Déficit en vitamine D et fractures

Introduction: Le déficit en vitamine D est un facteur de risque de fracture par ses effets osseux et extra osseux. En Suisse, 49,7% des patientes ostéoporotiques ont un déficit en vitamine D. L'objectif de ce travail était d'analyser le statut vitaminique D des patients hospitalisés pour fracture en fonction de la saison, du type de fracture et des caractéristiques individuelles. Méthode: Nous avons dosé la vitamine D des patients hospitalisés au CHUV pour une fracture entre le 1er novembre 2008 et le 31 juillet 2009 et vus dans le cadre de la filière de la fracture. Définition: insuffisance (10 et 30 μg/l) et carence (<10 μg/l) en vitamine D. Résultats: Le taux moyen de vitamine D était de 16,2 μg/l chez les 184 patients (femmes 86%, âge moyen 76ans). 167 patients (91%) avaient une insuffisance et 70 (38%) une carence. 59 patients bénéficiaient d'une supplémentation vitamino-calcique. Leur taux moyen était significativement plus élevé que ceux ne bénéficiant pas de supplémentation (22,9 vs 13,1 μg/l; p <0,05). Les proportions d'insuffisance (74,6% vs 94,4%) et de carence (3,4% vs 54,4%) étaient significativement plus basses. Le taux de vitamine D n'était pas différent entre les fractures traumatiques et non traumatiques (13,9 vs 16,4 μg/l; p = 0,4). Les patients avec une fracture de l'humérus avaient un taux plus bas que lors d'une autre fracture (9,0 vs 16,7 μg/l; p = 0,032). En distinguant les périodes hivernale et estivale, il n'existait pas de différence (16,13 vs 16,34; p = 0,90), ni en terme de carence (38% vs 37,9%; p = 0,99) ou d'insuffisance (86,7% vs 89,9%; p = 0,51). Aucune différence n'a été mise en évidence en fonction des classes d'âge (de 40 à >90 ans) ou du sexe. Les taux moyens de vitamine D étaient significativement plus bas lors d'IMC <18,5 ou >35. Conclusion: Cette analyse souligne l'importance du déficit en vitamine D dans une population de patients fracturés. Elle met en lumière le risque particulier couru par les patients aux deux extrêmes de l'IMC. Par ailleurs, les patients avec une supplémentation ont des taux sanguins de vitamine D insuffisants traduisant ou une compliance insuffisante ou la nécessité de prescrire des doses plus élevées.

Acute post-exercise oxygen uptake, hormone and plasma metabolite response in obese men.

This study aimed to compare oxygen uptake (  V˙O2), hormone and plasma metabolite responses during the 30 min after submaximal incremental exercise (Incr) performed at the same relative/absolute exercise intensity and duration in lean (L) and obese (O) men. Eight L and 8 O men (BMI: 22.9±0.4; 37.2±1.8 kg · m(-2)) completed Incr and were then seated for 30 min.   V˙O2 was monitored during the first 10 min and from the 25-30(th) minutes of recovery. Blood samples were drawn for the determination of hormone (catecholamines, insulin) and plasma metabolite (NEFA, glycerol) concentrations. Excess post-exercise oxygen consumption (EPOC) magnitude during the first 10 min was similar in O and in L (3.5±0.4; 3.4±0.3 liters, respectively, p=0.86). When normalized to percent change (  V˙O2END=100%), %   V˙O2END during recovery was significantly higher from 90-120 s in O than in L (p≤0.04). There were no significant differences in catecholamines (p≥0.24), whereas insulin was significantly higher in O than in L during recovery (p=0.01). The time-course of glycerol was similar from 10-30 min of recovery (-42% for L; -41% for O, p=0.85), whereas significantly different patterns of NEFA were found from 10-30 min of recovery between groups (-18% for L; +8% for O, p=0.03). Despite similar EPOC, a difference in   V˙O2 modulation between groups was observed, likely due to faster initial rates of   V˙O2 decline in L than in O. The different patterns of NEFA between groups may suggest a lower NEFA reesterification during recovery in O, which was not involved in the rapid EPOC component.

Muscle protein waste in tumor-bearing rats is effectively antagonized by a beta 2-adrenergic agonist (clenbuterol). Role of the ATP-ubiquitin-dependent proteolytic pathway.

