No abstract

High-resolution infrared and microwave spectra of He(N)-carbonyl sulfide (He(N)-OCS) clusters with N ranging from 2 to 8 have been detected and unambiguously assigned. The spectra show the formation of a solvation layer beginning with an equatorial "donut" of five helium atoms around the OCS molecule. The cluster moment of inertia increases as a function of N and overshoots the liquid droplet limit for N > 5, implying that even atoms in the first solvation shell are decoupled from the OCS rotation in helium nanodroplets. To the extent that this is due to superfluidity, the results directly explore the microscopic evolution of a phenomenon that is formally macroscopic in nature.

High resolution microwave and infrared spectra of He(N)-N2O clusters were studied in the range N=3 to 12. The apparent cluster moments of inertia increase from N=3 to 6, but then decrease, showing oscillatory behavior for N=7 to 12. This provides direct experimental evidence for the decoupling of helium atoms from the rotation of the dopant molecule in this size regime, signaling the transition from a molecular complex to a quantum solvated system and directly exploring the microscopic evolution of "molecular superfluidity."

We present high resolution spectra of He(N)-OCS clusters with N up to 39 in the microwave and 72 in the infrared regions, observed with apparatus-limited line widths of about 15 kHz and 0.001 cm(-1), respectively. The derived rotational constant, B (proportional to the inverse moment of inertia), passes through a minimum at N=9, then rises due to onset of superfluid effects, and exhibits broad oscillations with maxima at N=24, 47 and minima at 36, 62. We interpret these unexpected oscillations as a manifestation of the aufbau of a nonclassical helium solvation shell structure. These results bridge an important part of the gap between individual molecules and bulk matter with atom by atom resolution, providing new insight into microscopic superfluidity and a critical challenge for theory.

Background-Chemokines play an important role in atherogenesis and in ischemic injury and repair; however, prospective data on individual chemokines in unstable angina pectoris (UAP) are scarce. Therefore, we assessed chemokine patterns in a prospective cohort of patients with UAP. Methods and Results-Plasma samples of 54 patients with Braunwald class IIIB UAP were examined at baseline for 11 chemokines and 5 inflammatory mediators via multiplex analysis. Levels of CC chemokine ligand (CCL)-5 (also known as RANTES [regulated on activation, normally T-cell expressed, and secreted]; 32.7 versus 23.1 ng/mL, Pϭ0.018) and CCL18 (also known as PARC [pulmonary and activation-regulated chemokine]; 104.4 versus 53.7 ng/mL, Pϭ0.011) were significantly elevated in patients with refractory ischemic symptoms versus stabilized patients. Temporal monitoring by ELISA of CCL5, CCL18, and soluble CD40 ligand (sCD40) levels revealed a drop in CCL5 and sCD40L levels in all UAP patients from day 2 onward (CCL5 12.1 ng/mL, PϽ0.001; sCD40L 1.35 ng/mL, PϽ0.05), whereas elevated CCL18 levels were sustained for at least 2 days, then were decreased at 180 days after inclusion (34.5 ng/mL, PϽ0.001). Peripheral blood mononuclear cells showed increased protein expression of chemokine receptors CCR3 and CCR5 in CD3 ϩ and CD14 ϩ cells at baseline compared with 180 days after inclusion, whereas mRNA levels were downregulated, which was attributable in part to a postischemic release of human neutrophil peptide-3-positive neutrophils and in part to negative feedback. Finally, elevated CCL5 and CCL18 levels predicted future cardiovascular adverse events, whereas C-reactive protein and sCD40L levels did not. Conclusions-We are the first to report that CCL18 and CCL5 are transiently raised during episodes of UAP, and peak levels of both chemokines are indicative of refractory symptoms. Because levels of both chemokines, as well as of cognate receptor expression by circulating peripheral blood mononuclear cells, are increased during cardiac ischemia, this may point to an involvement of CCL5/CCL18 in the pathophysiology of UAP and/or post-UAP responses.