Uranium speciation and distribution on the surface of Shewanella putrefaciens in the presence of inorganic phosphate and zero-valent iron under anaerobic conditions.

Shewanella putrefaciens (S. putrefaciens) is one of the main microorganisms in soil bioreactors, which mainly immobilizes uranium through reduction and mineralization processes. However, the effects of elements such as phosphorus and ZVI, which may be present in the actual environment, on the mineralization and reduction processes are still not clearly understood and the environment is mostly in the absence of oxygen. In this study, we ensure that all experiments are performed in an anaerobic glove box, and we elucidate through a combination of macroscopic experimental findings and microscopic characterization that the presence of inorganic phosphates enhances the mineralization of uranyl ions on the surface of S. putrefaciens, while zero-valent iron (ZVI) facilitates the immobilization of uranium by promoting the reduction of uranium by S. putrefaciens. Interestingly, when inorganic phosphates and ZVI co-exist, both the mineralization and reduction of uranium on the bacterial surface are simultaneously enhanced. However, these two substances exhibit a certain degree of antagonism in terms of uranium immobilization by S. putrefaciens. Furthermore, it is found that the influence of pH on the mineralization and reduction of uranyl ions is far more significant than that of inorganic phosphates and ZVI. This study contributes to a better understanding of the environmental fate of uranium in real-world settings and provides valuable theoretical support for the bioremediation and risk assessment of uranium contamination.

Reference values of the carotid elastic modulus using shear wave elastography and arterial stiffness change in coronary slow flow.

PURPOSE: Shear wave elastography (SWE) accurately and sensitively evaluates arterial wall stiffness by quantifying the elastic modulus (EM); however, the absence of reference values has precluded its widespread clinical application. This prospective cohort study aimed to establish reference values for the carotid EM using SWE; investigate the main determinants of the EM; and evaluate EM changes in coronary slow flow (CSF), which is characterized by delayed coronary opacification without evident obstructive lesion in epicardial coronary artery on angiography. METHOD: This study enrolled 169 healthy volunteers and 30 patients with CSF. The carotid maximum EM (EMmax), mean EM, and minimum EM were measured using SWE. CSF was diagnosed by thrombolysis in the myocardial infarction frame count during coronary angiography. RESULTS: No differences were found in the EM between the left and right carotid arteries and between men and women. Multiple linear regression analysis revealed that age was independently correlated with the EMmax, which progressively increased with age. Moreover, smoking had an independent influence on the EM after adjusting for age; smokers had higher EM than non-smokers. Age-specific reference values for the carotid EM were established. The EM was higher in patients with CSF than in controls after adjusting for age and smoking status. CONCLUSIONS: This study first established the reference values for the carotid EM using SWE. Age and smoking status were the main determinants of the EM. Patients with CSF had high EM. SWE can effectively and noninvasively evaluate arterial stiffness in patients with CSF.

A human immunodeficiency virus-seronegative acquired immunodeficiency syndrome patient with opportunistic infections: A case report.

BACKGROUND: In rare cases, people living with chronic human immunodeficiency virus (HIV) infection do not develop antibodies despite demonstrable infection. Delayed or missed diagnosis of HIV infection leads to a lack of timely therapy, resulting in rapid disease progression with opportunistic infections or malignancies. CASE REPORT: A 44-year-old Chinese man presented with sore throat, oral leukoplakia, fever, dyspnoea and diffuse ground glass-like lesions in both lungs. Serum cytomegalovirus DNA was detectable, and CD4+ T-cell count was low. The patient was suspected of being a person living with HIV despite of the repeatedly negative HIV antibody tests using enzyme-linked immunsorbent assay and Western blot. Subsequently, high-plasma HIV RNA viral load was found on two repeated tests, while HIV DNA was also positive. Thus, the patient was confirmed as presenting with HIV-seronegative acquired immunodeficiency syndrome (AIDS). The symptoms improved in response to effective anti-fungal and anti-retroviral therapy after diagnosis. CONCLUSION: This is the third reported case of an HIV-seronegative AIDS patient in China, which are also rarely reported globally. HIV nucleic acid testing is important to screen out HIV infection, especially in those who present with severe immunodeficiency but remain HIV serogenative.