Tissue protein hypercatabolism (TPH) is a most important feature in cancer cachexia, particularly with regard to the skeletal muscle. The rat ascites hepatoma Yoshida AH-130 is a very suitable model system for studying the mechanisms involved in the processes that lead to tissue depletion, since it induces in the host a rapid and progressive muscle waste mainly due to TPH (Tessitore, L., G. Bonelli, and F. M. Baccino. 1987. Biochem. J. 241:153-159). Detectable plasma levels of tumor necrosis factor-alpha associated with marked perturbations in the hormonal homeostasis have been shown to concur in forcing metabolism into a catabolic setting (Tessitore, L., P. Costelli, and F. M. Baccino. 1993. Br. J. Cancer. 67:15-23). The present study was directed to investigate if beta 2-adrenergic agonists, which are known to favor skeletal muscle hypertrophy, could effectively antagonize the enhanced muscle protein breakdown in this cancer cachexia model. One such agent, i.e., clenbuterol, indeed largely prevented skeletal muscle waste in AH-130-bearing rats by restoring protein degradative rates close to control values. This normalization of protein breakdown rates was achieved through a decrease of the hyperactivation of the ATP-ubiquitin-dependent proteolytic pathway, as previously demonstrated in our laboratory (Llovera, M., C. García-Martínez, N. Agell, M. Marzábal, F. J. López-Soriano, and J. M. Argilés. 1994. FEBS (Fed. Eur. Biochem. Soc.) Lett. 338:311-318). By contrast, the drug did not exert any measurable effect on various parenchymal organs, nor did it modify the plasma level of corticosterone and insulin, which were increased and decreased, respectively, in the tumor hosts. The present data give new insights into the mechanisms by which clenbuterol exerts its preventive effect on muscle protein waste and seem to warrant the implementation of experimental protocols involving the use of clenbuterol or alike drugs in the treatment of pathological states involving TPH, particularly in skeletal muscle and heart, such as in the present model of cancer cachexia.

Muscle protein waste in tumor-bearing rats is effectively antagonized by a beta 2-adrenergic agonist (clenbuterol). Role of the ATP-ubiquitin-dependent proteolytic pathway.

Tissue protein hypercatabolism (TPH) is a most important feature in cancer cachexia, particularly with regard to the skeletal muscle. The rat ascites hepatoma Yoshida AH-130 is a very suitable model system for studying the mechanisms involved in the processes that lead to tissue depletion, since it induces in the host a rapid and progressive muscle waste mainly due to TPH (Tessitore, L., G. Bonelli, and F. M. Baccino. 1987. Biochem. J. 241:153-159). Detectable plasma levels of tumor necrosis factor-alpha associated with marked perturbations in the hormonal homeostasis have been shown to concur in forcing metabolism into a catabolic setting (Tessitore, L., P. Costelli, and F. M. Baccino. 1993. Br. J. Cancer. 67:15-23). The present study was directed to investigate if beta 2-adrenergic agonists, which are known to favor skeletal muscle hypertrophy, could effectively antagonize the enhanced muscle protein breakdown in this cancer cachexia model. One such agent, i.e., clenbuterol, indeed largely prevented skeletal muscle waste in AH-130-bearing rats by restoring protein degradative rates close to control values. This normalization of protein breakdown rates was achieved through a decrease of the hyperactivation of the ATP-ubiquitin-dependent proteolytic pathway, as previously demonstrated in our laboratory (Llovera, M., C. García-Martínez, N. Agell, M. Marzábal, F. J. López-Soriano, and J. M. Argilés. 1994. FEBS (Fed. Eur. Biochem. Soc.) Lett. 338:311-318). By contrast, the drug did not exert any measurable effect on various parenchymal organs, nor did it modify the plasma level of corticosterone and insulin, which were increased and decreased, respectively, in the tumor hosts. The present data give new insights into the mechanisms by which clenbuterol exerts its preventive effect on muscle protein waste and seem to warrant the implementation of experimental protocols involving the use of clenbuterol or alike drugs in the treatment of pathological states involving TPH, particularly in skeletal muscle and heart, such as in the present model of cancer cachexia.

Muscle protein waste in tumor-bearing rats is effectively antagonized by a beta 2-adrenergic agonist (clenbuterol). Role of the ATP-ubiquitin-dependent proteolytic pathway.

