Characterization of the effects of macronutrient deficiencies in mangabeira seedlings

Knowledge of the mineral nutrition requirements of mangabeira (Hancornia speciosa Gomes) is relatively scarce and rudimentary because there is a lack of consistent data concerning its nutritional demands at different developmental stages. The aim of this research was to characterize the visual symptoms of macronutrient deficiencies and to evaluate the effects of these deficiencies on the growth, the production of dry matter, and the leaf content of mangabeira. To achieve this goal, a greenhouse experiment was conducted at the Goiano Federal Institute (Instituto Federal Goiano) in Rio Verde - GO, from January to June 2011 in which mangabeira plants were arranged in a random block design and grown in nutrient solutions. This experiment was replicated four times. The plants were treated with either a complete nutrient solution or a nutrient solution from which the individual macronutrient of interest (nitrogen (N), phosphorous (P), potassium (K), magnesium (Mg), calcium (Ca), or sulfur (S) had been omitted. The omission of a macronutrient from the nutrient solution resulted in morphological alterations that were characteristic symptoms of the particular nutritional deficiency and caused decreases in growth and dry matter mass production. The accumulation of macronutrients displayed the following order in mangabeira leaves: N>K>Ca>P>S>Mg.

FGFR1 and PROKR2 rare variants found in patients with combined pituitary hormone deficiencies.

The genetic aetiology of congenital hypopituitarism (CH) is not entirely elucidated. FGFR1 and PROKR2 loss-of-function mutations are classically involved in hypogonadotrophic hypogonadism (HH), however, due to the clinical and genetic overlap of HH and CH; these genes may also be involved in the pathogenesis of CH. Using a candidate gene approach, we screened 156 Brazilian patients with combined pituitary hormone deficiencies (CPHD) for loss-of-function mutations in FGFR1 and PROKR2. We identified three FGFR1 variants (p.Arg448Trp, p.Ser107Leu and p.Pro772Ser) in four unrelated patients (two males) and two PROKR2 variants (p.Arg85Cys and p.Arg248Glu) in two unrelated female patients. Five of the six patients harbouring the variants had a first-degree relative that was an unaffected carrier of it. Results of functional studies indicated that the new FGFR1 variant p.Arg448Trp is a loss-of-function variant, while p.Ser107Leu and p.Pro772Ser present signalling activity similar to the wild-type form. Regarding PROKR2 variants, results from previous functional studies indicated that p.Arg85Cys moderately compromises receptor signalling through both MAPK and Ca(2) (+) pathways while p.Arg248Glu decreases calcium mobilization but has normal MAPK activity. The presence of loss-of-function variants of FGFR1 and PROKR2 in our patients with CPHD is indicative of an adjuvant and/or modifier effect of these rare variants on the phenotype. The presence of the same variants in unaffected relatives implies that they cannot solely cause the phenotype. Other associated genetic and/or environmental modifiers may play a role in the aetiology of this condition.

Biochemical and physiological responses of sugarcane cultivars to soil water deficiencies

Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)

Effects of some mineral deficiencies on the development of the soybean plant, Glycine max (L.) Merril cv Santa Rosa

The present work studies Ca, B and Zn omission on the development of soybean plants (Glycine max (L.) Merrill cv Santa Rosa). The experiment was carried out as hydroponic culture, viith complete Hoagland & Arnon nutrient solution nr. 2 (C), lacking calcium (-Ca), lacking boron (-B) or lacking zinc (-Zn), a total of 4 treatments. Seven samplings were made to determine: total dry matter (g), root dry matter (g), stem dry matter (g) and leaf dry matter (g). Results showed that Ca and B omissions decreased dry weight. Lack of Zn did not affect dry weight.

Virtues and limitations of census maps for identifying critical deficiencies

Includes bibliography

Raúl Prebisch on ECLAC's achievements and deficiencies: an unpublished interview

Includes bibliography

Progressive dopamine and hypocretin deficiencies in Parkinson's disease: is there an impact on sleep and wakefulness?

Sleep-wake disturbances are frequent in patients with Parkinson's disease, but prospective controlled electrophysiological studies of sleep in those patients are surprisingly sparse, and the pathophysiology of sleep-wake disturbances in Parkinson's disease remains largely elusive. In particular, the impact of impaired dopaminergic and hypocretin (orexin) signalling on sleep and wakefulness in Parkinson's disease is still unknown. We performed a prospective, controlled electrophysiological study in patients with early and advanced Parkinson's disease, e.g. in subjects with presumably different levels of dopamine and hypocretin cell loss. We compared sleep laboratory tests and cerebrospinal fluid levels with hypocretin-deficient patients with narcolepsy with cataplexy, and with matched controls. Nocturnal sleep efficiency was most decreased in advanced Parkinson patients, and still lower in early Parkinson patients than in narcolepsy subjects. Excessive daytime sleepiness was most severe in narcolepsy patients. In Parkinson patients, objective sleepiness correlated with decrease of cerebrospinal fluid hypocretin levels, and repeated hypocretin measurements in two Parkinson patients revealed a decrease of levels over years. This suggests that dopamine and hypocretin deficiency differentially affect sleep and wakefulness in Parkinson's disease. Poorer sleep quality is linked to dopamine deficiency and other disease-related factors. Despite hypocretin cell loss in Parkinson's disease being only partial, disturbed hypocretin signalling is likely to contribute to excessive daytime sleepiness in Parkinson patients.

[Interdisciplinary AWMF guideline for the treatment of primary antibody deficiencies]

Currently, management of antibody deficient patients differs significantly among caregivers. Evidence and consensus based (S3) guidelines for the treatment of primary antibody deficiencies were developed to improve the management of these patients.

Liver degeneration and lymphoid deficiencies in mice lacking suppressor of cytokine signaling-1

SOCS-1, a member of the suppressor of cytokine signaling (SOCS) family, was identified in a genetic screen for inhibitors of interleukin 6 signal transduction. SOCS-1 transcription is induced by cytokines, and the protein binds and inhibits Janus kinases and reduces cytokine-stimulated tyrosine phosphorylation of signal transducers and activators of transcription 3 and the gp130 component of the interleukin 6 receptor. Thus, SOCS-1 forms part of a feedback loop that modulates signal transduction from cytokine receptors. To examine the role of SOCS-1 in vivo, we have used gene targeting to generate mice lacking this protein. SOCS-1−/− mice exhibited stunted growth and died before weaning with fatty degeneration of the liver and monocytic infiltration of several organs. In addition, the thymus of SOCS-1−/− mice was reduced markedly in size, and there was a progressive loss of maturing B lymphocytes in the bone marrow, spleen, and peripheral blood. Thus, SOCS-1 is required for in vivo regulation of multiple cell types and is indispensable for normal postnatal growth and survival.