Blockade of adenosine A2A receptor alleviates cognitive dysfunction after chronic exposure to intermittent hypoxia in mice.

Obstructive sleep apnea-hypopnea syndrome (OSAHS) is widely known for its multiple systems damage, especially neurocognitive deficits in children. Since their discovery, adenosine A2A receptors (A2ARs) have been considered as key elements in signaling pathways mediating neurodegenerative diseases such as Huntington's and Alzheimer's, as well as cognitive function regulation. Herein, we investigated A2AR role in cognitive impairment induced by chronic intermittent hypoxia (CIH). Mice were exposed to CIH 7 h every day for 4 weeks, and intraperitoneally injected with A2AR agonist CGS21680 or A2AR antagonist SCH58261 half an hour before IH exposure daily. The 8-arm radial arm maze was utilized to assess spatial memory after CIH exposures.To validate findings using pharmacology, the impact of intermittent hypoxia was investigated in A2AR knockout mice. CIH-induced memory dysfunction was manifested by increased error rates in the radial arm maze test. The behavioral changes were associated with hippocampal pathology, neuronal apoptosis, and synaptic plasticity impairment. The stimulation of adenosine A2AR exacerbated memory impairment with more serious neuropathological damage, attenuated long-term potentiation (LTP), syntaxin down-regulation, and increased BDNF protein. Moreover, apoptosis-promoting protein cleaved caspase-3 was upregulated while anti-apoptotic protein Bcl-2 was downregulated. Consistent with these findings, A2AR inhibition with SCH58261 and A2AR deletion exhibited the opposite result. Overall, these findings suggest that A2AR plays a critical role in CIH-induced impairment of learning and memory by accelerating hippocampal neuronal apoptosis and reducing synaptic plasticity. Blockade of adenosine A2A receptor alleviates cognitive dysfunction after chronic exposure to intermittent hypoxia in mice.

Diallyl disulfide improves lipid metabolism by inhibiting PCSK9 expression and increasing LDL uptake via PI3K/Akt-SREBP2 pathway in HepG2 cells.

BACKGROUND AND AIM: Diallyl disulfide (DADS), a volatile sulfide extracted from garlic, has been suggested as a chemical of anti-atherosclerotic drugs, while its molecular mechanism for this benefit has not fully been understood. The aim of the present study was to investigate the effects of DADS on lipid metabolism and its potential mechanisms in HepG2 cells induced by lipopolysaccharides (LPS). METHODS AND RESULTS: HepG2 cells were treated with LPS with or without different concentrations of DADS (0, 20, 40, 80, 160 µg/ml) for 24 h. The cell activity was detected by CCK8, and Dil-LDL uptake assay was used to examine the LDL uptake. Real-time PCR and Western blot were used to detect the expression of LDLR, PCSK9 SREBP2 and HMGCR. In addition, we examined the effect of the combination of DADS with atorvastatin on PCSK9 expression. The results showed that LPS significantly increased PCSK9 and SREBP2 expressions in a dose-dependent manner in HepG2 cells. DADS attenuated PCSK9, SREBP2 and HMGCR expressions and up-regulated the expression of LDLR. Moreover, DADS reversed the expressions of PCSK9, SREBP2, HMGCR and LDLR induced by LPS and DADS could promote the LDL uptake in HepG2 cells. Furthermore, DADS decreased the expression of PCSK9 by activating the PI3K/Akt-SREBP2 signal pathway. Notably, DADS could reduce PCSK9 expression induced by atorvastatin in HepG2 cells. CONCLUSION: DADS could significantly attenuated PCSK9 expression in a dose-dependent manner induced by LPS and increased the LDLR expression in HepG2 cells, which was associated with the activation of PI3K/Akt-SREBP2 signaling pathway.

