Sub-bandgap photo-response of black silicon fabricated by femtosecond laser irradiation under water.

Here we propose a method to fabricate black Si without the need for any chalcogenide doping, accomplished by femtosecond (fs) laser irradiation in a liquid environment, aiming to fabricate the infrared detector and investigating their optoelectronic performance. Multi-scale laser-induced periodical surface structures (LIPSSs), containing micron sized grooves decorated with low spatial frequency ripples on the surface, can be clearly observed by SEM and 3D confocal microscope. The generated black Si demonstrates superior absorption capabilities across a broad wavelength range of 200-2500 nm, achieving an average absorptance of up to 71%. This represents a notable enhancement in comparison to untreated Si, which exhibits an average absorption rate of no more than 20% across the entire detectable spectrum. A metal-semiconductor-metal (MSM) type photodetector was fabricated based on this black Si, demonstrating remarkable optoelectronic properties, specifically, it attains a responsivity of 50.2 mA/W@10 V and an external quantum efficiency (EQE) of 4.02% at a wavelength of 1550 nm, significantly outperforming the unprocessed Si by more than five orders of magnitude. The great enhancement in infrared absorption as well as the optoelectronic performance can be ascribed to the synergistic effect of the multi-scale LIPSSs and the generated intermediate energy levels. On one hand, the multi-scale structures contribute to an anti-reflection and light trapping property; on the other hand, the defects levels generated through fs laser ablation process under water may narrow the band gap of the Si. The results therefore underscore the remarkable potential of black Si processed by fs laser under water for the application of photodetection, especially in the near-infrared band.

Direct Fabrication of Te-Doped Black Si with an Enhanced Photoelectric Performance by Femtosecond Laser Irradiation under Water.

Tellurium (Te)-doped black silicon (Si) with enhanced absorption and photoelectric performance over a broad wavelength range of 0.2-2.5 µm was obtained using femtosecond (fs) laser irradiation in liquid water. Prior to laser irradiation, the Si sample was covered with a Te thin film (thickness 200 nm) over an adhesion layer of Cr (thickness 5 nm). Surface analyses by scanning electron microscopy and three-dimensional confocal microscopy evidence the presence of hierarchical surface structures combining quasi-periodic stripes with a spatial period of about 5 µm and subwavelength laser-induced periodic surface structures directed in directions parallel and perpendicular to the direction of the laser polarization, respectively. Moreover, the incorporation of Te generates intermediate levels within the Si bandgap. The Te-doped black Si shows a significant enhancement of the absorption, which reaches values of about 48% in the UV and visible (0.2-1.1 µm) and 70% in the near-infrared (1.1-2.5 µm) spectral ranges, respectively, due to the synergistic effects of multiscale surface structures and Te incorporation. Moreover, the surface reflectance is reduced to almost zero across the entire spectrum. The Te-doped black Si sample is used to realize a photodetector which displays an impressive photoelectric capability, being characterized by a responsivity of 328 mA/W, and an external quantum efficiency of 49.27% at a voltage bias of -10 V for 1064 nm light illumination, with rising and falling times of 55 and 67 ms, respectively. These figures remarkably outperform the response of unprocessed Si under the same experimental conditions.

B1-cell-produced anti-phosphatidylserine antibodies contribute to lupus nephritis development via TLR-mediated Syk activation.

Autoantibodies produced by B cells play a pivotal role in the pathogenesis of systemic lupus erythematosus (SLE). However, both the cellular source of antiphospholipid antibodies and their contributions to the development of lupus nephritis (LN) remain largely unclear. Here, we report a pathogenic role of anti-phosphatidylserine (PS) autoantibodies in the development of LN. Elevated serum PS-specific IgG levels were measured in model mice and SLE patients, especially in those with LN. PS-specific IgG accumulation was found in the kidney biopsies of LN patients. Both transfer of SLE PS-specific IgG and PS immunization triggered lupus-like glomerular immune complex deposition in recipient mice. ELISPOT analysis identified B1a cells as the main cell type that secretes PS-specific IgG in both lupus model mice and patients. Adoptive transfer of PS-specific B1a cells accelerated the PS-specific autoimmune response and renal damage in recipient lupus model mice, whereas depletion of B1a cells attenuated lupus progression. In culture, PS-specific B1a cells were significantly expanded upon treatment with chromatin components, while blockade of TLR signal cascades by DNase I digestion and inhibitory ODN 2088 or R406 treatment profoundly abrogated chromatin-induced PS-specific IgG secretion by lupus B1a cells. Thus, our study has demonstrated that the anti-PS autoantibodies produced by B1 cells contribute to lupus nephritis development. Our findings that blockade of the TLR/Syk signaling cascade inhibits PS-specific B1-cell expansion provide new insights into lupus pathogenesis and may facilitate the development of novel therapeutic targets for the treatment of LN in SLE.