Tissue protein hypercatabolism (TPH) is a most important feature in cancer cachexia, particularly with regard to the skeletal muscle. The rat ascites hepatoma Yoshida AH-130 is a very suitable model system for studying the mechanisms involved in the processes that lead to tissue depletion, since it induces in the host a rapid and progressive muscle waste mainly due to TPH (Tessitore, L., G. Bonelli, and F. M. Baccino. 1987. Biochem. J. 241:153-159). Detectable plasma levels of tumor necrosis factor-alpha associated with marked perturbations in the hormonal homeostasis have been shown to concur in forcing metabolism into a catabolic setting (Tessitore, L., P. Costelli, and F. M. Baccino. 1993. Br. J. Cancer. 67:15-23). The present study was directed to investigate if beta 2-adrenergic agonists, which are known to favor skeletal muscle hypertrophy, could effectively antagonize the enhanced muscle protein breakdown in this cancer cachexia model. One such agent, i.e., clenbuterol, indeed largely prevented skeletal muscle waste in AH-130-bearing rats by restoring protein degradative rates close to control values. This normalization of protein breakdown rates was achieved through a decrease of the hyperactivation of the ATP-ubiquitin-dependent proteolytic pathway, as previously demonstrated in our laboratory (Llovera, M., C. García-Martínez, N. Agell, M. Marzábal, F. J. López-Soriano, and J. M. Argilés. 1994. FEBS (Fed. Eur. Biochem. Soc.) Lett. 338:311-318). By contrast, the drug did not exert any measurable effect on various parenchymal organs, nor did it modify the plasma level of corticosterone and insulin, which were increased and decreased, respectively, in the tumor hosts. The present data give new insights into the mechanisms by which clenbuterol exerts its preventive effect on muscle protein waste and seem to warrant the implementation of experimental protocols involving the use of clenbuterol or alike drugs in the treatment of pathological states involving TPH, particularly in skeletal muscle and heart, such as in the present model of cancer cachexia.

Crystal size distribution of periclase in contact metamorphic dolomite marbles from the southern Adamello Massif, Italy

Crystal size distributions (CSD) of periclase in contact metamorphic dolomite marbles are presented for two profiles near the Cima Uzza summit in the southern Adamello Massif (Italy). The database was combined with geochemical and petrological information to deduce the controls on the periclase-forming reaction. The contact metamorphic dolomite marbles are exposed at the contact of mafic intrusive rocks and are partially surrounded by them. Brucite is retrograde and pseudomorphs spherical periclase crystals. Prograde periclase growth is the consequence of limited infiltration of water-rich fluid at T near 605C. Stable isotope data show depletion in (13)C and (18)O over a narrow region (40 cm) near the magmatic contact, whereas the periclase-forming reaction front extends up to 4 m from the contact. CSD analyses along the two profiles show that the median grain size of the periclase crystals does not change, but that there is a progressively greater distribution of grain sizes, including a greater proportion of larger grains, with increasing distance from the contact. A qualitative model, based on the textural and geochemical data, attributes these variations in grain size to changing reaction affinities along a kinetically dispersed infiltration front. This study highlights the need to invoke disequilibrium processes for metamorphic mineral growth and expands the use of CSDs to systems of mineral formation driven by fluid infiltration.

Levosimendan as rescue therapy after surgery for congenital heart disease

Objectives: Levosimendan, a calcium-sensitizing agent has been reported as useful for the management of patients with low cardiac output state. We report here our experience, safety and efficacy of use of levosimendan as rescue therapy after surgery for congenital heart disease. Methods: Retrospective cohort study on patients necessitating levosimendan therapy for post operative low cardiac output or severe post operative systolic and diastolic dysfunction. Twelve patients with a mean age of 2.1 years (range 7 days - 14 years old) received levosimendan. Type of surgery: 3 arterial switch, 3 correction of complete abnormal pulmonary venous return, 3 closure of VSD and correction of aortic coarctation, 3 Tetralogy of Fallot, one correction of truncus arteriosus and one palliation for single ventricle. The mean time of ECC was 203 +/- 81min. Ten patients received levosimendan for low cardiac output not responding to conventional therapy in these cases (milrinone, dopamine and noradrenaline) in the first 6 hours following entry in the ICU and 3 patients received levosimendan 3-4 days after surgery for severe systolic and diastolic dysfunction. Levosimendan was given as a drip for 24-48 hours at the dose of 0.1-0.2 mcg/ kg/min, without loading dose. Results: Significant changes were noted on mean plasmatic lactate (3.3 +/- 1.7mmole/L vs 1.8 +/-0.6mmole/L, p+0.01), mean central venous saturation (55 +/- 11% vs 68 +/- 10%, p+0.01) and mean arterio-venous difference in CO2 (9.6 +/- 4.9mmHg vs 6.7 +/- 2.1mmHg, p+0.05) for values before and at the end of levosimendan administration. There was no significant changes on heart rate, systolic pressure or central venous pressure. No adverse effect was observed. Conclusion: Levosimendan, used as rescue therapy after surgery for congenital heart disease, is safe and improves cardiac output as demonstrated with improvement of parameters commonly used clinically.