Effect of pericardial incision on left ventricular morphology and systolic function in patients during coronary artery bypass grafting.

BACKGROUND: Accurate assessment of left ventricular (LV) systolic function is important after coronary artery bypass grafting (CABG). LV ejection fraction (LVEF) is conventionally used to evaluate LV systolic function; deformation parameters can be used to detect subtle LV systolic dysfunction. It is unclear whether an incised pericardium without sutures during CABG could affect LV morphology and function. We investigated the effect of pericardial incision on LV morphology and systolic function during CABG. METHODS: Intraoperative transesophageal echocardiography was performed in 27 patients during elective off-pump beating heart CABG 5 min before and after pericardial incision. LV longitudinal and mid-cavity transversal diameters, sphericity index, volumes, and LVEF were measured. LV global longitudinal strain (GLS), global circumferential strain (GCS), global radial strain (GRS), and twist obtained by two-dimensional speckle tracking echocardiography were measured simultaneously. RESULTS: LV mid-cavity transversal diameter increased, while the LV sphericity index decreased (P < 0.001) immediately after pericardial incision. The GLS, GCS, and twist significantly decreased, while the GRS notably increased (P < 0.001). The LV volumes and LVEF remained unchanged. CONCLUSIONS: Pericardial incision immediately transformed LV morphology from an ellipsoid to sphere, with decreased longitudinal and circumferential strain and twist, and increased radial strain, while LVEF remained unchanged. This should be considered when evaluating LV systolic function in patients after CABG.

Case Report: Multi-Modality Imaging of a Right Atrial Pseudoaneurysm in a Patient With Breast Cancer.

Cardiac pseudoaneurysms occur when a blood vessel wall is injured and the leaking blood is collected in the surrounding tissue. They are very rare events and have a high risk of rupture and poor prognosis. We report a case of right atrial pseudoaneurysm in a 54-year-old female patient diagnosed with breast cancer and lung metastasis. The patient underwent five intrapericardial infusions of cisplatin and nine cycles of systemic chemotherapy. Non-contrast-enhanced computed tomography (CT) was performed at follow-up evaluation during the chemotherapeutic process as this patient was contraindicated to iodine. CT without contrast and ultrasonography showed a crescent-shaped lesion near the right atrium but its nature could not be determined. Cardiac magnetic resonance (CMR) imaging with gadolinium contrast provided important information as an alternative enhanced imaging modality. By combining CT, ultrasonography and CMR images with the medical history of the patient, we inferred that the lesion was a pseudoaneurysm in the right atrium. This condition was related to the erosion of metastasized tumor cells or the accumulated cardiac toxicity of multiple cycles of chemotherapy or pericardiocentesis. This single case report suggests that cardiac rupture should be considered as a potential complication in patients with suspected pericardial metastasis. CMR imaging is an excellent tool for the detection of right atrial rupture.

Liraglutide improves lipid metabolism by enhancing cholesterol efflux associated with ABCA1 and ERK1/2 pathway.

