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.

Positive-Parity Linear-Chain Molecular Band in

An inelastic excitation and cluster-decay experiment ^{2}H(^{16}C,^{4}He+^{12}Be or ^{6}He+^{10}Be)^{2}H was carried out to investigate the linear-chain clustering structure in neutron-rich ^{16}C. For the first time, decay paths from the ^{16}C resonances to various states of the final nuclei were determined, thanks to the well-resolved Q-value spectra obtained from the threefold coincident measurement. The close-threshold resonance at 16.5 MeV is assigned as the J^{π}=0^{+} band head of the predicted positive-parity linear-chain molecular band with (3/2_{π}^{-})^{2}(1/2_{σ}^{-})^{2} configuration, according to the associated angular correlation and decay analysis. Other members of this band were found at 17.3, 19.4, and 21.6 MeV based on their selective decay properties, being consistent with the theoretical predictions. Another intriguing high-lying state was observed at 27.2 MeV which decays almost exclusively to ^{6}He+^{10}Be(∼6 MeV) final channel, corresponding well to another predicted linear-chain structure with the pure σ-bond configuration.

[Experimental study on substance P in the regulation of degranulation of cultured murine mast cells].

Objective: To investigate the effect of interleukin-4 (IL-4) stimulation on the expression of FcεRⅠα and NK-1R on mature mast cells(MC) cultured and differentiated from mouse bone marrow stem cells, and then to study if these MC also respond to substance P (SP) both in FcεRⅠα and NK-1R dependent manners. Methods: Bone marrow cells were aseptically flushed from BALB/c mouse femurs into complete RPMI 1640, followed by culture with stem cell factor (SCF 100 µg/L), IL-3 (15 µg/L) and IL-4 (0, 10, 15, 20 and 25 µg/L, respectively). The culture medium was changed once a week. The morphological changes of culture cells were observed under inverted microscope. After 4 weeks culture, the cells were collected and appraised by toluidine blue staining and flow cytometry. The expressions of surface CD117, FcεRⅠα and NK-1R on these cells were detected by flow cytometry and Western blot. Bone marrow MC were activated with SP (0, 0.01, 0.1, 1.0 and 10 mg/L, respectively) for 30 min. The histamine released into the supernatant and stored in the protoplasm was quantified by enzyme linked immunosorbent assay (ELISA). The percentage of histamine release was calculated as a percent of total histamine content. Results: When different concentrations of IL-4 (0, 10, 15, 20, 25 µg/L)were added into RPMI 1640, the positive rates of CD117 on MC surface were expressed as (94.8±1.3)%, (95.7±2.5)%, (94.1±1.3)%, (96.6±1.0)%, and (96.6±1.1)%, respectively, and there was no significant difference among these groups (F=8.51, P>0.05). The positive rates of FcεRⅠα were expressed as (81.5±2.6)%, (84.2±1.8)%, (91.8±2.0)%, (91.6±1.6)%, and (93.0±2.6)%, respectively, and there was statistically increasing among these groups (F=15.76, P<0.05). Then MC were activated by SP (0, 0.01, 0.1, 1.0, 10 mg/L), histamine from 20 µg/L IL-4 group were released (20.08±1.50)%, (32.76±2.99)%, (42.90±3.36)%、(50.21±1.29)%, (56.10±3.60)%, as similar as from 0 µg/L IL-4 were (19.37±2.02), (19.50±1.50), (21.77±1.91), (32.00±2.50), (33.56±1.25), there was significantly different when compared with each other (all P<0.05). Bone marrow MC were shown to have the highest expression of FcεRⅠα and NK-1R in culture of 20 µg/L IL-4 by the detection of Western blot, meanwhile these MC could be activated to degranulate by a lower concentration of SP (0.01 mg/L), with the release rate of histamine from MC showing a positive correlation with SP concentrations. On the other hand, MC with high expression of FcεRⅠα and little expression of NK-1R cultured with 0 µg/L IL-4, could also be activated by a much higher concentration of SP (1.0 mg/L). Conclusions: Bone marrow mast cells were shown to be successfully differentiated and to express NK-1R and FcεRⅠα upon co-culture with SCF and IL-3 or SCF, IL-3 and IL-4.When IL-4 was added into RPMI 1640, bone marrow MC could highly produce FcεRⅠα and NK-1R, thus building a better model of MC degranulation regulated by SP. And SP-controlled MC degranulation may be mediated through both FcεRⅠα (immunologically) and NK-1R (non-IgE mediated or non-immunologically) pathway.

