Discovery of the shape coexisting 0+ state in 32 Mg by a two neutron transfer reaction.

The "island of inversion" nucleus 32 Mg has been studied by a (t, p) two neutron transfer reaction in inverse kinematics at REX-ISOLDE. The shape coexistent excited 0+ state in 32 Mg has been identified by the characteristic angular distribution of the protons of the Δ L=0 transfer. The excitation energy of 1058 keV is much lower than predicted by any theoretical model. The low γ-ray intensity observed for the decay of this 0+ state indicates a lifetime of more than 10 ns. Deduced spectroscopic amplitudes are compared with occupation numbers from shell-model calculations.

Interplay between single-particle and collective effects in the odd-A Cu isotopes beyond N=40.

Collective properties of the low-lying levels in the odd-A 67-73Cu were investigated by Coulomb excitation with radioactive beams. The beams were produced at ISOLDE and postaccelerated by REX-ISOLDE up to 2.99 MeV/u. In 67,69Cu, low-lying 1/2(-), 5/2(-), and 7/2(-) states were populated. In 71,73Cu, besides the known transitions deexciting the single-particle-like 5/2(-) and core-coupled 7/2(-) levels, gamma rays of 454 and 135 keV, respectively, were observed for the first time. Based on a reanalysis of beta-decay work and comparison with the systematics, a spin 1/2(-) is suggested for these excited states. Three B(E2) values were determined in each of the four isotopes. The results indicate a significant change in the structure of the odd-A Cu isotopes beyond N=40 where single-particle-like and collective levels are suggested to coexist at very low excitation energies.

Coulomb excitation of 68,70Cu: first use of postaccelerated isomeric beams.

We report on the first low-energy Coulomb excitation measurements with radioactive Ipi=6- beams of odd-odd nuclei 68,70Cu. The beams were produced at ISOLDE, CERN and were post-accelerated by REX-ISOLDE to 2.83 MeV/nucleon. Gamma rays were detected with the MINIBALL spectrometer. The 6- beam was used to study the multiplet of states (3-, 4-, 5-, 6-) arising from the pi2p3/2 nu 1g9/2 configuration. The 4- state of the multiplet was populated via Coulomb excitation and the B(E2;6--->4-) value was determined in both nuclei. The results obtained illustrate the fragile stability of the Z=28 shell and N=40 subshell closures. A comparison with large-scale shell-model calculations using the 56Ni core shows the importance of the proton excitations across the Z=28 shell gap to the understanding of the nuclear structure in the neutron-rich nuclei with N approximately 40.

Compound and rotational damping in warm deformed rare-earth nuclei.

The gamma decay in the quasicontinuum from selected configurations of the rotational nucleus 163Er has been measured with the EUROBALL array. A new analysis technique has allowed for the first time to directly measure the compound and rotational damping widths Gamma (micro) and Gamma (rot). Values of Gamma (micro) approximately 20 keV and Gamma (rot) approximately 200 keV are obtained in the spin region I approximately 30-40 variant Planck's over 2pi, in good agreement with microscopic cranked shell model calculations. A dependence of Gamma (micro) and Gamma (rot) on the K-quantum number of the nuclear states is also presented.

Increased expression of nerve growth factor (NGF) and high affinity NGF receptor (p140 TrkA) in human osteoarthritic chondrocytes.

OBJECTIVE: We aimed to investigate the expression of nerve growth factor (NGF) and high affinity NGF receptor (p140 TrkA) on chondrocytes from human healthy and osteoarthritic cartilage. METHODS: We recruited 12 patients with osteoarthritis (OA) undergoing surgical knee replacement. Articular cartilage was split into two zones showing macroscopically and histologically the lowest (MIN) and highest (MAX) degree of osteoarthritic damage. Additional specimens of cartilage were obtained from three healthy donors. Chondrocytes were isolated by enzymatic digestion and freshly processed for NGF protein, Trk A detection and mRNA extraction. NGF-beta mRNA was determined by a reverse transcriptase-polymerase chain reaction (RT-PCR). NGF-beta and TrkA expression was evaluated by immunofluorescence and flow cytometry analysis. RESULTS: NGF-beta-specific mRNA was detected in normal and osteoarthritic chondrocytes. NGF-beta protein levels were low in normal chondrocytes, increased in MIN osteoarthritic cartilage and further enhanced in MAX osteoarthritic cartilage. Likewise, TrkA was scarcely expressed on normal chondrocytes and progressively increased on osteoarthritic chondrocytes based on the extent of anatomic damage. CONCLUSIONS: This is the first study showing that human chondrocytes synthesize NFG-beta and express on their surface the high affinity NGFR (p140 TrkA). Of note, NGF-beta and TrkA were upregulated in osteoarthritic chondrocytes suggesting a role of NGF in the pathophysiology of OA. We can speculate that NGF, like other growth factors, stimulates chondrocyte metabolism in the osteoarthritic process.

Interleukin-10 and interleukin-10 receptor in human osteoarthritic and healthy chondrocytes.