Self-powered photoelectrochemical sensor for chlorpyrifos detection in fruit and vegetables based on metal-ligand charge transfer effect by Ti3C2 based Schottky junction.

Herein, a high-performance self-powered photoelectrochemical (PEC) sensor was fabricated for chlorpyrifos (CPF) assay based on the noble-metal-free AgBr/Ti3C2 Schottky interface in fruit and vegetables. The Schottky barrier could provide an electron-transfer irreversible passage from AgBr to Ti3C2 nanosheets, and thus improving the light absorption and efficiency of charge separation. Such Schottky interface exhibited an ultrasensitive and selective photocurrent response for CPF due to the metal-ligand charge transfer effect. Because Ti3C2 MXene nanosheet had coordinative interaction with CPF and thus suppressed its photocurrent response of the Schottky interface, which was further confirmed by the electrochemical impedance spectra and X-ray photoelectron spectroscopy. The developed self-powered PEC sensor showed wide linear range (1 × 10-3 âˆ¼ 1 ng L-1), low detection limit (0.33 pg L-1), limit of quantitation (1 pg L-1), good reproducibility and stability. The sensor was applied for the determination of CPF in river water, apple and cucumber samples with good satisfactory results.

The IL-21-TET2-AIM2-c-MAF pathway drives the T follicular helper cell response in lupus-like disease.

Systemic lupus erythematosus (SLE) is a chronic autoimmune disease that involves T follicular helper (TFH ) cell-mediated humoral immune responses. Absent in melanoma 2 (human AIM2 and murine Aim2) is a well-known component of the inflammasome in the innate immune system. Surprisingly, we observed that in SLE patients, upregulated levels of AIM2 expression were found in peripheral blood and skin lesions, with the highest levels detected in TFH -like cells. In the CD4cre Aim2fl/fl conditional knockout mice, a markedly reduced TFH cell response was observed, with significantly lower levels of serum autoantibodies and proteinuria, as well as profoundly reduced renal IgG deposition in pristane-induced lupus mice. Mechanistically, IL-21 was found to recruit hydroxymethyltransferase ten-eleven translocation 2 (TET2) to the AIM2 promoter, resulting in DNA demethylation and increased transcription of AIM2. In addition, AIM2 could regulate c-MAF expression to enhance IL-21 production, which consequently promoted TFH cell differentiation. Our results have identified a role of AIM2 in promoting the TFH cell response and further revealed that the IL-21-TET2-AIM2-c-MAF signalling pathway is dysregulated in lupus pathogenesis, which provides a potential therapeutic target for SLE.

Non-noble metal plasmonic enhanced photoelectrochemical sensing of chlorpyrifos based on 1D TiO2-x/3D nitrogen-doped graphene hydrogel heterostructure.

Low-cost and resource-rich non-noble metal plasmonic materials have attracted tremendous attention as potential substitutes for plasmonic noble metals. Herein, 3D nitrogen-doped graphene hydrogels (NGH) decorated with Ti3+ self-doped 1D rod-shaped titanium dioxide nanorods (TiO2-x NR), 10-25 nm in size, were prepared by a facile one-step method. It was found that the as-fabricated TiO2-x NR/NGH showed a synergistic effect, displaying enhanced photoelectrochemical (PEC) activity by controlling the nanoscale architecture and improving the electronic properties, while also producing abundant oxygen vacancies, which extended the light harvesting and suppressed the recombination of electron-hole pairs induced by the non-noble metal surface plasmon resonance (SPR) effect. In particular, the transient-state photocurrent intensity of the TiO2-x NR/NGH composites was 5.1 times as high as that of pure TiO2. Therefore, the TiO2-x NR/NGH composites could serve as a substrate material for PEC sensing, providing a good basis for selective and sensitive detection of chlorpyrifos. Under optimal conditions, the constructed PEC sensor was found to have several advantages including a broad linear range (0.05 ng/mL-0.5 µg/mL), low detection limit (0.017 ng/mL), and considerable stability, demonstrating that the sensor may offer a promising route in the field of environmental analysis.

