Observation of the Exotic 0_{2}

We report here the first observation of the 0_{2}^{+} state of ^{8}He, which has been predicted to feature the condensatelike α+^{2}n+^{2}n cluster structure. We show that this state is characterized by a spin parity of 0^{+}, a large isoscalar monopole transition strength, and the emission of a strongly correlated neutron pair, in line with theoretical predictions. Our finding is further supported by the state-of-the-art microscopic α+4n model calculations. The present results may lead to new insights into clustering in neutron-rich nuclear systems and the pair correlation and condensation in quantum many-body systems under strong interactions.

Observation of enhanced monopole strength and clustering in (12)Be.

In a recent breakup-reaction experiment using a Be12 beam at 29 MeV/nucleon, the 0+ band head of the expected He4+He8 molecular rotation was clearly identified at about 10.3 MeV, from which a large monopole matrix element of 7.0±1.0 fm2 and a large cluster-decay width were determined for the first time. These findings support the picture of strong clustering in Be12, which has been a subject of intense investigations over the past decade. The results were obtained thanks to a specially arranged detection system around zero degrees, which is essential in determining the newly emphasized monopole strengths to signal the cluster formation in a nucleus.

The effects of SOCS-1 on liver endotoxin tolerance development induced by a low dose of lipopolysaccharide are related to dampen NF-kappaB-mediated pathway.

BACKGROUND: Endotoxin tolerance is an important mechanism to maintain the homeostasis of liver. It was reported that suppressors of cytokine signalling-1 was a negative regulator of lipopolysaccharide-induced macrophages activation, however, the mechanism underlying endotoxin tolerance and suppressors of cytokine signalling-1 has not been fully elucidated. AIM: Our aim here is to clarify whether suppressors of cytokine signalling-1 was involved in the mechanisms of endotoxin tolerance in liver through dampening nuclear factor-kappaB-mediated pathway. METHODS: Endotoxin tolerance models of C57BL/6J mice and isolated Kupffer cells were established by pretreating them with a low dose of lipopolysaccharide to observe the changes of suppressors of cytokine signalling-1 expression during endotoxin tolerance inducement. Moreover, a vector-based short hairpin RNA expression system was used to specifically inhibit suppressors of cytokine signalling-1 expression in RAW264.7 macrophage cells to further explore the role of suppressors of cytokine signalling-1 in endotoxin tolerance inducement. The expression of suppressors of cytokine signalling-1 was analysed by immunohistochemistry, reverse transcription-polymerase chain reaction and Western blotting, respectively. The responses to lipopolysaccharide were assessed by the activation of nuclear factor-kappaB and the production of tumour necrosis factor-alpha, which were analysed by ELISA. RESULTS: The histopathologic changes in the liver of the non-endotoxin tolerance group were more serious than those of the endotoxin tolerance group. The phagocytic activity of Kupffer cells were depressed and suppressors of cytokine signalling-1 expression in the endotoxin tolerance group obviously increased. Endotoxin tolerance also led to a hyporesponse of Kupffer cells to lipopolysaccharide with less activation of nuclear factor-kappaB, less production of tumour necrosis factor-alpha and more expression of suppressors of cytokine signalling-1 than those of non-endotoxin tolerance group. Moreover, the inhibitive effect was partly refracted in pSOCS-1-short hairpin RNA transfected RAW264.7 cells. CONCLUSIONS: Endotoxin tolerance induced by lipopolysaccharide pretreatment was accompanied with upregulation of suppressors of cytokine signalling-1 and the silence of suppressors of cytokine signalling-1 by RNA interference obviously attenuated this inhibitive effect, indicating that the absence of suppressors of cytokine signalling-1 caused abnormal enhancement of inflammatory cytokine production and suppressors of cytokine signalling-1 was involved in endotoxin tolerance inducement through dampening nuclear factor-kappaB-mediated pathway. Therefore, suppressors of cytokine signalling-1 may be a new target for the clinical treatment of sepsis.

[Study on adriamycin-porous tricalcium phosphate ceramic drug delivery system and its drug release test in vivo].

OBJECTIVE: To manufacture adriamycin-porous tricalcium phosphate (A-PTCP) ceramic drug delivery system (DDS) as a possible method for bone defect treatment after bone tumor operation. METHODS: A-PTCP DDS was made from putting adriamycin into PTCP. Thirty rabbits were divided randomly into group A(24 rabbits) and group B(6 rabbits). A-PTCP was implanted in the greater trochanter of the right femur in group A. Adriamycin were injected into veins in group B. Muscle around A-PTCP and plasma were taken out at different period. Adriamycin concentrations in muscle and plasma were measured by high performance liquid chromatography (HPLC). RESULTS: A-PTCP could gradually release adriamycin over 10 weeks. Adriamycin concentrations in the muscle were higher than that in plasma. CONCLUSION: A-PTCP may be a new method for repairing bone defects after bone tumor operation.

[The effect of cefazolin loaded bone matrix gelatin on repairing large segmental bone defects and preventing infection after operation].

OBJECTIVE: To explore the possibility of repair long segmental bone defects and preventing infection with cefazolin loaded bone matrix gelatin (C-BMG). METHODS: C-BMG was made from putting cefazolin into BMG by vacuum adsorption and freeze-drying techniques. The sustaining period of effective drug concentration in vitro and in vivo was detected by inhabition bacteria, and the drug concentration in local tissues (bone and muscle) and plasma after implantation of C-BMG was examined by high performance liquid chromatography(HPLC). RESULTS: The effective inhibition time to staphylococcus aureus of C-BMG was 22 days in vitro, while 14 days in vivo. The drug concentration in local tissues(bone and muscle) were higher than that of plasma, and the drug concentration in local tissues was higher in early stage, later it kept stable low drug release. It suggested that C-BMG had excellent ability to repair segmental long bone defects. CONCLUSION: C-BMG can gradually release cefazolin with effective drug concentration and has excellent ability to repair segmental long bone defects. It may be a novel method to repair segmental long bone defects and prevent infection after the operation.