CRESCIMENTO E PRODUÇÃO DO MARACUJAZEIRO-AMARELO EM SOLO COM BIOFERTILIZANTES E ADUBAÇÃO MINERAL COM NPK

Yellow passion fruit crop (Passiflora edulis f. flavicarpa Deg.) and natural insume use on agriculture are increasing in Remígio county Paraíba State, Brazil. In this direction was carried out an experiment, during July 2005 to December 2006 in randomized blocks in order to evaluate the effects of absence and presence of biofertilizers comum (bovine manure fertilizer fresh and water) and supermagro (bovine manure, water, macronutrients and micronutrients), applied to soil on liquid form, in level of 2.4 L plant-1, 30 days before and two months after transplanting, in the absence and presence of mineral fertilizer with NPK, with three repetition and six plantas per set using a factorial designs 3x2. The biofertilizers show more reliable to growth than fruit production of yellow passion fruit. Biggest production corresponded to treatments with the use of mineral fertilizer, specially in the first production. Comum and supermagro biofertilizer gave significative effects on vegetative growth of plants of yellow passion fruit plant but had no influence on fruits production

Clinical And Molecular Spectrum Of Patients With 17β-hydroxysteroid Dehydrogenase Type 3 (17-β-hsd3) Deficiency.

The enzyme 17β-hydroxysteroid dehydrogenase type 3 (17-β-HSD3) catalyzes the conversion of androstenedione to testosterone in the testes, and its deficiency is a rare disorder of sex development in 46,XY individuals. It can lead to a wide range of phenotypic features, with variable hormonal profiles. We report four patients with the 46,XY karyotype and 17-β-HSD3 deficiency, showing different degrees of genital ambiguity, increased androstenedione and decreased testosterone levels, and testosterone to androstenedione ratio G novel mutation, and c.277+4A>T mutation, both located within the intron 3 splice donor site of the HSD17B3 gene, were identified in case 3. In addition, homozygosis for the missense p.Ala203Val, p.Gly289Ser, p.Arg80Gln mutations were found upon HSD17B3 gene sequencing in cases 1, 2, and 4, respectively.56533-

Espectro clínico e molecular de pacientes com deficiência de 17β-hidroxiesteroide desidrogenase tipo 2 (17-β-HSD3)

The enzyme 17&#946;-hydroxysteroid dehydrogenase type 3 (17-&#946;-HSD3) catalyzes the conversion of androstenedione to testosterone in the testes, and its deficiency is a rare disorder of sex development in 46,XY individuals. It can lead to a wide range of phenotypic features, with variable hormonal profiles. We report four patients with the 46,XY karyotype and 17-&#946;-HSD3 deficiency, showing different degrees of genital ambiguity, increased androstenedione and decreased testosterone levels, and testosterone to androstenedione ratio < 0.8. In three of the patients, diagnosis was only determined due to the presence of signs of virilization at puberty. All patients had been raised as females, and female gender identity was maintained in all of them. Compound heterozygosis for c.277+2T&gt;G novel mutation, and c.277+4A&gt;T mutation, both located within the intron 3 splice donor site of the HSD17B3 gene, were identified in case 3. In addition, homozygosis for the missense p.Ala203Val, p.Gly289Ser, p.Arg80Gln mutations were found upon HSD17B3 gene sequencing in cases 1, 2, and 4, respectively. Arq Bras Endocrinol Metab. 2012;56(8):533-9A enzima 17&#946;-hidroxiesteroide desidrogenase tipo 3 (17-&#946;-HSD3) catalisa a conversão de androstenediona a testosterona nos testículos, e sua deficiência é uma forma rara de distúrbio do desenvolvimento do sexo em indivíduos 46,XY. A desordem apresenta um amplo espectro de características fenotípicas e de resultados de dosagens laboratoriais. Neste trabalho, são relatados quatro casos de deficiência da 17-&#946;-HSD3 com cariótipo 46,XY, ambiguidade genital em diversos graus, androstenediona aumentada, testosterona diminuída, e relação testosterona e androstenediona < 0,8. Em três das pacientes, o diagnóstico foi suspeitado devido à presença de sinais de virilização na puberdade. Todos os pacientes foram criados como mulheres, e a identidade de gênero feminino foi mantida em todas elas. A heterozigose composta da mutação nova c.277+2T&gt;G e da mutação c.277+4A&gt;T, ambas localizadas no sítio doador de splicing do íntron 3 do gene HSD17B3, foi identificada no caso 3. Além dessas, as mutações missense p.Ala203Val, p.Gly289Ser, p.Arg80Gln foram identificadas em homozigose pelo sequenciamento do gene HSD17B3 dos casos 1, 2 e 4, respectivamente. Arq Bras Endocrinol Metab. 2012;56(8):533-953353