OBJECTIVE: To evaluate the expression of interleukin-10 (IL-10) and interleukin-10 receptor (IL-10R) on chondrocytes from healthy, osteoarthritic, and foetal cartilage from human subjects. METHODS: Articular cartilage was obtained from 12 patients with osteoarthritis (OA) undergoing surgical knee replacement. Chondrocytes were isolated from the two zones of cartilage showing macroscopically and histologically the lowest (MIN) and highest (MAX) extent of osteoarthritic damage. Additional specimens of cartilage were obtained from 3 healthy donors and 3 human foetuses. IL-10 mRNA expression was determined by a reverse transcriptase-polymerase chain reaction (RT-PCR). For detection of intracellular IL-10 protein, chondrocytes were permeabilized and then incubated with R-phycoerythrin (PE) conjugated rat anti-human IL-10 mAb. Cell surface IL-10R was detected by incubation with biotinylated recombinant human IL-10; after washing, bound IL-10 was revealed by fluorescein (FITC) conjugated streptavidin. Positive chondrocytes were analysed by flowcytometry. RESULTS: IL-10 mRNA expression was higher in osteoarthritic than in normal chondrocytes. IL-10 protein intracellular levels were significantly higher in MAX than in MIN osteoarthritic cartilage or in healthy cartilage. Cell surface IL-10R was expressed on osteoarthritic chondrocytes with no difference in the degree of cartilage damage. The highest levels of IL-10 protein and IL-10R were found in foetal cartilage. CONCLUSION: Human chondrocytes synthesise IL-10 and express on their surface IL-10R. Since IL-10 inhibits IL-1 and TNF-alpha expression, its upregulation in osteoarthritic chondrocytes may counteract the detrimental effects of these catabolic cytokines. However, the functions of IL-10 in cartilage may go beyond those activities established in the immunological setting. The high levels of IL-10 and IL-10R in foetal cartilage, an active growing tissue, suggest that IL-10 may play a role in controlling chondrocyte metabolism under physiological conditions.

Chondrocyte phenotyping in human osteoarthritis.

Cell-ECM (extracellular matrix) interactions are believed to play a key role in maintaining the normal structure of tissues such as cartilage. Cell surface adhesion molecules have been reported to mediate chondrocyte binding to ECM proteins in human normal cartilage but the behaviour of these molecules in human osteoarthritic cartilage is unknown. We studied receptor matrix proteins on freshly isolated chondrocytes obtained from 10 patients with osteoarthritis (OA). Chondrocytes were isolated by enzymatic digestion from three zones of the articular cartilage with a different degree of macroscopic and microscopic damage and chondrocyte phenotype was defined by flow cytometry. Chondrocytes strongly expressed beta1, integrin but not beta3 integrin. LFA-1 (CD18/CD11a) and ICAM-1 (CD54) antigens were almost undetectable. Interestingly, beta1 expression was significantly higher in the minimally damaged zone than in the zones with medium and maximum damage. These data show that beta1-integrin-mediated chondrocyte-ECM interactions decrease in osteoarthritic cartilage suggesting that perturbations of chondrocyte-matrix signalling occurs during OA.

Integrin expression on chondrocytes: correlations with the degree of cartilage damage in human osteoarthritis.

OBJECTIVE: To verify the distribution of different types of beta 1 integrin on the plasma membrane of chondrocytes and to correlate the pattern of integrin expression to the severity of osteoarthritis (OA). METHODS: The articular cartilage of ten OA patients who had undergone surgical knee replacement for "genu varum" were studied. The cartilage was separated into three zones that macroscopically and microscopically showed a decreasing degree of anatomic lesions. After enzymatic digestion, the isolated chondrocytes were immediately challenged with monoclonal antibodies against the beta 1, alpha 1-6 and alpha v chains. The phenotypic study was paralleled by a cell cycle analysis performed by flow cytometry on chondrocytes stained with propidium iodide. RESULTS: Chondrocytes isolated from the articular cartilage of osteoarthritic patients expressed, in different percentages, all the alpha chains (alpha 1-6 and alpha v) of the beta 1 integrins. The alpha chain most frequently expressed was alpha 1, followed by alpha 3, alpha 5, alpha 2 and alpha v, with lesser amounts of alpha 4 and alpha 6. The beta 1 chain was expressed (on average) on the 40% of the chondrocytes regardless of the zone they were isolated from. Differential phenotypic analysis of the three zones showed that beta 1 integrins correlate inversely with the severity of the anatomic lesions and the cycle phase of the chondrocytes (the G0/G1 phase prevailed in the anatomically normal cartilage of the least damaged zone, and the S-phase in the most damaged zone). CONCLUSIONS: This study provides evidence of the existence of beta 1 integrins on the surface of chondrocytes from human OA cartilage, all of the alpha chains being represented, although in different percentages. Moreover, an inverse correlation was demonstrated between the severity of the anatomical changes found in the zones and the phenotypic/metabolic changes of the cells. These results, together with the well known inside-out signaling function of the adhesion molecules, highlight the key role of matrix interactions in the pathogenesis of the anatomic changes in OA.