BACKGROUND: Reverse cholesterol transport (RCT) is an important cardioprotective mechanism and the decrease in cholesterol efflux can result in the dyslipidemia. Although liraglutide, a glucagon like peptide-1 analogue, has mainly impacted blood glucose, recent data has also suggested a beneficial effect on blood lipid. However, the exact mechanism by which liraglutide modulates lipid metabolism, especially its effect on RCT, remain undetermined. Hence, the aim of the present study was to investigate the potential impacts and potential underlying mechanisms of liraglutide on the cholesterol efflux in both db/db mice and HepG2 cells. METHODS: Six-week old db/db mice with high fat diet (HFD) and wild type mice were administered either liraglutide (200 µg/kg) or equivoluminal saline subcutaneously, twice daily for 8 weeks and body weight was measured every week. After the 8-week treatment, the blood was collected for lipid evaluation and liver was obtained from the mice for hematoxylin-eosin (HE) staining, red O staining and Western blotting. Cholesterol efflux was assessed by measuring the radioactivity in the plasma and feces after intraperitoneal injection of 3H-labeled cholesterol. HepG2 Cells were treated with different concentrations of glucose (0, 5, 25, and 50 mmol/L) with or without liraglutide (1000 nmol/L) for 24 h. The intracellular cholesterol efflux was detected by BODIPY-cholesterol fluorescence labeling. Real-time PCR or Western blotting was used to examine the expression levels of ABCA1, ABCG1 and SR-B1. RESULTS: Liraglutide significantly decreased blood glucose, serum total cholesterol (TC), triglyceride (TG) and low-density lipoprotein cholesterol (LDL-C). It also reduced liver lipid deposition in db/db mice fed with HFD. Moreover, the movement of 3H-cholesterol from macrophages to plasma and feces was significantly enhanced in db/db mice fed with HFD after liraglutide adminstration. In vitro study, liraglutide could promote the cholesterol efflux of HepG2 cells under high glucose, and also increase the expression of ABCA1 by activating the ERK1/2 pathway. CONCLUSIONS: Liraglutide could improve lipid metabolism and hepatic lipid accumulation in db/db mice fed with HFD by promoting reversal of cholesterol transport, which was associated with the up-regulation of ABCA1 mediated by the ERK1/2 phosphorylation.

Liraglutide downregulates hepatic LDL receptor and PCSK9 expression in HepG2 cells and db/db mice through a HNF-1a dependent mechanism.

BACKGROUND: Proprotein convertase subtilisin/kexin type 9 (PCSK9), a major regulator of cholesterol homeostasis, is associated with glucose metabolism. Liraglutide, a glucagon-like peptide-1 receptor agonist, can increase insulin secretion in a glucose-dependent manner and lower blood glucose. We aimed to investigate the relationship between liraglutide and PCSK9. METHODS: At the cellular level, the expressions of PCSK9 and hepatocyte nuclear factor 1 alpha (HNF1α) protein in HepG2 cells stimulated by liraglutide was examined using Western blot. Seven-week old db/db mice and wild type (WT) mice were administered either liraglutide (200 µg/kg) or equivoluminal saline subcutaneously, twice daily for 7 weeks. Fasting glucose level, food intake and body weight were measured every week. After the 7-week treatment, the blood was collected for lipid and PCSK9 levels detection and the liver was removed from the mice for oil red O staining, immunohistochemical analysis, immunofluorescence test and Western bolt. RESULTS: Firstly, liraglutide suppressed both PCSK9 and HNF1α expression in HepG2 cells in a time and concentration dependent manner. Secondly, liraglutide induced weight loss in WT and db/db mice, decreased serum PCSK9, glucose and lipid levels and improved hepatic accumulation in db/db but not WT mice. Thirdly, liraglutide reduced both hepatic PCSK9 and low-density lipoprotein receptor (LDLR) expression with a decrease in HNF1α in db/db mice but not in WT mice. CONCLUSIONS: Liraglutide suppressed PCSK9 expression through HNF1α-dependent mechanism in HepG2 cells and db/db mice, and decreased LDLR possibly via PCSK9-independent pathways in db/db mice.

Anti-atherosclerotic effect of traditional fermented cheese whey in atherosclerotic rabbits and identification of probiotics.

