Institution
Sapienza University of Rome
Education•Rome, Lazio, Italy•
About: Sapienza University of Rome is a education organization based out in Rome, Lazio, Italy. It is known for research contribution in the topics: Population & Medicine. The organization has 62002 authors who have published 155468 publications receiving 4397244 citations. The organization is also known as: La Sapienza & Università La Sapienza di Roma.
Topics: Population, Medicine, Context (language use), Cancer, Nonlinear system
Papers published on a yearly basis
Papers
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TL;DR: It is suggested that WBV influences proprioceptive feedback mechanisms and specific neural components, leading to an improvement of neuromuscular performance.
Abstract: The aim of this study was to evaluate the acute responses of blood hormone concentrations and neuromuscular performance following whole-body vibration (WBV) treatment. Fourteen male subjects [mean (SD) age 25 (4.6) years] were exposed to vertical sinusoidal WBV, 10 times for 60 s, with 60 s rest between the vibration sets (a rest period lasting 6 min was allowed after 5 vibration sets). Neuromuscular performance tests consisting of counter-movement jumps and maximal dynamic leg presses on a slide machine, performed with an extra load of 160% of the subjects body mass, and with both legs were administered before and immediately after the WBV treatment. The average velocity, acceleration, average force, and power were calculated and the root mean square electromyogram (EMGrms) were recorded from the vastus lateralis and rectus femoris muscles simultaneously during the leg-press measurement. Blood samples were also collected, and plasma concentrations of testosterone (T), growth hormone (GH) and cortisol (C) were measured. The results showed a significant increase in the plasma concentration of T and GH, whereas C levels decreased. An increase in the mechanical power output of the leg extensor muscles was observed together with a reduction in EMGrms activity. Neuromuscular efficiency improved, as indicated by the decrease in the ratio between EMGrms and power. Jumping performance, which was measured using the counter-movement jump test, was also enhanced. Thus, it can be argued that the biological mechanism produced by vibration is similar to the effect produced by explosive power training (jumping and bouncing). The enhancement of explosive power could have been induced by an increase in the synchronisation activity of the motor units, and/or improved co-ordination of the synergistic muscles and increased inhibition of the antagonists. These results suggest that WBV treatment leads to acute responses of hormonal profile and neuromuscular performance. It is therefore likely that the effect of WBV treatment elicited a biological adaptation that is connected to a neural potentiation effect, similar to those reported to occur following resistance and explosive power training. In conclusion, it is suggested that WBV influences proprioceptive feedback mechanisms and specific neural components, leading to an improvement of neuromuscular performance. Moreover, since the hormonal responses, characterised by an increase in T and GH concentration and a decrease in C concentration, and the increase in neuromuscular effectiveness were simultaneous but independent, it is speculated that the two phenomena might have common underlying mechanisms.
533 citations
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TL;DR: The findings suggest that the Gcn5p bromodomain may discriminate between different acetylated lysine residues depending on the context in which they are displayed.
Abstract: The bromodomain is an approximately 110 amino acid module found in histone acetyltransferases and the ATPase component of certain nucleosome remodelling complexes. We report the crystal structure at 1.9 A resolution of the Saccharomyces cerevisiae Gcn5p bromodomain complexed with a peptide corresponding to residues 15-29 of histone H4 acetylated at the zeta-N of lysine 16. We show that this bromodomain preferentially binds to peptides containing an N:-acetyl lysine residue. Only residues 16-19 of the acetylated peptide interact with the bromodomain. The primary interaction is the N:-acetyl lysine binding in a cleft with the specificity provided by the interaction of the amide nitrogen of a conserved asparagine with the oxygen of the acetyl carbonyl group. A network of water-mediated H-bonds with protein main chain carbonyl groups at the base of the cleft contributes to the binding. Additional side chain binding occurs on a shallow depression that is hydrophobic at one end and can accommodate charge interactions at the other. These findings suggest that the Gcn5p bromodomain may discriminate between different acetylated lysine residues depending on the context in which they are displayed.
532 citations
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U. Bhawandeep1, Vardan Khachatryan, Albert M. Sirunyan, Armen Tumasyan +2289 more•Institutions (147)
TL;DR: In this paper, the trigger system consists of two levels designed to select events of potential physics interest from a GHz (MHz) interaction rate of proton-proton (heavy ion) collisions.