Is vertebroplasty a risk factor for subsequent vertebral fracture, meta-analysis of published evidence?

UNLABELLED: In our paper, we systemically retrieved the eligible study evaluating whether increased incidence of subsequent vertebral fracture is associated with vertebroplasty. Main effect sizes were vertebral fracture rates reported in terms of hazard ratio (HR) for time-to-event data or relative risk (RR) for dichotomous outcome. Our results do not support the hypothesis that vertebroplasty contributes to increased risk of subsequent vertebral fracture, neither adjacent nor total vertebral fracture. INTRODUCTION: Vertebroplasty has been implicated in significant changes in vertebral strength, vertebral shape, and consequently increased risk for subsequent vertebral fracture, especially the adjacent level. Here, we further tested the hypothesis whether new-onset vertebral fracture is a natural result of osteoporosis or consequence of cement augmentation. METHODS: Relevant literatures were retrieved using PubMed, Web of Knowledge, and Cochrane Central Register of Controlled Trials (CENTRAL), supplemented by a hand-search of the reference lists of selected articles. Eligible studies assessed whether increased morbidity of subsequent vertebral fracture is associated with vertebroplasty. Main effect sizes were vertebral fracture rates reported in terms of hazard ratio (HR) for time-to-event data or relative risk (RR) for dichotomous outcome. Random-effects model was used to account for clinical or methodological heterogeneity across studies. RESULTS: Thirteen studies with a number of 2,551 individuals (1,631 in vertebroplasty group and 920 in control group) were suitable for this meta-analysis. In trials that reported adjacent vertebral fracture as time-to-event data (two trials, n = 328), we found a similar incidence of vertebral fracture in percutaneous vertebroplasty (PVP) group compared to conservative therapy (HR 0.60, 95% confidence interval 0.29 to 1.26; P = 0.18). In trials that reported overall vertebral fracture as time-to-event data (three trials, n = 704), vertebroplasty was associated with a slightly increased but non-significant risk for vertebral fracture (HR 1.14, 95% confidence interval 0.65 to 2.00; P = 0.65). The outcome was further confirmed in the secondary meta-analysis of studies that reported vertebral fracture as dichotomous data. Subgroup analysis according to study design revealed no difference either. CONCLUSIONS: Our results do not support the hypothesis that vertebroplasty contributes to increased risk of subsequent vertebral fracture, neither adjacent nor total vertebral fracture. However, adequately designed randomized controlled trials are warranted to confirm the present findings.

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.

A novel sequence-based coa genotyping method to discriminate nosocomial methicillin-resistant Staphylococcus aureus isolates.

AIM: To evaluate a novel sequence-based coa typing method in classification for nosocomial methicillin-resistant Staphylococcus aureus. METHOD: D1 and D2 regions of coa gene were used to discriminate methicillin-resistant Staphylococcus aureus and compared with other classical sequence-based methods with discriminate power. RESULTS: All MRSA isolates were divided into 11 types and about 20 subtypes with coa typing method here. The discriminate power of this coa typing method was better than MLST or spa method. CONCLUSION: It was demonstrated that this coa method is a simple, rapid, and effective technique applicable for outbreak or local nosocomial MRSA investigations in the future.

Chronic lumbar paraspinal compartment syndrome: a case report and review of the literature.