The Multiple Roles of B Cells in the Pathogenesis of Sjögren's Syndrome.

Primary Sjögren's syndrome (pSS) is a chronic autoimmune disease characterized by lymphocytic infiltration and tissue destruction of exocrine glands such as salivary glands. Although the formation of ectopic lymphoid tissue in exocrine glands and overproduction of autoantibodies by autoreactive B cells highlight the critical involvement of B cells in disease development, the precise roles of various B cell subsets in pSS pathogenesis remain partially understood. Current studies have identified several novel B cell subsets with multiple functions in pSS, among which autoreactive age-associated B cells, and plasma cells with augmented autoantibody production contribute to the disease progression. In addition, tissue-resident Fc Receptor-Like 4 (FcRL4)+ B cell subset with enhanced pro-inflammatory cytokine production serves as a key driver in pSS patients with mucosa-associated lymphoid tissue (MALT)-lymphomas. Recently, regulatory B (Breg) cells with impaired immunosuppressive functions are found negatively correlated with T follicular helper (Tfh) cells in pSS patients. Further studies have revealed a pivotal role of Breg cells in constraining Tfh response in autoimmune pathogenesis. This review provides an overview of recent advances in the identification of pathogenic B cell subsets and Breg cells, as well as new development of B-cell targeted therapies in pSS patients.

IL-17 drives salivary gland dysfunction via inhibiting TRPC1-mediated calcium movement in Sjögren's syndrome.

OBJECTIVES: This study aims to determine a role of interleukin-17A (IL-17) in salivary gland (SG) dysfunction and therapeutic effects of targeting IL-17 in SG for treating autoimmune sialadenitis in primary Sjögren's syndrome (pSS). METHODS: Salivary IL-17 levels and IL-17-secreting cells in labial glands of pSS patients were examined. Kinetic changes of IL-17-producing cells in SG from mice with experimental Sjögren's syndrome (ESS) were analysed. To determine a role of IL-17 in salivary secretion, IL-17-deficient mice and constructed chimeric mice with IL-17 receptor C (IL-17RC) deficiency in non-hematopoietic and hematopoietic cells were examined for saliva flow rates during ESS development. Both human and murine primary SG epithelial cells were treated with IL-17 for measuring cholinergic activation-induced calcium movement. Moreover, SG functions were assessed in ESS mice with salivary retrograde cannulation of IL-17 neutralisation antibodies. RESULTS: Increased salivary IL-17 levels were negatively correlated with saliva flow rates in pSS patients. Both IL-17-deficient mice and chimeric mice with non-hematopoietic cell-restricted IL-17RC deficiency exhibited no obvious salivary reduction while chimeric mice with hematopoietic cell-restricted IL-17RC deficiency showed significantly decreased saliva secretion during ESS development. In SG epithelial cells, IL-17 inhibited acetylcholine-induced calcium movement and downregulated the expression of transient receptor potential canonical 1 via promoting Nfkbiz mRNA stabilisation. Moreover, local IL-17 neutralisation in SG markedly attenuated hyposalivation and ameliorated tissue inflammation in ESS mice. CONCLUSION: These findings identify a novel function of IL-17 in driving salivary dysfunction during pSS development and may provide a new therapeutic strategy for targeting SG dysfunction in pSS patients.

IL-17 sustains the plasma cell response via p38-mediated Bcl-xL RNA stability in lupus pathogenesis.