BACKGROUND: Traditional fermented cheese whey (TFCW), containing probiotics, has been used both as a dairy food with ethnic flavor and a medicine for cardiovascular disease, especially regulating blood lipid among Kazakh. We therefore investigated anti-atherosclerotic effects of TFCW in atherosclerotic rabbits and identified lactic acid bacteria (LAB) and yeasts in TFCW. METHODS: Atherosclerotic rabbits were induced by administration of atherosclerotic diet for 12 weeks and divided randomly into three groups and treated for 4 weeks with Simvastatin (20 mg/kg) or TFCW (25 mg/kg) and (50 mg/kg). In addition, a normal control group and an atherosclerotic group were used for comparison. All drugs were intragastrical administered once daily 10 mL/kg for 4 weeks. Body weight (BW), lipid profiles, C-reactive protein (CRP), vascular cell adhesion molecule-1 (VCAM-1), and intercellular adhesion molecule-1 (ICAM-1) were tested and theromatous plaques and the number of foam cells and infiltrating fibroblast cells in the thoracic aorta endothelium was evaluated by hematoxylin and eosin stainin. LAB and yeasts were isolated and purified by conventional techniques and identified using morphological and biochemical properties as well as gene sequences analysis. RESULTS: After 4 weeks of treatment, high and low dose TFCW decreased serum TC, TG, LDLC, CRP, VCAM-1 and ICAM-1 (P < 0.05) compared to atherosclerotic group, and increased HDL-C (P < 0.05) compared to normal controls. Histological analysis showed TFCW reduced VCAM-1 expression and formation of atheromatous plaques on the aortic endothelium of atherosclerotic rabbits. CONCLUSION: Seven classes of LBA from two different genera including Lactobacillus brevis, Lactobacillus kefianofaciens, Lactobacillus helveticus, Lactobacillus Casei, Lactobacillus plantarum, Lactobacillus kefiri and Lactococcus lactic as well as 2 classes of yeasts from two different genera including Saccharomyces unisporus and Issatchenkia orientalis were isolated and identified from TFCW. In summary, TFCW, containing 7 classes of LBA and 2 classes of yeasts, has significant anti-atherosclerotic potential in atherosclerotic rabbits and may modulate lipid metabolism and protect aorta in the atherosclerotic condition, which might be related to various probiotics acting through reducing the CRP, VCAM-1 and ICAM-1 levels and protecting the aortic endothelium.

Dimethyl fumarate induces necroptosis in colon cancer cells through GSH depletion/ROS increase/MAPKs activation pathway.

BACKGROUND AND PURPOSE: Dimethyl fumarate (DMF) is a newly approved drug for the treatment of relapsing forms of multiple sclerosis and relapsing-remitting multiple sclerosis. Here, we investigated the effects of DMF and its metabolites mono-methylfumarate (MMF and methanol) on different gastrointestinal cancer cell lines and the underlying molecular mechanisms involved. EXPERIMENTAL APPROACH: Cell viability was measured by the MTT or CCK8 assay. Protein expressions were measured by Western blot analysis. LDH release, live- and dead-cell staining, intracellular GSH levels, and mitochondrial membrane potential were examined by using commercial kits. KEY RESULTS: DMF but not MMF induced cell necroptosis, as demonstrated by the pharmacological tool necrostatin-1, transmission electron microscopy, LDH and HMGB1 release in CT26 cells. The DMF-induced decrease in cellular GSH levels as well as cell viability and increase in reactive oxygen species (ROS) were inhibited by co-treatment with GSH and N-acetylcysteine (NAC) in CT26 cells. DMF activated JNK, p38 and ERK MAPKs in CT26 cells and JNK, p38 and ERK inhibitors partially reversed the DMF-induced decrease in cell viability. GSH or NAC treatment inhibited DMF-induced JNK, p38, and ERK activation in CT26 cells. DMF but not MMF increased autophagy responses in SGC-7901, HCT116, HT29 and CT26 cancer cells, but autophagy inhibition did not prevent the DMF-induced decrease in cell viability. CONCLUSION AND IMPLICATIONS: DMF but not its metabolite MMF induced necroptosis in colon cancer cells through a mechanism involving the depletion of GSH, an increase in ROS and activation of MAPKs.

DMH1 increases glucose metabolism through activating Akt in L6 rat skeletal muscle cells.

