threefold rotation axis and is surrounded by six O atoms from three opc anions. The opc anions link the Mn and Na cations, forming a three-dimensional polymeric structure. The uncoordinated water mol-ecule, located on a threefold rotation axis, is equally disordered over two sites. The three-dimensional network is consolidated by N-H⋯O hydrogen bonds.

Circular RNA profile in diabetic peripheral neuropathy: analysis of coexpression networks of circular RNAs and mRNAs.

Aim: To study the expression pattern of circular RNAs in diabetic peripheral neuropathy. Materials & methods: Transmission electron microscopy was used to observe the ultrastructure of sciatic nerves and dorsal root ganglion (DRGs). circRNAs in DRGs were identified with high-throughput RNA sequencing. Whole-genome mRNAs were detected by a chip scan. Results: The ultrastructure of sciatic nerves and DRGs in diabetes mellitus mice changed significantly. A total of 11,004 circRNAs and 15 differentially expressed circRNAs, as well as 35,368 mRNAs and 133 differentially expressed mRNAs were identified in DRGs between wild-type and diabetes mellitus mice. 11 circRNAs and 14 mRNAs have a significant correlation using strict coexpression analysis. The expression of circRNA.4614 was validated to be upregulated significantly. Conclusion: Our study suggested that circRNAs might be involved in the regulation of mRNA expressions in diabetic peripheral neuropathy.

Alpha-lipoic acid downregulates TRPV1 receptor via NF-κB and attenuates neuropathic pain in rats with diabetes.

AIMS: Painful diabetic neuropathy (PDN) is a refractory complication of diabetes. The study aimed to investigate the role of α-lipoic acid (ALA) on the regulation of transient receptor potential vanilloid-1 (TRPV1) in dorsal root ganglion (DRG) neurons of rats with diabetes. METHODS: Whole-cell patch-clamp recordings were employed to measure neuronal excitability in DiI-labeled DRG neurons of control and streptozotocin (STZ)-induced diabetic rats. Western blotting and immunofluorescence assays were used to determine the expression and location of NF-κBp65 and TRPV1. RESULTS: STZ-induced hindpaw pain hypersensitivity and neuronal excitability in L4-6 DRG neurons were attenuated by intraperitoneal injection with ALA once a day lasted for one week. TRPV1 expression was enhanced in L4-6 DRGs of diabetic rats compared with age-matched control rats, which was also suppressed by ALA treatment. In addition, TRPV1 and p65 colocated in the same DRG neurons. The expression of p65 was upregulated in L4-6 DRGs of diabetic rats. Inhibition of p65 signaling using recombinant lentiviral vectors designated as LV-NF-κBp65 siRNA remarkably suppressed TRPV1 expression. Finally, p65 expression was downregulated by ALA treatment. CONCLUSION: Our findings demonstrated that ALA may alleviate neuropathic pain in diabetes by regulating TRPV1 expression via affecting NF-κB.

Poly[octa-µ-aqua-tetra-aqua-bis(µ-5-sul-fon-atobenzene-1,3-dicarboxyl-ato)cobalt(II)tetra-sodium].

The title compound, [CoNa(4)(C(8)H(3)O(7)S)(2)(H(2)O)(12)](n), is a three-dimensional coordination polymer bridged by sulfoisophthalate trianions and water mol-ecules. The Co(II) atom, located on an inversion centre, is coordinated by two carboxyl-ate groups of the sulfoisophthalate trianions and by four water mol-ecules in a distorted CoO(6) octa-hedral geometry. Two independent Na(I) atoms also have a distorted octa-hedral coordination geometry formed by water, carboxyl-ate O and sulfonate O atoms. An extensive O-H⋯O and C-H⋯O hydrogen-bonding network is present in the crystal structure, as well as weak π-π stacking [centroid-centroid distance = 3.9553 (11) Å].

Poly[octa-µ-aqua-tetra-aqua-bis(µ(4)-5-sulfonatobenzene-1,3-dicarboxyl-ato)nickel(II)tetra-sodium].

In the crystal structure of the title compound, [Na(4)Ni(C(8)H(3)O(7)S)(2)(H(2)O)(12)](n), the Ni(II) cation occupies an inversion centre and is coordinated by the carboxyl groups of the sulfoisophthalate trianions and water mol-ecules in a distorted octa-hedral geometry. Two independent Na(I) atoms are connected by the carboxyl and sulfonate groups of the sulfoisophthalate ligands anions and water mol-ecules in a distorted octa-hedral geometry. The sulfoisophthalate ligands and coordinated water mol-ecules bridge the Ni(II) and Na(I) cations, forming a three-dimensional polymeric structure. Weak π-π stacking is present between parallel benzene rings [centroid-centroid distance = 3.9349 (10) Å]. Extensive O-H⋯O and C-H⋯O hydrogen bonding helps to stabilize the crystal structure.

Poly[bis-(µ(2)-pyrimidine-2-carboxyl-ato-κO,N:O',N')calcium].

In the crystal structure of the title polymeric complex, [Ca(C(5)H(3)N(2)O(2))(2)](n), the Ca(II) cation has site symmetry m2 and is N,O-chelated by four pyrimidine-2-carboxyl-ate anions in a square-anti-prismatic geometry. The planar pyrimidine-2-carboxyl-ate anion is located on a crystallographic special position, three C atoms have site symmetry 2mm, while the carboxyl O atom, the pyrimidine N atom and the other C atom have site symmetry m. Each pyrimidine-2--carboxyl-ate anion bridges two Ca(II) cations, forming polymeric sheets extending parallel to (001). π-π stacking exists between parallel pyrimidine rings [centroid-centroid distance = 3.6436 (6) Å] of adjacent polymeric sheets. Weak C-H⋯O hydrogen bonding is also observed between these sheets.

