Ultrastructure of oogenesis in two tropical oviparous Demospongiae (Porifera): Cinachyrella apion and Tethya maza.

Reproduction is a key step for propagation of any species. Consequently, gametogenesis is crucial, as it links one generation to the other. Oogenesis is influenced by different factors, but it is usually related to the quality and quantity of the food and the capacity of the female to convert these resources into egg production. In Demospongiae (Porifera), oocytes vary in several aspects (e.g., origin, size, and vitellogenic pathways). However, data on oocyte morphology is still fragmentary, and the ultrastructural organization of reproductive cells has been investigated only in a few species, mainly of viviparous sponges. Here, we aimed to comprehend the oogenesis of two tropical oviparous demosponges (Cinachyrella apion and Tethya maza) using light and electron microscopy. In both species, oocytes seemed to originate from archaeocytes. Oocytes of C. apion were surrounded by a collagenous matrix and nurse cells containing many lipid vesicles. The increase of biosynthetic organelles, concomitantly with the presence of yolk vesicle in the ooplasm, indicated that the vitellogenesis was carried out through the mixed pathway. The oocytes of T. maza were surrounded by a follicle cell membrane and nurse cells containing yolk vesicles. The absence of characteristic biosynthetic organelles in the egg of this species indicated that vitellogenesis occured through the heterosynthetic pathway. The oogenesis of C. apion is similar to other species of the genus, while the follicle membrane and nurse cells surrounding the oocytes of T. maza are not observed in any other species of Tethya. These accessory cells were considered to have a trophic role during the oogenesis of the studied species. Moreover, the presence of these accessory cells may have ecological significance, as they accelerate the egg's production through trophic support of the growing oocyte.

Vascular endothelial growth factor (VEGF) and endothelial nitric oxide synthase (NOS3) polymorphisms are associated with high relapse risk in childhood acute lymphoblastic leukemia (ALL).

BACKGROUND: Angiogenesis has been shown as an important process in hematological malignancies. It consists in endothelial proliferation, migration, and tube formation following pro-angiogenic factors releasing, specially the vascular endothelial growth factor (VEGF), which angiogenic effect seems to be dependent on nitric oxide (NO). We examined the association among functional polymorphisms in these two angiogenesis related genes: VEGF (-2578C>A, -1154G>A, and -634G>C) and NOS3 (-786T>C, intron 4 b>a, and Glu298Asp) with prognosis of childhood acute lymphoblastic leukemia (ALL). METHODS: The genotypes were determined and haplotypes estimated in 105 ALL patients that were divided in 2 groups: high risk (HR) and low risk of relapse (LR) patients. In addition, event-free survival curves according to genotypes were assessed. RESULTS: The group HR compared to the LR showed a higher frequency of the alleles -2578C and -634C and the haplotype CGC for VEGF (0.72 vs. 0.51, p<0.008; 0.47 vs. 0.26, p<0.008; and 42.1 vs. 14.5, p<0.006; respectively) and a lower frequency of the haplotype CbGlu (0.4 vs. 8.8,p<0.006), for NOS3. CONCLUSION: Polymorphisms of VEGF and NOS3 genes are associated with high risk of relapse, therefore may have a prognostic impact in childhood ALL.

Endothelial nitric oxide synthase haplotypes associated with hypertension do not predispose to cardiac hypertrophy.

Left ventricular hypertrophy (LVH) is a complication that may result from chronic hypertension. While nitric oxide (NO) deficiency has been associated with LVH, inconsistent results have been reported with regards to the association of endothelial NO synthase (eNOS) polymorphisms and LVH in hypertensive patients. This study aims to assess whether eNOS haplotypes are associated with LVH in hypertensive patients. This study included 101 healthy controls and 173 hypertensive patients submitted to echocardiography examination. Genotypes for three eNOS polymorphisms were determined: a single-nucleotide polymorphism in the promoter region (T-786C) and in exon 7 (Glu298Asp), and variable number of tandem repeats in intron 4. We found no significant association between eNOS genotypes and hypertension or with LVH (all p > 0.05). However, while we found two eNOS haplotypes associated with variable risk of hypertension (all p < 0.05), we found no significant associations between eNOS haplotypes and LVH (all p > 0.05), even after adjustment in multiple linear regression analysis. These findings suggest that eNOS haplotypes that have been associated with variable susceptibility to hypertension were not associated with LVH in hypertensive patients. Further studies are necessary to examine whether other genes downstream may interact with eNOS polymorphisms and predispose to LVH in hypertensive patients.

Functional polymorphisms in the promoter of the matrix metalloproteinase-9 (MMP-9) gene are not linked with significant plasma MMP-9 variations in healthy subjects.

BACKGROUND: Matrix metalloproteinase-9 (MMP-9) is involved in the degradation of the extracellular matrix during physiological and pathological processes. Two functional polymorphisms [C(-1562)T and microsatellite (CA)13-25] in the promoter region of the MMP-9 gene have been associated with several diseases. The aim of this study was to examine whether these MMP-9 polymorphisms and haplotypes are linked with plasma MMP-9 variations in healthy subjects. METHODS: We studied 177 healthy male white volunteers (age range 20-55 years) who were non-smokers and not taking any medication. Genomic DNA was extracted from whole blood and genotypes for the C(-1562)T and the microsatellite (CA)n polymorphisms were determined. MMP-9 levels were measured in plasma samples by gelatin zymography. RESULTS: The frequency of the alleles C and T for the C(-1562)T polymorphism were 90% and 10%, respectively. The frequency of the alleles with less than 21 CA repeats (L) and with 21 repeats or higher (H) were 47% and 53%, respectively. We found no differences in plasma MMP-9 levels among the genotype groups or among different haplotypes (all p>0.05). CONCLUSIONS: These findings suggest that functional polymorphisms in the promoter of the MMP-9 gene are not linked with significant plasma MMP-9 variations in healthy subjects.