DMH1(4-[6-(4-Isopropoxyphenyl)pyrazolo [1,5-a]pyrimidin-3-yl] quinoline) is a compound C analogue with the structural modifications at the 3- and 6-positions in pyrazolo[1,5-a]pyrimidine backbone. Compound C was reported to inhibit both AMPK and Akt. Our preliminary work found that DMH1 activated Akt. Since Akt was involved in glucose metabolism, we aimed to identify the effects of DMH1 on glucose metabolism in L6 rat muscle cells and the potential mechanism. Results showed that DMH1 increased lactic acid release and glucose consumption in L6 rat muscle cells in a dose-dependent manner. DMH1 activated Akt in L6 cells. Akt inhibitor inhibited DMH1-induced Akt activation and DMH1-induced increases of glucose uptake and consumption. DMH1 had no cytotoxicity in L6 cells, but inhibited mitochondrial function and reduced ATP production. DMH1 showed no effect on AMPK, but in the presence of Akt inhibitor, DMH1 significantly activated AMPK. Compound C inhibited DMH1-induced Akt activation in L6 cells. Compound C inhibited DMH1-induced increase of glucose uptake, consumption and lactic acid release in L6 cells. DMH1 inhibited PP2A activity, and PP2A activator forskolin reversed DMH1-induced Akt activation. We concluded that DMH1 increased glucose metabolism through activating Akt and DMH1 activated Akt through inhibiting PP2A activity in L6 rat muscle cells. In view of the analogue structure of DMH1 and compound C and the contrasting effects of DMH1 and compound C on Akt, the present study provides a novel leading chemical structure targeting Akt with potential use for regulating glucose metabolism.

[Preparation of cobalt oxide mesoporous metallic oxide-clay composites and their catalytic performance in the oxidation of benzene].

Laponite clays composited with alumina, ceria and zirconia etc. were prepared using polyoxocations or simple metal ions as precursors, and then cobalt oxide was loaded onto them to obtain the catalysts. The results showed that compared with laponite clays, the as-prepared laponite had wide range of pore size distribution and increased pore volume. The pore volumes of laponite clays composited with alumina and ceria were more than 0.75 cm3 · g(-1). N2 isotherm type was maintained after Co3O4 loading, however, the N2 adsorption decreased with the increase of Co3 O4 loading, indicating the decrease of pore volume, which was caused by the blockage of metallic oxide/clay composites support. Furthermore, dispersion and catalytic performance of the catalysts were significantly influenced by the composited metallic elements. It was shown that according to the diffraction peak half-width of 311 crystal facet and scherrer equation, when the Co loading was 21.3% at laponite clays composited with Fe, Zr, Ce, Al, the average sizes of Co3O4 were 17.2, 16.0, 16.5 and 18.0 nm, respectively. Alumina composited clay with 21.3% Co loading showed high catalytic activity, the complete conversion temperature of benzene was 350°C. Among metallic oxide/laponite composites, the ZrO composited laponite with 21.3% Co loading exhibited the best catalytic performance, which could completely convert benzene at 310°C.

[Changes and clinical significance of CD8(+) T cell subset in patients with aplastic anemia, myelodysplastic syndrome and acute myeloid leukemia].

