Repeated Sprint Ability in Young Basketball Players (Part 2): The Chronic Effects of Multidirection and of One Change of Direction Are Comparable in Terms of Physiological and Performance Responses

The aim of this study was to examine the effects of a 5-week training program, consisting of repeated 30-m sprints, on two repeated sprint ability (RSA) test formats: one with one change of direction (RSA) and the other with multiple changes of direction (RSM). Thirty-six young male and female basketball players (age 16.1 \ub1 0.9 years), divided into two experimental groups, were tested for RSA, RSM, squat jump, counter-movement jump, and the Yo-Yo Intermittent Recovery-Level-1 (Yo-Yo IR1) test, before and after a 4-week training program and 1 week of tapering. One group performed 30-m sprints with one change of direction (RSA group, RSAG), whereas the other group performed multidirectional 30-m sprints (RSM group, RSMG). Both groups improved in all scores in the post-intervention measurements (P < 0.05), except for the fatigue index in the RSM test. However, when comparing the two groups, similar effects were found for almost all parameters of the tests applied, except for RPE in the RSA test, which had a greater decrease in the RSAG (from 8.7 to 5.9) than in the RSMG (from 8.5 to 6.6, P = 0.021). We can conclude that repeated 30-m sprints, either with one change of direction or multidirectional, induce similar physiological and performance responses in young basketball players, but have a different psycho-physiological impact

RNase Y cleavage sites fall within or near the genes encoding components of the putative degradosome, as defined by [17], and show sequence preference for guanosines.

<p>Predicted transcription start sites (TSS), detected RNase Y cleavage sites (Y-cleav.) and predicted transcriptional terminators (TransTerm) are indicated. Thin dotted lines show the sequence amplified by RT-PCR to demonstrate that RNase Y cleavage sites and ORFs are potentially on the same RNA molecules. (A) <i>SA0941-rnjA</i> operon, encoding a hypothetical protein and RNase J1. (B) <i>rnjB</i> gene encoding RNase J2 (<i>pnpA</i> encodes PNPase). (C) <i>pfkA-pykA</i> operon, encoding phosphofructokinase and pyruvate kinase. (D) The RNase Y gene (<i>cvfA</i>) with the putative RNase Y cleavage site at position +24. (E) RNase Y cleaves preferentially after a purine. 25 nucleotides on each side of the 99 RNase Y sites (see <a href="http://www.plosgenetics.org/article/info:doi/10.1371/journal.pgen.1005577#pgen.1005577.s012" target="_blank">S2 Table</a>) were extracted from the <i>S</i>. <i>aureus</i> N315 genome, and a frequency plot was generated. The RNase Y cleavage site (thick vertical dotted line), and the position detected by EMOTE (Y+1) are indicated. The preference for a guanosine residue immediately prior to the RNase Y cleavage sites is evident. Additionally, there is an enrichment of A's at position Y–6 and of pyrimidines at position Y+5. Finally, it appears that A's or U's are favoured in the region from 11 nt upstream to 7 nt downstream of the cleavage site, however this could also be due to the over-all nucleotide composition of <i>S</i>. <i>aureus</i>, which has 33% G+C (thin horizontal dotted line).</p

Mutated nucleophosmin detects clonal multilineage involvement in acute myeloid leukemia: Impact on WHO classification.

Because of a lack of specific clonality markers, information on lineage involvement and cell of origin of acute myeloid leukemia with normal karyotype (AML-NK), is missing. Because Nucleophosmin (NPM) gene is frequently mutated in AML-NK and causes aberrant NPM cytoplasmic localization (NPMc+), it was used as an AML lineage clonality marker. Clonal NPM exon 12 mutations were detected in myeloid, monocytic, erythroid, and megakaryocytic cells but not in fibroblasts or endothelia that were laser-microdissected from 3 patients with NPMc+ AML. Aberrant cytoplasmic expression of mutated NPM proteins was identified with anti-NPM antibodies in 2 or more myeloid hemopoietic cell lineages in 99 (61.5%) of 161 of NPMc+ AML paraffin-embedded bone marrow biopsies; lymphoid involvement was excluded in 3 investigated cases. These findings suggest that NPMc+ AML derives from either a common myeloid or earlier progenitor. Immunohistochemical studies show that varying combinations and ratios of NPMc+ leukemic cells from distinct lineages are responsible for heterogeneity within each French-American-British (FAB) classification type and for NPMc+ AML falling into different FAB categories. These findings question the value of FAB criteria in subdividing the WHO category of "AML not otherwise characterized" and suggest that, for clinical use, NPMc+ AML be provisionally regarded as a separate AML with prognostic significance

Immunohistochemistry predicts nucleophosmin (NPM) mutations in acute myeloid leukemia