Outcomes in neurosurgical patients who develop venous thromboembolism: a review of the RIETE registry.

OBJECTIVES: Registro Informatizado de Enfermedad TromboEmbólica (RIETE) database was used to investigate whether neurosurgical patients with venous thromboembolism (VTE) were more likely to die of bleeding or VTE and the influence of anticoagulation on these outcomes. METHODS: Clinical characteristics, treatment details, and 3-month outcomes were assessed in those who developed VTE after neurosurgery. RESULTS: Of 40 663 patients enrolled, 392 (0.96%) had VTE in less than 60 days after neurosurgery. Most patients in the cohort (89%) received initial therapy with low-molecular-weight heparin, (33% received subtherapeutic doses). In the first week, 10 (2.6%) patients died (8 with pulmonary embolism [PE], no bleeding deaths; P = .005). After the first week, 20 (5.1%) patients died (2 with fatal bleeding, none from PE). Overall, this cohort was more likely to develop a fatal PE than a fatal bleed (8 vs 2 deaths, P = .058). CONCLUSIONS: Neurosurgical patients developing VTE were more likely to die from PE than from bleeding in the first week, despite anticoagulation.

The genome sequence of taurine cattle: a window to ruminant biology and evolution.

To understand the biology and evolution of ruminants, the cattle genome was sequenced to about sevenfold coverage. The cattle genome contains a minimum of 22,000 genes, with a core set of 14,345 orthologs shared among seven mammalian species of which 1217 are absent or undetected in noneutherian (marsupial or monotreme) genomes. Cattle-specific evolutionary breakpoint regions in chromosomes have a higher density of segmental duplications, enrichment of repetitive elements, and species-specific variations in genes associated with lactation and immune responsiveness. Genes involved in metabolism are generally highly conserved, although five metabolic genes are deleted or extensively diverged from their human orthologs. The cattle genome sequence thus provides a resource for understanding mammalian evolution and accelerating livestock genetic improvement for milk and meat production.

Pneumopathie interstitielle dans la polyarthrite rhumatoïde [Interstitial lung disease in rheumatoid arthritis].

Interstitial lung disease (ILD) is found in up to 30% of patients with rheumatoid arthritis (RA) and is clinically manifest in 5 to 10%, resulting in significant morbidity and mortality. The most frequent histopathological forms are usual interstitial pneumonia and nonspecific interstitial pneumonia. Another recently described presentation is combined pulmonary fibrosis and emphysema. Similarly to idiopathic pulmonary fibrosis, acute exacerbation of ILD may occur in RA and is associated with severe prognosis. Smoking is a known risk factor of RA and may also play a role in the pathogenesis of RA-associated ILD, in combination with genetic and immunologic mechanisms. Several treatments of RA may also lead to drug-induced ILD.

Unexpected genomic variability in clinical and environmental strains of the pathogenic yeast Candida parapsilosis

Invasive candidiasis is the most commonly reported invasive fungal infection worldwide. Although Candida albicans remains the main cause, the incidence of emerging Candida species, such as C. parapsilosis is increasing. It has been postulated that C. parapsilosis clinical isolates result from a recent global expansion of a virulent clone. However, the availability of a single genome for this species has so far prevented testing this hypothesis at genomic scales. We present here the sequence of three additional strains from clinical and environmental samples. Our analyses reveal unexpected patterns of genomic variation, shared among distant strains, that argue against the clonal expansion hypothesis. All strains carry independent expansions involving an arsenite transporter homolog, pointing to the existence of directional selection in the environment, and independent origins of the two clinical isolates. Furthermore, we report the first evidence for the existence of recombination in this species. Altogether, our results shed new light onto the dynamics of genome evolution in C. parapsilosis.

