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Creatine is the object of growing interest in the scientific literature. This is because of the widespread use of creatine by athletes, on the one hand, and to some promising results regarding its therapeutic potential in neuromuscular disease on the other. In fact, since the late 1900s, many studies have examined the effects of creatine supplementation on exercise performance. This article reviews the literature on creatine supplementation as an ergogenic aid, including some basic aspects relating to its metabolism, pharmacokinetics and side effects. The use of creatine supplements to increase muscle creatine content above approximately 20 mmol/kg dry muscle mass leads to improvements in high-intensity, intermittent high-intensity and even endurance exercise (mainly in nonweightbearing endurance activities). An effective supplementation scheme is a dosage of 20 g/day for 4-6 days, and 5 g/day thereafter. Based on recent pharmacokinetic data, new regimens of creatine supplementation could be used. Although there are opinion statements suggesting that creatine supplementation may be implicated in carcinogenesis, data to prove this effect are lacking, and indeed, several studies showing anticarcinogenic effects of creatine and its analogues have been published. There is a shortage of scientific evidence concerning the adverse effects following creatine supplementation in healthy individuals even with long-term dosage. Therefore, creatine may be considered as a widespread, effective and safe ergogenic aid.

In spite of all the advances in sport nutrition and the importance of an adequate food intake in order to improve sport performance, both recreational and professional athletes forget frequently to include planning an optimum diet and fluid intake in their global strategy for performance. Physiological and metabolic adaptations produced as a consequence of physical exercise lead to the necessity of increasing caloric (in accordance to energy output) and protein (based on the trophic needs of the organism) intake. Likewise, paying major attention to vitamin and mineral intake, specifically B vitamins and zinc and chromium, is required, in order to optimize carbohydrate metabolism, the ultimate limiting factor for sport performance. During the training phase, 60% of calories should come from carbohydrates, protein intake should be 1.2-2 g/kg/day and athletes should follow the recommendations of the food guide pyramid. During the pre-, per- and post-competition phase the healthy aspect of the diet passes to a second level, in order to obtain good sport performance and to guarantee a fast and effective recovery. Again, carbohydrates with a high or medium glycaemic index and water are the nutrients which have to be calculated more thoroughly. In conclusion, athletes have to follow a diet that is adequate to their higher energy output and to their higher metabolic turnover. The food guide pyramid is a graphic expression which facilitates the comprehension and following of a healthy diet. In the present article, the authors introduce the pyramid adapted to the characteristics of sports nutrition, with easy-to-follow practical recommendations regarding the kind and amounts of foodstuffs that should be consumed in order to cover nutrient needs of people who exercise regularly.

The (C(n)H(2n+6)N(2))[Mn(3)(HPO(3))(4)] (n = 3-8) compounds have been prepared by hydrothermal synthesis and characterized by X-ray diffraction data and spectroscopic techniques. The crystal structure of (C(3)H(12)N(2))[Mn(3)(HPO(3))(4)] has been solved from single-crystal X-ray diffraction. The unit-cell parameters are a = 9.502(1), b = 5.472(1), c = 14.523(4) A, beta = 95.01(3) degrees, monoclinic, C2/m, with Z = 2. The compound shows a layered structure stacked along the c-axis with the alkyldiammonium cations placed in the interlayer space. The sheets are formed by Mn(3)O(12) trimer units extended in the ab-plane and connected by (HPO(3))(2-) anions. The study of the (C(n)H(2n+6)N(2))[Mn(3)(HPO(3))(4)] (n = 4-8) phases by X-ray powder diffraction indicates an isotype relation with the propanediammonium compound. The Dq and Racah parameters calculated for (C(3)H(12)N(2))[Mn(3)(HPO(3))(4)] are Dq = 880, B = 660 and C = 3610 cm(-1). The ESR spectra show isotropic signals with a g-value of 2.008. Magnetic measurements indicate the presence of antiferromagnetic interactions inside the [Mn(3)(HPO(3))(4)](2-) sheets. The J/K value has been estimated to be -15 K by considering that the system behaves like an isolated trimer at high temperatures.

A new iron(III) arsenate templated by ethylenediamine, (C2H10N2) [Fe(HAsO4)2(H2AsO4)](H2O), has been prepared by hydrothermal synthesis. The unit-cell parameters are a = 8.705(3) A, b = 16.106(4) A, c = 4.763(1) A, beta = 90.63(3) degrees; monoclinic, P2(1) with Z = 2. The compound exhibits a chain structure along the c-axis with the ethylenediammonium cations as counterion. The chains show isolated FeO6 octahedra with two HAsO4 and one H2AsO4 tetrahedra per FeO6 octahedron. The ESR spectrum at 5.0 K is isotropic with a g-value of 2.0, which remains practically unchanged at room temperature. Magnetic measurements indicate the presence of antiferromagnetic interactions. A value of -0.835 K for the J-exchange parameter has been calculated by fitting the magnetic data to a model for antiferromagnetic chains of spin S = 5/2.

By means of the polymerase chain reaction (PCR) it was obtained a probe for the gen that codifies the subunit B of cholerae toxin (CTxB), which carried a Vibrio cholerae 01 reference strain. The checking of the amplified product was performed by using the hybridization techniques in colonies. This product hybridized with the gen that codifies for the subunit B of cholerae toxin isolated from Peru and Ecuador, representing the present epidemics in Latin America, but it did not so with the phylogenetically related strains.

The microscopic polyarteritis is a vasculitis related to necrotizing glomerolunephritis. It always damages at renal and systemic level (a third of the cases presented hemorrhage alveolar). We have showed a case that took place with hemoptysis and renal progressive insufficiency. Among the patient antecedents, we can find arterial hypertension hematuria, rhinitis, epistaxis and artromyalgias. Just before his admittance it showed edemas on lower limbs and eyelids, dysnea, severe hemoptysis, paresthesias and general malaise. The immunologic analysis: Acs. glomerular basal antimembrane: negative, ANCA positive with antimieloperoxidasa specificity. The renal biopsy: focal necrotizing glomerulonephritis with semilunar and negative immunofluorescent. The nasas biopsy: unspecified chronic rhinitis. From the clinic point of view, the patient seemed to have the Wegener granulomatosis apart from the fact that he had hemoptysis which is a rare sign in this cases. However, we could not find any granuloma anatomopatologically, which did not clarify this diagnosis. We diagnosed microscopis Poliarteritis, as a third of the cases presented intrapulmonary haemorrhage. Moreover the renal damage it is identical than in the in Wegener granulomatosis. On the top of that, often we can find p-ANCA, which confirms the diagnosis in 99% of cases. Despite our doubt according to the diagnosis the therapeutical treatment of both illnesses is nowadays identical. This means that we were able to begin a precocious treatment with plasmapheresis, metilprednisolona and ciclofosfamida. After a week treatment there was an evident improvement. Five moth later the illness relapsed.