A 25-year-old male weightlifter felt increasing intractable low back pain during training but denied any acute injury. The physical examination, blood parameters, radiographs and MRI were unremarkable. He had been treated non-operatively by various means, with only temporary relief. The pressures in the lumbar paraspinal compartment were abnormally high and he was treated by surgical decompression. This gave rapid relief, he returned to training, and one year later the pain had not recurred.

Immune strategies using single-component LipL32 and multi-component recombinant LipL32-41-OmpL1 vaccines against leptospira

Genes encoding lipoproteins LipL32, LipL41 and the outer-membrane protein OmpL1 of leptospira were recombined and cloned into a pVAX1 plasmid. BALB/c mice were immunized with LipL32 and recombined LipL32-41-OmpL1 using DNA-DNA, DNA-protein and protein-protein strategies, respectively. Prime immunization was on day 1, boost immunizations were on day 11 and day 21. Sera were collected from each mouse on day 35 for antibody, cytokine detection and microscopic agglutination test while spleen cells were collected for splenocyte proliferation assay. All experimental groups (N = 10 mice per group) showed statistically significant increases in antigen-specific antibodies, in cytokines IL-4 and IL-10, as well as in the microscopic agglutination test and splenocyte proliferation compared with the pVAX1 control group. The groups receiving the recombined LipL32-41-OmpL1 vaccine induced anti-LipL41 and anti-OmpL1 antibodies and yielded better splenocyte proliferation values than the groups receiving LipL32. DNA prime and protein boost immune strategies stimulated more antibodies than a DNA-DNA immune strategy and yielded greater cytokine and splenocyte proliferation than a protein-protein immune strategy. It is clear from these results that recombination of protective antigen genes lipL32, lipL41, and ompL1 and a DNA-protein immune strategy resulted in better immune responses against leptospira than single-component, LipL32, or single DNA or protein immunization.

Immune strategies using single-component LipL32 and multi-component recombinant LipL32-41-OmpL1 vaccines against leptospira.

Genes encoding lipoproteins LipL32, LipL41 and the outer-membrane protein OmpL1 of leptospira were recombined and cloned into a pVAX1 plasmid. BALB/c mice were immunized with LipL32 and recombined LipL32-41-OmpL1 using DNA-DNA, DNA-protein and protein-protein strategies, respectively. Prime immunization was on day 1, boost immunizations were on day 11 and day 21. Sera were collected from each mouse on day 35 for antibody, cytokine detection and microscopic agglutination test while spleen cells were collected for splenocyte proliferation assay. All experimental groups (N = 10 mice per group) showed statistically significant increases in antigen-specific antibodies, in cytokines IL-4 and IL-10, as well as in the microscopic agglutination test and splenocyte proliferation compared with the pVAX1 control group. The groups receiving the recombined LipL32-41-OmpL1 vaccine induced anti-LipL41 and anti-OmpL1 antibodies and yielded better splenocyte proliferation values than the groups receiving LipL32. DNA prime and protein boost immune strategies stimulated more antibodies than a DNA-DNA immune strategy and yielded greater cytokine and splenocyte proliferation than a protein-protein immune strategy. It is clear from these results that recombination of protective antigen genes lipL32, lipL41, and ompL1 and a DNA-protein immune strategy resulted in better immune responses against leptospira than single-component, LipL32, or single DNA or protein immunization.

Sulfatide-tenascin interaction mediates binding to the extracellular matrix and endocytic uptake of liposomes in glioma cells.

Tenascin-C is an extracellular matrix glycoprotein, whose expression is highly restricted in normal adult tissues, but markedly up-regulated in a range of tumors, and therefore serves as a potential receptor for targeted anticancer drug or gene delivery. We describe here a liposomal carrier system in which the targeting ligand is sulfatide. Experiments with tenascin-C-expressing glioma cells demonstrated that binding of liposomes to the extracellular matrix relied essentially on the sulfatide-tenascin-C interaction. Following binding to the extracellular matrix, the sulfatide-containing liposomes were internalized via both caveolae/lipid raft- and clathrin-dependent pathways, which would ensure direct cytoplasmic release of the cargoes carried in the liposomes. Such natural lipid-guided intracellular delivery targeting at the extracellular matrix glycoproteins of tumor cells thus opens a new direction for development of more effective anticancer chemotherapeutics in future.

