Increased homocysteine plasma levels in breast cancer patients of a Mexican population

Aim: Hyperhomocysteinemia has been associated with different pathologies, including cardiovascular diseases, hypertension, diabetes, and breast cancer (BC). To examine the differences in total homocysteine (tHcy) plasma levels, we compared healthy women to BC patients from a Mexican population. Materials and Methods: The tHcy plasma levels were measured using high-performance liquid chromatography with a fluorescence detector in 89 female controls and 261 BC patients. Results: The observed plasma tHcy levels were significantly higher among the BC patients (11.1019 ± 5.9161 µmol/l) compared to the controls (9.1046 ± 1.3213 µmol/l) (p = 0.002), and these differences were evident when stratified by age (≥ 50 years old), menopause status, overweight and obesity, miscarriages, node metastases, progression, subtype classification (luminal, Her2 and triple negative) and nonresponse to chemotherapy. Conclusions: The tHcy plasma levels could be a good marker for the progression and chemosensitivity of BC in the analyzed sample from a Mexican population. Key Words: plasma levels, homocysteine, HPLC, breast cancer, Mexican population

Qualitative and quantitative determination of urinary glycosaminoglycans in patients with osteochondrodysplasias [Determinaci�n cualitativa y cuantitativa de glucosaminoglucanos urinarios en pacientes con osteocondrodisplasias.]

A quantitative and qualitative assay of urinary glycosaminoglycans (GAGs) was performed, by means of spectrophotometry and electrophoresis in 37 patients with a suspected diagnosis of osteo-chondrodysplasia. Levels were increased in 70.2% of the cases. One patient showed an electrophoretic pattern which was different and could not be identified in accord with the standard used

Qualitative and quantitative determination of urinary glycosaminoglycans in patients with osteochondrodysplasias [Determinación cualitativa y cuantitativa de glucosaminoglucanos urinarios en pacientes con osteocondrodisplasias.]

A quantitative and qualitative assay of urinary glycosaminoglycans (GAGs) was performed, by means of spectrophotometry and electrophoresis in 37 patients with a suspected diagnosis of osteo-chondrodysplasia. Levels were increased in 70.2% of the cases. One patient showed an electrophoretic pattern which was different and could not be identified in accord with the standard used

Spondyloepimetaphyseal dysplasia (SEMD) Shohat type

Recently a distinct spondyloepimetaphyseal dysplasia (SEMD) was reported in three members of a Jewish family. We present a 3.5-year-old Mexican boy with disproportionate short stature, peculiar face, short neck, small chest, abdominal distension, lumbar lordosis, short limbs, marked genua vara, and joint laxity. Roentgenologic findings include short long bones, wide and flared metaphyses with irregularities, delayed epiphyseal ossification, platyspondyly and morphological changes of vertebral bodies and fibular overgrowth. The striking resemblance of this patient to those previously reported confirms this form of SEMD as a distinct entity. Autosomal recessive inheritance is supported and the designation SEMD Shohat type is proposed

Genotoxicity produced by disease and drugs

In humans, DNA damage or genotoxicity may be caused by exposure to outsideagents like radiation, pesticides, combustion of hydrocarbons products as well asantineoplastic drugs. But also DNA damage could be come from inside of the body,determined mainly for excessive free radicals production generated by some diseaseprocess and that their increase exceed the natural defense systems responsible forremoving free radicals. In either case, the important thing is to identify the genotoxicityand try to protect the body, this may as simply as removing the source of exposure orprovide protection against such agents. In this chapter, we address some ways of how it has been identified genotoxiccompounds by direct analyses, basically micronucleogenics ones expressed quantitativelyby number of micronuclei in peripheral blood erythrocytes and micronucleated cells fromoral mucosa, the genotoxicity of some antineoplastic drugs as well as the identification ofsome diseases that are "genotoxic" to the individual that suffers it and that under certainconditions can also result in potentially teratogenic for children to mothers who hadsuffered some of these disorders. © 2009 Nova Science Publishers, Inc. All rights reserved

Genotoxicity produced by disease and drugs

In humans, DNA damage or genotoxicity may be caused by exposure to outsideagents like radiation, pesticides, combustion of hydrocarbons products as well asantineoplastic drugs. But also DNA damage could be come from inside of the body,determined mainly for excessive free radicals production generated by some diseaseprocess and that their increase exceed the natural defense systems responsible forremoving free radicals. In either case, the important thing is to identify the genotoxicityand try to protect the body, this may as simply as removing the source of exposure orprovide protection against such agents. In this chapter, we address some ways of how it has been identified genotoxiccompounds by direct analyses, basically micronucleogenics ones expressed quantitativelyby number of micronuclei in peripheral blood erythrocytes and micronucleated cells fromoral mucosa, the genotoxicity of some antineoplastic drugs as well as the identification ofsome diseases that are "genotoxic" to the individual that suffers it and that under certainconditions can also result in potentially teratogenic for children to mothers who hadsuffered some of these disorders. � 2009 Nova Science Publishers, Inc. All rights reserved

The TP53 16-bp duplication polymorphism is enriched in endometriosis patients

Background/Aim: The TP53 tumor suppressor gene encodes the nuclear phosphoprotein p53, which plays an important role in cell cycle regulation, apoptosis, DNA repair and angiogenesis. The TP53 gene contains common genetic polymorphisms that influence gene activity. Clinical implications of TP53 polymorphisms have been reported for several diseases, including a variety of solid tumors and endometriosis. We evaluated the association of a TP53 duplication polymorphism with endometriosis. Methods: We evaluated the role of the TP53 16-bp duplication polymorphism by comparing the genotypes of 204 healthy women (controls with surgically excluded endometriosis) to the genotypes of 151 women with endometriosis in the Mexican population. Results: The observed genotype frequencies for controls and endometriosis patients were 0.5 and 5% for 16 bp+/+, 11 and 21% for 16 bp+/-, and 88.5 and 77% for 16 bp-/-, respectively. The odds ratio (OR) was 9.8 (95% CI 1.2-446.8; p = 0.01). The association was more evident when we compared the distribution of genotype 16 bp+/+ to genotype 16 bp+/-. In patients with moderate/severe endometriosis, the OR was 4.0 (95% CI 1.6-9.8; p = 0.003). Conclusion: Our data suggest that the 16-bp duplication polymorphism in TP53 contributes significantly to endometriosis susceptibility in the Mexican population. Copyright � 2012 S. Karger AG, Basel

SNPs in human β-defensin 1 gene (DEFB1): Frequencies in a Mexican population and new PCR-RFLPs assays

Polymerase chain reaction-restriction fragment length polymorphism assays for two single nucleotide polymorphisms in the human β-defensin 1 gene have been validated with real-time PCR in 101 healthy individuals from western Mexico. Allele frequencies were 52.5% (692-A) and 98.5% (1836-A). These assays can be confidently used as a cheaper alternative genotyping method for these sites. © 2006 The Authors