The r-Process in Supersonic Neutrino-Driven Winds: The Roll of Wind Termination Shock

Recent hydrodynamic studies of core-collapse supernovae imply that the neutrino-heated ejecta from a nascent neutron star develops to supersonic outflows. These supersonic winds are influenced by the reverse shock from the preceding supernova ejecta, forming the wind termination shock. We investigate the effects of the termination shock in neutrino-driven winds and its roll on the r-process. Supersonic outflows are calculated with a semi-analytic neutrino-driven wind model. Subsequent termination-shocked, subsonic outflows are obtained by applying the Rankine-Hugoniot relations. We find a couple of effects that can be relevant for the r-process. First is the sudden slowdown of the temperature decrease by the wind termination. Second is the entropy jump by termination-shock heating, up to several 100NAk. Nucleosynthesis calculations in the obtained winds are performed to examine these effects on the r-process. We find that 1) the slowdown of the temperature decrease plays a decisive roll to determine the r-process abundance curves. This is due to the strong dependences of the nucleosynthetic path on the temperature during the r-process freezeout phase. Our results suggest that only the termination-shocked winds with relatively small shock radii (~500km) are relevant for the bulk of the solar r-process abundances (A~100-180). The heaviest part in the solar r-process curve (A~180-200), however, can be reproduced both in shocked and unshocked winds. These results may help to constrain the mass range of supernova progenitors relevant for the r-process. We find, on the other hand, 2) negligible roles of the entropy jump on the r-process. This is a consequence that the sizable entropy increase takes place only at a large shock radius (~10,000km) where the r-process has already ceased.Comment: 11 pages, 7 figures, submitted to ApJ, revised following referee's comments,Accepted for publication in Ap

The phenotype of infiltrating macrophages influences arteriosclerotic plaque vulnerability in the carotid artery

Background: Proinflammatory (M1) macrophages and anti-inflammatory (M2) macrophages have been identified in atherosclerotic plaques. While these macrophages have been speculated to be related to plaque vulnerability, there are limited studies investigating this relationship. Therefore, we examined the association between macrophage phenotype (M1 versus M2) and plaque vulnerability and clinical events. Methods: Patients undergoing carotid endarterectomy received an ultrasound of the carotid artery before surgery. Plaques were processed for analysis by immunohistochemistry, Western blotting, and real-time polymerase chain reaction studies. Medical history and clinical data were obtained from medical records. Results: Patients were divided into 2 groups: those suffering from acute ischemic attack (symptomatic, n = 31) and those that did not present with symptoms (asymptomatic, n = 34). Ultrasound analysis revealed that plaque vulnerability was greater in the symptomatic group (P= .033; Chi-square test). Immunohistochemistry revealed that plaques from the symptomatic group had a greater concentration of M1 macrophages (CD68-, CD11c-positive) while plaques from the asymptomatic group had more M2 macrophages (CD163-positive). This observation was confirmed by Western blotting. Characterization by real-time polymerase chain reaction studies revealed that plaques from the symptomatic group had increased expression of the M1 markers CD68 and CD11c, as well as monocyte chemoattractive protein-1, interleukin-6, and matrix metalloproteinase-9. In addition, more M1 macrophages expressed in unstable plaques were defined by ultrasound analysis, while more M2 macrophages were expressed in stable plaques. Conclusions: Our data show that M1 macrophage content of atherosclerotic plaques is associated with clinical incidence of ischemic stroke and increased inflammation or fibrinolysis. We also show the benefits of using ultrasound to evaluate vulnerability in the plaques