Recent studies have demonstrated a central role for plasma cells in the development of autoimmune diseases, such as systemic lupus erythematosus (SLE). Currently, both the phenotypic features and functional regulation of autoreactive plasma cells during SLE pathogenesis remain largely unclear. In this study, we first found that a major subset of IL-17 receptor-expressing plasma cells potently produced anti-dsDNA IgG upon IL-17A (IL-17) stimulation in SLE patients and lupus mice. Using a humanized lupus mouse model, we showed that the transfer of Th17 cell-depleted PBMCs from lupus patients resulted in a significantly reduced plasma cell response and attenuated renal damage in recipient mice compared to the transfer of total SLE PBMCs. Moreover, long-term BrdU incorporation in lupus mice detected highly enriched long-lived BrdU+ subsets among IL-17 receptor-expressing plasma cells. Lupus mice deficient in IL-17 or IL-17 receptor C (IL-17RC) exhibited a diminished plasma cell response and reduced autoantibody production with attenuated renal damage, while the adoptive transfer of Th17 cells triggered the plasma cell response and renal damage in IL-17-deficient lupus mice. In reconstituted chimeric mice, IL-17RC deficiency resulted in severely impaired plasma cell generation but showed no obvious effect on germinal center B cells. Further mechanistic studies revealed that IL-17 significantly promoted plasma cell survival via p38-mediated Bcl-xL transcript stabilization. Together, our findings identified a novel function of IL-17 in enhancing plasma cell survival for autoantibody production in lupus pathogenesis, which may provide new therapeutic strategies for the treatment of SLE.

Multiple Functions of B Cells in the Pathogenesis of Systemic Lupus Erythematosus.

Systemic lupus erythematosus (SLE) is an autoimmune disease characterized by excessive autoantibody production and multi-organ involvement. Although the etiology of SLE still remains unclear, recent studies have characterized several pathogenic B cell subsets and regulatory B cell subsets involved in the pathogenesis of SLE. Among pathogenic B cell subsets, age-associated B cells (ABCs) are a newly identified subset of autoreactive B cells with T-bet-dependent transcriptional programs and unique functional features in SLE. Accumulation of T-bet+ CD11c+ ABCs has been observed in SLE patients and lupus mouse models. In addition, innate-like B cells with the autoreactive B cell receptor (BCR) expression and long-lived plasma cells with persistent autoantibody production contribute to the development of SLE. Moreover, several regulatory B cell subsets with immune suppressive functions have been identified, while the impaired inhibitory effects of regulatory B cells have been indicated in SLE. Thus, further elucidation on the functional features of B cell subsets will provide new insights in understanding lupus pathogenesis and lead to novel therapeutic interventions in the treatment of SLE.

Antifungal activity of spider venom-derived peptide lycosin-I against Candida tropicalis.

Candida species are a major cause of human mucosal and deep tissue fungal infections, but few antifungal treatments are available. Here, we showed that lycosin-I, a peptide isolated from venom of the spider Lycosa singoriensis, acted as a potent antifungal inhibitor against Candida species. The MIC50 values of lycosin-I reached 8 µg/mL to treat fluconazole-susceptible and fluconazole-resistant C. tropicalis isolates. Time-kill kinetics assays revealed that after a 2-hour exposure, lycosin-I reduced colony-forming units/mL in fluconazole-susceptible and fluconazole-resistant C. tropicalis isolates approximately 70%. Furthermore, salinity tolerance assays suggested that even in the presence of Mg2+, lycosin-I maintained its potent antifungal ability at a high concentration. When the concentration of lycosin-I was increased from 1 × MIC to 8 × MIC, a significant decrease of the biofilm metabolic activity was observed in both fluconazole-susceptible and fluconazole-resistant C. tropicalis isolates. Moreover, the biofilm inhibitory concentration 50 (BIC50) and the biofilm eradicating concentration 50 (BEC50) were approximately 32 µg/mL and 128 µg/mL, respectively. Confocal laser scanning microscopy showed the localization of CY5-labeled lycosin-I mainly in the cell cytoplasm, and lycosin-I was likely to be localized in the cytoplasm after its transportation across the cell wall and membrane. Overall, our work shows that lycosin-I is a potent antifungal agent with a high efficacy, a high salinity tolerance, and potent anti-biofilm properties.

TLR4+CXCR4+ plasma cells drive nephritis development in systemic lupus erythematosus.

