Lifetime of the Bose gas with resonant interactions.

We study the lifetime of a Bose gas at and around unitarity using a Feshbach resonance in lithium 7. At unitarity, we measure the temperature dependence of the three-body decay coefficient L(3). Our data follow a L(3)=λ(3)/T(2) law with λ(3)=2.5(3)(stat)(6)(syst)×10(-20) (µK)(2) cm(6) s(-1) and are in good agreement with our analytical result based on zero-range theory. Varying the scattering length a at fixed temperature, we investigate the crossover between the finite-temperature unitary region and the previously studied regime where |a| is smaller than the thermal wavelength. We find that L(3) is continuous across the resonance, and over the whole a<0 range our data quantitatively agree with our calculation.

2.1-watts intracavity-frequency-doubled all-solid-state light source at 671 nm for laser cooling of lithium.

We present an all-solid-state laser source emitting up to 2.1 W of single-frequency light at 671 nm developed for laser cooling of lithium atoms. It is based on a diode-pumped, neodymium-doped orthovanadate (Nd:YVO(4)) ring laser operating at 1342 nm. Optimization of the thermal management in the gain medium results in a maximum multi-frequency output power of 2.5 W at the fundamental wavelength. We develop a simple theory for the efficient implementation of intracavity second harmonic generation, and its application to our system allows us to obtain nonlinear conversion efficiencies of up to 88%. Single-mode operation and tuning is established by adding an etalon to the resonator. The second-harmonic wavelength can be tuned over 0.5 nm, and mode-hop-free scanning over more than 6 GHz is demonstrated, corresponding to around ten times the laser cavity free spectral range. The output frequency can be locked with respect to the lithium D-line transitions for atomic physics applications. Furthermore, we observe parametric Kerr-lens mode-locking when detuning the phase-matching temperature sufficiently far from the optimum value.

Interleukin 4 co-stimulates the PDGF-BB- and bFGF-mediated proliferation of mesangial cells and myofibroblasts.

BACKGROUND: Although many mediators involved in the pathogenesis of fibrosis are known, its precise mechanism is still unknown. In vitro experiments may contribute to the recognition of cellular changes which also take place during fibrosis. METHODS: Renal tubular epithelial cells (EPC), mesangial cells (MC) and glomerular endothelial cells (GEDC) as well as endothelial cells (EDC) and myofibroblasts (MF) from cattle were isolated to measure the proliferation and protein synthesis in the presence of individual and combined cytokines/growth factors in cell cultures. RESULTS: Cytokines stimulating or permitting the proliferation of myofibroblast-like cells (MFLC) (MC and MF), caused damage of endothelial cells (EDC, GEDC), whereas EPC were stable. The proliferation of MFLC was strongly stimulated by PDGF-BB and bFGF and elevated more than twofold in the presence of interleukin 4 (IL-4), but IL-4 alone had no effect. Furthermore, the proliferation of transdifferentiated endothelial cells (TEC), obtained by incubation of EDC with TNFalpha and bFGF, was stimulated with both PDGF-BB/IL-4 and bFGF/IL-4 in the same way and proved to be stable with respect to TNFalpha. CONCLUSION: Interleukin 4 co-stimulates the PDGF-BB- and bFGF-mediated proliferation of MC, MF, and TEC. TNFalpha does not inhibit the proliferation of extracellular matrix-synthesizing cells, but has an inhibitory or even toxic effect on EDC and GEDC. It may be concluded that cytokines released in inflamed renal tissue influence tubulointerstitial cells in different ways, resulting in progressive tissue damage and fibrosis in which the EDC would be the most sensitive cells. Thus, we speculate that microvascular injury in these areas leads to ischemia and malnutrition of tubular EPC and may be responsible for ongoing tubular damage and resulting renal interstitial fibrosis.

Expression of beta2-microglobulin and c-fos mRNA: is there an influence of high- or low-flux dialyzer membranes?

BACKGROUND: Dialysis-related amyloidosis is an important complication of long-term hemodialysis (HD) therapy with several pathogenetic factors. One of them is the influence of the dialyzer membrane type on the synthesis of beta2-microglobulin (beta2m). In vitro results are controversial. Thus, the hypothesis of whether in vivo beta2m generation is induced by the HD procedure and whether this induction depends on the type of the used dialyzer membrane should be tested. The aim of the present study was to investigate the influence of "biocompatible" high-flux versus "bioincompatible" low-flux HD on in vivo beta2m generation as well as the induction of the early activation gene c-fos in peripheral blood cells. METHODS: Six nondiabetic HD patients [mean age 46 (21 to 69) years; Kt/V> 1.2] were included in a randomized crossover study using either a low-flux (cellulosic/cuprophan) or a high-flux (polyamide) dialyzer membrane. At the end of a four-week run-in period for each membrane, whole blood samples were taken before, immediately at, and four hours after the end of the dialysis session. MRNA was extracted, and after transcription to cDNA, quantitative polymerase chain reaction was performed for the beta2m gene, the early response gene c-fos, and the GAP-DH housekeeping gene. RESULTS: Based on the applied method for detection of specific mRNA, the results were given as ratio of beta2m or c-fos cDNA per GAP-DH cDNA. General cell activation during HD was indicated by increasing mRNA expression of c-fos related to the time course of the dialysis session, whereas beta2m did not change significantly. However, no difference was found when comparing the low-flux and the high-flux dialyzer membranes. Despite the evidence for activation of peripheral blood cells, as indicated by increasing c-fos message, no sign of beta2m mRNA induction during HD procedure with different dialyzer membranes was seen. CONCLUSIONS: Our results suggest that there is post-transcriptional regulation of beta2m generation and/or release as well as the influence of the dialyzer membrane type on post-translational processes, that is, advance glycation end products (AGE) or conformational modification of the beta2m protein. Furthermore, our data demonstrate that gene expression patterns during dialysis and/or uremia are not homogenous and need to be investigated further, especially with respect to the proinflammatory role of early leukocyte activation signals.

Time course of cytokine mRNA expression in kidneys of rats with unilateral ureteral obstruction.

The development of renal interstitial fibrosis (RIF) is related to the expression and excretion of cytokines and growth factors. Thus, we investigated the time course of mRNA expression of cytokines known as causative factors in a model of RIF in rats before and on day 10 after unilateral ureteral obstruction (UUO), when first signs of fibrosis were visible, as well as during progressive RIF. UUO causes a fivefold increase in mRNA expression of monocyte chemoattractant protein 1 15 days after surgery as compared with contralateral kidneys. The level remains elevated about three-fold up to day 25. The mRNA of the fibrogenic cytokine transforming growth factor beta 1 (TGF-beta1) is increased two- to threefold during the time course, whereas the mRNAs of platelet-derived growth factor B chain (PDGF-B) and its receptor beta (PDGF-Rbeta) increase after UUO, reaching their maxima on days 10-15. PDGF-B mRNA increase up to day 15, marking the onset of fibrosis, and decreases thereafter, whereas the expression of the PDGF-Rbeta mRNA remains elevated more than threefold over the entire study period. Incubation of cultured renal fibroblasts with TGF-beta1 and/or PDGF-B suggests that their specific action on cell growth and proliferation is maintained even when they are used in combination. The sustained elevation of TGF-beta1 and PDGF-B/PDGF-Rbeta mRNA levels confirms the assumption of a particular involvement of these cytokines in the pathogenesis of RIF. The mRNA expression of the gap junctional protein connexin 43 in ureteral ligated kidneys is increased sixfold already 5 days after UUO. In this way, the increased connexin 43 mRNA levels indicate a possible function in the remodeling of the kidney tissue after tubular damage and fibrosis.