Large-area fabrication of periodic Fe nanorings with controllable aspect ratios in porous alumina templates.

Highly uniform Fe nanoring arrays in porous anodic alumina templates are fabricated by physical vapour deposition and grazing ion milling techniques. The nanorings have aspect ratios ranging from 0.8 to 4, depending on the deposition conditions. The outer diameter of the individual nanorings, and the area density and distribution patterns are completely determined by the template used. Selected-area electron diffraction reveals that these nanorings have a polycrystalline microstructure. The nanoring fabrication method demonstrated here can be extended to other materials.

Mechanism of clofibrate hepatotoxicity: mitochondrial damage and oxidative stress in hepatocytes.

Peroxisome proliferators have been found to induce hepatocarcinogenesis in rodents, and may cause mitochondrial damage. Consistent with this, clofibrate increased hepatic mitochondrial oxidative DNA and protein damage in mice. The present investigation aimed to study the mechanism by which this might occur by examining the effect of clofibrate on freshly isolated mouse liver mitochondria and a cultured hepatocyte cell line, AML-12. Mitochondrial membrane potential (Delta Psi(m)) was determined by using the fluorescent dye 5,5',6,6'-tetrachloro-1,1', 3,3'-tetraethyl-benzimidazolylcarbocyanine iodide (JC-1) and tetramethylrhodamine methyl ester (TMRM). Application of clofibrate at concentrations greater than 0.3 mM rapidly collapsed the Delta Psi(m) both in liver cells and in isolated mitochondria. The loss of Delta Psi(m) occurred prior to cell death and appeared to involve the mitochondrial permeability transition (MPT), as revealed by calcein fluorescence studies and the protective effect of cyclosporin A (CsA) on the decrease in Delta Psi(m). Levels of reactive oxygen species (ROS) were measured with the fluorescent probes 5-(and-6)-carboxy-2',7'-dichlorofluorescein diacetate (DCFDA) and dihydrorhodamine 123 (DHR123). Treatment of the hepatocytes with clofibrate caused a significant increase in intracellular and mitochondrial ROS. Antioxidants such as vitamin C, deferoxamine, and catalase were able to protect the cells against the clofibrate-induced loss of viability, as was CsA, but to a lesser extent. These results suggest that one action of clofibrate might be to impair mitochondrial function, so stimulating formation of ROS, which eventually contribute to cell death.

Effect of cardiolipin on proton permeability of phospholipid liposomes: the role of hydration at the lipid-water interface.

The effect of cardiolipin on the proton permeability of dipalmitoyl-phosphatidylcholine small unilamellar vesicles was examined by utilizing the pH-dependent fluorescence emission of 5- (and 6-) carboxyfluorescein. It has been found that the proton permeability of the phospholipid bilayer was greatly enhanced in the presence of cardiolipin, an acidic phospholipid mainly found in the inner mitochondrial membranes. In the presence of bovine heart cardiolipin, the bilayer surface hydration, as assessed with the fluorescence lifetime of 1-anilinonaphthalene-8-sulfonic acid, was increased, while hydration in the acyl chain region was not altered. In addition, the bilayer fluidity was also not affected. Taken together, these results suggest that the lipid-water interface is the major energy barrier for proton permeation of the bilayer vesicles, and alteration to properties of this interface by cardiolipin headgroup appears to be responsible for the enhanced proton permeability.

Lipid peroxidation in small and large phospholipid unilamellar vesicles induced by water-soluble free radical sources.

