Cryptococcosis in México is caused by both species of the Cryptococcus species complex i.e., Cryptococcus neoformans and C. gattii. The current study was aimed to determine genetic variability of 72 Mexican clinical isolates using PCR-fingerprinting with the primer M13. PCR fingerprinting revealed 55 VNI, five VNII, three VNIII, one VNIV, two VGI, two VGII, two VGIII and two VGIV isolates among those studied. The results show that most cryptococcosis cases in México are AIDS related and are caused by C. neoformans var. grubii, genotypes VNI and VNII. In addition this study revealed for the first time the presence of genotypes VNIV and VGII among Mexican clinical isolates. The present data show that all genotypes that have been described for the Cryptococcus species complex are found in México, indicating a much wider geographic distribution of genotypes than previously reported. The molecular analysis of Mexican cryptococcal isolates generated PCR-fingerprinting patterns which will provide references for future typing studies to allow the integration of Mexican cryptococcal genotypes into the ongoing global genotyping study of the Cryptococcus species complex.

The degradation of a mono azo dye in an automated and controlled anaerobic-aerobic sequencing batch reactor (SBR) is described in this work. The experiments were conducted with a synthetic wastewater containing acid orange 7 as the model compound to degrade and glucose as the co-substrate in a molar relationship 1:40 (substrate/co-substrate). It was possible to control the anaerobic and aerobic stages, using the redox potential (ORP) as the only control variable. The strategy detects an inflection point in the ORP signal, indicating the end of the reaction. The efficiency of removal of total organic carbon was between 85% and 90%. Azo dye was removed with 85% efficiency during the anaerobic stage.

Severe maternal zinc deficiency has a devastating effect on pregnancy outcome. Studies of humans and experimental animals show that maternal zinc deficiency can cause infertility, prolonged labor, intrauterine growth retardation, teratogenesis, severe immunological deficiencies, or fetal death. The additional need for zinc during pregnancy can be met by an increase in zinc intake. An increase in zinc supplements, when excessive, can cause a decrease in copper. Therefore, it is important to determine the zinc and copper concentrations in embryonic tissue in experimental models and their relationship with embryo number and viability. BALB/c mice were divided into groups according to zinc oral supplementation and gestational age. Phagocytosis was assessed in peritoneal macrophages from dams. The zinc and copper concentrations were obtained by inductively coupled plasma-optical emission spectrometry. Zn and Cu data concentrations in all the analyzed samples were above the detection limits. No spectral interferences were found in both elements. Zinc concentrations show a tendency to increase in embryos (14 gestational days and 21 gestational days) supplemented with zinc. Copper concentrations showed a noticeable tendency to diminish (36% and 27%, respectively) in the same period. In contrast, in placenta Zn values were increased by 30% and Cu values were decreased by 26%. We suggest a pivotal role of the placenta metabolism with its homeostatic mechanisms, in these findings. An important increment appeared in the +Zn embryo number (40%) relative to control (-Zn) embryos at 21 d gestational age. Embryo mortality was at 6% in +Zn embryos and at 20% in -Zn embryos. We consider these findings, both in the number and in the viability of +Zn embryos, outstanding.