Abstract: This paper describes the CMS trigger system and its performance during Run 1 of the LHC. The trigger system consists of two levels designed to select events of potential physics interest from a GHz (MHz) interaction rate of proton-proton (heavy ion) collisions. The first level of the trigger is implemented in hardware, and selects events containing detector signals consistent with an electron, photon, muon, tau lepton, jet, or missing transverse energy. A programmable menu of up to 128 object-based algorithms is used to select events for subsequent processing. The trigger thresholds are adjusted to the LHC instantaneous luminosity during data taking in order to restrict the output rate to 100 kHz, the upper limit imposed by the CMS readout electronics. The second level, implemented in software, further refines the purity of the output stream, selecting an average rate of 400 Hz for offline event storage. The objectives, strategy and performance of the trigger system during the LHC Run 1 are described.
532 citations
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TL;DR: It is shown that a wide variety of different mutations in the parkin gene are a common cause of autosomal recessive parkinsonism in Europe and that different types of point mutations seem to be more frequently responsible for the disease phenotype than are deletions.
Abstract: Autosomal recessive juvenile parkinsonism (AR-JP, PARK2; OMIM 602544), one of the monogenic forms of Parkinson's disease (PD), was initially described in Japan. It is characterized by early onset (before age 40), marked response to levodopa treatment and levodopa-induced dyskinesias, The gene responsible for AR-JP was recently identified and designated parkin, We have analysed the 12 coding exons of the parkin gene in 35 mostly European families with early onset autosomal recessive parkinsonism. In one family, a homozygous deletion of exon 4 could be demonstrated. By direct sequencing of the exons in the index patients of the remaining 34 families, eight previously undescribed point. mutations (homozygous or heterozygous) were detected in eight families that included 20 patients, The mutations segregated with the disease in the families and were not detected on 110-166 control chromosomes. Four mutations caused truncation of the parkin protein. Three were frameshifts (202-203delAG, 255delA and 321-322insGT) and one a nonsense mutation (Trp453Stop). The other four were missense mutations (Lys161Asn, Arg256Cys, Arg275Trp and Thr415Asn) that probably affect amino acids that are important for the function of the parkin protein, since they result in the same phenotype as truncating mutations or homozygous exon deletions. Mean age at onset was 38 +/- 12 years, but onset up to age 58 was observed. Mutations in the parkin gene are therefore not invariably associated with early onset parkinsonism. In many patients, the phenotype is indistinguishable from that of idiopathic PD. This study has shown that a wide variety of different mutations in the parkin gene are a common cause of autosomal recessive parkinsonism in Europe and that different types of point mutations seem to be more frequently responsible for the disease phenotype than are deletions.
532 citations
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TL;DR: The risk of major bleeding during induction chemotherapy in adolescents and adults with acute myeloid leukemia (except acute promyelocytic leukemia, which the authors did not study) was similar with platelet-transfusion thresholds of 20,000 per cubic millimeter and 10,000 each.
Abstract: Background Prophylactic platelet transfusions are usually administered to patients receiving myelotoxic chemotherapy when their platelet count falls below 20,000 per cubic millimeter. Some observations suggest that lower platelet counts can be appropriate in patients in stable condition, but the safety of lower thresholds is uncertain. Methods We evaluated 255 adolescents and adults (age, 16 to 70 years) with newly diagnosed acute myeloid leukemia (but not acute promyelocytic leukemia), who were treated in 21 centers. One hundred thirty-five patients were randomly assigned to receive a transfusion when their platelet count fell below 10,000 per cubic millimeter (or 10,000 to 20,000 per cubic millimeter in those with a temperature above 38°C, with active bleeding, or a need for invasive procedures), and 120 patients were assigned to receive a transfusion when their platelet count was less than 20,000 per cubic millimeter. Results Patients in the group with a threshold of 10,000 platelets per cubic millimet...
532 citations
Authors
Showing all 62745 results
Name | H-index | Papers | Citations |
---|---|---|---|
Charles A. Dinarello | 190 | 1058 | 139668 |
Gregory Y.H. Lip | 169 | 3159 | 171742 |
Peter A. R. Ade | 162 | 1387 | 138051 |
H. Eugene Stanley | 154 | 1190 | 122321 |
Suvadeep Bose | 154 | 960 | 129071 |
P. de Bernardis | 152 | 680 | 117804 |
Bart Staels | 152 | 824 | 86638 |
Alessandro Melchiorri | 151 | 674 | 116384 |
Andrew H. Jaffe | 149 | 518 | 110033 |
F. Piacentini | 149 | 531 | 108493 |
Subir Sarkar | 149 | 1542 | 144614 |
Albert Bandura | 148 | 255 | 276143 |
Carlo Rovelli | 146 | 1502 | 103550 |
Robert C. Gallo | 145 | 825 | 68212 |
R. Kowalewski | 143 | 1815 | 135517 |