RESUMEN

OBJECTIVE: Glucocorticoid (GC)-induced adverse reactions (ARs) have been extensively studied due to their potential impact on patients' health. This study aimed to examine the potential correlation between two polymorphisms [adenosine triphosphate-binding cassette B1 (ABCB1) C3435T and plasminogen activator inhibitor-1 (PAI-1) 4G/5G] and various GC-induced ARs in nephrotic syndrome (NS) patients. METHODS: In this study, 513 NS patients who underwent GC treatment were enrolled. Then, the patients were divided into two groups based on ABCB1 C3435T and PAI-1 4G/5G genotyping, and intergroup comparisons of clinicopathological data and GC-induced ARs were performed. Univariate and multivariate logistic analyses were subsequently conducted to identify potential risk factors for GC-induced ARs, and a nomogram was subsequently established and validated via the area under the ROC curve (AUC), calibration curve and decision curve analysis (DCA). RESULTS: We identified ABCB1 C3435T as an independent risk factor for the development of steroid-associated avascular necrosis of the femoral head (SANFH) (OR: 2.191, 95% CI: 1.258-3.813, P=0.006) but not as a risk factor for the occurrence of steroid diabetes mellitus (S-DM). On the other hand, PAI-1 4G/5G was identified as an independent risk factor for the development of both SANFH (OR: 2.198, 95% CI: 1.267-3.812, P=0.005) and S-DM (OR: 2.080, 95% CI: 1.166-3.711, P=0.013). Notably, no significant correlation was found between the two gene polymorphisms and other GC-induced ARs. In addition, two nomograms were established and validated to demonstrate strong calibration capability and clinical utility. CONCLUSION: Assessing ABCB1 C3435T and PAI-1 4G/5G before steroid treatment in NS patients could be useful for identifying patients at a high risk of developing SANFH and S-DM.

RESUMEN

BACKGROUND: Obstructive sleep apnea-hypopnea syndrome (OSAHS) is a common chronic disorder which is followed by various complications. Calpain-10 belongs to a commonly expressed member of the Calpain-like cysteine protease family, which acts as risk marker for some diseases. The purpose of this study is to elucidate correlation between Calpain-10 single-nucleotide polymorphisms (SNPs) and the incidence of OSAHS followed by ischemic stroke (IS). METHODS: OSAHS patients were divided as OSAHS + IS, OSAHS, and control groups, respectively. Immunohistochemistry was performed for Calpain-10 protein expression, polymerase chain reaction (PCR)-restriction fragment length polymorphism for detection of gene polymorphisms of SNP 43 and SNP 19, and PCR-allele specific amplification for SNP 44. Polysomnography was conducted to check the nocturnal polysomnography indicators, and also Montreal Cognitive Assessment (MoCA), Scientific Data System scores cognition and anxiety of patients, respectively. Logistic analysis was used for the risky factors for OSAHS. RESULTS: Calpain-10 protein expression was significantly increased in the OSAHS + IS and OSAHS groups compared with the control group. Significant differences in SNP 43 and SNP 44 genotype, and also allele frequency were observed in 3 groups, among which the OSAHS + IS group had higher SNP 43 and SNP 44 allele frequency than the control and OSAHS groups. There were differences regarding apnea-hypopnea index, minimum fingertip blood oxygen saturation (LSaO2 [%]), oxygen reduction index (ODI) between patients with different genotypes of SNP 43 and SNP 44 in OSAHS patients, and also GC and AT frequency in the OSAHS + IS and OSAHS groups. As compared with the OSAHS group, the MoCA scores and MoCA subitems in the OSAHS + IS group were declined, whereas the Scientific Data System scores were elevated. Additionally, GG 43 genotype, high apnea-hypopnea index, and body mass index were detected as the risk factors of OSAHS. CONCLUSION: These findings indicate that the Calpain-10 SNP 43 may be related to OSAHS with IS, with SNP 43 GG genotype as a risk factor for OSAHS with IS.

Asunto(s)

Calpaína/genética , Apnea Obstructiva del Sueño/complicaciones , Apnea Obstructiva del Sueño/genética , Accidente Cerebrovascular/complicaciones , Accidente Cerebrovascular/genética , Pueblo Asiatico , Ensayo de Inmunoadsorción Enzimática , Femenino , Frecuencia de los Genes , Humanos , Masculino , Persona de Mediana Edad , Oxígeno/sangre , Reacción en Cadena de la Polimerasa , Polimorfismo de Longitud del Fragmento de Restricción , Polimorfismo de Nucleótido Simple , Polisomnografía

RESUMEN

In the title compound, {[Cu(C(18)H(12)N(6))]NO(3)·H(2)O}(n), the Cu(I) ion is coordinated by three N atoms [Cu-N 1.962 (3)-2.019 (3) Å] from three 2,4,6-tri-4-pyridyl-1,3,5-triazine (L) ligands. Each L ligand bridges three Cu(I) atoms, generating a positively charged three-dimensional polymeric network with voids propagated along the b axis. These voids are filled with NO(3) (-) anions with a shortest Cu⋯O distance of 2.645 (3) Šand water mol-ecules, which are linked into negatively charged helical chains via inter-molecular O-H⋯O hydrogen bonds.

RESUMEN

In the title compound, [Ni(CHO(2))(2)(C(18)H(12)N(6))(H(2)O)(2)](n), the Ni(II) ion, lying on a crystallographic inversion center, has a distorted octa-hedral coordination comprising two water ligands, two O-atom donors from formate ligands and two N-atom donors from the 2,4,6-tris-(4-pyrid-yl)-1,3,5-triazine ligands. These ligands bridge the Ni(II) complex units, forming zigzag chains along the c axis. Adjacent chains are linked by O-H⋯O hydrogen bonds, forming a three-dimensional supra-molecular network.