OBJECTIVES: In patients with systemic lupus erythematosus (SLE), immune tolerance breakdown leads to autoantibody production and immune-complex glomerulonephritis. This study aimed to identify pathogenic plasma cells (PC) in the development of lupus nephritis. METHODS: PC subsets in peripheral blood and renal tissue of patients with SLE and lupus mice were examined by flow cytometry and confocal microscopy, respectively. Sorting-purified PCs from lupus mice were adoptively transferred into Rag2-deficient recipients, in which immune-complex deposition and renal pathology were investigated. In culture, PCs from lupus mice and patients with SLE were treated with a TLR4 inhibitor and examined for autoantibody secretion by enzyme-linked immunospot assay (ELISPOT). Moreover, lupus mice were treated with a TLR4 inhibitor, followed by the assessment of serum autoantibody levels and glomerulonephritis activity. RESULTS: The frequencies of TLR4+CXCR4+ PCs in peripheral blood and renal tissue were found significantly increased with the potent production of anti-dsDNA IgG, which were associated with severe renal damages in patients with SLE and mice with experimental lupus. Adoptive transfer of TLR4+CXCR4+ PCs from lupus mice led to autoantibody production and glomerulonephritis development in Rag2-deficient recipients. In culture, TLR4+CXCR4+ PCs from both lupus mice and patients with SLE showed markedly reduced anti-dsDNA IgG secretion on TLR4 blockade. Moreover, in vivo treatment with TLR4 inhibitor significantly attenuated autoantibody production and renal damages in lupus mice. CONCLUSIONS: These findings demonstrate a pathogenic role of TLR4+CXCR4+ PCs in the development of lupus nephritis and may provide new therapeutic strategies for the treatment of SLE.

Characteristics of lipid metabolism including serum apolipoprotein M levels in patients with primary nephrotic syndrome.

BACKGROUND: Apolipoprotein M (apoM) is a 26-kD apolipoprotein that is mainly expressed in specific cell types, such as human liver parenchymal cells and kidney proximal renal tubular epithelial cells. ApoM can regulate the formation of pre-ß-HDL and the reverse cholesterol transport and thus plays an important role in the metabolism of lipids and lipoproteins, meaning that it can affect the development of lipid metabolism disorders. Significantly elevated serum apoM levels are detected in patients with hyperlipidemia. However, few studies have shown how apoM is expressed in primary nephrotic syndrome (PNS), which is often accompanied with hyperlipidemia, and the underlying mechanism is poorly understood. This study was aimed at examining the apoM levels in patients with PNS and at determining the effects of PNS on serum apoM levels in these patients. METHODS: This study included patients with hyperlipidemia (n = 37), the PNS with hyperlipidemia group (n = 62), PNS without hyperlipidemia group (n = 33), and healthy controls (n = 73). The age and body-mass index (BMI) matched among the groups of participants. Their serum apoM concentrations were measured by an enzyme-linked immunosorbent assay. Serum levels of conventional lipids and renal function indices were assessed using an automatic biochemical analyzer. The data were analyzed by means of Pearson's correlation coefficient (continuous variables) or Student's t test (mean differences). RESULTS: The average serum apoM concentrations were higher in the hyperlipidemia group (61.1 ± 23.2 mg/L, P = 0.004) than in the healthy controls (31.6 ± 18.92 mg/L). The serum apoM concentrations were lower in the PNS with hyperlipidemia group (25.1 ± 16.31 mg/L, P = 0.007) and in the PNS without hyperlipidemia group (21.00 ± 17.62 mg/L, P = 0.003) than in the healthy controls. The serum apoM concentrations in the PNS with hyperlipidemia group did not differ significantly from those in the PNS without hyperlipidemia group (P = 0.083). Moreover, serum apoM levels positively correlated with serum high-density lipoprotein cholesterol (HDL-C) and apoA1 levels and negatively correlated with proteinuria in PNS patients (r = 0.458, P = 0.003; r = 0.254, P = 0.022; r = -0.414, P = 0.028). CONCLUSION: Serum apoM concentrations are higher in patients with hyperlipidemia than in healthy controls. Low serum apoM levels in patients with PNS are likely caused by PNS.

Low apolipoprotein M serum levels correlate with Systemic lupus erythematosus disease activity and apolipoprotein M gene polymorphisms with Lupus.