This study was purposed to detect the balance and the activity change of cytotoxic T cell subsets in aplastic anemia (AA) patients, myelodysplastic syndrome (MDS) patients and acute myeloid leukemia (AML) patients, and to explore the cellular immune mechanism for abnormal hematopoiesis of the three diseases, so as to provide experimental basis for the choice of clinical treatment. The proportion of the cytotoxic T cells and part of the T-cells subsets in peripheral blood were detected by flow cytometry in 35 cases of MDS, including 19 refractory anemia (MDS-RA), 16 refractory anemia with excess blasts (MDS-RAEB), 17 AA, 15 AML patients and 10 normal donors respectively. The results showed that compared with the control group, the percentage of Tc1, Tc1/Tc2, CD8(+)HLA-DR(+), CD3(+)CD8(+)CD28(+), CD8(+)CD45RO(+) cells was significantly higher and the percentage of CD8(+)CD45RA(+) was significantly lower in AA and MDS-RA group. There was no difference in the percentage of Tc2 cells between AA/MDS-RA and normal controls; the percentage of CD8(+)CD45RO(+) cells was significantly higher and the percentage of Tc1, CD3(+)CD8(+)CD28(+), CD8(+)HLA-DR(+) was significantly lower in MDS-RAEB group, the percentage of CD8(+)CD45RA(+) was lower but the difference was not significant, and there was no difference in the percentage of Tc, Tc1/Tc2 cells between MDS-RAEB group and the control group. The percentage of Tc2 cells was significantly higher and the percentage of other parameters was significantly lower in AML group than those of normal controls. It is concluded that the cellular immune statuses in AA, the different stages of MDS and AML are different. In AA and the early stage of MDS, the balance of Tc1/Tc2 shifts to Tc1, and the activation of T-cell subsets increases. In the late stage of MDS and AML, the balance of Tc1/Tc2 shifts to Tc2, the activation of T-cell subsets decreases. The former may be closely related to bone marrow failure while the latter may be one of the important mechanisms in which the malignant clones escape from immune effect.

Elevated plasma level of HMGB1 is associated with disease activity and combined alterations with IFN-α and TNF-α in systemic lupus erythematosus.

Recent studies indicate that high-mobility group box protein 1 (HMGB1) contributes to the pathogenesis of diverse autoimmune disorders. It induces the production of interferon-alpha (IFN-alpha) and tumor necrosis factor alpha (TNF-alpha) in vitro. In the present study, plasma HMGB1, TNF-alpha, and IFN-alpha were determined with ELISA in 37 patients with systemic lupus erythematosus (SLE) and 39 age- and sex-matched healthy controls (HC). The possible associations of these cytokines with disease activities, autoantibodies, and certain laboratory parameters were also explored. The plasma levels of HMGB1, TNF-alpha, and IFN-alpha were increased in SLE patients compared with those of HC (P < 0.05). Moreover, the levels of HMGB1 and TNF-alpha in the active SLE patients were elevated compared with those in inactive patients and HC. Additionally, plasma HMGB1 was positively correlated with peripheral neutrophils, and plasma TNF-alpha was positively correlated with anti-Sm, ESR and CRP, while plasma IFN-alpha was inversely correlated with the age and platelet level in SLE patients. Our data indicated that increased plasma HMGB1 was associated with disease activity in SLE, which was similar to TNF-alpha. High level of plasma IFN-alpha may be related to nephritis and thrombocytopenia in SLE.

Mesoporous Co3O4 and Au/Co3O4 catalysts for low-temperature oxidation of trace ethylene.

Low-temperature catalysts of mesoporous Co(3)O(4) and Au/Co(3)O(4) with high catalytic activities for the trace ethylene oxidation at 0 degrees C are reported in this paper. The catalysts were prepared by using the nanocasting method, and the mesostructure was replicated from three-dimensional (3D) cubic KIT-6 silicas. High resolution transmission electron microscopy (HRTEM) studies revealed that {110} facets were the exposed active surfaces in the mesoporous Co(3)O(4), whereas the Co(3)O(4) nanosheets prepared by the precipitation method exhibited the most exposed {112} facets. We found that the mesoporous Co(3)O(4) was significantly more active for ethylene oxidation than the Co(3)O(4) nanosheets. The results indicated that the crystal facet {110} of Co(3)O(4) played an essential role in determining its catalytic oxidation performance. The synthesized Au/Co(3)O(4) materials, in which the gold nanoparticles were assembled into the pore walls of the Co(3)O(4) mesoporous support, exhibited stable, highly dispersed, and exposed gold sites. Gold nanoparticles present on Co(3)O(4) readily produced surface-active oxygen species and promoted ethylene oxidation to achieve a 76% conversion at 0 degrees C, which is the highest conversion reported yet.