The susceptibility of small and large egg yolk phosphatidylcholine unilamellar vesicles to Fe(2+)/histidine-Fe(3+)- and Fenton reagent (Fe(2+)-H(2)O(2))-induced lipid peroxidation was evaluated by measuring the formation of thiobarbituric acid reactive substances (TBARS). It has been found that surface curvature or phospholipid packing exerts significant effect on the oxidative susceptibility of the unsaturated lipid bilayers and the highly curved and loosely packed small unilamellar vesicles (SUVs) exhibit much less resistance to the oxidative stress induced by the water-soluble free radical sources. The presence of lipid hydroperoxides in sonicated vesicles was excluded as the cause for higher level of lipid peroxidation in the phospholipid SUVs. Instead, the experimental results can be explained by the difference in ability of the water-soluble oxidants to penetrate the two types of lipid membranes. This hypothesis is supported by data obtained from fluorescence lifetime and quenching studies.

Caloric restriction prevents oxidative damage induced by the carcinogen clofibrate in mouse liver.

Long-term caloric restriction in rodents is known to decrease levels of oxidative damage, which may contribute to an 'anti-ageing' effect. We show here that a shorter period (10 months) of caloric restriction had only small effects on levels of oxidative DNA and protein damage in the livers of mice, but completely attenuated increased oxidative damage caused by the carcinogen clofibrate. Since clofibrate is thought to exert its actions by increasing oxidative damage, our data suggest that 10 months of caloric restriction can increase the resistance of tissues to agents inducing oxidative stress. This may be an important factor in explaining how caloric restriction decreases cancer incidence.

Mitochondrial damage by the "pro-oxidant" peroxisomal proliferator clofibrate.

Clofibrate is a peroxisome proliferator that can cause hepatic cancer in rodents. It has been suggested that oxidative damage is involved in this hepatocarcinogenesis, although the data are conflicting. We confirmed that clofibrate causes oxidative damage in nuclei from the livers of mice treated with this substance, measured both as protein carbonyls and levels of 8-hydroxy-2'-deoxyguanosine (8-OHdG) in DNA. In addition, clofibrate also affects mitochondria, causing elevated levels of carbonyls and 8-OHdG, increased state 4 respiration and decreased adenosine triphosphatase (ATPase) activity. No evidence for clofibrate-induced lipid peroxidation in mitochondria was obtained. We propose that mitochondria may be a major target of injury and a source of oxidative stress in clofibrate-treated animals.

Ca2+-induced fusion of sulfatide-containing phosphatidylethanolamine small unilamellar vesicles.

The fusogenic properties of sulfatide-containing 1,2-dioleoyl-3-sn -phosphatidylethanolamine (DOPE) small unilamellar vesicles (SUVs) in the presence of CaCl2 were studied by mixing membrane lipids based on an assay of fluorescence resonance energy transfer (FRET). Fusion of the vesicles was also confirmed by mixing aqueous contents with the Tb/dipicolinate (DPA) assay. The half-times of lipid mixing revealed that the fusion rate decreased with increasing molar concentration of sulfatide. This inhibitory effect was more obvious at sulfatide concentrations higher than 30 mol%, where hydration at the membrane surface reached its maximum and the fusion was no longer pH-sensitive in the range of pH 6.0 - 9.0. Similar inhibitory effect was also observed in Ca2+-induced fusion of DOPE/ganglioside GM1 vesicles but at a lower concentration of the glycosphingolipid (20 mol%). In contrast, increasing the concentration of phosphatidylserine (PS) in DOPE/PS SUVs resulted in an increase in the rate of Ca2+-induced lipid mixing and the pH sensitivity of this system was not affected. These results are consistent with an increasing steric hindrance to membrane fusion at higher molar concentration and larger headgroup size of the glycosphingolipids. Interestingly, the pH sensitivity of the sulfatide-containing liposomes was retained when they were allowed to fuse with synaptosomes in the absence of Ca2+ by a mechanism involving protein mediation.

Hydration and stability of sulfatide-containing phosphatidylethanolamine small unilamellar vesicles.

