Complexes containing benzimidazolyl-phenol ligands and Ln(III) ions: Synthesis, spectroscopic studies and preliminary cytotoxicity evaluation.

Fourteen new complexes were obtained from Ln(III)(NO3)3∙n-H2O and the chromophores 2-(1H-benzo[d]imidazol-2-yl)-phenol (Bzp1) or 2-(5-methyl-1H-benzo[d]imidazol-2-yl)-phenol (Bzp2). The complete characterization allowed us to assign unequivocally the structures of all the complexes. The techniques used for this purpose were Ultraviolet-Visible (UV-Vis) and Fourier-Transform Infrared (FT-IR) spectroscopies, High-Resolution Mass Spectrometry (HRMS), Magnetic Susceptibility (MS), Elemental Analysis (EA) and Molar Conductivity (MC). HRMS allowed us to find the molecular ion and its isotopic pattern. The FT-IR spectral data suggested that benzimidazolyl-phenol ligands coordinate with Ln(III) ions through iminic nitrogen and phenolic oxygen. Thermogravimetric Analysis (TGA) studies of NdBzp1 and GdBzp2 complexes indicate the presence of lattice water along with three nitrates and two benzimidazolyl-phenol ligands; the thermal decomposition was consistent with the minimal formula suggested by EA. The coordination type of the benzimidazolyl-phenol ligands, the geometry and the structural organization of these coordination complexes have been interpreted by Density Functional Theory (DFT) calculations, and they coincided with the physicochemical data suggesting a coordination number eight for the Ln(III) ions. The cytotoxicity of the chromophores and their coordination complexes was tested against a cancer cell line (HeLa), as compared with structure/support cells (NIH-3T3) and defense cells (J774A.1), revealing that three coordination complexes showed moderate cytotoxicity against the cell lines studied.

Prospective assessment of diagnostic tests for pediatric penicillin allergy: From clinical history to challenge tests.

BACKGROUND: Diagnostic guidelines for penicillin allergy in children recommend cumbersome protocols based partially on data from adults, which may be suboptimal for pediatric use. OBJECTIVE: To assess the accuracy of tools for diagnosis of penicillin allergy in children. METHODS: A prospective, multicenter study was conducted in children with reported adverse events related to penicillin, excluding severe reactions. All patients underwent a uniform diagnostic protocol that consisted of clinical history, skin tests, serum specific IgE (sIgE), and, regardless of these results, drug provocation tests (DPTs). RESULTS: A total of 732 children (mean age, 5.5 years; 51.2% males) completed the allergy workup, including DPTs. Amoxicillin triggered 96.9% of all reactions. None of the patients with an immediate index reaction (IR) developed a reaction on DPT. Penicillin allergy was confirmed in 35 children (4.8%): 6 immediate reactions (17%) and 29 nonimmediate reactions (83%) on the DPT. No severe reactions were recorded. The allergist diagnosis based on the clinical history was not associated with the DPT final outcome. In 30 of 33 allergic patients (91%), the results of all skin tests and sIgE tests were negative. A logistic regression model identified the following to be associated with penicillin allergy: a family history of drug allergy (odds ratio [OR], 3.03; 95% confidence interval [CI], 1.33-6.89; P = .008), an IR lasting more than 3 days vs 24 hours or less (OR, 8.96; 95% CI, 2.01-39.86; P = .004), and an IR treated with corticosteroids (OR, 2.68; 95% CI, 1.30-5.54; P = .007). CONCLUSION: Conventional predictors of allergy to penicillin performed weakly. The authors propose straightforward penicillin provocation testing in controlled, experienced centers for the diagnosis of nonsevere penicillin allergy in children.

Crystal structure of catena-poly[[[tri-aqua-(4-cyano-benzoato-κO)nickel(II)]-µ-4,4'-bi-pyridine-κ(2) N:N'] 4-cyano-benzoate].

In the title polymeric complex salt, {[Ni(C8H4NO2)(C10H8N2)(H2O)3](C8H4NO2)} n , the Ni(II) cation is coordinated by a 4-cyano-benzoate anion, two 4,4'-bi-pyridine ligands and three water mol-ecules in a distorted N2O4 octa-hedral geometry. The 4,4'-bi-pyridine ligands bridge the Ni(II) cations to form polymeric chains of the title complex cations, propagating along the c-axis direction. The dihedral angle between the pyridine rings of the 4,4'-bi-pyridine ligand is 24.9 (6)°. In the crystal, the uncoordinating 4-cyano-benzoate anions link with the complex cations via O-H⋯O hydrogen bonds into a three-dimensional supra-molecular architecture. Weak C-H⋯O, C-H⋯N inter-actions and π-π stacking [centroid-to-centroid distances = 3.566 (4) and 3.885 (4) Å] are also observed in the crystal.

Bis(µ2-benzoato-κ(2) O:O')bis-[(benzoato-κ(2) O,O')bis(4,4'-bi-pyridine-κN)cobalt(II)]-benzoic acid (1/6).

In the title compound, [Co2(C7H5O2)4(C10H8N2)4]·6C6H5COOH, the centrosymmetric cobalt dimer co-crystallizes with six mol-ecules of benzoic acid. Each Co(II) atom is coordinated by four O atoms in a distorted square-planar arrangement while the N atoms are located in apical positions. The dihedral angles between the rings comprising each of the 4,4'-bipyridyl ligands are 25.2 (2) and 22.8 (2)°. In the crystal, the three-dimensional network is assembled by O-H⋯O and C-H⋯O hydrogen bonds.