BACKGROUND: Sequence variation in gene promoters is often associated with disease risk. In this study, we tested the hypothesis that common promoter variation in the APOM gene is associated with systemic lupus erythematosus (SLE) risk and SLE-related clinical phenotypes in a Chinese cohort. Meanwhile, we investigated the expression of apolipoprotein M (APOM) in the serum of patients with systemic lupus erythematosus (SLE) and its relationship with disease activity. METHODS: We used a case-control design and genotyped 52 SLE patients and 52 healthy controls for 19 APOM promoter single nucleotide polymorphism (SNP) (rs113947529, rs1143030, rs114826514, rs116715239, rs12525463, rs1266078, rs2273612, rs28432254, rs34490746, rs4947251, rs55880811, rs707921, rs74890500, rs75629491, rs76611345, rs76794541, rs805264, rs805297, rs9267528). Genotyping was done by matrix-assisted laser desorption/ionization time-of-flight mass spectrometry (MALDI-TOF MS). The blood serum concentration of APOM was measured by an enzyme-linked immunosorbent assay in SLE patients and controls. RESULTS: The average concentration of APOM in serum was significantly lower in SLE patients compared to controls and APOM levels in SLE patients with positive anti-dsDNA antibodies were dramatically lower than that of patients with negative anti-dsDNA antibodies (P = 0.011). It was interesting that APOM levels correlated with systemic lupus erythematosus disease activity index (SLEDAI) scores (r = -0.396, P = 0.004). No association between APOM and SLE susceptibility was detected in our Han Chinese cohort. CONCLUSIONS: Our results demonstrated that lower APOM levels in SLE patients and correlated with disease activity.

Urinary NGAL for the diagnosis of the renal injury from multiple myeloma.

OBJECTIVES: Neutrophil gelatinase-associated lipocalin (NGAL) has been proved as a sensitive biomarker in acute and chronic renal injury. Renal impairment is a common complication of multiple myeloma (MM). We attempt to assess the value of NGAL for the early and accurate diagnosis of renal injury in MM patients. METHODOLOGY: Forty-five MM patients with CKD stage I to V(MM-renal group), 20 MM patients with normal kidney function (MM-non-renal group), and 37 healthy volunteers (healthy control) were compared for serum and urinary NGAL and other renal injury biomarkers (Creatinine[CRE]; Cystatin-C [CysC]; N-acetyl-beta-D-glucosaminidase [NAG]). Other biomarkers reflect the inflammation and tumor burden like high-sensitivity C-reactive protein(hs-CRP) and urine free light chain were also detected. RESULTS: Among the biomarkers of renal injury, the assessment of serum CysC, CRE and NGAL was a reliable tool to distinguish MM-renal from MM-non-renal. Both serum and urinary NGAL levels were higher in MM-renal patients than in MM-non-renal or healthy controls (187.10 (45.60-699.60) vs 136.70 (47.70-216.50) vs 117.7 (69.3-192.3), P< 0.01; 37.50 (6.30-412.10) vs 18.00 (0.50-66.50) vs 11.2 (0.9-69.1), P< 0.01). Univariate analysis showed that both serum (Odds Ratio = 1.009; 95%CI 1.002-1.017; P= 0.018) and urinary NGAL (Odds Ratio = 1.038; 95%CI 1.003-1.073; P= 0.031) as well as serum CysC (Odds Ratio = 9.875; 95%CI 1.685-57.882; P= 0.011) were strong predictors for the risk of renal injury in MM patients. Moreover, the urinary NGAL level was negatively correlated with estimated glomerular filtration rate (eGFR) (r= -0.586, P= 0.00003) and has a tendency towards positive correlation with urine free light chain (r = 0.235, P = 0.124) and hs-CRP (r = 0.379, P = 0.074). CONCLUSIONS: The present study demonstrated that urinary NGAL was not superior to serum NGAL in distinguishing MM-renal group from MM-non-renal group. And it could be considered an independent predictor of renal injury from multiple myeloma reflecting active kidney damage, tumor burden, and inflammation.

High apolipoprotein M serum levels correlate with chronic obstructive pulmonary disease.