Nucleophosmin (NPM) exon-12 mutations occur in 50% to 60% of adult acute myeloid leukemia (AML) with normal karyotype and are predictors of favorable prognosis. We evaluated bone marrow or peripheral blood samples from 450 adult patients with AML of the GIMEMA (Gruppo Italiano Malattie Ematologiche Maligne dell'Adulto)/AML12 EORTC (European Organization for Research and Treatment of Cancer) trial to (1) search for new exon-12 NPM mutations; (2) determine whether NPM immunostaining on paraffin-embedded biopsies predicts NPM mutations; and (3) investigate altered nucleocytoplasmic NPM traffic in primary AML cells. Fourteen NPM mutations, including 8 new variants, were identified. All 200 AML cases expressing cytoplasmic NPM (NPMc(+) AML) carried NPM mutations. None of the 250 cases with nucleus-restricted NPM (NPMc(-) AML) was mutated. At the C-terminus, NPM leukemic mutants carried mutations of only tryptophan 290 or of both tryptophans 288 and 290 and a new nuclear export signal (NES) motif, which appear to underlie their nuclear export. The specific Crm1/exportin-1 inhibitor leptomycin-B relocated NPM mutants from cytoplasm to nucleus of primary NPMc(+) AML cells, demonstrating that nuclear export is NES dependent. NPM mutants bound and recruited wild-type NPM into leukemic cell cytoplasm. Because alterations at C-terminus of leukemic NPM mutants are similar, immunohistochemistry detects all exon-12 NPM mutations and is a valuable, inexpensive tool in the diagnostic-prognostic work-up of patients with AML with normal karyotype.status: publishe

Immunohistochemistry predicts nucleophosmin (NPM) mutations in acute myeloid leukemia

Nucleophosmin (NPM) exon-12 mutations occur in 50% to 60% of adult acute myeloid leukemia (AML) with normal karyotype and are predictors of favorable prognosis. We evaluated bone marrow or peripheral blood samples from 450 adult patients with AML of the GIMEMA (Gruppo Italiano Malattie Ematologiche Maligne dell'Adulto)/AML12 EORTC (European Organization for Research and Treatment of Cancer) trial to (1) search for new exon-12 NPM mutations; (2) determine whether NPM immunostaining on paraffin-embedded biopsies predicts NPM mutations; and (3) investigate altered nucleocytoplasmic NPM traffic in primary AML cells. Fourteen NPM mutations, including 8 new variants, were identified. All 200 AML cases expressing cytoplasmic NPM (NPMc(+) AML) carried NPM mutations. None of the 250 cases with nucleus-restricted NPM (NPMc(-) AML) was mutated. At the C-terminus, NPM leukemic mutants carried mutations of only tryptophan 290 or of both tryptophans 288 and 290 and a new nuclear export signal (NES) motif, which appear to underlie their nuclear export. The specific Crm1/exportin-1 inhibitor leptomycin-B relocated NPM mutants from cytoplasm to nucleus of primary NPMc(+) AML cells, demonstrating that nuclear export is NES dependent. NPM mutants bound and recruited wild-type NPM into leukemic cell cytoplasm. Because alterations at C-terminus of leukemic NPM mutants are similar, immunohistochemistry detects all exon-12 NPM mutations and is a valuable, inexpensive tool in the diagnostic-prognostic work-up of patients with AML with normal karyotype

Immunohistochemistry predicts nucleoplasmin (NPM) mutations in acute myeloid leukemia.

Nucleophosmin (NPM) exon-12 mutations occur in 50% to 60% of adult acute myeloid leukemia (AML) with normal karyotype and are predictors of favorable prognosis. We evaluated bone marrow or peripheral blood samples from 450 adult patients with AML of the GIMEMA (Gruppo Italiano Malattie Ematologiche Maligne dell'Adulto)/AML12 EORTC (European Organization for Research and Treatment of Cancer) trial to (1) search for new exon-12 NPM mutations; (2) determine whether NPM immunostaining on paraffin-embedded biopsies predicts NPM mutations; and (3) investigate altered nucleocytoplasmic NPM traffic in primary AML cells. Fourteen NPM mutations, including 8 new variants, were identified. All 200 AML cases expressing cytoplasmic NPM (NPMc(+) AML) carried NPM mutations. None of the 250 cases with nucleus-restricted NPM (NPMc(-) AML) was mutated. At the C-terminus, NPM leukemic mutants carried mutations of only tryptophan 290 or of both tryptophans 288 and 290 and a new nuclear export signal (NES) motif, which appear to underlie their nuclear export. The specific Crm1/exportin-1 inhibitor leptomycin-B relocated NPM mutants from cytoplasm to nucleus of primary NPMc(+) AML cells, demonstrating that nuclear export is NES dependent. NPM mutants bound and recruited wild-type NPM into leukemic cell cytoplasm. Because alterations at C-terminus of leukemic NPM mutants are similar, immunohistochemistry detects all exon-12 NPM mutations and is a valuable, inexpensive tool in the diagnostic-prognostic work-up of patients with AML with normal karyotype