Risk of vertical HIV transmission combines the 'B35-Cw4 disadvantage' and the 'pattern of inheritance' theories of progression.

Mother-to-child transmission during pregnancy provides a unique system for studying the correlation between HLA phenotype and susceptibility to HIV infection. We studied this relationship in a Spanish cohort. We determined frequencies of HLA class I and II alleles in 120 infants born to HIV-infected mothers and 67 HIV-infected mothers. Although there was no statistical difference in the frequency of HLA-B35 between transmitting and non-transmitting mothers, the allele was more frequent in infected children than in uninfected children. HLA-B35 has been consistently reported as a risk factor in the progression to AIDS. In addition, it has been proposed that whether a given allele can confer susceptibility to, or protection against, progression depends on maternal versus paternal inheritance patterns, since the child inherits a virus that reflects the history of CTL encounters of the mother. Our results on vertical HIV transmission combine for the first time the 'HLA-B35 disadvantage' and the 'pattern of inheritance' theories.

Endothelial function in HIV-infected patients with low or mild cardiovascular risk.

BACKGROUND: Highly active antiretroviral therapy for HIV-infected patients is associated with metabolic side effects, which could cause an increased cardiovascular risk in these patients. Non-invasive study of endothelial function by brachial artery ultrasound can detect subclinical atherosclerosis. Several studies have assessed endothelial function in HIV-infected patients with associated cardiovascular risk factors. OBJECTIVES: The aim of this study is to determine endothelial function in HIV-infected patients under antiretroviral therapy with low or mild coronary risk and lipid levels within the normal range. METHODS: Transversal study including 28 HIV-infected adults (15 receiving antiretroviral therapy and 13 naive) with low or mild cardiovascular risk and 12 healthy controls. Subjects with diabetes mellitus, hypertension, cardiovascular disease, obesity, high cholesterol or high triglyceride levels were excluded. Endothelial function was determined with flow-mediated dilation (FMD) of the brachial artery by ultrasound study. RESULTS: Treated HIV-infected patients had significantly lower FMD (5.93 +/- 3.56) than healthy controls (10.64 +/- 3.08, P = 0.008). Naive patients had an intermediate FMD, but this was not statistically significant. CONCLUSIONS: HIV-infected patients receiving antiretroviral therapy who have low or mild cardiovascular risk and lipid levels within the normal range have endothelial dysfunction compared with healthy controls.

PTEN and DMBT1 homozygous deletion and expression in medulloblastomas and supratentorial primitive neuroectodermal tumors.

Medulloblastoma, which accounts for 20-25% of all childhood brain tumors, is defined as a primitive neuroectodermal tumor (PNET) located in the cerebellum. Supratentorial PNET are less frequent than medulloblastoma. But their clinical outcome is worse than in medulloblastomas. Chromosome 10q contains at least 2 tumor suppressor genes that might play a role in brain tumor development: PTEN and DMBT1. The aim of this study was to compare the status of homozygous deletion and expression of PTEN and DMBT1 genes in PNET primary tumor samples and cell lines. Homozygous deletions of PTEN and DMBT1 were studied in 32 paraffin-embedded PNET samples (23 medulloblastomas and 9 supratentorial PNET) and in 7 PNET cell lines, by differential PCR and by FISH. PTEN homozygous losses were demonstrated in 7 medulloblastomas (32%) and in no supratentorial PNET, while homozygous deletions of DMBT1 appeared in 1 supratentorial PNET (20%) and in 7 medulloblastomas (33%). No homozygous deletion of PTEN or DMBT1 was detected in any of the PNET cell lines either by differential PCR or by FISH. Expression study of the 2 genes was performed in the 7 PNET cell lines by RT-PCR. One PNET cell line lacked PTEN and DMBT1 expression, while 2 medulloblastoma cell lines did not express DMBT1. Our results add some positive data to the hypothesis that supratentorial PNETs and medulloblastomas might be genetically different.

Association of NOS3 gene with metabolic syndrome in hypertensive patients.

Recent data from animal models indicate that the eNOS null mice present a phenotype that resemble the human metabolic syndrome (hypertension, insulin resistance and hypertriglyceridemia). In this work, we have studied whether NOS3 gene, previously related to endothelial dysfunction, might have a role in metabolic syndrome susceptibility in hypertensive patients. To carry out the study, we genotyped 105 hypertensive patients < or = 60 years old with two polymorphisms of NOS3 gene: 1132 T>C and 7164 G>T (GeneBank:AF519768.1). To check the allelic frequency of these polymorphisms in our geographical area, we also genotyped 94 unselected healthy controls (control group). To perform sample genotyping, we designed a novel FRET system coupled to real time PCR. There were no differences in genotypic distribution or allelic frequency between hypertensive patients and the control group. However, we observed that 786CC genotype was significantly more frequent in hypertensive patients with metabolic syndrome than in those without the syndrome (p=0.0022). When both polymorphisms were analyzed, we identified the 786C894G as the risk haplotype for metabolic syndrome susceptibility (p=0.011). These data suggest a role of the NOS3 gene in the pathogenesis of metabolic syndrome in hypertensive patients.