Aqua-(2,2'-bipyridine)bis-(4-hydroxy-benzoato)zinc(II).

In the title complex, [Zn(C(7)H(5)O(3))(2)(C(10)H(8)N(2))(H(2)O)], the Zn(II) ion is coordinated by two 4-hydroxy-benzoate anions, one 2,2'-bipyridine mol-ecule and one water mol-ecule and displays a distorted octa-hedral geometry. One Zn-O bond [2.5300 (15) Å] is much longer than the others in the mol-ecule. In the crystal structure, the face-to-face separation of 3.547 (9) Šsuggests no π-π stacking between parallel bipyridine ring systems, and an extensive O-H⋯O hydrogen-bonding network between the coordinated water molecule, the phenol group and carboxylate O atoms is present.

Bis[4-(4-pyridyl)pyridinium] µ-4,4'-bipyridine-bis-[tetra-aqua-(4,4'-bipyridine)manganese(II)] bis-(5-sulfonatobenzene-1,3-dicarboxyl-ate) 4,4'-bipyridine solvate penta-deca-hydrate.

The crystal structure of the title compound, (C(10)H(9)N(2))(2)[Mn(2)(C(10)H(8)N(2))(3)(H(2)O)(8)](C(8)H(3)O(7)S)(2)·C(10)H(8)N(2)·15H(2)O, consists of dinuclear Mn(II) complex cations, sulfonato-benzene-dicarboxyl-ate trianions, 4-(4-pyridyl)pyridinium cations, uncoordin-ated 4,4'-bipyridine and uncoordinated water mol-ecules. One 4,4'-bipyridine mol-ecule bridges two Mn atoms, forming a centrosymmetric dinuclear complex; the mid-point of the C-C bond linking the pyridine rings of the bridging ligand is located on an inversion center. Each Mn(II) atom is coordinated by four water and two 4,4'-bipyridine mol-ecules in a distorted octa-hedral geometry. The Mn(II) atom deviates by 0.591 (5) and 0.209 (2) Šfrom the mean planes of the coordinated pyridine rings. In the 4-(4-pyridyl)pyridinium cation, the two pyridine rings are twisted with respect to each other, making dihedral angle of 34.78 (17)°. The uncoordinated bipyridine mol-ecule is also centrosymmetric. One of uncoordinated water mol-ecules has site symmetry 2, and the other uncoordinated water mol-ecule is located close to an inversion center and its one H atom is disordered equally over two sites. Extensive π-π stacking between pyridine rings is observed and an extensive hydrogen-bonding network of the types N-H⋯N, O-H⋯N and O-H⋯O is present.

Bis(1H-imidazole-κN)bis-(2-oxidopyridinium-3-carboxyl-ato-κO,O)nickel(II).

In the crystal structure of the title Ni(II) complex, [Ni(C(6)H(4)NO(3))(2)(C(3)H(4)N(2))(2)], the Ni(II) atom is located on a twofold rotation axis and is chelated by two oxidopyridiniumcarboxyl-ate anions and further cis-coordinated by two imidazole ligands in a distorted cis-N(2)O(4) octa-hedral geometry. The C-O bond distance of 1.2573 (19) Šfound for the non-coordinating O atom of the carboxyl-ate group indicates significant delocalization of π-electron density over this residue. Similarly, the C-O bond distance of 1.260 (2) Šin the heteroaromatic ring indicates delocalization between the deprotonated hydr-oxy group and the pyridinium ring. The uncoordinated carboxyl-ate O atom links with the imidazole and pyridinium rings of adjacent mol-ecules via N-H⋯O and C-H⋯O hydrogen bonding, leading to a two-dimensional array parallel to (100).

Bis(1H-imidazole-κN)bis-(2-oxidopyridinium-3-carboxyl-ato-κO,O)cobalt(II).

In the mol-ecule of the title Co(II) complex, [Co(C(6)H(4)NO(3))(2)(C(3)H(4)N(2))(2)], the Co(II) atom is located on a twofold rotation axis and chelated by two oxidopyridiniumcarboxyl-ate anions and further cis-coordinated by two imidazole ligands in a distorted octa-hedral geometry. The shorter C-O bond distance of 1.260 (2) Šsuggests electron delocalization between the oxido group and the pyridinium ring. The uncoordinated carboxyl-ate O atom links with the imidazole and pyridinium rings of adjacent mol-ecules via N-H⋯O hydrogen bonding. Weak C-H⋯O hydrogen bonding is also present in the crystal structure.

4-Acetyl-pyridine-fumaric acid (2/1).

In the crystal structure of the title cocrystal, 2C(7)H(7)NO·C(4)H(4)O(4), the complete fumaric acid mol-ecule is generated by a crystallographic inversion centre. The two components of the cocrystal are linked by an O-H⋯N hydrogen bond.

Tetra-aqua-bis(pyridine-3-sulfonato-κN)nickel(II).

In the mol-ecule of the title compound, [Ni(C(5)H(4)NO(3)S)(2)(H(2)O)(4)], the Ni(II) cation is located on an inversion center and is coordinated by four water mol-ecules and two pyridine-3-sulfonate anions with an NiN(2)O(4) distorted octa-hedral geometry. The face-to-face separation of 3.561 (5) Šbetween parallel pyridine rings indicates the existence of weak π-π stacking between the pyridine rings. The structure also contains inter-molecular O-H⋯O hydrogen bonding and weak C-H⋯O hydrogen bonding.