Association between allergic diseases and epilepsy: A systematic review and meta-analysis.

OBJECTIVE: A number of studies have suggested a pathophysiological link between allergic diseases and epilepsy. Understanding the association between allergic diseases and epilepsy can help establish healthcare policies, implement prevention strategies, and provide a new direction for treatment. The study aimed to examine the association between allergic diseases and epilepsy. METHODS: PubMed, EMBASE, and Web of Science were searched for relevant primary articles. Two individuals independently conducted abstract screening, full-text review, data extraction, and quality assessment. Random-effects models were used to pool the risk estimates. RESULTS: From the 3124 citations identified, 32 were reviewed in full text. Finally, 11 studies with a total of 3,312,033 subjects were eligible for the analyses. Few studies reported the type of epilepsy, and there were inconsistent attempts to control for confounding. The pooled result showed that there was an 81% increase in the prevalence of epilepsy among individuals with asthma compared with those without asthma (odds ratio: 1.81, 95% confidence interval [CI]:1.47-2.21). The incidence of epilepsy in patients with eczema was 2.57 (95%CI: 1.54-4.27). Sensitivity analyses confirmed that no single study qualitatively influenced the pooled OR. All funnel plots were asymmetric upon visual inspection, suggesting publication bias. CONCLUSION: Our findings suggest that patients with allergic diseases might have a high risk of epilepsy. Additional high-quality primary studies are required to confirm the association, obtain information regarding the mechanism of association, and determine prevention opportunities.

[Research advances in neonatal hyperbilirubinemia and gene polymorphisms].

Hyperbilirubinemia is a prevalent disease in neonates and is also a main reason for hospitalization within the first week after birth, and this disease is mainly caused by the imbalance between production and elimination of bilirubin. Uridine diphosphate glucuronosyltransferase 1A1 (UGT1A1), organic anion transporter polypeptide 2 (OATP2), heme oxygenase 1 (HO-1), and biliverdin reductase A (BLVRA) play crucial roles in the metabolism of bilirubin. More and more studies have revealed the association between the variation of the encoding genes for these enzymes and hyperbilirubinemia. This article reviews the research advances in the association between the gene polymorphisms of bilirubin metabolic enzymes and hyperbilirubinemia.

Poly[[(1,10-phenanthroline)(µ-l-tartrato)zinc] hexa-hydrate].

The title compouand {[Zn(C(4)H(4)O(6))(C(12)H(8)N(2))]·6H(2)O}(n), has a linear chain structure parallel to [100] with Zn(C(4)H(4)O(6))(C(12)H(8)N(2)) repeat units; the asymmetric unit consists of one Zn(2+) cation, one l-tartrate dianion, one 1,10-phenanthroline and six free water mol-ecules. The Zn atom is in a distorted octa-hedral ZnN(2)O(4) coordination environment. The crystal structure is stabilized by O-H⋯O hydrogen bonds and π-π stacking of the phenanthroline units [centroid-centroid distances in the range 3.552 (2)-3.625 (2)Å] occurs between the chains. The title compound is isotypic with the Cu and Mn analogues.

Bis(2-propyl-1H-imidazol-3-ium) bis-(pyridine-2,6-dicarboxyl-ato-κO,N,O)cadmate(II).

The title salt, (C(6)H(11)N(2))(2)[Cd(C(7)H(3)NO(4))(2)], displays a discrete mononuclear structure, in which the central Cd(II) atom is six-coordinated in a distorted octa-hedral coordination geometry by two N and four O atoms from two different pyridine-2,6-dicarboxyl-ate anions in an O(2),N,O(6)-tridentate chelation mode. The crystal packing is stabilized by N-H⋯O hydrogen bonds and π-π inter-actions [centroid-centroid distance = 3.576 (5) Å].

[µ-1,4-Bis(1,2,4-triazol-1-ylmeth-yl)benzene]-bis-[aqua-(pyridine-2,6-dicarboxyl-ato)copper(II)] monohydrate.

The title compound, [Cu(2)(C(7)H(3)NO(4))(2)(C(12)H(12)N(6))(H(2)O)(2)]·H(2)O, displays a discrete dinuclear structure, in which the central Cu(II) atom is five-coordinated in a distorted square-based pyramidal coordination geometry and the flexible ligand 1,4-bis-(1,2,4-triazol-1-ylmeth-yl)benzene adopts a bis-monodentate bridging mode linking the Cu(II) atoms. It is further assembled by O-H⋯O hydrogen-bond inter-actions involving both the coordinated and uncoordinated water molecules. The latter exhibits half-occupancy.

Hexa-kis-(1-benzyl-1H-imidazole-κN)manganese(II) bis-(perchlorate).

In the title compound, [Mn(C(10)H(10)N(2))(6)](ClO(4))(2), the Mn(II) ion, located on an inversion center, is coordinated by six N atoms from three pairs of symmetry-related 1-benzyl-1H-imidazole ligands in a distorted octa-hedral geometry. In the crystal, weak inter-molecular C-H⋯O hydrogen bonds link the complex cations and perchlorate anions.

1,1'-[1,4-Phenyl-enebis(methyl-ene)]bis-(2-methyl-1H-imidazol-3-ium) 2,4-dicarb-oxy-benzene-1,5-dicarboxyl-ate monohydrate.

In the dication of the title compound, C(16)H(20)N(4) (2+)·C(10)H(4)O(8) (2-)·H(2)O, the dihedral angles formed by mean planes of the imidazolium rings and the benzene ring are 69.05 (18) and 89.1 (2)°. In the crystal, the components are linked into a three-dimensional network by inter-molecular N-H⋯O and O-H⋯O hydrogen bonds.