Results of An International Study of Quantitative BCR/ABL Assays Using Defined RNA Samples

Molecular monitoring of BCR/ABL transcripts by real time quantitative reverse transcription PCR (qRT-PCR) is an essential technique for clinical management of patients with BCR/ABL-positive CML and ALL. Though quantitative BCR/ABL assays are performed in hundreds of laboratories worldwide, results among these laboratories cannot be reliably compared due to heterogeneity in test methods, data analysis, reporting, and lack of quantitative standards. Recent efforts towards standardization have been limited in scope. Aliquots of RNA were sent to clinical test centers worldwide in order to evaluate methods and reporting for e1a2, b2a2, and b3a2 transcript levels using their own qRT-PCR assays. Total RNA was isolated from tissue culture cells that expressed each of the different BCR/ABL transcripts. Serial log dilutions were prepared, ranging from 100 to 10-5, in RNA isolated from HL60 cells. Laboratories performed 5 independent qRT-PCR reactions for each sample type at each dilution. In addition, 15 qRT-PCR reactions of the 10-3 b3a2 RNA dilution were run to assess reproducibility within and between laboratories. Participants were asked to run the samples following their standard protocols and to report cycle threshold (Ct), quantitative values for BCR/ABL and housekeeping genes, and ratios of BCR/ABL to housekeeping genes for each sample RNA. Thirty-seven (n=37) participants have submitted qRT-PCR results for analysis (36, 37, and 34 labs generated data for b2a2, b3a2, and e1a2, respectively). The limit of detection for this study was defined as the lowest dilution that a Ct value could be detected for all 5 replicates. For b2a2, 15, 16, 4, and 1 lab(s) showed a limit of detection at the 10-5, 10-4, 10-3, and 10-2 dilutions, respectively. For b3a2, 20, 13, and 4 labs showed a limit of detection at the 10-5, 10-4, and 10-3 dilutions, respectively. For e1a2, 10, 21, 2, and 1 lab(s) showed a limit of detection at the 10-5, 10-4, 10-3, and 10-2 dilutions, respectively. Log %BCR/ABL ratio values provided a method for comparing results between the different laboratories for each BCR/ABL dilution series. Linear regression analysis revealed concordance among the majority of participant data over the 10-1 to 10-4 dilutions. The overall slope values showed comparable results among the majority of b2a2 (mean=0.939; median=0.9627; range (0.399 - 1.1872)), b3a2 (mean=0.925; median=0.922; range (0.625 - 1.140)), and e1a2 (mean=0.897; median=0.909; range (0.5174 - 1.138)) laboratory results (Fig. 1-3)). Thirty-four (n=34) out of the 37 laboratories reported Ct values for all 15 replicates and only those with a complete data set were included in the inter-lab calculations. Eleven laboratories either did not report their copy number data or used other reporting units such as nanograms or cell numbers; therefore, only 26 laboratories were included in the overall analysis of copy numbers. The median copy number was 348.4, with a range from 15.6 to 547,000 copies (approximately a 4.5 log difference); the median intra-lab %CV was 19.2% with a range from 4.2% to 82.6%. While our international performance evaluation using serially diluted RNA samples has reinforced the fact that heterogeneity exists among clinical laboratories, it has also demonstrated that performance within a laboratory is overall very consistent. Accordingly, the availability of defined BCR/ABL RNAs may facilitate the validation of all phases of quantitative BCR/ABL analysis and may be extremely useful as a tool for monitoring assay performance. Ongoing analyses of these materials, along with the development of additional control materials, may solidify consensus around their application in routine laboratory testing and possible integration in worldwide efforts to standardize quantitative BCR/ABL testing.

PhylomeDB v4: zooming into the plurality of evolutionary histories of a genome

Phylogenetic trees representing the evolutionary relationships of homologous genes are the entry point for many evolutionary analyses. For instance, the use of a phylogenetic tree can aid in the inference of orthology and paralogy relationships, and in the detection of relevant evolutionary events such as gene family expansions and contractions, horizontal gene transfer, recombination or incomplete lineage sorting. Similarly, given the plurality of evolutionary histories among genes encoded in a given genome, there is a need for the combined analysis of genome-wide collections of phylogenetic trees (phylomes). Here, we introduce a new release of PhylomeDB (http://phylomedb.org), a public repository of phylomes. Currently, PhylomeDB hosts 120 public phylomes, comprising >1.5 million maximum likelihood trees and multiple sequence alignments. In the current release, phylogenetic trees are annotated with taxonomic, protein-domain arrangement, functional and evolutionary information. PhylomeDB is also a major source for phylogeny-based predictions of orthology and paralogy, covering >10 million proteins across 1059 sequenced species. Here we describe newly implemented PhylomeDB features, and discuss a benchmark of the orthology predictions provided by the database, the impact of proteome updates and the use of the phylome approach in the analysis of newly sequenced genomes and transcriptomes.