The effect of sulfatide on membrane hydration of 1, 2-dioleoyl-sn-glycero-3-phosphoethanolamine (DOPE) small unilamellar vesicles (SUVs) was investigated using steady-state and time-resolved fluorescence spectroscopy. The degree of hydration in the headgroup region of the bilayer lipids was assessed with the fluorescence lifetime of N-(5-dimethylaminonaphthalene-1-sulfonyl)dipalmitoylphosphatidylethan olamine along with the ratio of its fluorescence intensities measured in samples prepared either in D2O- or in H2O-based buffers. Similarly, hydration of acyl chains near the headgroup region and that close to the bilayer center were studied using 1-(4-trimethylammoniumphenyl)-6-phenyl-1,3,5-hexatriene and 1-palmitoyl-2-[2-[4-(6-phenyl-trans-1,3, 5-hexatrienyl)phenyl]ethyl]carbonyl]-3-sn-phosphatidylcholine as probes. Increasing sulfatide concentration up to 30 mol% resulted in an increase in surface hydration and a decrease in interchain hydration. These were correlated with an increase in bilayer stability of the DOPE/sulfatide SUVs. Moreover, variation of pH was found to affect the hydration and stability of the bilayer vesicles. No further change in headgroup hydration and interchain hydration near the bilayer center was observed at sulfatide concentrations >/=30 mol%. At such high sulfatide concentrations, bilayer hydration and stability were no longer pH-sensitive. The effects of sulfatide on hydration and stability of DOPE bilayer vesicles are discussed by taking into account the electrostatic and geometrical properties of the sulfated galactosyl headgroups.

Steady-state fluorescence quenching for detecting acyl chain interdigitation in phosphatidylcholine vesicles.

In the present study we have demonstrated the detection of the transition of 1,2-dipalmitoyl-sn-glycero-3-phosphocholine (DPPC) multilamellar vesicles from the noninterdigitated gel to the fully interdigitated gel phase in the presence of ethanol or ethylene glycol (EG) using the method of fluorescence quenching. This method is based on the change of accessibility of 2-(12-(7-nitrobenz-2-oxa-1, 3-diazol-4-yl)amino)dodecanoyl-1-hexadecanoyl-sn-glycero-3- phosphatidyl-choline (NBD-PC), a membrane-buried fluorophore, to iodide, a quencher in the aqueous solution, during the phase transition. It is found that accessible fluorophore appears to increase at ethanol and EG concentrations known for inducing DPPC interdigitation. This increase in accessibility is either due to the relocation of the fluorescent moiety closer to the lipid-water interface or an increase in the ability of the quencher to penetrate into the loosely packed headgroup region of the interdigitated domain or both. Our results suggest the coexistence of interdigitated and noninterdigitated phases in the phospholipid vesicles and the method of fluorescence quenching might be useful in quantitating the percentage of phospholipids which are interdigitated.

Stability and pH sensitivity of sulfatide-containing phosphatidylethanolamine small unilamellar vesicles.

The bilayer stabilization effect of sulfatide and the pH sensitivity of sulfatide-containing 1,2-dioleoyl-sn-glycero-3-phosphoethanolamine (DOPE) small unilamellar vesicles were examined by light scattering and the release of entrapped calcein. At 30 mol% sulfatide, stable DOPE/sulfatide vesicles were formed at the physiological pH and their stability was preserved in the presence of human plasma. These vesicles were found to be pH-sensitive and became leaky at pH 6.0 or when there was a pH-gradient across the membrane bilayer. Under such conditions, the amount of calcein released after 24 h incubation at 37 degrees C was increased by one-fold compared to that found at pH 7.4. Our results suggest that the hydration and partial dehydration of the headgroup of sulfatide upon changing pH play an essential role in determining the pH sensitivity of DOPE/sulfatide vesicles, while the importance of the condensing effect of the glycolipid on membrane bilayer is less significant.