BACKGROUND: Recently, variations in a component of high-density lipoprotein (HDL), namely apolipoprotein M (apoM), were found to be associated with chronic obstructive pulmonary disease (COPD). The aim of this study was to evaluate the association between apoM and COPD severity. Factors associated with apoM, COPD, or coronary artery disease (CAD) were also assessed. METHODS: A total of 110 COPD patients and 110 age- and sex-matched non-COPD controls were included. Among them, thirty COPD patients and seven non-COPD controls had CAD. ApoM and pentraxin-3 levels were measured by ELISA. Additionally, the levels of high-sensitivity C-reactive protein (hs-CRP), cholesterol, and triglyceride were assessed using an automatic biochemical analyzer. RESULTS: Serum apoM levels increased gradually with COPD severity, with the most prominent apoM elevation observed in very severe COPD cases. In addition, ApoM was correlated with percent-predicted forced expiratory volume in one second (% predicted FEV1) (r = -0.38, P < 0.001), low-density lipoprotein cholesterol (LDL-C) (r = 0.23, P < 0.017), and hs-CRP (r = 0.24, P = 0.01) in COPD patients. Furthermore, apoM was shown to be a risk factor for COPD onset (OR = 1.095, 95% CI = 1.034-1.160, P = 0.002), but not associated with CAD in COPD patients. CONCLUSIONS: Serum apoM was elevated in COPD patients and increased gradually with COPD severity. However, there was no association between apoM and CAD development in COPD patients.

[Association of serum level of apolipoprotein M with disease activity in systemic lupus erythematosus].

OBJECTIVE: To explore the association of serum level of apolipoprotein M with disease activity in systemic lupus erythematosus (SLE). METHODS: A total of 65 patients with SLE, who came to Second Xiangya Hospital for treatment from April to November in 2013 (SLE group) and 120 age-and sex-matched controls (control group) were studied. The SLE group was further divided into three groups according to systemic lupus erythematosus disease activity index (SLEDAI): a mild activity group, a moderate activity group and a severe activity group (n=16, 16, 33, respectively). The control group was also divided into a disease control group (n=60) and a healthy control group (n=60). The serum levels of apo M were measured by enzyme-linked immunosorbent assay (ELISA). Other indicators including TC, TG, HDL, LDL, apo A1, apo B, and anti-dsDNA antibody were detected. The correlation between SLEDAI or anti-dsDNA antibody and apo M was assessed. RESULTS: Compared with the healthy control group, the expression levels of apo M and HDL were decreased significantly (both P<0.05), and the expression levels of anti-dsDNA antibody, TG, apo B were increased significantly in the SLE group (all P<0.05). Comparison among the three subgroups, no significant differences in apo M were found (all P>0.05). The serum concentration of apo M was significant negatively correlated with SLEDAI and anti-dsDNA antibody (r=-0.551, -0.562, both P<0.01). CONCLUSION: Compared with the healthy control group, the serum levels of apo M in patients with SLE are significantly decreased. The apo M is closely correlated with disease activity of SLE and it might be used as an indicator to monitor the disease activity of SLE.

Identifying atomic geometry and electronic structure of (2 x 3)-Sr/Si(100) surface and its initial oxidation.

We present a joint experimental and theoretical study on the geometric and electronic states and the initial oxidation of the (2x3)-Sr/Si(100) surface. With scanning tunneling microscopy/scanning tunneling spectroscopy (STM/STS) measurements combined with ab initio calculations, the atomic geometry and the electronic states of the (2x3)-Sr/Si(100) surface are identified. The dimerization of the Si atoms in the single atom row based on a (1x3) Si substrate model plays a critical role in stabilization of the surface structure and in determining the electronic properties. At the very initial oxidation of the surface, four features corresponding to the primary adsorption and oxidation sites are determined. Three of them are corresponding to the most favored oxidation sites with single oxygen molecules, whose local density of states gives semiconducting behavior. One is corresponding to the oxidation site with two oxygen molecules, whose local density of states gives metallic behavior. These features all exhibit dark spots with different shapes in the occupied state images but display either dark spots or bright protrusions depending on the different oxidation sites in the empty state images. Compared with the theoretical calculations, the plausible adsorption and oxidation models are proposed.