Obesity-related phenotypes are associated to parental longevity in a Swiss population-based study

METHODS. We analyzed data from a population-based sample of 2561 participants (1163 men and 1398 women) aged 55-75 years from the city of Lausanne, Switzerland (CoLaus study). Participants were stratified by the number of parents (0, 1, 2) who survived to 85 years or more. Trend across these strata was assessed using a non-parametric kmean test. The associations of parental age (independent covariate used as a proxy for longevity) with fasting blood glucose, blood pressures, blood lipids, body mass index (BMI), weight, height or liver enzymes (continuous dependent variables) were analyzed using multiple linear regressions. Models were adjusted for age, sex, alcohol consumption, smoking and educational level, and BMI for liver enzymes. RESULTS. For subjects with 0 (N = 1298), 1 (N = 991) and 2 (N = 272) long-lived parents, median BMI (interquartile range) was 25.4 (6.5), 24.9 (6.1) and 23.7 (4.8) kg/m2 in women (P <0.001), and 27.3 (4.8), 27.0 (4.5) and 25.9 (4.9) kg/m2 in men (P = 0.04), respectively; median weight was 66.5 (16.1), 65.0 (16.4) and 63.4 (13.7) kg in women (P = 0.003), and 81.5 (17.0), 81.4 (16.4) and 80.3 (17.1) kg in men (P = 0.36). Median height was 161 (8), 162 (9) and 163 (8) cm in women (P = 0.005) and 173 (9), 174 (9) and 174 (11) cm in men (P = 0.09). The corresponding medians for AST (Aspartate Aminotransferase) were 31 (13), 29 (11) and 28 (10) U/L (P = 0.002), and 28 (17), 27 (14) and 26 (19) U/L for ALT (Alanin Aminotransferase, P = 0.053) in men. In multivariable analyses, greater parental longevity was associated with lower BMI, lower weight and taller stature in women (P < 0.01) and lower AST in men (P = 0.011). No significant associations were observed for the other variables analyzed. Sensitivity analyses restricted to subjects whose parents were dead (N = 1844) led to similar results, with even stronger associations of parental longevity with liver enzymes in men. CONCLUSIONS. In women, increased parental longevity was associated with smaller BMI, attributable to lower weight and taller stature. In men, the association of increased parental longevity with lower liver enzymes, independently of BMI, suggests that parental longevity may be associated with decreased nonalcoholic fatty liver disease.

EFEITO DA RETIRADA DA INFLORESCÊNCIA MASCULINA NA PRECOCIDADE DA COLHEITA E PRODUÇÃO DA BANANEIRA-'PRATA-ANÃ' SOB IRRIGAÇÃO NA REGIÃO NORTE DE MINAS GERAIS

O trabalho foi desenvolvido na região Norte de Minas Gerais, em uma área pertencente a EPAMIG - CTNM, localizada no Perímetro Irrigado do Jaíba. O delineamento experimental utilizado foi inteiramente casualizado , com dois tratamentos e 22 repetições, e cada parcela constituída por três plantas. Objetivou-se avaliar o efeito da retirada da inflorescência masculina na precocidade de colheita e produção da bananeira-'Prata-Anã', avaliando-se os três primeiros ciclos. Houve redução no período entre a retirada da inflorescência e a colheita, quando se eliminou a inflorescência masculina, sendo que, no primeiro ciclo, promoveu aumento no peso total de frutos, peso médio de frutos, peso médio de pencas, diâmetro e peso do fruto central e espessura de casca do fruto central da segunda penca, peso da penca 2, peso da penúltima penca, peso do engaço e peso e comprimento da ráquis. Não promoveu aumento de peso total do cacho, no comprimento do fruto central da segunda penca, peso da penca 1 e peso da última penca. No segundo ciclo, apesar de tendência de aumento, não houve diferença estatística para os parâmetros de produção. Já no terceiro ciclo, houve aumento no peso do cacho, além de aumento nos parâmetros de produção, concordando com os resultados obtidos na primeira colheita