Insulin-like growth factor-1 promotes cell cycle progression via upregulation of cyclin D1 expression through the phosphatidylinositol 3-kinase/nuclear factor-kappaB signaling pathway in FRTL thyroid cells.

AIM: Insulin-like growth factor-1 (IGF-1) is an important hypertrophic and cell cycle progression factor for a number of cell types. It has been proven that IGF-1 is involved in the regulation of thyroid proliferation and cell cycle progression; however, the exact mechanism of this regulation has not been fully elucidated. In the present study, we investigated the effect of IGF-1 on the expression of cyclin D1, an important cell cycle regulatory protein, and a signaling pathway involved in IGF-1's effect on cyclinD1 expression in FRTL thyroid cells. METHODS: FRTL thyroid cells were treated with IGF-1 or vector control for 24 h. As appropriate to individual experiments, a phosphatidylinositol 3-kinase (PI3K) inhibitor, LY294002, and/or a nuclear factor-kappaB (NF-kappaB) inhibitor, BAY11-7082, were added 1 h prior to IGF-1 treatment. Western blotting was used to detect cyclin D1 protein expression. Immunofluorescence was performed to analyze the expression of IkappaBalpha, an NF-kappaB inhibitory protein. Cell cycle analysis was performed by fluorescence activated cell sorting (FACS). RESULTS: IGF-1 increased the cyclin D1 expression in thyroid cells. This increase was blocked by pretreatment with LY294002 or BAY11-7082. Further studies showed that IGF-1 specifically induced NF-kappaB activity. Treatment with IGF-1 could accelerate cell cycle progression from G(0)/G(1) to S phase, whereas this progression was inhibited by the presence of LY294002 or BAY11-7082. CONCLUSION: In summary, the results of the present study show that in FRTL cells, IGF-1 promotes cell cycle progression via an upregulation of cyclin D1 expression, at least partially through the PI3K/NF-kappaB signaling pathway.

Poly[[aqua-(1-naphthyl-acetato)cadmium(II)]-µ(3)-pyridin-3-olato].

In the title complex, [Cd(C(5)H(4)NO)(C(12)H(9)O(2))(H(2)O)](n), each Cd(II) atom is coordinated by two carboxylate O atoms from one 1-naphthyl-acetate ligand, two hydroxyl O atoms from two pyridin-3-olate ligands, one N atom from another pyridin-3-olate ligand and one water mol-ecule, and displays a distorted octa-hedral coordination geometry. The compound forms infinite chains of pyridin-3-olate ligands bridging 1-naphthyl-acetate-Cd(II) units parallel to the b axis, with a Cd⋯Cd separation of 3.578 (2) Å. The chains are further self-assembled into a supra-molecular network through inter-molecular O-H⋯O hydrogen-bonding inter-actions.

[Selection and interaction of Ni2+ metal-binding peptides].

Ni2+ binding peptides were selected from phage random dodecapeptide library by metal affinity chromatography. After four rounds of biopanning, phage amplification and DNA sequencing, a group of peptide sequences were obtained. GenBank blast found no homogenous sequences, Clustal W analysis showed no motifs but they were really riched in histidines and contained di- or more histidines(his). Affinity assays of selected metal-binding phages for various metal-charged NTA resins and the experiments of E. coli suppression and detoxification gave positive results for Ni2+ binding peptides: strong affinities for Ni2+ were found for Ni2+ binding peptide displayed phages, as well as for other metals (Cu2+, Co2+, Zn2+, Cr2+, Cd2+); affinities of the binding peptides for Cu2+, Ni2+, Co2+ and Zn2+ were much higher than that of Cd2+ and Cr2+; in addition, Ni2+ binding peptides displayed phages had effects on E. coli as to enhance the tolerance and detoxification of E. coli for heavy metals when exposed to Ni2+ and Cd2+. The interactions of meal binding peptides for heavy metals were also disclosed by microscopic observation. The research offered great values for the study of the interaction between metals and peptides, as well as in other areas such as heavy metal bioremediation.