The Relationship Between Serum Homocysteine Levels and Vertebral Fractures

Serum homocysteine and pentosidine levels have attracted attention as associated markers of bone quality, which affects bone strength. We examined the relationship of serum homocysteine levels with existing vertebral fractures and renal function. We evaluated 279 of 960 osteoporosis outpatients (12 men, 267 women; mean age, 72 years) whose serum homocysteine levels had been measured in our department. Using a glomerular filtration rate (GFR)-based chronic renal failure severity classification system, we divided patients into three groups: G1/G2, G3a/G3b/G4, and G5. We further divided the patients in the G1/G2 and G3a/G3b/G4 groups into two subgroups on the basis of the presence of fractures. Vertebral fractures were significantly more frequent when serum homocysteine levels were high in the G1/G2 group (P = 0.002). Serum homocysteine levels were lower in patients in the G1/G2 group than the G3a/G3b/G4 group despite the presence or absence of vertebral fractures (P < 0.001). Significant differences in serum homocysteine levels were also seen between patients with and without vertebral fractures in both the G1/G2 and G3a/G3b/G4 groups (P = 0.02). There were also significant correlations between GFR and serum homocysteine levels in both the G1/G2 and G3a/G3b/G4 groups (correlation coefficients, −0.43 and −0.65, respectively; P < 0.001). A negative correlation was observed between serum homocysteine levels and GFR in the G1/G2 and G3a/G3b/G4 groups, and we were able to reaffirm that serum homocysteine levels are affected by renal function. In the G1/G2 group, the prevalence of vertebral fractures was significantly higher in patients with high serum homocysteine levels. Even if renal function was poor, serum homocysteine levels were significantly higher in patients with vertebral fractures. Thus, serum homocysteine is a valid marker of bone quality

Teriparatide Treatment for An Atypical Fracture of the Femoral Shaft: A Case Report

An 82-year-old woman had been taking alendronate for 5 years and 5 months, which had been prescribed for osteoporosis at a local clinic. Severe left thigh pain began without any trauma. X-ray, computed tomography and magnetic resonance imaging findings showed atypical femoral fracture（AFF）. Treatment with teriparatide and weight-bearing therapy was selected. Bone union was achieved without surgery. Teriparatide has been reported to promote AFF healing. At four years and 9 months from the beginning of treatment, our patient has no left femoral pain and no impairment to activities of daily living. Careful follow-up will be necessary as long-term outcomes of conservative AFF treatment have not been reported to date

Nel positively regulates the genesis of retinal ganglion cells by promoting their differentiation and survival during development

Peer reviewedPublisher PD

Crystal structures of Lymnaea stagnalis AChBP in complex with neonicotinoid insecticides imidacloprid and clothianidin

Neonicotinoid insecticides, which act on nicotinic acetylcholine receptors (nAChRs) in a variety of ways, have extremely low mammalian toxicity, yet the molecular basis of such actions is poorly understood. To elucidate the molecular basis for nAChR–neonicotinoid interactions, a surrogate protein, acetylcholine binding protein from Lymnaea stagnalis (Ls-AChBP) was crystallized in complex with neonicotinoid insecticides imidacloprid (IMI) or clothianidin (CTD). The crystal structures suggested that the guanidine moiety of IMI and CTD stacks with Tyr185, while the nitro group of IMI but not of CTD makes a hydrogen bond with Gln55. IMI showed higher binding affinity for Ls-AChBP than that of CTD, consistent with weaker CH–π interactions in the Ls-AChBP–CTD complex than in the Ls-AChBP–IMI complex and the lack of the nitro group-Gln55 hydrogen bond in CTD. Yet, the NH at position 1 of CTD makes a hydrogen bond with the backbone carbonyl of Trp143, offering an explanation for the diverse actions of neonicotinoids on nAChRs

Energy renormalization of exciton complexes in GaAs quantum dots

Using GaAs/AlGaAs self-assembled quantum dots we study the few-particle dynamics of fully confined systems, which is associated with purely Coulomb interaction and is not affected by the internal strain field. Systematic evolution in the binding energies of positive and negative trions, as well as biexcitons, with dot size is interpreted in terms of a balance between the Hartree mean-field corrections on single-particle states and the interparticle correlations which lead to a nonseparable dynamics. The experimental behaviors are well reproduced by exact many-body calculations within the framework of the quantum Monte Carlo approach